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Azygos ( impar ), from the Greek άζυξ, refers to an anatomical structure that is unpaired. This is relatively unusual, as most elements of anatomy reflect bilateral symmetry . Azygos may refer to:
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https://en.wikipedia.org/wiki/Azygos
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The Azzopardi phenomenon , or Azzopardi effect , is the presence of DNA in necrotic venules . [ 1 ] It can occur in small cell carcinomas and in some high-grade malignant neoplasms . [ 1 ] [ 2 ] The effect is well known in diagnostic surgical pathology . [ 3 ] The phenomenon is named after the pathologist, John G. Azzopardi . [ 4 ] [ 5 ] [ 6 ]
Azzopardi was able to correctly characterize the effect as due to DNA; it had been thought previously but incorrectly to be calcium. [ 4 ] Necrosis results in the release of cellular DNA , which adheres in patches to the walls of blood vessels, showing as intensely basophilic material on hematoxylin-eosin stain. [ 1 ]
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https://en.wikipedia.org/wiki/Azzopardi_phenomenon
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A B-cell leukemia is any of several types of lymphoid leukemia which affect B cells . [ 1 ]
Types include (with ICD-O code): [ citation needed ]
aggressive: Sézary disease
This oncology article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/B-cell_leukemia
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BMC Cancer is a peer-reviewed open access medical journal that publishes original research on cancer and oncology . It was established in 2001 at a time when open access publishing was in its infancy, and is published by BioMed Central . It was one of the first journals to be open access and exclusively published online. [ 1 ]
The journal is abstracted and indexed by PubMed , MEDLINE , CAS , EMBASE , Scopus , Current Contents , and CABI . [ 2 ] According to the Journal Citation Reports , its 2-year impact factor was 3.4 in 2023. [ 3 ]
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https://en.wikipedia.org/wiki/BMC_Cancer
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The BODE index , for B ody-mass index, airflow O bstruction , D yspnea , and E xercise , is a multidimensional scoring system and capacity index used to test patients who have been diagnosed with chronic obstructive pulmonary disease (COPD) and to predict long-term outcomes for them. The index uses the four factors to predict risk of death from the disease.
The BODE index will result in a score of zero to ten dependent upon FEV 1 or "forced expiratory volume in one second" (the greatest volume of air that can be breathed out in the first second of a breath), body-mass index, the distance walked in six minutes, and the modified MRC dyspnea scale . [ 1 ] [ 2 ] Significant weight loss is a bad sign. [ 3 ] Results of spirometry are also good predictors of the future progress of the disease, but they are not as good as the test results of the BODE index. [ 3 ] [ 4 ]
This medical article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/BODE_index
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1JM7 , 1JNX , 1N5O , 1OQA , 1T15 , 1T29 , 1T2U , 1T2V , 1Y98 , 2ING , 3COJ , 3K0H , 3K0K , 3K15 , 3PXA , 3PXB , 3PXC , 3PXD , 3PXE , 4IFI , 4IGK , 4JLU , 4OFB , 4U4A , 4Y18 , 4Y2G
672
12189
ENSG00000012048
ENSMUSG00000017146
P38398
P48754
NM_007299 NM_007300 NM_007301 NM_007302 NM_007303 NM_007305 NM_007306
NM_009764
NP_009225 NP_009228 NP_009229 NP_009230 NP_009231
NP_033894
Breast cancer type 1 susceptibility protein is a protein that in humans is encoded by the BRCA1 ( / ˌ b r æ k ə ˈ w ʌ n / ) gene . [ 5 ] Orthologs are common in other vertebrate species, whereas invertebrate genomes may encode a more distantly related gene. [ 6 ] BRCA1 is a human tumor suppressor gene [ 7 ] [ 8 ] (also known as a caretaker gene ) and is responsible for repairing DNA . [ 9 ]
BRCA1 and BRCA2 are unrelated proteins, [ 10 ] but both are normally expressed in the cells of breast and other tissues, where they help repair damaged DNA , or destroy cells if DNA cannot be repaired. They are involved in the repair of chromosomal damage with an important role in the error-free repair of DNA double-strand breaks . [ 11 ] [ 12 ] If BRCA1 or BRCA2 itself is damaged by a BRCA mutation , damaged DNA is not repaired properly, and this increases the risk for breast cancer . [ 13 ] [ 11 ] BRCA1 and BRCA2 have been described as "breast cancer susceptibility genes" and "breast cancer susceptibility proteins". The predominant allele has a normal, tumor-suppressive function, whereas high penetrance mutations in these genes cause a loss of tumor-suppressive function, which correlates with an increased risk of breast cancer. [ 14 ]
BRCA1 combines with other tumor suppressors, DNA damage sensors and signal transducers to form a large multi-subunit protein complex known as the BRCA1 -associated genome surveillance complex (BASC). [ 15 ] The BRCA1 protein associates with RNA polymerase II , and through the C-terminal domain, also interacts with histone deacetylase complexes. Thus, this protein plays a role in transcription, and DNA repair of double-strand DNA breaks [ 11 ] ubiquitination , transcriptional regulation as well as other functions. [ 16 ]
Methods to test for the likelihood of a patient with mutations in BRCA1 and BRCA2 developing cancer were covered by patents owned or controlled by Myriad Genetics . [ 17 ] [ 18 ] Myriad's business model of offering the diagnostic test exclusively led from Myriad being a startup in 1994 to being a publicly traded company with 1200 employees and about $500 million in annual revenue in 2012; [ 19 ] it also led to controversy over high prices and the inability to obtain second opinions from other diagnostic labs, which in turn led to the landmark Association for Molecular Pathology v. Myriad Genetics lawsuit. [ 20 ]
The chromosomal location of BRCA1 was discovered by Mary-Claire King 's team at UC Berkeley in 1990. [ 21 ] After an international race to refine the precise location of BRCA1 , [ 22 ] the gene was cloned in 1994 by scientists at University of Utah, National Institute of Environmental Health Sciences (NIEHS) and Myriad Genetics . [ 17 ] [ 23 ]
BRCA1 orthologs have been identified in most vertebrates for which complete genome data are available. [ 6 ]
The BRCA1 protein contains the following domains: [ 24 ]
This protein also contains nuclear localization signals and nuclear export signal motifs. [ 25 ]
The human BRCA1 protein consists of four major protein domains: the Znf C3HC4- RING domain , the BRCA1 serine domain and two BRCT domains. These domains encode approximately 27% of BRCA1 protein. There are six known isoforms of BRCA1, [ 26 ] with isoforms 1 and 2 comprising 1863 amino acids each. [ citation needed ]
BRCA1 is unrelated to BRCA2 , i.e. they are not homologs or paralogs . [ 10 ]
The RING motif , a Zn finger found in eukaryotic peptides, is 40–60 amino acids long and consists of eight conserved metal-binding residues, two quartets of cysteine or histidine residues that coordinate two zinc atoms. [ 28 ] This motif contains a short anti-parallel beta-sheet , two zinc-binding loops and a central alpha helix in a small domain. This RING domain interacts with associated proteins, including BARD1 , which also contains a RING motif, to form a heterodimer. The BRCA1 RING motif is flanked by alpha helices formed by residues 8–22 and 81–96 of the BRCA1 protein. It interacts with a homologous region in BARD1 also consisting of a RING finger flanked by two alpha-helices formed from residues 36–48 and 101–116. These four helices combine to form a heterodimerization interface and stabilize the BRCA1-BARD1 heterodimer complex. [ 29 ] Additional stabilization is achieved by interactions between adjacent residues in the flanking region and hydrophobic interactions. The BARD1/BRCA1 interaction is disrupted by tumorigenic amino acid substitutions in BRCA1, implying that the formation of a stable complex between these proteins may be an essential aspect of BRCA1 tumor suppression. [ 28 ]
The RING domain is an important element of ubiquitin E3 ligases , which catalyze protein ubiquitination. Ubiquitin is a small regulatory protein found in all tissues that directs proteins to compartments within the cell. BRCA1 polypeptides, in particular, Lys-48-linked polyubiquitin chains are dispersed throughout the resting cell nucleus, but at the start of DNA replication , they gather in restrained groups that also contain BRCA2 and BARD1. BARD1 is thought to be involved in the recognition and binding of protein targets for ubiquitination. [ 30 ] It attaches to proteins and labels them for destruction. Ubiquitination occurs via the BRCA1 fusion protein and is abolished by zinc chelation . [ 28 ] The enzyme activity of the fusion protein is dependent on the proper folding of the RING domain. [ citation needed ]
BRCA1 serine cluster domain (SCD) spans amino acids 1280–1524. A portion of the domain is located in exons 11–13. High rates of mutation occur in exons 11–13. Reported phosphorylation sites of BRCA1 are concentrated in the SCD, where they are phosphorylated by ATM/ATR kinases both in vitro and in vivo . ATM/ATR are kinases activated by DNA damage . Mutation of serine residues may affect the localization of BRCA1 to sites of DNA damage and DNA damage response. [ 27 ]
The dual repeat BRCT domain of the BRCA1 protein is an elongated structure approximately 70 Å long and 30–35 Å wide. [ 31 ] The 85–95 amino acid domains in BRCT can be found as single modules or as multiple tandem repeats containing two domains. [ 32 ] Both of these possibilities can occur in a single protein in a variety of different conformations. [ 31 ] The C-terminal BRCT region of the BRCA1 protein is essential for repair of DNA, transcription regulation, and tumor-suppressor function. [ 33 ] In BRCA1, the dual tandem repeat BRCT domains are arranged in a head-to-tail fashion in the three-dimensional structure, burying 1600 Å of hydrophobic, solvent-accessible surface area in the interface. These all contribute to the tightly packed knob-in-hole structure that comprises the interface. These homologous domains interact to control cellular responses to DNA damage . A missense mutation at the interface of these two proteins can perturb the cell cycle , resulting in a greater risk of developing cancer. [ citation needed ]
BRCA1 is part of a complex that repairs double-strand breaks in DNA. The strands of the DNA double helix are continuously breaking as they become damaged. Sometimes only one strand is broken, sometimes both strands are broken simultaneously. DNA cross-linking agents are an important source of chromosome/DNA damage. Double-strand breaks occur as intermediates after the crosslinks are removed, and indeed, biallelic mutations in BRCA1 have been identified to be responsible for Fanconi Anemia , Complementation Group S (FA-S), [ 34 ] a genetic disease associated with hypersensitivity to DNA crosslinking agents. BRCA1 is part of a protein complex that repairs DNA when both strands are broken. When this happens, it is difficult for the repair mechanism to "know" how to replace the correct DNA sequence, and there are multiple ways to attempt the repair. The double-strand repair mechanism in which BRCA1 participates is homology-directed repair , where the repair proteins copy the identical sequence from the intact sister chromatid . [ 35 ] FA-S is almost always a lethal condition in utero; only a handful cases of biallelic BRCA1 mutations have been reported in literature despite the high carrier frequencies in the Ashkenazim, and none since 2013. [ 36 ]
In the nucleus of many types of normal cells, the BRCA1 protein interacts with RAD51 during repair of DNA double-strand breaks. [ 37 ] These breaks can be caused by natural radiation or other exposures, but also occur when chromosomes exchange genetic material (homologous recombination, e.g., "crossing over" during meiosis). The BRCA2 protein, which has a function similar to that of BRCA1, also interacts with the RAD51 protein. By influencing DNA damage repair, these three proteins play a role in maintaining the stability of the human genome. [ 38 ]
BRCA1 is also involved in another type of DNA repair, termed mismatch repair . BRCA1 interacts with the DNA mismatch repair protein MSH2 . [ 39 ] MSH2, MSH6 , PARP , and some other proteins involved in single-strand repair are reported to be elevated in BRCA1-deficient mammary tumors. [ 40 ]
A protein called valosin-containing protein (VCP, also known as p97) plays a role in recruiting BRCA1 to the damaged DNA sites. After ionizing radiation, VCP is recruited to DNA lesions and cooperates with the ubiquitin ligase RNF8 to orchestrate assembly of signaling complexes for efficient DSB repair. [ 41 ] BRCA1 interacts with VCP. [ 42 ] BRCA1 also interacts with c-Myc , and other proteins that are critical to maintain genome stability. [ 43 ]
BRCA1 directly binds to DNA, with a higher affinity for branched DNA structures. This ability to bind to DNA contributes to its ability to inhibit the nuclease activity of the MRN complex as well as the nuclease activity of Mre11 alone. [ 44 ] This may explain a role for BRCA1 to promote lower fidelity DNA repair by non-homologous end joining (NHEJ). [ 45 ] BRCA1 also colocalizes with γ-H2AX (histone H2AX phosphorylated on serine-139) in DNA double-strand break repair foci, indicating it may play a role in recruiting repair factors. [ 16 ] [ 46 ]
Formaldehyde and acetaldehyde are common environmental sources of DNA cross-links that often require repairs mediated by BRCA1-containing pathways. [ 47 ]
This DNA repair function is essential; mice with loss-of-function mutations in both BRCA1 alleles are not viable, and as of 2015, only two adults were known to have loss-of-function mutations in both alleles (leading to FA-S); both had congenital or developmental issues, and both had cancer. One was presumed to have survived to adulthood because one of the BRCA1 mutations was hypomorphic . [ 48 ]
BRCA1 was shown to co-purify with the human RNA polymerase II holoenzyme in HeLa extracts, implying it is a component of the holoenzyme. [ 49 ] Later research, however, contradicted this assumption, instead showing that the predominant complex including BRCA1 in HeLa cells is a 2 megadalton complex containing SWI/SNF . [ 50 ] SWI/SNF is a chromatin remodeling complex. Artificial tethering of BRCA1 to chromatin was shown to decondense heterochromatin , though the SWI/SNF interacting domain was not necessary for this role. [ 46 ] BRCA1 interacts with the NELF-B ( COBRA1 ) subunit of the NELF complex. [ 46 ]
Certain variations of the BRCA1 gene lead to an increased risk for breast cancer as part of a hereditary breast–ovarian cancer syndrome . Researchers have identified hundreds of mutations in the BRCA1 gene, many of which are associated with an increased risk of cancer. Females with an abnormal BRCA1 or BRCA2 gene have up to an 80% risk of developing breast cancer by age 90; increased risk of developing ovarian cancer is about 55% for females with BRCA1 mutations and about 25% for females with BRCA2 mutations. [ 52 ]
These mutations can be changes in one or a small number of DNA base pairs (the building blocks of DNA), and can be identified with PCR and DNA sequencing. [ 53 ]
In some cases, large segments of DNA are rearranged. Those large segments, also called large rearrangements, can be a deletion or a duplication of one or several exons in the gene. Classical methods for mutation detection (sequencing) are unable to reveal these types of mutation. [ 54 ] Other methods have been proposed: traditional quantitative PCR , [ 55 ] multiplex ligation-dependent probe amplification (MLPA), [ 56 ] and Quantitative Multiplex PCR of Short Fluorescent Fragments (QMPSF). [ 57 ] Newer methods have also been recently proposed: heteroduplex analysis (HDA) by multi-capillary electrophoresis or also dedicated oligonucleotide array based on comparative genomic hybridization (array-CGH). [ 58 ]
Some results suggest that hypermethylation of the BRCA1 promoter , which has been reported in some cancers, could be considered as an inactivating mechanism for BRCA1 expression. [ 59 ]
A mutated BRCA1 gene usually makes a protein that does not function properly. Researchers believe that the defective BRCA1 protein is unable to help fix DNA damage, leading to mutations in other genes. These mutations can accumulate and may allow cells to grow and divide uncontrollably to form a tumor. Thus, BRCA1 inactivating mutations lead to a predisposition for cancer. [ citation needed ]
BRCA1 mRNA 3' UTR can be bound by an miRNA , Mir-17 microRNA . It has been suggested that variations in this miRNA, along with Mir-30 microRNA could confer susceptibility to breast cancer. [ 60 ]
In addition to breast cancer, mutations in the BRCA1 gene also increase the risk of ovarian and prostate cancers . Moreover, precancerous lesions ( dysplasia ) within the fallopian tube have been linked to BRCA1 gene mutations. Pathogenic mutations anywhere in a model pathway containing BRCA1 and BRCA2 greatly increase risks for a subset of leukemias and lymphomas. [ 11 ]
Women who have inherited a defective BRCA1 or BRCA2 gene are at a greatly elevated risk of developing breast and ovarian cancer. Their risk of developing breast and/or ovarian cancer is so high, and so specific to those cancers, that many mutation carriers choose to have prophylactic surgery . There has been much conjecture to explain such striking tissue specificity. Major determinants of where BRCA1/2 hereditary cancers occur are related to tissue specificity of the cancer pathogen, the agent that causes chronic inflammation, or the carcinogen. The target tissue may have receptors for the pathogen, may become selectively exposed to an inflammatory process, or a carcinogen. An innate genomic deficit in a tumor suppressor gene impairs normal responses and exacerbates the susceptibility to disease in organ targets. This theory also fits data for several tumor suppressors beyond BRCA1 or BRCA2. A major advantage of this model is that it suggests there may be some options in addition to prophylactic surgery. [ 61 ]
As aforementioned, biallelic and homozygous inheritance of the BRCA1 gene leads to FA-S, which is almost always an embryonically lethal condition.
BRCA1 expression is reduced or undetectable in the majority of high-grade, ductal breast cancers. [ 62 ] It has long been noted that loss of BRCA1 activity, either by germ-line mutations or by down-regulation of gene expression, leads to tumor formation in specific target tissues. In particular, decreased BRCA1 expression contributes to both sporadic and inherited breast tumor progression. [ 63 ] Reduced expression of BRCA1 is tumorigenic because it plays an important role in the repair of DNA damages, especially double-strand breaks, by the potentially error-free pathway of homologous recombination. [ 64 ] Since cells that lack the BRCA1 protein tend to repair DNA damages by alternative more error-prone mechanisms, the reduction or silencing of this protein generates mutations and gross chromosomal rearrangements that can lead to progression to breast cancer. [ 64 ]
Similarly, BRCA1 expression is low in the majority (55%) of sporadic epithelial ovarian cancers (EOCs) where EOCs are the most common type of ovarian cancer, representing approximately 90% of ovarian cancers. [ 65 ] In serous ovarian carcinomas , a sub-category constituting about 2/3 of EOCs, low BRCA1 expression occurs in more than 50% of cases. [ 66 ] Bowtell [ 67 ] reviewed the literature indicating that deficient homologous recombination repair caused by BRCA1 deficiency is tumorigenic. In particular, this deficiency initiates a cascade of molecular events that sculpt the evolution of high-grade serous ovarian cancer and dictate its response to therapy. Especially noted was that BRCA1 deficiency could be the cause of tumorigenesis, whether due to BRCA1 mutation or any other event that causes a deficiency of BRCA1 expression.
In addition to its role in repairing DNA damages, BRCA1 facilitates apoptosis in breast and ovarian cell lines when cells are stressed by agents, including ionizing radiation , that cause DNA damages . [ 68 ] Repair of DNA damages and apoptosis are two enzymatic processes essential for maintaining genome integrity in humans. Cells that are deficient in DNA repair tend to accumulate DNA damages , and when such cells are also defective in apoptosis, they tend to survive even with excess DNA damage. [ 69 ] Replication of DNA in such cells leads to mutations and these mutations may cause cancer. Thus, BRCA1 appears to have two roles related to the prevention of cancer, where one role is to promote repair of a specific class of damages and the second role is to induce apoptosis if the level of such DNA damage is beyond the cell's repair capability [ 69 ]
Only about 3%–8% of all women with breast cancer carry a mutation in BRCA1 or BRCA2. [ 70 ] Similarly, BRCA1 mutations are only seen in about 18% of ovarian cancers (13% germline mutations and 5% somatic mutations ). [ 71 ]
Thus, while BRCA1 expression is low in the majority of these cancers, BRCA1 mutation is not a major cause of reduced expression. Certain latent viruses, which are frequently detected in breast cancer tumors, can decrease the expression of the BRCA1 gene and cause the development of breast tumors. [ 72 ]
BRCA1 promoter hypermethylation was present in only 13% of unselected primary breast carcinomas. [ 73 ] Similarly, BRCA1 promoter hypermethylation was present in only 5% to 15% of EOC cases. [ 65 ]
Thus, while BRCA1 expression is low in these cancers, BRCA1 promoter methylation is only a minor cause of reduced expression.
There are several specific microRNAs , when overexpressed, that directly reduce expression of specific DNA repair proteins (see MicroRNA section DNA repair and cancer ) In the case of breast cancer, microRNA-182 (miR-182) specifically targets BRCA1. [ 74 ] Breast cancers can be classified based on receptor status or histology, with triple-negative breast cancer (15%–25% of breast cancers), HER2+ (15%–30% of breast cancers), ER+ / PR+ (about 70% of breast cancers), and Invasive lobular carcinoma (about 5%–10% of invasive breast cancer). All four types of breast cancer were found to have an average of about 100-fold increase in miR-182, compared to normal breast tissue. [ 75 ] In breast cancer cell lines, there is an inverse correlation of BRCA1 protein levels with miR-182 expression. [ 74 ] Thus, it appears that much of the reduction or absence of BRCA1 in high-grade ductal breast cancers may be due to over-expressed miR-182.
In addition to miR-182, a pair of almost identical microRNAs, miR-146a and miR-146b-5p, also repress BRCA1 expression. These two microRNAs are over-expressed in triple-negative tumors and their over-expression results in BRCA1 inactivation. [ 76 ] Thus, miR-146a and/or miR-146b-5p may also contribute to reduced expression of BRCA1 in these triple-negative breast cancers.
In both serous tubal intraepithelial carcinoma (the precursor lesion to high grade serous ovarian carcinoma (HG-SOC) ), and in HG-SOC itself, miR-182 is overexpressed in about 70% of cases. [ 77 ] In cells with over-expressed miR-182, BRCA1 remained low, even after exposure to ionizing radiation (which normally raises BRCA1 expression). [ 77 ] Thus, much of the reduced or absent BRCA1 in HG-SOC may be due to over-expressed miR-182.
Another microRNA known to reduce the expression of BRCA1 in ovarian cancer cells is miR-9. [ 65 ] Among 58 tumors from patients with stage IIIC or stage IV serous ovarian cancers (HG-SOG), an inverse correlation was found between expressions of miR-9 and BRCA1, [ 65 ] so that increased miR-9 may also contribute to reduced expression of BRCA1 in these ovarian cancers.
DNA damage appears to be the primary underlying cause of cancer, [ 78 ] and deficiencies in DNA repair appear to underlie many forms of cancer. [ 79 ] If DNA repair is deficient, DNA damage tends to accumulate. Such excess DNA damage may increase mutational errors during DNA replication due to error-prone translesion synthesis . Excess DNA damage may also increase epigenetic alterations due to errors during DNA repair. [ 80 ] [ 81 ] Such mutations and epigenetic alterations may give rise to cancer . The frequent microRNA-induced deficiency of BRCA1 in breast and ovarian cancers likely contributes to the progression of those cancers.
All germ-line BRCA1 mutations identified to date have been inherited, suggesting the possibility of a large "founder" effect in which a certain mutation is common to a well-defined population group and can, in theory, be traced back to a common ancestor. Given the complexity of mutation screening for BRCA1, these common mutations may simplify the methods required for mutation screening in certain populations. Analysis of mutations that occur with high frequency also permits the study of their clinical expression. [ 82 ] Examples of manifestations of a founder effect are seen among Ashkenazi Jews . Three mutations in BRCA1 have been reported to account for the majority of Ashkenazi Jewish patients with inherited BRCA1-related breast and/or ovarian cancer: 185delAG, 188del11, and 5382insC in the BRCA1 gene. [ 83 ] [ 84 ] In fact, it has been shown that if a Jewish woman does not carry a BRCA1 185delAG, BRCA1 5382insC founder mutation, it is highly unlikely that a different BRCA1 mutation will be found. [ 85 ] Additional examples of founder mutations in BRCA1 are given in Table 1 (mainly derived from [ 82 ] ).
As women age, reproductive performance declines, leading to menopause. This decline is tied to a reduction in the number of ovarian follicles. Although about 1 million oocytes are present at birth in the human ovary, only about 500 (about 0.05%) of these ovulate. The decline in ovarian reserve appears to occur at a constantly increasing rate with age, [ 117 ] and leads to nearly complete exhaustion of the reserve by about age 52. As ovarian reserve and fertility decline with age, there is also a parallel increase in pregnancy failure and meiotic errors, resulting in chromosomally abnormal conceptions. [ 118 ]
Women with a germ-line BRCA1 mutation appear to have a diminished oocyte reserve and decreased fertility compared to normally aging women. [ 119 ] Furthermore, women with an inherited BRCA1 mutation undergo menopause prematurely. [ 120 ] Since BRCA1 is a key DNA repair protein, these findings suggest that naturally occurring DNA damages in oocytes are repaired less efficiently in women with a BRCA1 defect, and that this repair inefficiency leads to early reproductive failure. [ 119 ]
As noted above, the BRCA1 protein plays a key role in homologous recombinational repair. This is the only known cellular process that can accurately repair DNA double-strand breaks. DNA double-strand breaks accumulate with age in humans and mice in primordial follicles. [ 121 ] Primordial follicles contain oocytes that are at an intermediate (prophase I) stage of meiosis. Meiosis is the general process in eukaryotic organisms by which germ cells are formed, and it is likely an adaptation for removing DNA damages, especially double-strand breaks, from germ line DNA. [ 122 ] (Also see article Meiosis ). Homologous recombinational repair employing BRCA1 is especially promoted during meiosis. It was found that expression of four key genes necessary for homologous recombinational repair of DNA double-strand breaks ( BRCA1, MRE11, RAD51 and ATM ) decline with age in the oocytes of humans and mice, [ 121 ] leading to the hypothesis that DNA double-strand break repair is necessary for the maintenance of oocyte reserve and that a decline in efficiency of repair with age plays a role in ovarian aging.
Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide. At diagnosis, almost 70% of persons with NSCLC have locally advanced or metastatic disease. Persons with NSCLC are often treated with therapeutic platinum compounds (e.g., cisplatin, carboplatin, or oxaliplatin) that cause inter-strand cross-links in DNA. Among individuals with NSCLC, low expression of BRCA1 in the primary tumor correlated with improved survival after platinum-containing chemotherapy. [ 123 ] [ 124 ] This correlation implies that low BRCA1 in cancer, and the consequent low level of DNA repair, causes vulnerability of cancer to treatment by the DNA cross-linking agents. High BRCA1 may protect cancer cells by acting in a pathway that removes the DNA damage introduced by the platinum drugs. Thus, the level of BRCA1 expression is a potentially important tool for tailoring chemotherapy in lung cancer management. [ 123 ] [ 124 ]
The level of BRCA1 expression is also relevant to ovarian cancer treatment. Patients having sporadic ovarian cancer who were treated with platinum drugs had longer median survival times if their BRCA1 expression was low compared to patients with higher BRCA1 expression (46 compared to 33 months). [ 125 ]
A patent application for the isolated BRCA1 gene and cancer promoting mutations discussed above, as well as methods to diagnose the likelihood of getting breast cancer, was filed by the University of Utah, National Institute of Environmental Health Sciences (NIEHS) and Myriad Genetics in 1994; [ 17 ] over the next year, Myriad, (in collaboration with investigators at Endo Recherche, Inc., HSC Research & Development Limited Partnership, and University of Pennsylvania), isolated and sequenced the BRCA2 gene and identified key mutations, and the first BRCA2 patent was filed in the U.S. by Myriad and other institutions in 1995. [ 18 ] Myriad is the exclusive licensee of these patents and has enforced them in the US against clinical diagnostic labs. [ 20 ] This business model led from Myriad being a startup in 1994 to being a publicly traded company with 1200 employees and about $500M in annual revenue in 2012; [ 19 ] it also led to controversy over high prices and the inability to get second opinions from other diagnostic labs, which in turn led to the landmark Association for Molecular Pathology v. Myriad Genetics lawsuit. [ 20 ] [ 126 ] The patents began to expire in 2014.
According to an article published in the journal, Genetic Medicine , in 2010, "The patent story outside the United States is more complicated.... For example, patents have been obtained but the patents are being ignored by provincial health systems in Canada. In Australia and the UK, Myriad's licensee permitted use by health systems but announced a change of plans in August 2008. Only a single mutation has been patented in Myriad's lone European-wide patent, although some patents remain under review of an opposition proceeding. In effect, the United States is the only jurisdiction where Myriad's strong patent position has conferred sole-provider status." [ 127 ] [ 128 ] Peter Meldrum, CEO of Myriad Genetics, has acknowledged that Myriad has "other competitive advantages that may make such [patent] enforcement unnecessary" in Europe. [ 129 ]
As with any gene, finding variation in BRCA1 is not hard. The real value comes from understanding what the clinical consequences of any particular variant are. Myriad has a large, proprietary database of such genotype-phenotype correlations. In response, parallel open-source databases are being developed.
Legal decisions surrounding the BRCA1 and BRCA2 patents will affect the field of genetic testing in general. [ 130 ] A June 2013 article, in Association for Molecular Pathology v. Myriad Genetics (No. 12-398), quoted the US Supreme Court 's unanimous ruling that, "A naturally occurring DNA segment is a product of nature and not patent eligible merely because it has been isolated," invalidating Myriad's patents on the BRCA1 and BRCA2 genes. However, the Court also held that manipulation of a gene to create something not found in nature could still be eligible for patent protection. [ 131 ] The Federal Court of Australia came to the opposite conclusion, upholding the validity of an Australian Myriad Genetics patent over the BRCA1 gene in February 2013. [ 132 ] The Federal Court also rejected an appeal in September 2014. [ 133 ] Yvonne D'Arcy won her case against US-based biotech company Myriad Genetics in the High Court of Australia . In their unanimous decision on October 7, 2015, the "high court found that an isolated nucleic acid, coding for a BRCA1 protein, with specific variations from the norm that are indicative of susceptibility to breast cancer and ovarian cancer was not a 'patentable invention.'" [ 134 ]
BRCA1 has been shown to interact with the following proteins:
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https://en.wikipedia.org/wiki/BRCA1
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1N0W , 3EU7
675
12190
ENSG00000139618
ENSMUSG00000041147
P51587
P97929
NM_000059
NM_001081001 NM_009765
NP_000050
NP_001074470 NP_033895
BRCA2 and BRCA2 ( / ˌ b r æ k ə ˈ t uː / [ 5 ] ) are human genes and their protein products, respectively. The official symbol (BRCA2, italic for the gene, nonitalic for the protein) and the official name (originally breast cancer 2 ; currently BRCA2, DNA repair associated ) are maintained by the HUGO Gene Nomenclature Committee . One alternative symbol, FANCD1 , recognizes its association with the FANC protein complex. Orthologs , styled Brca2 and Brca2, are common in other vertebrate species. [ 6 ] [ 7 ] BRCA2 is a human tumor suppressor gene [ 8 ] [ 9 ] (specifically, a caretaker gene ), found in all humans; its protein , also called by the synonym breast cancer type 2 susceptibility protein , is responsible for repairing DNA. [ 10 ]
BRCA2 and BRCA1 are normally expressed in the cells of breast and other tissue, where they help repair damaged DNA or destroy cells if DNA cannot be repaired. They are involved in the repair of chromosomal damage with an important role in the error-free repair of DNA double strand breaks. [ 11 ] [ 12 ] If BRCA1 or BRCA2 itself is damaged by a BRCA mutation , damaged DNA is not repaired properly, and this increases the risk for breast cancer . [ 13 ] [ 14 ] BRCA1 and BRCA2 have been described as "breast cancer susceptibility genes" and "breast cancer susceptibility proteins". The predominant allele has a normal tumor suppressive function whereas high penetrance mutations in these genes cause a loss of tumor suppressive function, which correlates with an increased risk of breast cancer. [ 15 ]
The BRCA2 gene is located on the long (q) arm of chromosome 13 at position 12.3 (13q12.3). [ 16 ] The human reference BRCA2 gene contains 27 exons, and the cDNA has 10,254 base pairs [ 17 ] coding for a protein of 3418 amino acids. [ 18 ] [ 19 ]
Although the structures of the BRCA1 and BRCA2 genes are very different, at least some functions are interrelated. The proteins made by both genes are essential for repairing damaged DNA (see Figure of recombinational repair steps). BRCA2 binds the single strand DNA and directly interacts with the recombinase RAD51 to stimulate [ 27 ] and maintain [ 28 ] strand invasion, a vital step of homologous recombination . The localization of RAD51 to the DNA double-strand break requires the formation of the BRCA1-PALB2-BRCA2 complex. PALB2 (Partner and localizer of BRCA2) [ 29 ] can function synergistically with a BRCA2 chimera (termed piccolo, or piBRCA2) to further promote strand invasion. [ 30 ] These breaks can be caused by natural and medical radiation or other environmental exposures, but also occur when chromosomes exchange genetic material during a special type of cell division that creates sperm and eggs ( meiosis ). Double strand breaks are also generated during repair of DNA cross links. By repairing DNA, these proteins play a role in maintaining the stability of the human genome and prevent dangerous gene rearrangements that can lead to hematologic and other cancers.
BRCA2 has been shown to possess a crucial role in protection from the MRE11 -dependent nucleolytic degradation of the reversed forks that are forming during DNA replication fork stalling (caused by obstacles such as mutations, intercalating agents etc.). [ 31 ]
Like BRCA1, BRCA2 probably regulates the activity of other genes and plays a critical role in embryo development.
Certain variations of the BRCA2 gene increase risks for breast cancer as part of a hereditary breast–ovarian cancer syndrome . Researchers have identified hundreds of mutations in the BRCA2 gene, many of which cause an increased risk of cancer. BRCA2 mutations are usually insertions or deletions of a small number of DNA base pairs in the gene. As a result of these mutations, the protein product of the BRCA2 gene is abnormal, and does not function properly. Researchers believe that the defective BRCA2 protein is unable to fix DNA damage that occurs throughout the genome. As a result, there is an increase in mutations due to error-prone translesion synthesis past un-repaired DNA damage, and some of these mutations can cause cells to divide in an uncontrolled way and form a tumor.
People who have two mutated copies of the BRCA2 gene have one type of Fanconi anemia . This condition is caused by extremely reduced levels of the BRCA2 protein in cells, which allows the accumulation of damaged DNA. Patients with Fanconi anemia are prone to several types of leukemia (a type of blood cell cancer); solid tumors, particularly of the head, neck, skin, and reproductive organs; and bone marrow suppression (reduced blood cell production that leads to anemia ). Women having inherited a defective BRCA1 or BRCA2 gene have risks for breast and ovarian cancer that are so high and seem so selective that many mutation carriers choose to have prophylactic surgery . There has been much conjecture to explain such apparently striking tissue specificity. Major determinants of where BRCA1 - and BRCA2 -associated hereditary cancers occur are related to tissue specificity of the cancer pathogen, the agent that causes chronic inflammation, or the carcinogen. The target tissue may have receptors for the pathogen, become selectively exposed to carcinogens and an infectious process. An innate genomic deficit impairs normal responses and exacerbates the susceptibility to disease in organ targets. This theory also fits data for several tumor suppressors beyond BRCA1 or BRCA2 . A major advantage of this model is that it suggests there are some options in addition to prophylactic surgery. [ 33 ]
In addition to breast cancer in men and women, mutations in BRCA2 also lead to an increased risk of ovarian , uterine tube , prostate and pancreatic cancer . In some studies, mutations in the central part of the gene have been associated with a higher risk of ovarian cancer and a lower risk of prostate cancer than mutations in other parts of the gene. Several other types of cancer [ which? ] have also been seen in certain families with BRCA2 mutations. [ citation needed ]
In general, strongly inherited gene mutations (including mutations in BRCA2 ) account for only 5-10% of breast cancer cases; the specific risk of getting breast or other cancer for anyone carrying a BRCA2 mutation depends on many factors. [ 34 ]
The BRCA2 gene was discovered in 1994 by a multi-institutional team of scientists, led by researchers at The Institute of Cancer Research, London. [ 35 ] [ 16 ] [ 36 ] In 1996, Kenneth Offit and his research group at Memorial Sloan Kettering Cancer Center successfully identified the most common mutation on the gene associated with breast and ovarian cancer among individuals of Ashkenazi Jewish ancestry. [ 37 ] [ 38 ] [ 39 ] [ 40 ]
The gene was first cloned by scientists at Myriad Genetics , Endo Recherche, Inc., HSC Research & Development Limited Partnership, and the University of Pennsylvania . [ 41 ]
Methods to diagnose the likelihood of a patient with mutations in BRCA1 and BRCA2 getting cancer were covered by patents owned or controlled by Myriad Genetics . [ 42 ] [ 43 ] Myriad's business model of exclusively offering the diagnostic test led from Myriad's beginnings as a startup in 1994 to its being a publicly traded company with 1200 employees and about $500M in annual revenue in 2012; [ 44 ] it also led to controversy over high test prices and the unavailability of second opinions from other diagnostic labs, which in turn led to the landmark Association for Molecular Pathology v. Myriad Genetics lawsuit. [ 45 ]
All germline BRCA2 mutations identified to date have been inherited, suggesting the possibility of a large "founder" effect in which a certain mutation is common to a well-defined population group and can theoretically be traced back to a common ancestor. Given the complexity of mutation screening for BRCA2, these common mutations may simplify the methods required for mutation screening in certain populations. Analysis of mutations that occur with high frequency also permits the study of their clinical expression. [ 46 ] A striking example of a founder mutation is found in Iceland, where a single BRCA2 (999del5) mutation accounts for virtually all breast/ovarian cancer families. [ 47 ] [ 48 ] This frame-shift mutation leads to a highly truncated protein product. In a large study examining hundreds of cancer and control individuals, this 999del5 mutation was found in 0.6% of the general population. Of note, while 72% of patients who were found to be carriers had a moderate or strong family history of breast cancer, 28% had little or no family history of the disease. This strongly suggests the presence of modifying genes that affect the phenotypic expression of this mutation, or possibly the interaction of the BRCA2 mutation with environmental factors. Additional examples of founder mutations in BRCA2 are given in the table below.
In the plant Arabidopsis thaliana , loss of the BRCA2 homolog AtBRCA2 causes severe defects in both male meiosis and in the development of the female gametocyte . [ 65 ] AtBRCA2 protein is required for proper localization of the synaptonemal complex protein AtZYP1 and the recombinases AtRAD51 and AtDMC1. Furthermore, AtBRCA2 is required for proper meiotic synapsis. Thus AtBRCA2 is likely important for meiotic recombination. It appears that AtBRCA2 acts during meiosis to control the single-strand invasion steps mediated by AtRAD51 and AtDMC1 occurring during meiotic homologous recombinational repair of DNA damages. [ 65 ]
Homologs of BRCA2 are also essential for meiosis in the fungus Ustilago maydis , [ 66 ] the worm Caenorhabditis elegans , [ 67 ] [ 68 ] and the fruitfly Drosophila melanogaster . [ 69 ]
Mice that produce truncated versions of BRCA2 are viable but sterile. [ 70 ] BRCA2 mutant rats have a phenotype of growth inhibition and sterility in both sexes. [ 71 ] Aspermatogenesis in these mutant rats is due to a failure of homologous chromosome synapsis during meiosis.
DMC1 (DNA meiotic recombinase 1) is a meiosis specific homolog of RAD51 that mediates strand exchange during homologous recombinational repair. DMC1 promotes the formation of DNA strand invasion products (joint molecules) between homologous DNA molecules. Human DMC1 interacts directly with each of a series of repeat sequences in the BRCA2 protein (called BRC repeats) that stimulate joint molecule formation by DMC1. [ 72 ] BRC repeats conform to a motif consisting of a sequence of about 35 highly conserved amino acids that are present at least once in all BRCA2-like proteins. The BRCA2 BRC repeats stimulate joint molecule formation by promoting the interaction of single-stranded DNA (ssDNA) with DMC1. [ 72 ] The ssDNA complexed with DMC1 can pair with homologous ssDNA from another chromosome during the synopsis stage of meiosis to form a joint molecule, a central step in homologous recombination . Thus the BRC repeat sequences of BRCA2 appear to play a key role in recombinational repair of DNA damages during meiotic recombination.
Overall, it appears that homologous recombination during meiosis functions to repair DNA damages, [ citation needed ] and that BRCA2 plays a key role in performing this function.
BRCA2 is required in the mouse for neurogenesis and suppression of medulloblastoma . [ 73 ] ‘’BRCA2’’ loss profoundly affects neurogenesis, particularly during embryonic and postnatal neural development. These neurological defects arise from DNA damage. [ 73 ]
Epigenetic alterations in expression of BRCA2 (causing over-expression or under-expression) are very frequent in sporadic cancers (see Table below) while mutations in BRCA2 are rarely found. [ 74 ] [ 75 ] [ 76 ]
In non-small cell lung cancer, BRCA2 is epigenetically repressed by hypermethylation of the promoter. [ 77 ] In this case, promoter hypermethylation is significantly associated with low mRNA expression and low protein expression but not with loss of heterozygosity of the gene.
In sporadic ovarian cancer, an opposite effect is found. BRCA2 promoter and 5'-UTR regions have relatively few or no methylated CpG dinucleotides in the tumor DNA compared with that of non-tumor DNA, and a significant correlation is found between hypomethylation and a >3-fold over-expression of BRCA2. [ 78 ] This indicates that hypomethylation of the BRCA2 promoter and 5'-UTR regions leads to over-expression of BRCA2 mRNA.
One report indicated some epigenetic control of BRCA2 expression by the microRNAs miR-146a and miR-148a. [ 79 ]
In eukaryotes , BRCA2 protein has an important role in homologous recombinational repair. In mice and humans, BRCA2 primarily mediates orderly assembly of RAD51 on single-stranded (ss) DNA, the form that is active for homologous pairing and strand invasion. [ 80 ] BRCA2 also redirects RAD51 from double-stranded DNA and prevents dissociation from ssDNA. [ 80 ] In addition, the four paralogs of RAD51 , consisting of RAD51B ( RAD51L1 ), RAD51C (RAD51L2), RAD51D ( RAD51L3 ), XRCC2 form a complex called the BCDX2 complex (see Figure: Recombinational repair of DNA). This complex participates in RAD51 recruitment or stabilization at damage sites. [ 26 ] The BCDX2 complex appears to act by facilitating the assembly or stability of the RAD51 nucleoprotein filament . RAD51 catalyses strand transfer between a broken sequence and its undamaged homologue to allow re-synthesis of the damaged region (see homologous recombination models ).
Some studies of cancers report over-expressed BRCA2 whereas other studies report under-expression of BRCA2 . At least two reports found over-expression in some sporadic breast tumors and under-expression in other sporadic breast tumors. [ 81 ] [ 82 ] (see Table).
Many cancers have epigenetic deficiencies in various DNA repair genes (see Frequencies of epimutations in DNA repair genes in cancers ). These repair deficiencies likely cause increased unrepaired DNA damages. The over-expression of BRCA2 seen in many cancers may reflect compensatory BRCA2 over-expression and increased homologous recombinational repair to at least partially deal with such excess DNA damages. Egawa et al. [ 83 ] suggest that increased expression of BRCA2 can be explained by the genomic instability frequently seen in cancers, which induces BRCA2 mRNA expression due to an increased need for BRCA2 for DNA repair.
Under-expression of BRCA2 would itself lead to increased unrepaired DNA damages. Replication errors past these damages (see translesion synthesis ) would lead to increased mutations and cancer.
BRCA2 has been shown to interact with
BRCA2 contains a number of 39 amino acid repeats that are critical for binding to RAD51 (a key protein in DNA recombinational repair) and resistance to methyl methanesulphonate treatment. [ 102 ] [ 109 ] [ 110 ] [ 118 ]
The BRCA2 helical domain adopts a helical structure, consisting of a four-helix cluster core (alpha 1, alpha 8, alpha 9, alpha 10) and two successive beta-hairpins (beta 1 to beta 4). An approximately 50-amino acid segment that contains four short helices (alpha 2 to alpha 4), meanders around the surface of the core structure . In BRCA2, the alpha 9 and alpha 10 helices pack with the BRCA2 OB1 domain through van der Waals contacts involving hydrophobic and aromatic residues, and also through side-chain and backbone hydrogen bonds . This domain binds the 70-amino acid DSS1 (deleted in split-hand/split foot syndrome) protein, which was originally identified as one of three genes that map to a 1.5-Mb locus deleted in an inherited developmental malformation syndrome. [ 116 ]
The BRCA OB1 domain assumes an OB fold , which consists of a highly curved five-stranded beta-sheet that closes on itself to form a beta-barrel . OB1 has a shallow groove formed by one face of the curved sheet and is demarcated by two loops, one between beta 1 and beta 2 and another between beta 4 and beta 5, which allows for weak single strand DNA binding . The domain also binds the 70-amino acid DSS1 (deleted in split-hand/split foot syndrome) protein. [ 116 ]
The BRCA OB3 domain assumes an OB fold , which consists of a highly curved five-stranded beta-sheet that closes on itself to form a beta-barrel . OB3 has a pronounced groove formed by one face of the curved sheet and is demarcated by two loops, one between beta 1 and beta 2 and another between beta 4 and beta 5, which allows for strong ssDNA binding . [ 116 ]
The Tower domain adopts a secondary structure consisting of a pair of long, antiparallel alpha-helices (the stem) that support a three-helix bundle (3HB) at their end. The 3HB contains a helix-turn-helix motif and is similar to the DNA binding domains of the bacterial site-specific recombinases , and of eukaryotic Myb and homeodomain transcription factors . The Tower domain has an important role in the tumour suppressor function of BRCA2, and is essential for appropriate binding of BRCA2 to DNA. [ 116 ] Studies shown that conformation of this tower domain is allosterically controlled by a small protein "DSS1", which interacts with helical, OB1 and OB2 domains of BRCA2. [ 119 ]
A patent application for the isolated BRCA1 gene and cancer-cancer promoting mutations, as well as methods to diagnose the likelihood of getting breast cancer, was filed by the University of Utah, National Institute of Environmental Health Sciences (NIEHS) and Myriad Genetics in 1994; [ 42 ] over the next year, Myriad, in collaboration with other investigators, isolated and sequenced the BRCA2 gene and identified relevant mutations, and the first BRCA2 patent was filed in the U.S. by Myriad and the other institutions in 1995. [ 41 ] Myriad is the exclusive licensee of these patents and has enforced them in the US against clinical diagnostic labs. [ 45 ] This business model led from Myriad being a startup in 1994 to being a publicly traded company with 1200 employees and about $500M in annual revenue in 2012; [ 44 ] it also led to controversy over high prices and the inability to get second opinions from other diagnostic labs, which in turn led to the landmark Association for Molecular Pathology v. Myriad Genetics lawsuit. [ 45 ] [ 120 ] The patents begin to expire in 2014.
Peter Meldrum, CEO of Myriad Genetics, has acknowledged that Myriad has "other competitive advantages that may make such [patent] enforcement unnecessary" in Europe. [ 121 ]
Legal decisions surrounding the BRCA1 and BRCA2 patents will affect the field of genetic testing in general. [ 122 ] In June 2013, in Association for Molecular Pathology v. Myriad Genetics (No. 12-398), the US Supreme Court unanimously ruled that, "A naturally occurring DNA segment is a product of nature and not patent eligible merely because it has been isolated," invalidating Myriad's patents on the BRCA1 and BRCA2 genes. However, the Court also held that manipulation of a gene to create something not found in nature could still be eligible for patent protection. [ 123 ] The Federal Court of Australia came to the opposite conclusion, upholding the validity of an Australian Myriad Genetics patent over the BRCA1 gene in February 2013, [ 124 ] but this decision is being appealed and the appeal will include consideration of the US Supreme Court ruling. [ 125 ]
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BT-20 is a breast cancer cell line derived from a 74-year-old human female in 1958 by E.Y. Lasfargues and L. Ozzello. [ 1 ] The cells technically came from a triple-negative breast cancer , which was caused by an invasive ductal carcinoma in the mammary gland . BT-20 cells are known to have amplified regions of chromosomes 6, 11, and 20, with most cells being hyperdiploid. [ 2 ] The cells express an estrogen receptor with a deletion of exon 5, and are used in preclinical studies of breast cancer.
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BW-247 is an antidepressant. [ 1 ] [ 2 ] BW-247 is a secondary amine, closely related in structure to the tricyclic antidepressants, which inhibits NA uptake in aortic strips [ 3 ] and rat cerebral cortex slices. [ 4 ] Unlike the tricyclic antidepressants, it is reported not to possess anticholinergic activity. [ 5 ]
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B symptoms are a set of symptoms , namely fever , night sweats , and unintentional weight loss , that can be associated with both Hodgkin lymphoma and non-Hodgkin lymphoma . These symptoms are not specific to lymphomas, especially each one considered individually, and even as a trio they are not pathognomonic for lymphomas, but the presence of the trio is sensitive enough for lymphomas to warrant diagnostic investigation and differential diagnosis . The presence or absence of B symptoms has prognostic significance in lymphomas and is reflected in their staging .
B symptoms are so called because Ann Arbor staging of lymphomas includes both a number (I–IV) and a letter (A or B). [ 1 ] "A" indicates the absence of systemic symptoms, while "B" indicates their presence.
B symptoms include:
The presence of B symptoms is a marker for more advanced disease with systemic, rather than merely local, involvement. B symptoms are a clear negative prognostic factor in Hodgkin lymphoma. [ 2 ] The relevance of B symptoms in non-Hodgkin lymphoma is less clear, although B symptoms tend to correlate with disease that is either more widespread or of a higher histologic grade. [ 3 ]
It has been suggested that, in Hodgkin lymphoma, fever and weight loss are much more prognostically significant than night sweats. In one series of patients with early-stage Hodgkin disease, the presence or absence of night sweats had no impact on cure rates and outcome. However, fever and weight loss had a pronounced negative impact on cure and survival rates, regardless of treatment modality. [ 4 ]
aggressive: Sézary disease
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B-type inclusions , formerly known as Guarnieri bodies / ɡ w ɑːr n ˈ j ɛər i / are cellular features found upon microscopic inspection of epithelial cells of individuals suspected of having poxvirus [ 1 ] (e.g. smallpox [ 2 ] or vaccinia ). In cells stained with eosin , they appear as pink blobs in the cytoplasm of affected epithelial cells. The absence of Guarnieri bodies cannot be used as to rule out smallpox , however, as more sensitive test need to be performed.
B-type inclusions are the sites of viral replication and are found in all poxvirus-infected cells, unlike A-type inclusions which are more strongly eosinophilic and only found in infections with certain poxviruses. [ 3 ]
They are named after the Italian physician Giuseppe Guarnieri.
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The concept of backward masking originated in psychoacoustics , referring to temporal masking of quiet sounds that occur moments before a louder sound.
In cognitive psychology , visual backward masking involves presenting one visual stimulus (a "mask" or "masking stimulus") immediately after a brief (usually 30 ms) "target" visual stimulus resulting in a failure to consciously perceive the first stimulus. [ 1 ] It is widely used in psychophysiological studies on fear and phobias that investigate the preattentive nonconscious reactions to fear-relevant stimuli. [ 2 ]
It is unknown how a later stimulus is able to block an earlier one. However, one theory for this phenomenon, known as the dual channel interaction theory, proposes that a fast signal created by the second stimulus is able to catch up to and overcome a slower signal sent from the first impulse. [ 3 ] A similar phenomenon can occur when a masking stimulus precedes a target stimulus rather than follows it: this is known as forward masking , [ 1 ] or visual forward masking when the stimulus is visual. While not consciously perceived, the masked stimulus can nevertheless still have an effect on cognitive processes such as context interpretation. It has been shown that visually masked stimuli can elicit motor responses in simple reaction-time tasks (e.g. response priming ) independent of their conscious visibility. [ 4 ]
It is a widespread belief that masked stimuli can be used for psychological manipulation (see subliminal messages , psychorama ). However, the empirical evidence for subliminal persuasion is limited.
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The trait of backward speech is described as an ability to spontaneously and accurately reverse words. Two strategies of word reversal were reported: reversal according to the phonetic structure of the words or reversal according to their spelling . [ 1 ] In the 1980s Nelson Cowan hypothesized that this ability is afforded by an extraordinary working memory . [ 2 ] Recent studies have provided evidence that the working memory is indeed involved in this ability and further suggested that genetic factors may contribute to this trait. [ 1 ]
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Bacterial adhesins are cell-surface components or appendages of bacteria that facilitate adhesion or adherence to other cells or to surfaces, usually in the host they are infecting or living in. Adhesins are a type of virulence factor .
Adherence is an essential step in bacterial pathogenesis or infection , required for colonizing a new host . [ 1 ] Adhesion and bacterial adhesins are also a potential target either for prophylaxis or for the treatment of bacterial infections. [ 2 ]
Bacteria are typically found attached to and living in close association with surfaces. During the bacterial lifespan, a bacterium is subjected to frequent shear-forces . In the crudest sense, bacterial adhesins serve as anchors allowing bacteria to overcome these environmental shear forces, thus remaining in their desired environment. However, bacterial adhesins do not serve as a sort of universal bacterial Velcro. Rather, they act as specific surface recognition molecules, allowing the targeting of a particular bacterium to a particular surface such as root tissue in plants, lacrimal duct tissues in mammals, or even tooth enamel. [ 3 ]
Most fimbria of gram-negative bacteria function as adhesins, but in many cases it is a minor subunit protein at the tip of the fimbriae that is the actual adhesin. In gram-positive bacteria, a protein or polysaccharide surface layer serves as the specific adhesin. To effectively achieve adherence to host surfaces, many bacteria produce multiple adherence factors called adhesins .
Bacterial adhesins provide species and tissue tropism . Adhesins are expressed by both pathogenic bacteria and saprophytic bacteria . This prevalence marks them as key microbial virulence factors in addition to a bacterium's ability to produce toxins and resist the immune defenses of the host.
Through the mechanisms of evolution, different species of bacteria have developed different solutions to the problem of attaching receptor specific proteins to the bacteria surface. Today many different types and subclasses of bacterial adhesins may be observed in the literature.
The typical structure of a bacterial adhesin is that of a fimbria or pilus . [ 3 ] The bacterial adhesin consists primarily of an intramembranous structural protein which provides a scaffold upon which several extracellular adhesins may be attached. [ 3 ] However, as in the case of the CFA1 fimbriae, the structural protein itself can sometimes act as an adhesin if a portion of the protein extends into the extracellular matrix (ECM).
The best characterized bacterial adhesin is the type 1 fimbrial FimH adhesin. This adhesin is responsible for D-mannose sensitive adhesion. [ 3 ] The bacterium synthesizes a precursor protein consisting of 300 amino acids then processes the protein by removing several signal peptides ultimately leaving a 279 amino acid protein. [ 3 ] Mature FimH is displayed on the bacterial surface as a component of the type 1 fimbrial organelle. [ 3 ]
In 1999, the structure of FimH was resolved via x-ray crystallography . FimH is folded into two domains. The N terminal adhesive domain plays the main role in surface recognition while the C-terminal domain is responsible for organelle integration. [ 5 ] A tetra-peptide loop links the two domains. Additionally, a carbohydrate-binding pocket has been identified at the tip of the N-terminal adhesive domain. [ 5 ] This basic structure is conserved across type 1 fimbrial adhesins though recent studies have shown that in vitro induced mutations can lead to the addition of C-terminal domain specificity resulting in a bacterial adhesion with dual bending sites and related binding phenotypes. [ 6 ]
The majority of bacterial pathogens exploit specific adhesion to host cells as their main virulence factor. "A large number of bacterial adhesins with individual receptor specificities have been identified." [ 3 ] Many bacterial pathogens are able to express an array of different adhesins. Expression of these adhesins at different phases during infection play the most important role in adhesion based virulence. [ 3 ] Numerous studies have shown that inhibiting a single adhesin in this coordinated effort can often be enough to make a pathogenic bacterium non-virulent . This has led to the exploration of adhesin activity interruption as a method of bacterial infection treatment.
The study of adhesins as a point of exploitation for vaccines comes from early studies which indicated that an important component of protective immunity against certain bacteria came from an ability to prevent adhesin binding. [ 7 ] Additionally, adhesins are attractive vaccine candidates because they are often essential to infection and are surface-located, making them readily accessible to antibodies .
The effectiveness of anti-adhesin antibodies is illustrated by studies with FimH, the adhesin of uropathogenic Escherichia coli (UPEC). Work with E. coli stems from observations of human acquired immunity. Children in third world countries may suffer from several episodes of E. coli associated diarrhea during the first three years of life. If the child survives this initial period of susceptibility, infection rates typically drop substantially. Field studies show that this acquired immunity is directed primarily against bacterial adhesins. [ 3 ]
Recent studies from Worcester Polytechnic Institute show that the consumption of cranberry juice may inhibit the action of UPEC adhesins. Using atomic force microscopy researchers have shown that adhesion forces decrease with time following cranberry juice consumption. [ 8 ] This research has opened the door to further exploration of orally administered vaccines which exploit bacterial adhesins.
A number of problems create challenges for the researcher exploring the anti-adhesin immunity concept. First, a large number of different bacterial adhesins target the same human tissues. Further, an individual bacterium can produce multiple different types of adhesin, at different times, in different places, and in response to different environmental triggers. [ 3 ] Finally, many adhesins present as different immunologically distinct antigenic varieties, even within the same clone (as is the case in Neisseria gonorrhoeae ). [ 9 ]
Despite these challenges, progress is being made in the creation of anti-adhesion vaccines. In animal models, passive immunization with anti FimH-antibodies and vaccination with the protein significantly reduced colonization by UPEC. [ 10 ] Moreover, the Bordetella pertussis adhesins FHA and pertactin are components of three of the four acellular pertussis vaccines currently licensed for use in the U.S. Additionally, anti-adhesion vaccines are being explored as a solution to urinary tract infection (UTI). The use of synthetic FimH adhesion peptides was shown to prevent urogenital mucosal infection by E. coli in mice. [ 11 ]
The Dr family of adhesins bind to the Dr blood group antigen component of decay-accelerating factor (DAF). [ 12 ] These proteins contain both fimbriated and afimbriated adherence structures and mediate adherence of uropathogenic Escherichia coli to the urinary tract. [ 13 ] They do so by inducing the development of long cellular extensions that wrap around the bacteria. [ 12 ] They also confer the mannose-resistant hemaglutination phenotype, which can be inhibited by chloramphenicol . The N-terminal portion of the mature protein is thought to be responsible for chloramphenicol sensitivity. [ 14 ] Also, they induce activation of several signal transduction cascades, including activation of PI-3 kinase . [ 12 ]
The Dr family of adhesins are particularly associated with cystitis and pregnancy-associated pyelonephritis . [ 12 ]
Multivalent adhesion molecules (MAMs) are a widespread family of adhesins found in Gram negative bacteria, including E. coli , Vibrio , Yersinia , and Pseudomonas aeruginosa . [ 15 ] MAMs contain tandem repeats of mammalian cell entry (MCE) domains which specifically bind to extracellular matrix proteins and anionic lipids on host tissues. Since they are abundant in many pathogens of clinical importance, multivalent adhesion molecules are a potential target for prophylactic or therapeutic anti-infectives. The use of a MAM targeting adhesion inhibitor was shown to significantly decrease the colonization of burn wounds by multidrug resistant Pseudomonas aeruginosa in rats. [ 16 ]
N. gonorrhoeae is host restricted almost entirely to humans. [ 3 ] "Extensive studies have established type 4 fimbrial adhesins of N. gonorrhoeae virulence factors." [ 3 ] These studies have shown that only strains capable of expressing fimbriae are pathogenic. High survival of polymorphonuclear neutrophils (PMNs) characterizes Neisseria gonorrhoeae infections. Additionally, recent studies out of Stockholm have shown that Neisseria can hitchhike on PMNs using their adhesin pili thus hiding them from neutrophil phagocytic activity. This action facilitates the spread of the pathogen throughout the epithelial cell layer. [ 17 ]
Escherichia coli strains most known for causing diarrhea can be found in the intestinal tissue of pigs and humans where they express the K88 and CFA1 [ 18 ] to attach to the intestinal lining. Additionally, UPEC causes about 90% of urinary tract infections. [ 19 ] Of those E. coli which cause UTIs, 95% express type 1 fimbriae. FimH in E. coli overcomes the antibody based immune response by natural conversion from the high to the low affinity state. Through this conversion, FimH adhesion may shed the antibodies bound to it. Escherichia coli FimH provides an example of conformation specific immune response which enhances impact on the protein. [ 19 ] By studying this particular adhesion, researchers hope to develop adhesion-specific vaccines which may serve as a model for antibody-mediation of pathogen adhesion. [ 19 ]
Adhesins are also used in cell communication, and bind to surface communicators. Can also be used to bind to other bacteria.
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Bacterial neuraminidase is type of neuraminidase and a virulence factor for many bacteria including Bacteroides fragilis and Pseudomonas aeruginosa .
Its function is to cleave a sialic acid residue off ganglioside- GM1 (a modulator of cell surface and receptor activity) turning it into asialo-GM1 to which type 4 pili (attachment factors) bind preferentially.
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A baffle is a surgically created tunnel or wall within the heart or major blood vessels used to redirect the flow of blood. [ 1 ] They are used in some types of heart abnormalities that a child is born with known as congenital heart defects . Baffles are usually constructed, at least in part, from a person's own heart tissue, while other methods of redirecting blood using artificial material are known by the more generic term 'conduits'. [ 1 ]
Baffles can be made between different structures depending on the heart condition that needs to be treated.
In dextro-transposition of the great arteries , at the initial arterial switch a Jatene procedure is normally done in conjunction to switch the coronary arteries as well, as they originate from the aorta . The Jatene procedure is ideally performed during the second week of life, before the left ventricle adjusts to the lower pulmonary pressure. In cases where the Jatene is not performed in time, the left ventricle weakens and is consequently unable to contract against the higher arterial pressures of systemic circulation. In this scenario, a second procedure with an atrial switch is done after recovery from the first intervention.
The atrial switch is done via either the Mustard procedure , in which the atrial septum is cut out and a baffle is made with the pericardial baffle, or a Senning procedure, in which the atrial septum itself is used to create the baffle. The effect of either procedure is a physiologic atrial switch, redirecting blood from the superior and inferior vena cava to the left ventricle and blood from the pulmonary veins to the right ventricle, to treat transposition of the great arteries . [ 2 ]
The lateral tunnel form of the Fontan procedure uses a baffle to redirect blood from the inferior vena cava to the pulmonary arteries . [ 3 ]
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Bagadilico , Basal Ganglia Disorders Linnaeus Consortium , is a research group in Lund , Sweden , and a Linnaeus environment, supported by the Swedish Research Council. The group comprises about 120 researchers at either Lund University or Lund University Hospital.
The name Bagadilico is an acronym formed using the two initial letters from the words Basal Ganglia Disorders Linnaeus Consortium.
The group's ultimate goal is to find new therapies for Parkinson's disease and Huntington's disease . These disorders have in common that they are caused by disturbances in the part of the brain called the basal ganglia . To achieve this goal, the group wants to establish and develop a strong, multidisciplinary research environment.
The program's ambition is to receive knowledge that improves the patients’ quality of life, through improved therapies and methods of diagnosis, and also improves the situation for the families.
Researchers from Lund University Medical Faculty, Faculty of Engineering, Cultural Sciences and Lund University Hospital make up the group. The aim of this collaboration is for new therapies to be made available to the patients more quickly, and for ethical and cultural aspects to be taken into consideration.
The medical part of the research focuses on cell transplantation, gene therapy and finding new drugs. New clinical trials where dopamine-producing cells will be transplanted into the brains of patients with Parkinson's disease are planned for 2010.
An important part of the program is acquiring knowledge of how therapies are best designed to benefit patients, their families and the society as a whole, and considering ethical and cultural aspects of progress in biomedical research.
Development of Restorative and Neuroprotective Treatment Strategies for Parkinsons Disease [1] The Neurobiology Unit aims at developing new restorative and neuroprotective treatments for neurodegenerative diseases using cell transplantation and direct in vivo gene delivery.
Neuronal Survival Unit [2] The Neuronal Survival Unit is focused on pathogenetic mechanisms and pharmacological treatment in cell and animal models of Parkinson's and Huntington's diseases.
Basal Ganglia Pathophysiology [3] The Basal Ganglia Pathophysiology team explores molecular and cellular plasticity in the basal ganglia after damage and/or pharmacological treatment.
Outcomes Research, Measurements and Evaluation in Parkinson's Disease [4] The research involves outcomes measures intended to reflect illness from the patients’ perspective, as well as clinical assessment tools. Ongoing work involves instruments tapping areas such as motor dysfunction, perceived health, distress, and functional status.
BRAINS Unit - Brain Repair and Imaging in Neural Systems [5] The BRAINS UNIT is focused on the development of new therapeutic strategies for neurodegenerative diseases. The research is a synthesis of mechanisms of repair in the brain and in vivo imaging at the systems level.
Nanobiotechnology and Lab-on-a-Chip [6] The research involves the Acoustic Trapping Project aimed at performing particle and cell trapping in a perfusion based microfluidics system. The technique will provide a platform for performing cellassays in a non-contact way using ultrasonic standing waves.
CNS Gene Therapy Research Group [7] The CNS Gene Therapy Team develop systems for sufficient and sustained expression of transgenes in the CNS. Gene transfer is used to express trophic factors or neurotransmitter-producing enzymes in animal models of neurodegenerative disease.
The Cultural Research Team [8] The Cultural Research Team looks at the cultural aspects on neurodegenerative disorders such as Parkinson's and Huntington's disease.
Translational Neuroendocrine Research Unit [9] The Translational Neuroendocrine Research Unit focuses on the neuropsychiatric Huntington's disease, and studies molecular mechanisms in the interface to depression, dementia and obesity.
Clinical Experimental Therapies in Neurodegenerative and Inflammatory Diseases [10] The projects aim at transferring preclinical results into a clinical experimental therapeutics programme in Parkinsons disease, and inflammatory disorders in the nervous system.
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Balanced anesthesia , also known as multimodal anesthesia (also spelt: anaesthesia ), is a technique used to induce and maintain anesthesia in patients undergoing surgery or certain medical procedures. This method employs a combination of anesthetic agents and other drugs – and techniques – to selectively target various aspects of the central nervous system , allowing for a tailored anesthetic experience based on the individual patient's needs and the specific requirements of the procedure. [ 1 ]
The specialist physician (in Canadian and American English : anesthesiologist ; in Commonwealth and British English : anaesthetist ) [ 2 ] or veterinarian evaluates various patient factors prior to selecting an anesthetic approach. These factors include major organ function, general condition, and compensatory capacity (ability to function despite stressors). In balanced anesthesia, appropriate agents are used in combination, at carefully-calibrated levels. [ 3 ] [ 4 ]
The concept of balanced anesthesia was first introduced by John Silas Lundy in 1926 [ 5 ] and has since become the predominant method of anesthesia in modern medical practice. [ 1 ]
The primary objectives of general anesthesia include inducing unconsciousness, providing analgesia , facilitating muscle relaxation, and the temporary suppression of motor reflexes . [ 6 ] Achieving muscle paralysis is often necessary for certain surgical procedures. Depending on the procedure to be undertaken, blocking transmission of nociception ( autonomic nervous system responses to noxious stimuli and its cardiac and hemodynamic effects – even in the absence of conscious pain perception), may be the aim of analgesia. Amnesia – induced through an altered state of consciousness – may be adequate or preferred over total unconsciousness. The physiological stability of the patient has to be maintained while all this is achieved. [ 1 ] [ 7 ] [ 8 ]
Balanced anesthesia is employed in a range of surgical procedures to optimize patient safety and comfort. [ 6 ] It is commonly used in major abdominal surgeries, such as bowel resections, liver surgery, and gastric bypass, where deep anesthesia and muscle relaxation are required. In cardiac surgery, balanced anesthesia facilitates precise control of heart rate and blood pressure, which is critical during these complex procedures. Additionally, orthopedic surgeries, including hip and knee replacements, utilize this approach to enhance muscle relaxation and pain management. Gynecological surgeries, such as hysterectomies and laparoscopic procedures, also benefit from balanced anesthesia to maintain patient stability and comfort throughout the operation. [ 1 ]
The scope of pharmacodynamics is the effects caused on the body by a medicine. The distribution of any pharmacologic agent, its concentration in tissues , blood or plasma , and its clearance from the body, are the pharmacokinetic features of a medicine. [ 9 ]
Unlike single-agent anesthesia, which can lead to increased adverse effects when higher doses of a single drug are administered, balanced anesthesia allows for the use of lower doses of multiple agents. This strategy minimizes the risk of side effects by enabling the anesthesiologist to target specific effects through the adjustment of individual agents. The pharmacodynamics of each agent—their effects on the body—can be finely controlled, while pharmacokinetics—how these agents are distributed and cleared from the body—plays a critical role in the effectiveness of the anesthesia. [ 8 ]
Injectable anesthetic agents may be administered by constant rate infusion (CRI) which is a portion of balanced anesthetic techniques, can be made like a single intermittent dose or as a single injection. [ 9 ] It should keep a during the time. Both the foreseeable pharmacodynamic effects and foreseeable concentration of plasma can be offered by the CRI of specific medicine. [ 9 ] It has similarity on keeping the invariable concentration of end-tidal by using the vaporous precise device, which can provide the volatile anesthetic . [ 9 ]
When the administration rate exceeds the clearance rate , a stable-state concentration has been achieved by delivering the medicine as a CRI. In addition, if the medicine has distributed fully at equilibrium in the body, which is called the volume of distribution at a stable state. [ 10 ] In case the loading dose was administered after the CRI, the time period of which will keep the concentration at a stable state equals 3 time constants or 5 terminal half-lives of the specific medicine. [ 11 ] The bolus dose can full with the volume of the medicine in an efficient and effective way so that the medicine can be cleared and delivered. This also can promote to achieve the stable state in a prompter approach. [ 9 ]
Administering a CRI has two important methods: targeting a specific infusion rate, and making the infusion rate constant.
Based on a 2010 review of injectable-agent use for short-duration anesthesia, the American Association of Equine Practitioners recommends the use of xylazine as a sedative for induction of anesthesia for durations of around 20 minutes or less. [ 12 ] In addition, diazepam and ketamine are recommended after the xylazine. [ 12 ] For longer duration anesthesia, those over 30 minutes, the most common anesthetics is the combination of guaifenesin , ketamine, and xylazine or isoflurane . [ 12 ]
The technique of balanced anesthetic has been applied widely with cats and dogs . [ failed verification ] [ 13 ]
When general anesthesia is used for cats and dogs, the most common method is inhalant agents because they are both easy to manage and the depth of anesthesia is predictable. The depth of anesthesia can be changed and recovered if some unexpected situation occurs during surgery. [ 13 ] Although inhaled anesthetics will cause an unconscious state in which cats and dogs will not recall or perceive pain, the depth of anesthesia may not prevent the variety of reflex reactions to harmful stimuli during the operation. [ 13 ] In order to prevent these reflex reactions, it may be required to increase the concentration of inhalant anesthetic agents; higher rates of inhalant administration are associated with higher cardiovascular and respiratory complications. Respiratory depression may result, [ 14 ] especially in young patients and those with preexisting systemic disease. This is associated with increased morbidity and mortality. [ 15 ]
With the balanced anesthetic technique, the low concentration of inhalant anesthetic agents and other medicines used during the operation can alter the perception of painful stimuli. In other words, using balanced anesthetic techniques for cats and dogs can decrease the morbidity and mortality effectively. [ 13 ] Therefore, in this situation, using balanced anesthetic techniques in cats and dogs is less risky for operation than using the general anesthesia. According to a report from a teaching hospital, the rate of complications resulting in death in cats and dogs using the balanced anesthesia are relatively low, at 1/9 and 1/233 respectively. [ 16 ]
Balanced anesthesia has various advantages in veterinary cases: In certain circumstances it is considerably cheaper than the usual anesthesia. Secondly, it can reduce the death rate. Furthermore, it offers more stable operating conditions for veterinarians . [ 17 ] It also increase animal safety and comfort. [ 18 ] Balanced anesthesia can make patients calm by using drugs such as: medetomidine , diazepam or midazolam , and acepromazine . [ 18 ] Keeping patients calm prior to surgery can avoid the unpredictable consequences of stress , such as tachypnea , hypertension and tachycardia which may be harmful to the anesthetized patients. [ 18 ] In addition, anxiety and stress may cause the nociceptive pain . [ 17 ] The balanced anesthesia therefore may therefore decrease those possible complications.
Another advantage of using balanced anesthesia is that it can decrease the chance of adverse effects . [ 18 ] All medicines may have adverse effect on patients; some serious adverse effects of anesthesia may be caused by inhalational anesthetic , although in general these medicines are highly safe and useful. [ 18 ] Using the correct amount of balanced anesthetic agents, the adverse effects can be reduced to some extent. [ 18 ]
Balanced anesthesia can also minimize the pain patients suffer. Pain may delay wound healing , decrease appetite, and even result in death. [ 17 ] Using the proper amount of analgesics can reduce the amount of inhalant anesthetics required and help patients reduce the pain. [ 18 ]
The quantity of a single anesthetic which is used for balanced techniques has similarity with that which is used for standing sedation. [ 9 ] However, compare to the doses used for TIVA (total intravenous anesthesia), which is always lower than using the single anesthetics. [ 9 ] The doses of anesthetics required differ, and depend on the required duration of anesthesia, the requirements for anesthesia to volatile, expected pain of injection of anesthesia, the experience the anesthetist using various medicines, and other factors. [ 9 ]
The pharmacokinetics of the two most common anesthetic agents, xylazine and ketamine, used during the surgical anasthesia are:
Xylazine is the most widely anesthetic agent used for short-duration operations in non-human animals. It does not have a medical use in humans.
Pharmacokinetics of xylazine may be influenced by anesthesia since after an intravenous therapy about 1.1 mg/kg, the half-life of xylazine will increase to 118 minutes and the clearance will decrease to 6 mL/kg/min. [ 19 ] Based on a recent study, if injecting the morphine , which is 0.1 or 0.2 mg/kg, in the vein at the same time can extend the terminal half-life to about 150 minutes and the clearance will not be influenced. [ 19 ]
Ketamine is the most widely anesthetic agent used for longer duration operations.
After an intravenous therapy, which is about 2.2 mg/kg, mixed with the 1.1 mg/kg xylazine the half-life of xylazine is approximately 66 minutes and the clearance is around 31 mL/kg/min when patients are halothane -anesthetized. [ 20 ] If only managing the xylazine and ketamine, the terminal half-life will be 42 minutes and its clearance will be 27 mL/kg/min. [ 20 ] When the CRI of ketamine is kept stable for an hour at 2.4 mg/kg/h, the terminal half-life will be 46 minutes and the clearance will be 32 mL/kg/min. [ 21 ]
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The Ballard Maturational Assessment , Ballard Score , or Ballard Scale , is a gestational age assessment technique. It was devised by Dr. Jeanne L. Ballard , professor emeritus of Pediatrics, Obstetrics and Gynecology at the University of Cincinnati College of Medicine . It was developed in 1979. [ 1 ]
The assessment scores various criteria, the sum of which is then extrapolated to the gestational age of the fetus . These criteria are divided into physical and neuromuscular criteria. This scoring allows for the estimation of age in the range of 26 weeks to 44 weeks. The New Ballard Score is an extension of the above to include extremely pre-term babies , i.e., up to 20 weeks.
The scoring relies on the intra-uterine changes the fetus undergoes during maturation. Whereas the neuromuscular criteria depend mainly upon muscle tone, the physical scale relies on anatomical changes. Neonate fetuses (less than 37 weeks of age) are in a state of physiological hypotonia , and, since muscle tone increases throughout the fetal growth period, it can be used to identify fetal maturation.
In the original Ballard Score, each of the criteria is scored from 0 – 5. The scores were then ranged 5 – 50, with the corresponding gestational ages being 26 weeks and 44 weeks. A score increase of 5 advances the estimated age by 2 weeks. The New Ballard Score allows scores of −1 for the criteria, hence making negative scores possible. The possible scores then range from −10 – 50 with the gestational range extending earlier to 20 weeks.
A simple formula to for age from the Ballard Score is
age = (2 * score + 120) / 5
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The ballistocardiograph ( BCG ) is a measure of ballistic forces generated by the heart. [ 1 ] The downward movement of blood through the descending aorta produces an upward recoil , moving the body upward with each heartbeat. [ 2 ] As different parts of the aorta expand and contract, the body continues to move downward and upward in a repeating pattern. [ 3 ] Ballistocardiography is a technique for producing a graphical representation of repetitive motions of the human body arising from the sudden ejection of blood into the great vessels with each heart beat. [ 4 ] It is a vital sign in the 1–20 Hz frequency range which is caused by the mechanical movement of the heart and can be recorded by noninvasive methods from the surface of the body . It was shown for the first time, after extensive research work by Isaac Starr , that the effect of main heart malfunctions can be identified by observing and analyzing the BCG signal. [ 5 ] Recent [ when? ] work also validates BCG could be monitored using camera in a non-contact manner. [ 6 ]
One example of the use of a BCG is a ballistocardiographic scale, which measures the recoil of the persons body who is on the scale. A BCG scale is able to show a person's heart rate as well as their weight. [ citation needed ]
The term ballistocardiograph originated from the Roman ballista , which is derived from the Greek word ballein (to throw), a machine for launching missiles, plus the Greek words for heart and writing. [ citation needed ]
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https://en.wikipedia.org/wiki/Ballistocardiography
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Balloon-occluded retrograde transvenous obliteration ( BRTO ) is an endovascular procedure used for the treatment of gastric varices . When performing the procedure, an interventional radiologist accesses blood vessels using a catheter, inflates a balloon (e.g. balloon occlusion) and injects a substance into the variceal blood vessels that causes blockage of those vessels. To prevent the flow of the agent out of the intended site (variceal blood vessels), a balloon is inflated during the procedure, which occludes.
BRTO is used for the treatment of bleeding from gastric varices. In addition to transjugular intrahepatic portosystemic shunt (TIPS), BRTO is a first line treatment for the prevention of recurrent bleeding from gastric varices (GOV2 or IGV1). [ 1 ] BRTO may be used for the treatment of ectopic varices. [ 1 ]
As BRTO results in a blockage of a portosystemic shunt, the procedure may result in increased portal hypertension, which may worsen esophageal varices or ascites. [ 2 ] [ 1 ]
BRTO was developed as a procedure in the early 1990s. [ 2 ] Initially, the procedure was performed using ethanolamine oleate as a sclerosant. [ 2 ] [ 3 ] Between 2006 and 2007, American physicians began using sodium tetradecyl sulfate (3% STS) as an alternative sclerosing agent. [ 2 ] [ 3 ]
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A balloon septostomy is the widening of the foramen ovale , a patent foramen ovale (PFO), or an atrial septal defect (ASD) via cardiac catheterization using a balloon catheter . This procedure allows for a greater amount of oxygenated blood to enter the systemic circulation in some cases of cyanotic congenital heart defect (CHD). [ citation needed ]
After the catheter is inserted, the deflated balloon catheter is passed from the right atrium through the foramen ovale, PFO, or ASD into the left atrium; it is then inflated and pulled back through to the right atrium, thereby enlarging the opening and allowing greater amounts of blood to pass through it. The resulting man-made opening is one of many forms of shunting , and is often referred to as an ASD.
This is normally a palliative procedure used to prepare a patient for, or sustain them until, a corrective surgery can be performed. At this time the ASD is closed using either sutures or a cardiac patch , depending on the size or nature of the opening. The procedure is often unsuccessful in infants and children older than one month because of a thickened septum. [ 1 ]
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Balthasar Gérard (alternative spellings Gerards or Gerardts ; c. 1557 – 14 July 1584) was the assassin of the Dutch revolt 's leader, William the Silent of the House of Orange (William the Silent, and later known as the "Father of the Fatherland"). He killed William the Silent in Delft on 10 July 1584, by shooting him twice with a pair of pistols, and was afterwards tried, convicted, tortured, and executed. Gérard was born in Franche-Comté (then belonging to Holy Roman Empire , afterwards to France ). He came from a Roman Catholic family with 11 children and was a great admirer of Philip II , king of Spain and the Netherlands. He studied law at the University of Dole . On 15 March 1580, King Philip had offered a reward of 25,000 crowns, peerage and an inheritable estate to anyone who killed or captured William the Silent, to whom he referred in his decree as a "pest on the whole of Christianity and the enemy of the human race." [ 1 ] [ 2 ]
After the reward offered by Philip was published, Gérard left for Luxembourg , where he learned that Juan de Jáuregui had already been preparing to attempt the assassination, but this attempt did not succeed. In March 1584 he went to Trier , where he put his plan before the regent of the Jesuits , but another Jesuit convinced him to change his original scheme and go to the prince of Parma . In Tournai , after holding counsel with a Franciscan , Father Gery, Gérard wrote a letter, a copy of which was deposited with the guardian of the convent , and the original presented personally to the Prince of Parma. In the letter Gérard wrote, in part, "The vassal ought always to prefer justice and the will of the king to his own life." [ 1 ]
At first the prince thought him unfit but after consulting Haultepenne and others with the letter he was assigned to Christoffel d'Assonleville, who spoke with Gérard, and asked him to put this in writing, which he did on 11 April 1584. He requested absolution from the prince of Parma "as he was about to keep company for some time with heretics and atheists, and in some sort to conform himself to their customs". [ 1 ]
For his first expenses he begged for 50 crowns, which were refused. "I will provide myself out of my own purse", Gérard told Assonleville, "and within six weeks you will hear of me." Assonleville responded: "Go forth, my son ... and if you succeed in your enterprise, the King will fulfill all his promises, and you will gain an immortal name besides." [ 1 ] On Sunday, 8 July 1584, Gérard loitered in the courtyard of the Prinsenhof examining the premises. A halberdier asked him why he was waiting there. He excused himself by saying that in his present shabby clothing and without new shoes he was unfit to join the congregation in the church opposite. The halberdier unsuspectingly arranged from the Prince of Orange himself a gift of 50 crowns for Gérard, who the following morning purchased a pair of pistols from a soldier, haggling the price for a long time because the soldier could not supply the particular chopped bullets or slugs he wanted. [ 1 ]
On 10 July 1584, as William the Silent climbed the stairs to the second floor, he was spoken to by the Welsh captain Roger Williams , who knelt before him. William put his hand on the bowed head of the old captain, at which moment Gérard jumped out of a dark corner. He drew his weapons and fired two shots at the stadtholder . William the Silent collapsed. His sister knelt beside him, but it was too late. The exact story surrounding the last moments before his death are lost to history, but according to legend he was asked whether he commended his soul to Christ, he answered in the affirmative. His last words were, Mon Dieu, ayez pitié de moi et de mon pauvre peuple ("My God, have mercy on me and on my poor people"). The contemporary consensus among Dutch historians is that William the Silent could not have said this, as he was most likely dead at the instant he was shot. However, his legendary final words remain a part of the Dutch historical canon.
Gérard fled through a side door and ran across a narrow lane, pursued by Roger Williams. Gérard had almost reached the ramparts, from which he intended to jump into the moat. On the other side a saddled horse stood ready. A pig's bladder around his waist was intended to help keep him afloat. However, he stumbled over a heap of rubbish. A servant and a halberdier of the prince who had raced after him caught him. When called a traitor by his captors, he is said to have replied, "I am no traitor; I am a loyal servant of my lord." "Which lord?", they asked. "Of my lord and master, the king of Spain". At the same time more pages and halberdiers of the prince appeared and dragged him back to the house under a rain of fists and beatings with the butt of a sword. Hearing his assailants chatter and convinced he heard the prince was still alive, he cried "Cursed be the hand that missed!" [ citation needed ]
The shooting is notable for being the first recorded political assassination of a head of state with a handheld firearm. [ 3 ] [ 4 ] After William the Silent's murder, more than 200 years would pass until another head of state was killed by a firearm, when Gustav III , King of Sweden , was fatally wounded at a midnight masquerade in 1792. [ 3 ]
At the house he immediately underwent a preliminary examination before the city magistrates . Upon being interrogated by the magistrates, he reportedly showed neither despair nor contrition, but rather a quiet exultation, stating: "Like David , he had slain Goliath of Gath ."
At his trial, Gérard was sentenced to be tortured and then executed, in a manner considered brutal even by the standards at the time. The magistrates decreed that the right hand of Gérard should be burned off with a red-hot iron, that his flesh should be torn from his bones with pincers in six different places, that he should be quartered and disemboweled alive, his heart torn from his bosom and flung in his face, and that, finally, his head should be taken off . [ 1 ]
Gérard's torture was extraordinarily brutal. On the first night of his imprisonment, Gérard was hung on a pole and lashed with a whip . Next, his wounds were smeared with honey and a goat was brought to lick the honey off his skin with its rough tongue. The goat, however, refused to touch his body. After several other forms of torture, he was left to pass the night with his hands and feet bound together , like a ball, so sleep would be difficult. During the following three days, he was repeatedly mocked and hung on a pole with his hands tied behind his back . Then, a weight of 300 metric pounds (150 kg) was attached to each of his big toes for half an hour.
Subsequently, Gérard was fitted with shoes made of well-oiled, uncured dog skin; the shoes were two fingers shorter than his feet. In this state, he was put before a fire. When the shoes warmed up, they contracted, crushing the feet inside them to stumps. When the shoes were removed, his half-broiled skin was torn off. After his feet were damaged, his armpits were branded. He was then dressed in a shirt soaked in alcohol. Lastly, burning bacon fat was poured over him and sharp nails were stuck between the flesh and the nails of his hands and feet. On 14 July, four days after the assassination, the sentence declared at the trial was carried out and Gérard was tortured and executed in the market square of Delft. His severed head was then displayed on a pike behind the Prinsenhof , [ 5 ] and his arms and legs displayed on four gates of the city. [ 6 ]
Philip II gave Gérard's parents, instead of the reward of 25,000 crowns, three country estates in Lievremont, Hostal, and Dampmartin in the Franche-Comté , and the family was raised to the peerage . Philip II would later offer the estates to Philip William , Orange's son and the next Prince of Orange, provided the prince continue to pay a fixed portion of the rents to the family of his father's murderer; the insulting offer was rejected. The estates remained with the Gérard family. The apostolic vicar Sasbout Vosmeer tried to have Gérard canonized , to which end he removed the dead man's head and showed it to church officials in Rome, but the idea was rejected.
The village of Vuillafans renamed the street where Gérard was born "Rue Gérard" in his memory.
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The Baly Medal is a biennial award awarded by the Royal College of Physicians of London.
Founded by a gift from Frederick Daniel Dyster (1809?–93) received in 1866, confirmed by deed 1930 – in memory of William Baly : £400 to provide a gold medal for the person deemed to have most distinguished himself in the science of physiology , especially during the previous two years. The award is made every alternate year on the recommendation of the President and Council at the Quarterly Meeting in July and presented on the occasion of the Harveian Oration .
Source 1871–1911 RCP Archived 2017-10-22 at the Wayback Machine
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The Band of Parents is a 501(c)(3) nonprofit organization . Formed in July 2007 and incorporated in October 2007, it was founded by approximately 100 parents of young children with neuroblastoma who were treated at Memorial Sloan Kettering Cancer Center (MSKCC). Its purpose is to fund the development of new therapies for neuroblastoma that would not otherwise be pursued by research institutions or the pharmaceutical industry . The organization has become the largest single funder of neuroblastoma research at MSKCC. [ 1 ] [ 2 ] [ 3 ] [ 4 ] [ 5 ] [ 6 ]
Neuroblastoma is a form of childhood cancer that can develop at any age but typically presents between the ages of 18 months and five years. It affects a little over 600 children per year in the United States . Most are diagnosed with stage IV disease, the most advanced form. Even with aggressive therapy, stage IV neuroblastoma carries a poor prognosis , with a three-year survival rate of 30–40%. [ 7 ]
Compared with other types of cancer , neuroblastoma is rare. Scientific advances have allowed the development of individualized treatments, with techniques such as immunotherapy being targeted to specific kinds of cancer. However, because of the rising cost of drug development, which is approaching $1 billion, pharmaceutical companies are not likely to develop drugs that are specific to neuroblastoma or other rare disorders. [ citation needed ]
The Band of Parents' first project was the development of a humanized antibody , Hu3F8.
In addition to surgery , chemotherapy and radiation , many neuroblastoma patients at MSKCC were treated with a murine (mouse-derived) monoclonal antibody called 3F8 . Given intravenously , 3F8 binds specifically to neuroblastoma cells and triggers an immune response , which destroys the cancerous cells. Because the antibody also binds to peripheral nerve cells , the treatment is painful, but it is generally without long-term complications. However, its use is limited by the body's eventual development of human anti-murine antibody, which neutralizes the effects. The Band of Parents raised $2–$3 million to fund the genetic engineering of the murine cell line that produces 3F8 so that it would produce a new antibody, Hu3F8, using human genes. Hu3F8 has the same benefits as 3F8, but because it is 98% human, it does not cause a neutralizing immune response. In theory, this should allow patients to be treated with it indefinitely. [ 8 ]
In March 2013, the Band of Parents led a group of nonprofit organizations in providing a $2 million grant to MSKCC to fund the development of a bispecific monoclonal antibody targeting neuroblastoma. [ 1 ]
The organization's other projects have included the Loneliest Road Campaign, [ 9 ] a 3,000-mile, 19-day bicycle ride across the US by six fathers of children in active treatment; a bake sale with cookies made by the children, their families and supporters; [ 10 ] and The BoP Shop, an online store featuring artwork by children with neuroblastoma.
In 2012, the Band of Parents began an annual gala event called the Evening of Hope, which has become its primary fundraiser. [ 11 ]
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The Bangladesh Medical and Dental Council ( BMDC ) is the professional regulatory body that monitors the practice of medicine in Bangladesh. It was formed under the Bangladesh Medical Council Act. The act was made in 1973, hence it is also called 1973 Act of Bangladesh Medical Council. [ 1 ] The act of 1973 was repealed in 1980 & Bangladesh Medical & Dental Council Act was passed by the parliament on 9 April 1980.
It is located in the capital of Bangladesh , Dhaka in 203, Shaheed Sayed Nazrul Islam Sarani (86, Bijoy Nagar). Its function is to give registration to MBBS & BDS doctors to practice medicine and dentistry in Bangladesh. It maintains the official register of medical practitioners, dental practitioner, and medical assistant practitioner within Bangladesh. Its chief responsibility is to "protect, promote and maintain the health and safety of the public" by controlling entry to the register, and suspending or removing members when necessary. It also sets the standards for medical colleges in Bangladesh. Unregistered, suspended or removed members are not allowed to practice medicine in Bangladesh. [ 1 ]
The Bangladesh Medical and Dental Council is the regulatory authority and the custodian of medical and dental education in Bangladesh . [ 1 ]
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A Bankart repair is an operation for habitual anterior shoulder dislocation . [ 1 ] The joint capsule is sewed to the detached glenoid labrum , without duplication of the subscapularis tendon .
The procedure is named for the Bankart lesion , a common name for the condition it addresses. The condition was named for British surgeon Arthur Sydney Blundell Bankart , who first described it in the British Medical Journal in 1923. [ 2 ]
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The Banting Medal , officially the Banting Medal for Scientific Achievement , is an annual award conferred by the American Diabetes Association (ADA), which is the highest award of ADA. Inaugurated in 1941, the prize is given in memory of Sir Frederick Banting , [ 1 ] a key discoverer of insulin and its therapeutic use. [ 1 ] [ 2 ]
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Bar code medication administration ( BCMA ) is a barcode system designed by Glenna Sue Kinnick to prevent medication errors in healthcare settings and to improve the quality and safety of medication administration. The overall goals of BCMA are to improve accuracy, prevent errors, and generate online records of medication administration.
BCMA was first implemented in 1995 [ 1 ] at the Colmery-O'Neil Veteran Medical Center in Topeka , Kansas, US. It was created by a nurse who was inspired by a car rental service using bar code technology. From 1999 to 2001, the Department of Veterans Affairs promoted the system to 161 facilities. [ 2 ] Cummings and others recommend the BCMA system for its reduction of errors. They suggest healthcare settings to consider the system first while they are waiting for radiofrequency identification (RFID). They also pointed out that adopting the system takes a careful plan and a deep change in work patterns. [ 3 ] As of the year 2004, hospitals were mandated by the federal government to start using BCMA for all prescription drugs. [ 4 ]
It consists of a bar code reader , a portable or desktop computer with wireless connection, a computer server, and some software. When a nurse gives medication to a patient in a healthcare setting, the nurse can scan the barcode on the patient's wristband on the patient to verify the patient's identity. The nurse can then scan the bar code on medication and use software to verify that he/she is administering the right medication to the right patient at the right dose, through the right route, and at the right time ("five rights of medication administration"). [ 5 ] Bar code medication administration was designed as an additional check to aid the nurse in administering medications; however, it cannot replace the expertise and professional judgment of the nurse. The implementation of BCMA has shown a decrease in medication administration errors in the healthcare setting. [ 6 ]
Bar codes on medication have federal government guidelines that are reflected within the bar code packaging. [ 7 ] The first few digits are used to identify the labeler , this code is issued by the Food and Drug Administration . The next section of the label contains the product code , known as the medication, and the last section of the bar code label lists the packager's code for the medication. [ 8 ]
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Baralyme is a mixture of 80% calcium hydroxide and 20% barium hydroxide compounds [ 1 ] [ 2 ] [ 3 ] that is used as an alternative to soda lime to absorb the exhaled carbon dioxide in a closed circuit anesthetic system. [ 4 ]
The substance has been used for carbon dioxide scrubbing in diving bells and the U.S Navy's engineered SEALAB 's I, II, and the failed SEALAB III. [ citation needed ]
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A barbed broach is a hand-operated endodontic tool used to remove the pulp tissue during root canal treatments. They have been in widespread use at least since the early 1900s, and their introduction allowed dentists to remove tissue from much smaller root canals than before. [ 1 ]
Barbed broaches are made from stainless steel with a plastic handle and tapered, round, soft iron wires, and the smooth surface is notched to form barbs. These barbs are designed to entangle the tissue so it can be removed intact from the canal wall. [ 2 ] Shorter barbed broaches were also used as of the early 1900s to file down canal walls. [ 3 ] Related are smooth broaches; originally used to dress or to wrap cotton to dry the root canal, they have since found broader use as pathfinders into the canal. [ 1 ] Often thinner than barbed broaches and sometimes made of carbon steel , they are less prone to collapsing in fine canals. [ 4 ] Hybrids of smooth and barbed broaches called "apex broaches" were also in use, with varying handle lengths. [ 1 ]
Barbed broaches were pioneered by Edward Maynard in the mid-1800s. When Maynard demonstrated their use in St. Petersburg in 1845, using a watch spring filed down to a hair's thickness, Czar Nicholas was so impressed that he offered to appoint Maynard as Actual Dentist to His Imperial Majesty. Maynard declined. [ 5 ]
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The barber surgeon was one of the most common European medical practitioners of the Middle Ages , generally charged with caring for soldiers during and after battle. In this era, surgery was seldom conducted by physicians. Instead, barbers , who possessed razors and dexterity, were responsible for tasks ranging from cutting hair to pulling teeth to amputating limbs.
In this period, surgical mortality was very high due to blood loss, shock and infection. Yet, since doctors thought that bloodletting to balance "humours" would improve health, barbers also used bloodletting razors and applied leeches . Meanwhile, physicians considered themselves to be above surgery. [ 1 ] Physicians mostly observed during surgery and offered consulting, but otherwise often chose academia or working in universities.
Due to religious and sanitary monastic regulations, monks had to maintain their tonsure (the traditional baldness on the top of the head of Catholic monks). This created a market for barbers, because each monastery had to train or hire a barber. They would perform bloodletting and minor surgeries, pull teeth and prepare ointments. The first barber surgeons to be recognized as such worked in monasteries around AD 1000. [ 1 ]
Because physicians performed surgery so rarely, the Middle Ages saw a proliferation of barbers, among other medical "paraprofessionals", including cataract couchers , herniotomists , lithotomists , midwives , and pig gelders [ broken anchor ] . In 1254, Bruno da Longobucco, an Italian physician who wrote about surgery, expressed concern about barbers performing phlebotomies and scarifications . [ 1 ]
In 16th century Paris , barber-surgery was divided into two categories: "Surgeons of the Short Robe" and "Surgeons of the Long Robe." [ 2 ] "Surgeons of the Long Robe", a qualification offered in institutions such as the College of St. Cosme, required students to take a formal exam. [ 3 ] This was opposed to "Surgeons of the Short Robe", who did not need to take an exam to qualify [ 2 ] and, alongside barbering, would perform minor surgical procedures. [ 3 ] However, despite the different education requirements, both types of surgeons were called "barber-surgeons". [ 2 ] This distinction between "short coat" and "long coat" continued in surgery until relatively recently [ 4 ] Eventually, in 1660, the barber surgeons recognized the physicians' dominance. [ 1 ]
From the 1540s in France, the translation into French of the works of ancient authors allowed progress in the transmission of knowledge: barber-surgeons could add to their manual skills, and ancient surgical knowledge could be conformed to actual practice. [ 5 ]
"If you want a servant to follow your orders, you can't give them in an unknown tongue."
New problems arose in war surgery, without equivalents in the past: wounds caused by firearms and mutilations caused by artillery . The barber-surgeon was required to treat all the effects on the surface of the body, the doctor treating those on the inside. [ 7 ]
There was already social mobility between surgeons and barber-surgeons. A surgeon's apprenticeship began with the practice of shaving. The young surgeon could thus have a source of income before mastering the surgery of his time. In the context of Renaissance humanism, this practical experience took place outside of academic scholasticism. The action is clearly sanctioned by the results, visible to all. For Michel de Montaigne , compared to medicine:
“Surgery seems to me much more certain, because it sees and handles what it does; there is less to conjecture and guess.” [ 8 ]
In Italy, barbers were not as common. The Salerno medical school trained physicians to be competent surgeons, as did the schools in Bologna and Padua. In Florence, physicians and surgeons were separate, but the Florentine Statute concerning the Art of Physicians and Pharmacists in 1349 gave barbers an inferior legal status compared to surgeons. [ 1 ]
Surgical practices in the Iberian Peninsula date back to the Megalithic era (2000 BC), with evidence of trepanation . Until the Renaissance, Spanish surgery followed Greek, Arab, and medieval traditions, with significant progress in the 16th century through anatomical studies. Despite this, military, naval, and barber-surgeons performed operations, as physicians distanced themselves from surgery. A royal decree regulated barber-surgeons in Spain . [ 9 ] There were active barber surgeons operating in Valencia in the 15th century. [ 10 ] One notable practitioner was Antonio Fernando de Medrano , a professional barber surgeon active in Madrid during the 17th century. [ 11 ]
The establishment of surgical chairs in Spanish universities in the late 16th century gave surgery social and academic recognition, but a standardized system emerged only in the 18th century with the Reales Colegios de Cirugía (Royal Colleges of Surgeons), founded by military surgeons. [ 12 ] The first institutions in Cádiz (1748) and Barcelona (1764), led by Virgili, were followed by Madrid (1780), founded by Antoni de Gimbernat . These colleges formally integrated surgery into medical education, solidifying its scientific status. [ 9 ]
Formal recognition of surgeons' skills (in England at least) goes back to 1540, [ 13 ] when the Fellowship of Surgeons (who existed as a distinct profession but were not "Doctors/Physicians" for reasons including that, as a trade, they were trained by apprenticeship rather than academically) merged with the Company of Barbers , a London livery company , to form the Company of Barber-Surgeons . However, the trade was gradually put under pressure by the medical profession and in 1745, the surgeons split from the Barbers' Company (which still exists) to form the Company of Surgeons . In 1800 a royal charter was granted to this company and the Royal College of Surgeons in London came into being. Later it was renamed to cover all of England—equivalent colleges exist for Scotland and Ireland as well as many of the old UK colonies (e.g., Canada ). [ 14 ]
There are few studies on barber surgeons in Finland . The first known account is that of Hinzikinus from 1324 to 1326, originating from Turku , a city in the southern region of the country, who provided medical preparation and wound care for Viceroy Matts Kettilmundson. The second barber surgeon documented was Henrik Bardskärare, who worked in the castle of Vyborg in Finland (currently a part of Russia ). Each company of 400–500 men in the Swedish Army was assigned a barber during the rule of King Gustav I Vasa in the 16th century. A barber surgeon was available to tend to the injured in almost every division. In 1571, the barbers organized into a professional guild that governed their training, jobs, pay, and the number of barbers. Barbers from other countries could join the guild as well. The guild mandated that barber surgeons receive their training from established masters as apprentices, and in order to receive their degrees, the apprentices had to pass an exam. The guild provided guidelines for the barber surgeons' fees or pay, which varied and occasionally depended on how many patients were treated and surgeries were carried out. [ 15 ]
Few traces of barbers' links with the surgical side of the medical profession remain. One is the traditional red and white barber's pole , or a modified instrument from a blacksmith, which is said to represent the blood and bandages associated with their historical role.
In the United Kingdom, Ireland, Australia, New Zealand, and South Africa, another vestige is the use of the titles Mr , Ms , Mrs , or Miss rather than Dr by physicians when they complete their surgery qualifications by, for example, the award of an MRCS or FRCS diploma. [ 16 ] This practice dates back to the days when surgeons were not required to obtain a university education in medicine, and is retained despite the fact that all surgeons in these countries
must earn a medical degree and spend additional years in surgical training and certification. [ 17 ]
Media related to Barber surgeons at Wikimedia Commons
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A bare-metal stent is a stent made of thin, uncoated (bare) metal wire that has been formed into a mesh-like tube. The first stents licensed for use in cardiac arteries were bare metal – often 316L stainless steel. More recent "second generation" bare-metal stents have been made of cobalt chromium alloy. [ 1 ] While plastic stents were first used to treat gastrointestinal conditions of the esophagus, gastroduodenum, biliary ducts, and colon, bare-metal stent advancements led to their use for these conditions starting in the 1990s. [ 2 ]
Drug-eluting stents are often preferred over bare-metal stents because the latter carry a higher risk of restenosis , the growth of tissue into the stent resulting in vessel narrowing. [ 3 ]
This medical treatment –related article is a stub . You can help Wikipedia by expanding it .
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Bariatric surgery (also known as metabolic surgery or weight loss surgery ) is a surgical procedure used to manage obesity and obesity-related conditions. [ 1 ] [ 2 ] Long term weight loss with bariatric surgery may be achieved through alteration of gut hormones, physical reduction of stomach size ( stomach reduction surgery ), [ 3 ] reduction of nutrient absorption, or a combination of these. [ 2 ] [ 4 ] Standard of care procedures include Roux en-Y bypass , sleeve gastrectomy , and biliopancreatic diversion with duodenal switch , from which weight loss is largely achieved by altering gut hormone levels responsible for hunger and satiety, leading to a new hormonal weight set point . [ 4 ]
In morbidly obese people, bariatric surgery is the most effective treatment for weight loss and reducing complications. [ 5 ] [ 6 ] [ 7 ] [ 8 ] [ 9 ] A 2021 meta-analysis found that bariatric surgery was associated with reduction in all-cause mortality among obese adults with or without type 2 diabetes . [ 10 ] This meta-analysis also found that median life-expectancy was 9.3 years longer for obese adults with diabetes who received bariatric surgery as compared to routine (non-surgical) care, whereas the life expectancy gain was 5.1 years longer for obese adults without diabetes. [ 10 ] The risk of death in the period following surgery is less than 1 in 1,000. [ 11 ] Bariatric surgery may also lower disease risk, including improvement in cardiovascular disease risk factors , fatty liver disease , and diabetes management. [ 12 ]
Stomach reduction surgery is frequently used for cases where traditional weight loss approaches, consisting of diet and physical activity, have proven insufficient, or when obesity already significantly affects well-being and general health. [ 3 ] [ 13 ] The weight-loss procedure involves reducing food intake. Some individuals might suppress bodily functions to reduce the absorption of carbohydrates , fats, calories , and proteins . The outcome is a significant reduction in BMI . [ 3 ] The efficacy of stomach reduction surgery varies depending on the specific type of procedure. [ 13 ] There are two primary divisions of surgery, specifically gastric sleeve surgery and gastric bypass surgery. [ 3 ]
As of October 2022, [update] the American Society of Metabolic and Bariatric Surgery and International Federation for the Surgery of Obesity recommended consideration of bariatric surgery for adults meeting two specific criteria: people with a body mass index (BMI) of more than 35 whether or not they have an obesity-associated condition, and people with a BMI of 30–35 who have metabolic syndrome . [ 12 ] [ 14 ] However, these designated BMI ranges do not hold the same meaning in particular populations, such as among Asian individuals, for whom bariatric surgery may be considered when a BMI is more than 27.5. [ 12 ] Similarly, the American Academy of Pediatrics recommends bariatric surgery for adolescents 13 and older with a BMI greater than 120% of the 95th percentile for age and sex. [ 15 ]
Bariatric surgery has proven to be the most effective obesity treatment option for enduring weight loss. [ 16 ] Along with this weight reduction, the procedure reduces risk of cardiovascular diseases, type 2 diabetes, fatty liver disease, depression syndromes, among others. [ 17 ] While often effective, numerous barriers to shared decision making between the medical provider and person affected include lack of insurance coverage or understanding how it functions, a lack of knowledge about procedures, conflicts with organizational priorities and care coordination , and tools supporting people who need the surgery. [ 18 ]
Historically, eligibility for bariatric surgery was defined as a BMI greater than 40, or a BMI more than 35 with an obesity-associated comorbidity, as based on the 1991 NIH Consensus Statement. [ 12 ] In the three decades that followed, obesity rates continued to rise, laparoscopic surgical techniques made the procedure safer, and high-quality research showed effectiveness at improving health among various conditions. [ 14 ] In October 2022, ASMBS/IFSO revised the eligibility criteria, which include all adult patients with a BMI greater than 35, and those with a BMI more than 30 with metabolic syndrome . [ 14 ] However, BMI is a limited measurement, for which factors such as ethnicity are not used in the BMI calculation. Eligibility criteria for bariatric surgery are modified for people who identify as a part of the Asian population with a BMI of more than 27.5. [ 12 ]
Stomach reduction surgeries were highly recommended for patients who meet these criteria: BMI>40 (type 3 obesity), BMI>35 (type 2 obesity), with specific comorbid conditions such as type 2 diabetes , hypertension , dyslipidemia , etc. [ 19 ]
As of 2019, [update] the American Academy of Pediatrics recommended bariatric surgery without age-based eligibility limits under the following indications: BMI more than 35 with severe comorbidity, such as obstructive sleep apnea (Apnea-Hypopnea Index above 0.5), type 2 diabetes, idiopathic intracranial hypertension , nonalcoholic steatohepatitis , Blount disease , slipped capital femoral epiphysis , gastroesophageal reflux disease , and idiopathic hypertension or a BMI above 40 without comorbidities. [ 20 ] Surgery is contraindicated with a medically correctable cause of obesity, substance abuse, concurrent or planned pregnancy, eating disorder , or inability to adhere to postoperative recommendations and mandatory lifestyle changes. [ 20 ]
When counseling a patient on bariatric procedures, providers take an interdisciplinary approach. Psychiatric screening is also critical for determining postoperative success. [ 21 ] [ 22 ] People with a BMI of 40 or greater have a 5-fold risk of depression, and half of bariatric surgery candidates are depressed. [ 21 ] [ 22 ] Among bariatric surgery candidates and those who undergo bariatric surgery, mental health-related conditions including anxiety disorders , eating disorders , and substance use are also more commonly reported. [ 23 ]
Elderly patients will face higher postoperative complications due to frailty of elderly patients. The adolescents who performed stomach reduction surgery showed better results and there is no negative impact on linear/ puberty growth. [ 19 ]
Stomach reduction surgery is not suitable for people with the following conditions:
In adults, malabsorptive procedures lead to more weight loss than restrictive procedures, but they have a higher risk profile. [ 26 ] Gastric banding is the least invasive, so it may offer fewer complications, while gastric bypass may offer the highest initial and most sustainable weight loss. [ 26 ] A single protocol is not superior to the other. In one 2019 systematic review, estimated weight loss (EWL) for each surgical protocol is as follows: 56.7% for gastric bypass, 45.9% for gastric banding, 74.1% for biliopancreatic bypass +/- duodenal switch and 58.3% for sleeve gastrectomy. [ 27 ] Most patients do remain obese (BMI 25-35) following surgery despite significant weight loss, and patients with BMI over 40 tended to lose more weight than those with BMI under 40. [ 28 ] [ 29 ]
Concerning metabolic syndrome , bariatric surgery patients were able to achieve remission 2.4 times as often as those who underwent nonsurgical treatment. [ 29 ] [ 28 ] No significant difference was noted for changes in cholesterol, or LDL, but HDL did increase in the surgical groups, and reduction in blood pressure was variable between studies. [ 29 ] [ 28 ]
Studies of bariatric surgery for type 2 diabetes ( T2DM ) within the obese population show that 58% prioritize the improvement of diabetes, while 33% pursued surgery for weight loss alone. [ 30 ] While weight loss is essential in T2DM management, sustaining improvements long-term is challenging; 50% to 90% of people struggle to achieve adequate diabetes control, suggesting the need for alternative interventions. [ 31 ] In this context, studies have reported an 85–90% resolution of T2DM after bariatric surgery, measured by reductions in fasting plasma glucose and HbA1C levels, and remission rates of up to 74% two years post-surgery. [ 31 ] [ 32 ] Bariatric surgery is considered for individuals with new-onset T2DM and obesity, although the level of improvement may be slightly less. [ 29 ]
The relative risk reductions associated with bariatric surgery are 61%, 64%, and 77% for the development of T2DM, hypertension, and dyslipidemia, respectively, highlighting the efficacy of bariatric surgery in prevention as well as resolution of chronic obesity. [ 29 ] Predictors for post-operative diabetes resolution include the current method of diabetes control, adequate blood sugar control, age, duration of diabetes, and waist circumference. [ 30 ]
Bariatric surgery likewise plays a role in the reduction of medication use. [ 29 ] During postoperative follow-up, 76% of people discontinued the use of insulin, while 62% no longer required T2DM medications at all. [ 29 ]
A 2021 meta-analysis found that bariatric surgery was associated with 59% and 30% reductions in all-cause mortality among obese adults with or without type 2 diabetes respectively. [ 10 ] It also found that median life expectancy was 9 years longer for obese adults with diabetes who received bariatric surgery as compared to routine (non-surgical) care, whereas the life expectancy gain was 5 years longer for obese adults without diabetes. [ 10 ] The overall cancer risk in bariatric surgery patients was decreased by 44%, especially in colorectal, endometrial, breast, and ovarian cancer. [ 33 ] Improvements in cardiovascular health are the most well-described changes after bariatric surgery, with notable reductions in the incidence of stroke (except in patients with T2DM), heart attack, atrial fibrillation, all-cause cardiovascular mortality, and ischemic heart disease. [ 33 ] [ 29 ]
Bariatric surgery in older patients is a safety concern; the relative benefits and risks in this population are not known. [ 34 ]
In 2017, the American Society for Metabolic and Bariatric Surgery stated that it was not clear whether medical weight-loss treatments or bariatric surgery affected subsequent treatments for infertility in both men and women. [ 35 ]
Bariatric surgery reduces the risk of gestational diabetes and hypertensive disorders of pregnancy in women who later become pregnant, but increases the risks of preterm birth and maternal anemia . [ 33 ] [ 36 ] A 2021 systematic review found that post-bariatric surgery normalized hormonal levels and menstrual cycles, and improved fertility, with no increased short-term risk of miscarriages or congenital malformations. [ 37 ]
For women with polycystic ovary syndrome , post-operatively there tends to be a reduction in menstrual irregularity, hirsutism , infertility, and the overall prevalence of polycystic ovary syndrome is reduced by bariatric surgery at 12 and 23 months. [ 33 ]
Among people seeking bariatric surgery, pre-operative mental health disorders are commonly reported. [ 38 ] [ 23 ] Some studies indicate that psychological health can improve after bariatric surgery, due in part to improved body image, self-esteem, and change in self-concept; these findings were found in children (see Considerations in adolescent patients below). [ 39 ] Bariatric surgery has consistently been associated with postoperative decreases in depression symptoms and reduced severity. [ 39 ]
Weight loss surgery in adults is associated with an elevated risk of complications compared to nonsurgical treatments for obesity. [ 40 ] [ 41 ] Complications can be separated into 2 stages, early complication (within 30 days after surgeries) and late complications (after 30 days). [ 42 ]
The overall risk of mortality is low in bariatric surgery at 0 to .01%. Severe complications, such as gastric perforation or necrosis, have been significantly reduced by improved surgical experience and training. Bariatric surgery morbidity is also low at 5%. [ 26 ] [ 29 ] [ 33 ] In fact, several studies have reported a reduced overall long-term all-cause mortality compared to controls. [ 26 ] [ 29 ] [ 33 ] However, obese populations maintain an elevated risk of disease and mortality compared to the general population even after surgery, therefore elevated mortality after surgery may be related to the ongoing complications of existing obesity-related disease. [ 26 ] [ 29 ] [ 33 ]
The percentage of procedures requiring reoperations due to complications was 8% for adjustable gastric banding , 6% after Roux-en-Y gastric bypass , 1% for sleeve gastrectomy , and 5% after biliopancreatic diversion. [ 28 ] Over a 10-year study while using a common data model to allow for comparisons, 9% of patients who received a sleeve gastrectomy required some form of reoperation within 5 years compared to 12% of patients who received a Roux-en-Y gastric bypass. Both of the effects were fewer than those reported with adjustable gastric banding. [ 43 ]
Laparoscopic bariatric surgery requires an average hospital stay of 2–5 days, barring potential complications. [ 44 ] Minimally invasive procedures (i.e. adjustable gastric band ) tend to have less complications than open procedures (i.e. Roux-en-Y ). [ 26 ] [ 33 ] Similar to other surgical procedures, there is a risk of atelectasis (collapse of small airways) and pleural effusion (fluid buildup in lungs), and pneumonia which tends to be less associated with minimally invasive procedures. [ 26 ] [ 33 ]
Complications specific to the laparoscopic gastric band procedure include esophageal perforation from the advancement of the calibration probe, gastric perforation from the creation of a retrograde gastric tunnel, esophageal dilation, and acute dilation of the gastric pouch due to malpositioning of the gastric band. [ 26 ] Gastric band malpositioning can be devastating, leading to gastric prolapse, overdistention, and resultingly, gastric ischemia and necrosis. [ 26 ] Erosion and migration of the band may also occur post-operatively, in which case, if over 50% of the circumference of the band migrates, then surgical repositioning is necessary. [ 26 ]
Risks of Roux-en-Y gastric bypass include anastomotic stenosis (narrowing of the intestine where the two segments are rejoined), bleeding, leaks, fistula formation, ulcers (ulcers near the rejoined segment), internal hernia, small bowel obstruction , kidney stones, and gallstones. [ 26 ] Bowel obstruction tends to be more difficult to diagnose in post-bariatric surgery patients due to their reduced ability to vomit; symptoms mainly involve abdominal pain and are intermittent due to twisting and untwisting of the intestinal mesentery . [ 26 ]
Sleeve gastrectomy also carries a small risk of stenosis, staple line leak, stricture formation, leaks, fistula formation, bleeding, and gastro-esophageal reflux disease (also known as GERD or heartburn). [ 17 ] [ 26 ]
Deficiencies of micronutrients like iron (15%), vitamin D, vitamin B12, fat-soluble vitamins, thiamine, and folate are common after bariatric procedures. [ 26 ] [ 28 ] Such deficiencies are potentiated by alterations in absorption and lack of appetite and often require supplementation. Notably, chronic vitamin D deficiency may contribute to osteoporosis ; insufficiency fractures, especially of the upper extremity, are of higher incidence in bariatric surgery patients. [ 26 ] [ 33 ] Sleeve gastrectomy leads to fewer long-term vitamin deficiencies compared to gastric banding.
Early complication: Bleeding is present in approximately 5% of cases of sleeve gastrectomy. Symptoms can vary widely, ranging from gastrointestinal bleeding to internal bleeding. Venous thromboembolism (VTE) may occur, causing a decrease in flow through the splenic system, potentially leading to system collapse or death. [ 42 ]
Late complications: They include gastric stenosis , nutrient deficiencies , and Gastroesophageal reflux disease. For gastric stenosis, the symptoms are food intolerance and vomiting. [ 42 ] For the gastroesophageal reflux disease , which due to post-surgery changes of reduced lower esophageal sphincter tension and increased intragastric pressure. Patients may suffer from heartburn after eating or upper abdominal pain . [ 45 ]
An early complication of Roux-En-Y Gastric Bypass: Small bowel obstruction , which can be caused by the internal hernias due to the laparoscopic RYGB surgery techniques that were used. And it is life-threatening to patients since it is hard to diagnose through clinical or radiographic imaging. [ 46 ] The symptoms included vomiting, abdominal pain and peritonitis . Common complications such as internal gastrointestinal hemorrhage (bleeding) and staple line leakage occur in both surgeries. [ 46 ]
Late complication: For the anastomotic stricture, [ 47 ] there is a 2.9%-23% chance for patients to experience gastrojejunal anastomosis . [ 46 ] This complication more often occurs in the laparoscopic era than open RYGB surgery. Symptoms such as difficulty swallowing and vomiting . [ 46 ]
The most common complication, especially after sleeve gastrectomy, is GERD, which may occur in up to 25% of cases. [ 48 ] Dumping syndrome (rapid emptying of undigested stomach contents) is another common complication of bariatric surgery, especially after Roux-en-Y, which is further classified into early and late dumping syndrome. [ 48 ] Dumping syndrome in some cases may be associated with more efficient weight loss, however, it can be uncomfortable. [ 48 ] Symptoms of dumping syndrome include nausea, diarrhea, painful abdominal cramps, bloating, and autonomic symptoms such as tachycardia, palpitations, flushing, and sweating. [ 48 ] Early dumping syndrome (emptying within 1 hour of eating) is also associated with a rapid drop in blood pressure, which may cause fainting. [ 48 ] Late dumping syndrome is characterized by low blood sugar 1–3 hours after a meal, presenting with palpitations, tremors, sweating, a feeling of faintness, and irritability. [ 48 ] Dumping syndrome is best mitigated by consuming small meals and avoiding high carb or high-fat foods. [ 48 ]
Rapid weight loss after obesity surgery can contribute to the development of gallstones , especially at 6 and 18 months. [ 26 ] [ 28 ] Estimates for prevalence of symptomatic gallstones after Roux-En-Y gastric bypass range from 3–13%. [ 17 ] The risk of gallstones following bariatric surgery has shown to be higher among those of the female sex. [ 49 ]
Kidney stones are common after Roux-En-Y gastric bypass, with estimates of prevalence ranging from 7-11%. [ 17 ] All surgical modalities are associated with a significant increase in the risk of kidney stones compared to nonsurgical weight loss treatment, with biliopancreatic diversion being the most associated at a ten-fold increase in one study. [ 50 ]
Bariatric surgery as a treatment for obesity can lead to vitamin deficiencies. Long-term follow-up reported deficiencies for vitamins D, E, A, K and B12. [ 51 ] There are guidelines for multivitamin supplementation, but adherence rates are reported to be less than 20%. [ 52 ]
Pregnancy in patients post-bariatric surgery must be carefully monitored. Infant mortality, preterm birth, small fetal size, congenital anomalies, and NICU admission are all elevated in bariatric surgery patients. This elevation in adverse outcomes is thought to be because of malnutrition. [ 53 ] Most notably, a reduction in serum folate and iron are well-established correlates to neural tube defects and preterm birth, respectively. People considering pregnancy should consult with their physician before conceiving to optimize their health and nutritional status before pregnancy. [ 53 ]
Bariatric procedures function by a variety of mechanisms, such as alteration of gut hormones, reduction of the gut size (reducing the amount of food that may pass through), and reduction or blockage of nutrient absorption. [ 2 ] [ 54 ] The distinction in these mechanisms, and which are at work for a particular bariatric procedure is not always clearly defined, as multiple mechanisms may be used by a single procedure. [ 2 ] [ 4 ] For instance, while sleeve gastrectomy (discussed below) was initially thought to work simply by reducing the size of the stomach, research has begun to elucidate changes in gut hormone signaling as well. [ 17 ] The two most frequently performed procedures are sleeve gastrectomy and Roux-en-Y gastric bypass (also called gastric bypass), with sleeve gastrectomy accounting for more than half of all procedures since 2014. [ 17 ]
Studies have shown that bariatric procedures may have additional effects on the hormones that affect hunger and satiety (such as ghrelin and leptin ), despite initial development to target reduction of food intake and/or nutrient absorption. [ 2 ] [ 17 ] [ 55 ] This is especially important when considering the durability of weight loss compared to lifestyle changes. While diet and exercise are essential for maintaining a healthy weight and physical fitness, metabolism typically slows as the individual loses weight, a process known as metabolic adaptation . [ 55 ] Thus, efforts for obese individuals to lose weight often stall, or result in weight re-gain. Bariatric surgery is thought to affect the weight "set point," leading to a more durable weight loss. This is not completely understood but may involve the cell-signaling pathways and hunger/satiety hormones. [ 4 ]
Procedures may reduce food intake by reducing the size of the stomach that is available to hold a meal (see below: gastric sleeve or stomach folding). Filling the stomach faster enables an individual to feel more full after a smaller meal. [ 2 ] [ 4 ] [ 56 ]
Procedures may reduce the amount of intestine that food passes through to decrease the absorption of nutrients from food. [ 2 ] [ 4 ] For example, a Roux-en-Y gastric bypass connects the stomach to a more distal part of the intestine, which reduces the ability of the intestines to absorb nutrients from the food. [ 4 ]
Roux-en-Y gastric bypass disrupts the gastric branches of the vagal nerve completely and sleeve gastrectomy does so partially. [ 57 ] Before current bariatriac was introduced, isolated vagotomy was used for the treatment of obesity. [ 58 ] Vagotomy leads to a reduction of gastric acid and consequently to a reduction in nutrient absorption and a delay in gastric emptying. In addition, the effect of the hunger hormone Ghrelin is reduced, because it acts through the vagal nerve. [ 59 ] This leads to a reduction of the hunger feeling and weight loss. [ 60 ]
Sleeve gastrectomy , also known as a gastric sleeve, is a surgical weight-loss procedure where the stomach size is reduced by the surgical removal of a large portion of the stomach, following along the major curve of the stomach. [ 2 ] The open edges are then attached (typically with surgical staples , sutures, or both) to leave the stomach shaped more like a tube, or a sleeve, with a banana shape. [ 17 ]
The procedure is performed laparoscopically and is not reversible. It has been found to produce a weight loss comparable to that of Roux-en-Y gastric bypass . [ 17 ] The risk of ulcers or narrowing of the gut due to intestinal strictures is less so with sleeve gastrectomy versus Roux-en-Y gastric bypass, but it is not as effective at treating GERD or type 2 diabetes. [ 17 ]
This was the most commonly performed bariatric surgery as of 2021 [update] in the United States, and is one of the two most commonly performed bariatric surgeries in the world. [ 2 ] [ 4 ] Though initially thought to work strictly by reducing the size of the stomach, recent research has shown that there are also changes in gut signaling hormones with this procedure leading to weight loss. [ 2 ] [ 56 ]
The sleeve gastrectomy mechanism works by creating a narrow gastric lumen which restricts food intake and prevents receptive relaxation, alongside ongoing research into hormonal changes, and gastrointestinal motility . [ 61 ] [ 62 ]
The physical mechanism that will make the SG stand out to other bariatric surgery is its reduction of the storage of the stomach significantly, allowing patients to control their calorie intakes. [ 61 ]
The mechanism related to hormone regulation, SG can help to improve Insulin sensitivity, aiming for better glucose regulation and contributing to the remission of type 2 diabetes in many patients. The levels of gut hormones such as GLP-1 and PYY increase after operation of SG. [ 62 ] GLP-1 enhances insulin secretion and has a satiety-inducing effect, while PYY helps reduce appetite . These hormonal changes are pivotal in the metabolic improvements observed after SG, including better control of blood sugar levels and reduced hunger. [ 61 ] [ 63 ]
SG will affect the metabolism and absorption of nutrients , hence causing an effect on nutrient dynamics. Postoperative observation shows patients' nutrient levels of Vitamin B1 and B12 have significantly declined, necessitating careful postoperative nutritional management to prevent deficiencies. [ 61 ]
Research suggests SG surgery can alter the composition of the gut microbiota , which plays a role in obesity and metabolic health. Changes in the gut microbial community post-SG may influence energy harvest from the diet, impact inflammatory pathways, and affect the host 's metabolic profile. [ 61 ]
The key mechanism is gastrointestinal motility adjustment of SG surgery, which impacts the speed and efficiency of food processing. [ 61 ] Studies have observed a modification in the pressure of the lower esophageal sphincter and an increase in intragastric pressure post-surgery, which collectively impact the gastrointestinal motility. [ 61 ]
Techniques:
After 1-3 postoperative days, patients begin oral intake, contingent on a successful gastrografin leak test, and receive continuous metabolic monitoring. [ 64 ] To reduce early respiratory risk, prophylactic measures such as oxygen support and ultrasound evaluations are employed. [ 64 ]
Late postoperative care involves careful observation for anastomotic leaks, patient change to a clear liquid diet, and managing potential nausea and vomiting . [ 64 ] After discharge, the focus shifts to dietary management, starting with a full liquid diet and gradually incorporating soft, solid foods. Monitoring includes regular check-ups for weight and blood pressure , along with comprehensive lab tests to ensure optimal recovery. [ 64 ]
Roux-en-Y gastric bypass surgery involves the creation of a new connection in the gastrointestinal tract , from a smaller portion of the stomach to the middle of the small intestine . [ 4 ]
The surgery is a permanent procedure that aims to decrease the absorption of nutrients due to the new, limited connection created. [ 4 ] The surgery also works by affecting gut hormones, resetting hunger and satiety levels. [ 4 ] The physically smaller stomach and increase in baseline satiety hormones help people to feel full with less food after the surgery. [ 4 ]
This is the most commonly performed operation for weight loss in the United States, with approximately 140,000 gastric bypass procedures performed in 2005. [ 17 ] A 2021 evidence update comparing the benefits and harms of bariatric procedures found that Roux-en-Y gastric bypass surgery and sleeve gastrectomy both effectively reduced weight and led to Type 2 diabetes remission. After five years, Roux-en-Y resulted in greater weight loss (26% compared to 19% for sleeve gastrectomy) and a 25% lower rate of diabetes relapse. However, Roux-en-Y patients had a higher likelihood of hospitalization and additional abdominal surgeries compared to sleeve gastrectomy. [ 65 ] Though, since 2013, sleeve gastrectomy has overtaken RYGB as the most common bariatric procedure. [ 17 ] RYGB remains one of the two most commonly performed bariatric surgeries in the world. [ 2 ] [ 4 ]
Gastric bypass is the most frequently employed technique for weight reduction, the abnormal absorption in the intestines and the physical restriction of the stomach. [ 3 ] [ 13 ] The types of surgeries can be categorized by the effects and the changes made. Reconstruction of the small intestine to reduce the mucosal area which is used to absorb nutrients is called the Malabsorption operation. [ 13 ] The jejunoileal bypass (JIB) is the most traditional technique for gastric bypass. [ 66 ] This procedure has no limitations in the flow and processing of food; [ 66 ] it only allows the transport of nutrients from the small intestine to the surrounding areas of the intestine. [ 66 ] The impact of weight loss is apparent and remarkable. [ 13 ] Individuals who undergo Roux-en-Y gastric bypass (RYGB) consume fewer snacks and meals compared to those who undergo JIB. [ 13 ] The RYGB procedure has been proved to be the most effective medical treatment for type 2 diabetes and weight loss. After performing gastric bypass surgery, the two hormones related to obesity, leptin and insulin , fall in levels and while lose weight. [ 13 ]
Roux-en-Y (RYGB) offers two surgical approaches for processing: an open technique or the laparoscopic technique. The majority of cases are still performed with laparoscopy. [ 13 ] The laparoscopic approach is a safe procedure that is associated with fewer problems resulting from wound inflammation . [ 13 ]
There are three main areas of techniques for performing laparoscopic RYGB: (1) Anastomotic technique [ 67 ] including Linear Circular stapler. 2) Alimentary limb configuration , such as Antecolic or Retrocolic and Antegastric or Retrogastric. 3) Limb-length of the bilio- pancreatic (BP) limb. [ 13 ]
Linear stapling: this technique has two variations. 1) Perform the jejuno -jejunal (JJ) anastomosis , then act on the gastro-jejunal (GJ) anastomosis. 2) reverse the first process. [ 13 ]
Jejuno-jejunal first: This technique is prevalent within gastric bypass surgery.
Other techniques include the Omega Loop Technique and Trans-abdominal technique employ different operating approaches along with different process orders. All of them will show positive weight loss results. [ 13 ]
The duration of the recuperation phase typically ranges from 2 to 4 weeks. The length of the period is dependent upon the self-perception of the patients and their future state of mental and physical ability. For patients to resume their normal activities, a minimum of 3-5 weeks recovery period is required. Doctors should determine the length of the recovery period based on a range of body mass index . [ 42 ]
The biliopancreatic diversion with duodenal switch (BPD/DS) is a slightly less common bariatric procedure, but is increasing in use with proven efficacy for sustainable weight loss. [ 68 ]
This procedure has multiple steps. First, a sleeve gastrectomy (see above section) is performed. This part of the procedure causes food intake restriction due to the physical reduction of the stomach size, and is permanent. [ 68 ] Next, the stomach is then disconnected from the upper part of the small intestine and connected to a farther part of the small intestine (ileum) , creating the alimentary limb. [ 68 ] The leftover section of the far part of the small intestine is then used to make a connection that brings digestive fluids from the gallbladder and pancreas to the alimentary limb. [ 68 ]
Weight loss following the surgery is largely due to the alteration of gut hormones that control hunger and satiety, as well as the physical restriction of the stomach and decrease in nutrient absorption. [ 69 ] Compared to the sleeve gastrectomy and Roux-en-Y gastric bypass, BPD/DS produces better results with lasting weight loss and resolution of type 2 diabetes. [ 69 ]
Vertical banded gastroplasty was more commonly used in the 1980s, and is not typically performed in the 21st century. [ 71 ]
In the vertical banded gastroplasty, a part of the stomach is permanently stapled to create a smaller, new stomach. [ 71 ] This new stomach is physically restricted, allowing people to feel full with smaller meals. [ 72 ] Short-term weight loss is similar to other bariatric procedures, but long-term complications may be higher. [ 72 ]
This procedure is similar to the sleeve gastrectomy surgery, but a sleeve is created by suturing , rather than physically removing stomach tissue. [ 73 ] This allows for the natural ability of the stomach to absorb nutrients to remain intact. [ 73 ] This procedure is reversible, is a less invasive procedure, and does not use hardware or staples. [ 74 ]
Gastric plication significantly reduces the volume of the patient's stomach, so smaller amounts of food provide a feeling of satiety. [ 74 ] In a 2020 review and meta-analysis, long-term weight loss was not as durable as other, more common bariatric techniques. [ 74 ] Gastric plication has not performed as well as the sleeve gastrectomy, with the sleeve gastrectomy associated with greater weight loss and fewer complications. [ 73 ]
The restriction of the stomach also can be created using a silicone band, which can be adjusted by the addition or removal of saline through a port placed just under the skin, a procedure called adjustable gastric band surgery. [ 34 ] This operation can be performed laparoscopically, and is commonly referred to as a "lap band". Weight loss is predominantly due to the restriction of nutrient intake that is created by the small gastric pouch and the narrow outlet. [ 34 ] It is considered somewhat of a safe surgical procedure, with a mortality rate of 0.05%. [ 34 ]
Intragastric balloon involves placing a deflated balloon into the stomach, and then filling it to decrease the amount of gastric space, resulting in the feeling of fullness after a smaller meal. [ 75 ] [ 76 ] The balloon can be left in the stomach for a maximum of 6 months and results in weight loss of 3 BMI or 3–8 kg within several study ranges. [ 75 ] [ 76 ] Weight loss with the gastric balloon tends to be more modest than other interventions. The intragastric balloon may be used before another bariatric surgery to assist the patient in reaching a weight that is suitable for surgery but can be used repeatedly and unrelated to other procedures. [ 76 ]
This procedure where a device similar to a heart pacemaker that is implanted by a surgeon, with the electrical leads stimulating the external surface of the stomach, was under preliminary research in 2015. [ 77 ] Electrical stimulation is thought to modify the activity of the enteric nervous system of the stomach, which is interpreted by the brain to give a sense of satiety, or fullness. Early evidence suggests that it is less effective than other forms of bariatric surgery. [ 77 ]
People are followed closely both before and after bariatric procedures by a healthcare team. The care team may include people in a variety of disciplines, such as social workers, dietitians, and medical weight management specialists. [ 34 ] Follow-up after surgery is typically focused on helping avoid complications and tracking the progress toward body weight goals. [ 34 ] Having a structure of social support in the post-operative time may be beneficial as people work through the changes that present physically and emotionally following surgery. [ 23 ]
Dietary restrictions after recovery from surgery depend in part on the type of surgery. In general, immediately after bariatric surgery, the person is restricted to a clear liquid diet, which includes foods such as broth , diluted fruit juices, or sugar-free drinks. [ 64 ] This diet is continued until the gastrointestinal tract begins to recover approximately 2–3 weeks after surgery. [ 64 ] The next stage provides a puréed liquid or soft-solid diet that is slightly increased in viscosity. This may consist of high protein, liquid, or soft foods such as protein shakes, soft meats, and dairy products. [ 34 ] [ 64 ] People in recovery are encouraged to compose their diet mainly of plant-based foods and soft proteins (1.0–1.5g/kg/day). [ 34 ] [ 64 ] During recovery, people must adapt to eating more slowly and avoid eating past fullness; overeating may lead to nausea and vomiting. [ 34 ] [ 64 ] Alcohol is avoided completely in the first 6 months to 1 year after surgery. [ 64 ] Some people may take a daily multivitamin to compensate for reduced absorption of essential nutrients. [ 34 ]
In general, women are advised to avoid pregnancy for 12–24 months after bariatric surgery to reduce the possibility of intrauterine growth restriction or nutrient deficiency, since a person having bariatric surgery will likely undergo significant weight loss and changes in metabolism. Over many years, the rates of potential adverse maternal and fetal outcomes have been reduced for mothers following bariatric surgery. [ 33 ] [ 36 ] [ 64 ]
After a person successfully loses weight following bariatric surgery, excess skin may occur. [ 78 ] Bariatric plastic surgery procedures, sometimes called body contouring, may be an option for people wishing to remove excess skin following the large change in weight. [ 79 ] Targeted areas include the arms, buttocks and thighs, abdomen, and breasts, with changes occurring slowly over years. [ 80 ]
The rising prevalence of lawsuits related to gastric bypass surgery is a legal concern in different countries. [ 81 ] The causes are complex, including the immature characteristics of this technology and an increasing number of patients. In the future, the number of emergent patients who have stomach reduction surgery, long-term complications, and the number of lawsuits due to non-eligible surgery will increase. [ 81 ]
In the 21st century, obesity rates increased globally, and with this, a proportional rise in related diseases and complication. [ 17 ] [ 82 ] In the United States during 2017-20, an estimated 40% of adults were obese, up from 30% in 1999-2000. [ 17 ] The costs of treating obesity and related conditions has a large economic impact globally. [ 83 ] [ 84 ] This economic impact results from direct treatment of obesity, treatment of obesity-related conditions, as well as other economic losses from decreased workforce productivity. [ 17 ] [ 84 ]
Bariatric surgery is cost-effective when compared to savings estimated from treatment or prevention of obesity-related conditions. [ 84 ] Cost-effectiveness occurs at the individual level due to fewer healthcare expenses for medications, and nationally with a reduction in the overall lifetime healthcare costs. [ 85 ] [ 84 ]
During the early 21st century, obesity among children and adolescents increased globally, as did treatment options including lifestyle changes, drug treatments, and surgical procedures. [ 86 ] [ 87 ] The medical complications and health concerns associated with childhood obesity may have short or long-term effects, with a growing concern of a potential decline in overall life expectancy . [ 87 ] [ 20 ] Childhood obesity may affect mental health and impact eating practices. [ 87 ]
Difficulties surrounding obesity treatment selection among children and adolescents include ethical considerations when obtaining consent from those who may be unable to do so without adult guidance or understanding the potential lasting effects of invasive procedures. [ 86 ] [ 88 ] Among high-quality randomized control trial data for surgical treatment of obesity, many studies are not specific to children and adolescents. [ 89 ] Concerns for bullying about overweight or body image exist for those with childhood obesity; self-harm among children and adolescents bullied for their weight also occurs. [ 87 ]
Bariatric surgical procedures available to adolescents include: Roux-en-Y gastric bypass, vertical sleeve gastrectomy, and adjustable gastric banding. [ 90 ] Multiple organizations have created guidelines for bariatric surgery indications in children and adolescents. In 2022-23, such guidelines overlapped with recommendations for potential bariatric surgical management in children and adolescents with a BMI of 40 or higher, or a BMI of 35 or higher while also experiencing related experiences. [ 91 ] [ 12 ] [ 92 ]
Reviews have shown similar weight loss in adolescents following bariatric surgery as in adults. [ 93 ] Reduction of eating disorders for several years after bariatric surgery has also been shown in adolescents after bariatric surgery. [ 93 ] Long-term reduction in or resolution of weight-related conditions, such as diabetes and high blood pressure , occurred in adolescents after bariatric surgery. [ 94 ] Long-term effects of bariatric surgery in adolescents remains under research, as of 2023. [ 93 ] [ 94 ]
Techniques for weight loss have been reported for decades, with a more formal transition to noting weight loss following surgical intervention in the 1950s when subsequent weight loss after surgical shortening of the small intestine in dogs and people was observed. [ 95 ] [ 96 ] Specifically, anastomosis between upper and lower portions of the small intestine to skip, or bypass, part of the small intestine led to what was called the jejuno-ileal bypass . [ 96 ] A modified version of this procedure showed long-term improvement of lipid levels in people with known high levels of cholesterol following the procedure. [ 96 ]
Further modification of the bypass procedure achieved weight loss in obesity, during which an anastomosis between the small intestine and upper lower intestine, known as a jejunocolic bypass , was performed. [ 95 ] During the late 1960s, the initiation of bariatric surgery followed the development of a procedure to bypass portions of the stomach – the gastric bypass . [ 95 ] [ 96 ] [ 97 ]
Sleeve gastrectomy (SG), is one of the most popular stomach reduction surgeries and was earliest performed in 1990 as a first-stage operation of duodenal switch (DS) surgery. Patients who go through SG typically experience substantial weight loss, preventing the need for the second phase of DS. [ 97 ]
Laparoscopic techniques revolutionized bariatric surgery, making procedures less invasive and recovery quicker. The first laparoscopic gastric bypass performed by Alan Wittgrove in 1994 exemplifies this leap in surgical innovation . [ 97 ] The SG laparoscopic version was first performed in 1999. [ 13 ]
Historically, the RYGBP is the best bariatric surgery for obese patients, but now being rivalled by the SG. The complication of RYGBP leads people to find less intricate and safer surgeries, the complication including internal hernias and anastomotic complications. [ 13 ] Nowadays, SG has a lower risk of complication, and the mortality rate has become the more favorable option for the patients. [ 71 ]
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Baricity refers to the ratio of the densities ( density ) of a substance, e.g., spinal local anesthetic, compared to the mean density of human cerebrospinal fluid , both at 37°C. Baricity is used in anesthesia to determine the manner in which a particular drug will spread in the intrathecal space.
The mean density of cerebrospinal fluid at 37°C is 1.0003 g litre −1 , with a range of 1.0000–1.0006 (± 2 standard deviations) g mlitre −1 . [ 1 ] Solutions that have a density very close to that of cerebrospinal fluid have a baricity approaching 1.0 and are referred to as isobaric . Hypobaricity is defined as a solution with a density lower than 3 standard deviations below the mean density of cerebrospinal fluid. [ 2 ] Thus, mathematically, a hypobaric solution has a baricity less than 0.99955 ((1.0003-0.00015*3)/1.0003). Hypobaric solutions are usually created by mixing the local anesthetic with distilled water. Theoretically, the lower boundary of hyperbaricity may be defined as 3 standard deviations above the mean, however, the actual density at which local anaesthetics behave consistently as a hyperbaric solution is less clear. [ 2 ] Hyperbaric solutions are created by mixing dextrose 5-8% with the desired local anesthetic; such mixtures tend to have densities far above the theoretical lower boundary. Plain (no distilled water or dextrose added) solutions of bupivacaine (a commonly used spinal anesthetic) with a density of 0.9993 g litre −1 at 37°C are hypobaric in all patients. [ 2 ]
Hyperbaric solutions will flow in the direction of gravity and settle in the most dependent areas of the intrathecal space. Conversely, hypobaric mixtures will rise in relation to gravitational pull. These properties allow the anesthesia provider to preferentially control the spread of the block by choice of mixture and patient positioning. [ 3 ]
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Barinthus Biotherapeutics plc (formerly Vaccitech plc) is a biotechnology company developing immunotherapies for infectious diseases, cancer and autoimmune diseases such as hepatitis B , HPV and prostate cancer . [ 1 ] [ 2 ] Formerly known as Vaccitech plc , in November 2023 the company announced that it had renamed itself to Barinthus Biotherapeutics plc. As of 2024, the company employs more than 100 people.
The company's platforms include Chimpanzee Adenovirus Oxford ( ChAdOx ) and Modified vaccinia Ankara (MVA), two viral vectors which safely mimic viral infection in human cells and elicit antibody and T cell responses to pathogens and tumours , [ 3 ] as well as two SNAP synthetic platforms, SNAP-TI (SNAP-Tolerance Immunotherapy) and SNAP-CI (SNAP-Cancer Immunotherapy), previously referred to collectively as SNAPvaxTM.
The company was founded in 2016 as a University spin-off by Sarah Gilbert and Adrian V. S. Hill at The Jenner Institute , University of Oxford . [ 4 ] [ 5 ] [ 6 ]
Vaccitech has been financed and supported by M&G Catalyst, Google Ventures (GV), Fosun International , Tencent , Huawei , Sequoia Capital , GeneMatrix , Liontrust Asset Management , Korea Investment Partners and Oxford Sciences Innovation (OSI). [ 7 ] [ 8 ] [ 9 ]
In early 2020, Vaccitech and the University of Oxford co-invented a vaccine for COVID-19 using the ChAdOx platform. [ citation needed ]
In July 2020, it was reported that people in Brazil, South Africa and the US had been recruited to populate the vaccine trials. [ 10 ]
In July 2020, Vaccitech scientists reported in The Lancet a "single-blind, randomised controlled trial in five trial sites in the UK of a chimpanzee adenovirus -vectored vaccine ( ChAdOx1 nCoV-19 ) expressing the SARS-CoV-2 spike protein." Several subjects needed prophylactic paracetamol to minimize their adverse reactions.
Vaccitech held an initial public offering of shares in 2021, listing on NASDAQ on 30 April 2021. [ 11 ]
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Bartholin gland carcinoma is a type of cancer of the vulva arising in the Bartholin gland . [ 2 ] It typically presents with a painless mass at one side of the vaginal opening in a female of middle-age and older, and can appear similar to a Bartholin cyst . [ 2 ] The mass may be big or small, may be deep under skin or appear nearer the surface with overlying ulceration . [ 2 ] Average age at presentation is 53-years. [ 3 ]
The tumor can become large before a woman is aware of symptoms . One of the first symptoms can be painful sex . In other instances, there may be a mass or ulcer in the vulva area. Many clinicians assume that an enlarged Bartholin gland is malignant in a postmenopausal woman until proven otherwise. The growth of the tumor can spread to nearby areas such as the ischiorectal fossa and inguinal lymph nodes . Approximately 50% of bartholin gland carcinomas originate from squamous cell carcinomas . Another uncommon characteristic of Bartholin gland malignancies is that the growth of a lesion originates from the three types of epithelial tissue present in the gland: mucinous , transitional , and squamous . [ 4 ]
It is rare, accounting for less than 1% of all female genital tract cancers and less than 5% of all vulva cancers . [ 2 ]
The cause is unknown. [ 2 ]
Bartholin gland can be differentiated by histology to determine whether the malignancy is due to squamous cell carcinoma, adenoid cystic carcinoma, or adenocarcinoma. [ 5 ]
Though Bartholin gland carcinoma is rare, along with other unusual Bartholin gland growths, it may not be the typical practice for clinicians to consider lesions malignant. Early diagnosis can help prevent the cancer from spreading from the glands to the surrounding area. Though malignancies of the Bartholin gland are rare, clinicians biopsy Bartholin gland lesions in older women or when the growth reoccurs or does not respond to the original treatment. [ 4 ]
The prognosis is optimistic if the growth has not metastasized to the lymph nodes. [ 4 ]
Bartholin glands were described in cattle by Casper Bartholin in 1677. Their existence in humans was postulated at that time. [ 4 ] Treatment can be a vulvectomy that results in the removal of the growth and an extensive removal of adjacent tissue. An inguinal lymphadenectomy often accompanies the vulvectomy. The tissue that is removed sometimes includes sections of the vagina and rectum . [ 6 ]
The adenoid cystic carcinoma of the Bartholin gland is another uncommon malignancy with symptoms that include local painful intermittent recurrences. The disease is slow to progress, but it can result in lung cancer after a long time after the initial treatment. Treatment consists of surgical removal of the growth. Sometimes, radiation and chemotherapy are performed. [ 7 ]
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Prof. Baruch Modan ( Hebrew : ברוך מודן) (1932-2001) [ 1 ] was an Israeli medical scientist . Modan made significant findings in the field of oncology and was an expert on the effects of radiation .
Modan worked with various types of cancer , and in 1974 demonstrated that the chances of getting breast cancer increase for anyone who has had X-ray dosages as low as 1.6 rem. He was an expert on treating cancer among children.
A professor at the University of Tel Aviv , Prof. Modan was Chairman of the Department of Epidemiology and Head of the Stanley Steyer Institute for Cancer Epidemiology and Research at the Sackler Faculty of Medicine . He was also Director-General of the Israeli Ministry of Health .
He was the father of Rutu Modan . [ citation needed ]
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Basal cell adenoma is a rare, low-grade benign salivary gland neoplasm . [ 1 ]
The most common involved site is the parotid gland , however other possible sites include the submandibular gland , [ 2 ] minor salivary glands of upper lip, buccal mucosa, palate and nasal septum. [ 1 ]
It appears as a slow-growing, firm and mobile mass. [ 1 ]
Treatment is by surgical excision with a margin of healthy tissue. [ 2 ] Although the recurrence rate is high, the prognosis is generally good. [ 1 ]
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A baseline in science (including medicine ) is the initial conditions found by observation and measurement at the beginning of a survey or clinical trial or which is used for comparison with later data collected during or after the survey or trial to identify and measure changes, often with the intention of assessing the effects of a treatment or procedure. [ 1 ] [ 2 ]
In environmental science a baseline study is necessary to be able to accurately determine impact by monitoring the environment and comparing the changing situation with the initial conditions after development has occurred. In some cases, baseline information already be available from previous surveys, but it may be necessary to gather data in the field. [ 3 ]
Example: If a patient with kidney failure (whose creatinine is usually 3.0 mg/dL) suddenly has a creatinine of 5.0 mg/dL, then his creatinine is out of his normal. For that person with kidney failure, absolute normal no longer applies because he will never again be able to obtain an absolutely normal creatinine level (0.5–1.2 mg/dL) with kidneys that no longer function properly.
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Basilar invagination is invagination (infolding) of the base of the skull that occurs when the top of the C2 vertebra migrates upward. It can cause narrowing of the foramen magnum (the opening in the skull where the spinal cord passes through to the brain ). It also may press on the lower brainstem . [ 1 ]
This is similar to Chiari malformation . That, however, is usually present at birth.
A doctor will base his or her diagnosis on the symptoms the patient has and the results of tests, including:
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The Baskerville effect , or the Hound of the Baskervilles effect , is the alleged self-fulfilling prophecy that there is an increase in rate of mortality through heart attacks on days considered unlucky because of the psychological stress this causes on superstitious people. The term derives from the Sherlock Holmes novel The Hound of the Baskervilles in which a hellish-looking dog chases Sir Charles Baskerville, sufferer of a chronic heart disease. According to legend, the dog cursed his family, Baskerville runs in great fear and dies of a heart attack "with an expression of horror in his face".
The Baskerville effect was named by David Phillips and his colleagues at the University of California, San Diego , on a paper where they reported that the daily number of deaths of Chinese and Japanese Americans from heart attacks between 1973 and 1998 was 7 percent higher on the fourth of the month compared to the average for the other days in that month, while this was not observed in the general American population. [ 1 ]
Four (四, formal writing: 肆, pinyin si4) is considered an unlucky number in Chinese , and hence in the Japanese and Korean , because it sounds like "death" (死 pinyin si3). Some Chinese and Japanese hotels and hospitals do not use it as a room number (the way that American architects don't use 13 as a floor number in office or hotel buildings). The authors, seeing how telephone line subscribers could choose the last four digits in their telephone numbers, found evidence that the number 4 is avoided among Chinese and Japanese Americans by searching the California Yellow Pages for telephone numbers of Chinese and Japanese restaurants, and finding that these had significantly fewer numbers 4 in this last section (366 out of 4748, or 7.71 percent) than it would be expected by chance (10 percent), a pattern not observed on restaurants listed as American. [ 1 ] An analysis of the 20,000 computerized death certificates of Asian-Americans in San Diego, Phillips discovered that there was a 13 percent uptick in death rates on the fourth of the month. [ 2 ] [ 3 ] The hypothesis was that the peak was caused by stress induced by the superstition surrounding this number. [ 1 ]
In 2002, Gary Smith commented that Phillips and colleagues had omitted data from several heart disease categories, picking only those that happened to have a higher rate on the fourth day, calling them "chronic heart diseases". Smith also pointed out that they had not done this on their previous studies of Jewish deaths near Passover and Chinese deaths near the Harvest Moon , where they had used all heart disease categories. [ 4 ]
Smith also found no statistically relevant peaks on day 4 in data from 1969–1988 and 1999–2001 for total coronary deaths, inpatients, or the subset of heart diseases used by Phillips and colleagues, adding that there were more deaths on day 5 in the 1969–1988 data, and more deaths on day 3 in the 1999–2001 data. [ 4 ]
In 2003, Nirmal Panesar and colleagues looked for this effect on the Chinese population of Hong Kong . They looked at mortality data from 1995 to 2000, comparing the days of the month with "deathly connotations" (4, 14 and 24) with the other days of the month on both the Lunar and Gregorian calendars, and found no statistically significant difference. [ 5 ]
In early 2018, Jonathan Jarry analysed this phenomenon, citing both Smith's and Panesar et al's papers, pointing out that, if the effect was real, a bigger effect would be seen in Asia, while the opposite occurs. [ 6 ] Jarry states that the peak observed on the original study appears because of what the researchers decided to compare it to, and quotes cardiologist Christopher Labos as concluding that "while the number of deaths on day 4 may be higher than average, it is not actually statistically higher than any individual day."
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The Batista procedure (also called a reduction left ventriculoplasty) was an experimental heart procedure that proposed the reversal of the effects of remodeling in cases of end-stage dilated cardiomyopathy refractory to conventional medical therapy. The hypothesis of the operation appears to be that reduction (resection) of marginally viable ventricular mass may result in superior geometric remodeling thus conferring better performance when faced with ventricular failure. In spite of promising initial results, the method was soon found to be of little if any benefit, and it is no longer considered a recommended treatment for the disease.
The Batista procedure was invented by Brazilian physician and cardiac surgeon Randas Batista in 1994 for use in patients with non-ischemic dilated cardiomyopathy . Many of his patients were victims of Chagas disease . Chagas disease represents a parasitic nonischemic cardiomyopathy targeting parasympathetic inflow to the heart. Chagas cardiomyopathy thus represents a unique method of study of diastolic heart failure. It may be addressed by removal of a portion of viable tissue from the left ventricle to reduce its size (partial left ventriculectomy), with or without repair or replacement of the mitral valve. [ 1 ]
Although several studies showed benefits from this surgery, studies at the Cleveland Clinic concluded that this procedure was associated with a high early and late failure rate. At 3 years only 26 percent were event-free and survival rate was only 60 percent. [ 2 ] Most hospitals in the US have abandoned this operation and it is no longer included in heart failure guidelines. [ 3 ] [ 4 ]
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The Bean prize , also known as the William B. Bean Student Research Award and named for William Bennett Bean , is awarded annually to medical students by the American Osler Society (AOS) for research in history of medicine and humanities . [ 1 ] [ 2 ] [ 3 ]
The Bean prize is named for William Bennett Bean , who was a resident physician under Sir William Osler . [ 4 ] Bean became the first president of the American Osler Society , who created the award for medical students. [ 4 ]
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A beating heart cadaver is a body that is pronounced dead in all medical and legal definitions, connected to a medical ventilator , and retains cardio-pulmonary functions. This keeps the organs of the body, including the heart , functioning and alive. [ 1 ] As a result, the period of time in which the organs may be used for transplantation is extended. The heart contains pacemaker cells that will cause it to continue beating even when a patient is brain-dead . Other organs in the body do not have this capability and need the brain to be functioning to send signals to the organs to carry out their functions. A beating heart cadaver requires a ventilator to provide oxygen to its blood, but the heart will continue to beat on its own even in the absence of brain activity . [ 2 ] This allows organs to be preserved for a longer period of time in the case of a transplant or donation. A small number of cases in recent years indicate that it can also be implemented for a brain-dead pregnant woman to reach the full term of her pregnancy. [ 2 ] There is an advantage to beating heart cadaver organ donation because doctors are able to see the vitals of the organs and tell if they are stable and functioning before transplanting to an ailing patient. [ 3 ]
The observed phenomena of lifelike qualities after death is not a new concept. In René Descartes ' Discourse on the Method , he notes that decapitated animals move and display characteristics of a living body a few seconds after decapitation which was published in 1637. [ 4 ] This continued into the French Revolution where it was observed that people who had been beheaded showed movements in facial muscles and hearts could continue to beat for almost an hour past the time of beheading. [ 5 ] The guillotine in some cases did not completely sever head from body. In 1875 an examiner named Pierre Jean Cabanis was assigned the duty of making sure a body was truly dead. [ 4 ] There were also stories involving beheadings where the victims would stand up and walk around before falling dead. The ambiguity around brain death and true death has followed it to present day. In an effort to clarify some of these gray areas, the Harvard Medical Committee developed criteria for identifying a body as dead in 1968. [ 4 ] [ 5 ] These criteria required patients to be completely unaware and unresponsive to external stimuli, have no spontaneous muscle movements, and exhibit no reflexive response even when manipulated. They also required that an electroencephalography ( EEG ) show no signs of activity. [ 4 ] The purpose of this report was to encourage physicians to distinguish brain death and irreversible coma from a persistent vegetative state where the patient still has some awareness and cycles through sleep and wakefulness. [ 6 ]
In 1971 similar Minnesota criteria were published eliminating the EEG, repeating the exam after 12 hours, a severe lesion in the brain, and increasing the duration of the apnea test to four minutes rather than Harvard's three minute guideline. Other slight changes in the next decades included the United Kingdom's decision to eliminate the repetition of the exam and change from a duration of the apnea test to specified levels of CO 2 in 1976. [ 5 ] Later, in 1981 the President's Commission reinstated the apnea test and the repeat exam. In a study done in 1989, only 35% of 195 physicians and nurses involved in organ procurement polled knew brain death criteria. These were not the same nurses and physicians who diagnose brain death. Presently, there is hot debate over the protocol for diagnosing someone as brain dead due to widespread disinformation and misinformation on the internet. [ 7 ]
The American Academy of Neurology created a prerequisite and neurological clinical assessment to be used as guidelines for determining brain death published in 2010. [ 6 ] To be considered for brain death the body must have a determinant cause of coma, have normal systolic blood pressure, and pass two neurological tests. These neurological assessments commonly consist of an apnea test, reflex tests where the body is manipulated or exposed to a stimulus and does not react, or be in a coma where there is complete unresponsiveness. [ 6 ] Cerebral angiography , electroencephalography, transcranial doppler ultrasonography, and cerebral scintigraphy are some of the tests that are used to test if there is any significant brain activity. [ 6 ]
Caring for a beating heart cadaver is similar to caring for a living patient. Since the brain has stopped functioning, the hormone levels and blood pressure must be regulated by intensive care unit (ICU) personnel. [ 8 ] The protocol for preserving the cadaver aims to prevent infection and maintain adequate oxygenation of tissue. [ 9 ] The cadaver's status must be continuously monitored, so that ICU staff can prevent organ failure or quickly operate to save threatened organs. [ 8 ]
A beating heart cadaver is kept alive in order to keep its organs from decaying before they can be transplanted. Surgeons will remove the organs, one after the other, and have them transferred to the recipients' treating teams. [ 1 ] The entire recovery process is usually completed within four hours. [ 9 ] This process was formerly known as an "organ harvest", but the name has since changed to the milder "organ recovery". [ 1 ] Many organs can be extracted, and many lives can be saved by one body. The bodies are generally those of organ donors , who have either given first-person consent to become an organ donor, presumptive consent by not explicitly declining to donate [ 10 ] or whose legal next-of-kin makes the decision to donate. [ 11 ] Some donated organs are taken from non-heart-beating donors . [ 12 ] Organs from brain deaths , however, have a better success rate, and currently most organ donation is from these deaths. [ 13 ]
How long the brain-dead person is kept on the ventilator may vary depending on the availability of surgical teams and the wishes of the family of that brain-dead person. An anesthesiologist is regularly present at organ donation surgical procedures, not for pain, but to monitor the vital signs and administer medications to optimize organ harvest. [ 14 ] Due to the results of the apnea test if a person lacks the brain function to breathe unassisted, it is concluded that it would also lack the brain function to relay the sensation of pain. [ 14 ] The anesthesiologist also ensures that muscle spasms or reflexes do not occur during the procedure. Though the brain may be dead, the pathway that reflexes follow does not pass from the stimulus in the body to the brain. Instead the spinal cord coordinates the knee-jerk reactions of reflexes including pulling back from the pain of putting a hand in an open flame or jerking away from an invasive incision. When the brain is dead these pathways remain intact and the anesthesiologist is present to ensure that these reactions do not complicate the procedure. [ 14 ]
Pregnancy can be prolonged after brain death. It is then possible to deliver the baby by means of caesarian section. [ 15 ] Cadavers have been reported to support a fetus for a period of 107 days. After delivering the baby, some cadavers have subsequently become organ donors. [ 16 ] Since 1981 there have been 22 recorded instances of keeping a mother declared brain dead in a beating heart cadaver state until the baby is delivered. [ 2 ]
A review of 11 of these unique circumstance pregnancies was conducted in 2000. Four of these cases involved a persistent vegetative state of the mother and in 7 maternal brain death was diagnosed. [ 17 ] The women that underwent these gestation periods all delivered preterm an average of 30.5 weeks, where a normal pregnancy is around 35 weeks for full term. [ 17 ] The mothers were observed to have severe hypotension once in the brain dead or vegetative state and in all but one case the baby was delivered by cesarian section. It has also been found that by the 24th week of pregnancy intensive care is not as necessary and the mother is more stable than treatment occurring before the 24th week. [ 17 ] Common complications involved inability to regulate temperature which is treated with heating and cooling blankets, as well as failure of the endocrine system which is important in maintaining a stable fetal environment. [ 17 ] Following the delivery of the baby, organs of the mother are harvested as well. [ 16 ]
From an ethical perspective the family and next of kin are often involved in the decision to terminate or prolong the pregnancy. This can be a difficult decision given the level of care required to keep the mothers living for the duration of their gestation which can vary. Intensive care of a vegetative state patient is not usually advised due to the dismal chances of recovery, but in the case that the fetus could survive this care is often justified and administered at the discretion of the family. [ 14 ] [ 17 ] Intense counseling and advisement by physicians and neonatal experts often accompanies these rare situations. [ 12 ]
Brain death is defined as irreversible cessation of all functions of the entire brain, including the brain stem: coma (with a known cause), absence of brainstem reflexes, and apnea. When doctors take away ventilation systems and patients fail to breathe, move, or show any signs of arousal on their own they are considered brain dead. [ 14 ] This test is called an apnea test. The ventilator is taken away and is reconnected only if the person decided to be an organ donor. This definition can create some cognitive dissonance because not responding to stimulation may show a problem with the central nervous system, yet when someone has a beating heart and lungs that will still function with the help of a ventilator it is difficult for some to accept as death. Brain death patients have characteristics of the living and the dead. [ 3 ]
Organ recovery from beating heart cadavers has remained ambiguous to the public. There is a guideline for organ transplantation consisting of two parts. It states that organ donors must be dead before removing the organs, and removing the organs is not the cause of death. [ 18 ] This clause is in place to ensure that organ donation is not exploited to use people purely as a means to an end. However, many believe that even with these guidelines in place the protocol for organ donation still has room for criticism. There is an opinion that negative views from public and medical personnel on this subject tend to stem from a lack of understanding of what it means to be considered brain dead and how these decisions are made, [ 19 ] but there are also legitimate concerns relating to the consciousness of the patient. [ 20 ] One social issue that is commonly brought up is the potential for conflict of interest for the medical team examining the body. [ 19 ] Another issue raising concerns in the organ donation by beating heart cadaver field is the administration of drugs to the patient that prevent clotting prior to the donation procedure. These drugs are not beneficial to the patient and are intended solely to help the recipient of the organs. [ 18 ] To alleviate some of these social concerns, there has been push for a standard in determining death and creating a normalized system for transplantation in these patients. [ 19 ]
From a religious standpoint, the encouragement of organ donation or acceptance may vary. The Catholic church with input from Pope John Paul II , identified transplantation from beating heart cadavers or living subjects as acceptable if there are no added risks to the donor. [ 21 ] This has been widely debated in Japan where the first heart transplant took place in 1968 and the patient died a few months after the procedure. [ 22 ] Since then, more transplantation procedures have taken place but it is still a controversial subject. Transplantation in naturalist religions and cultures such as those of the Native Americans, Buddhists , and Confucianists tend to dissuade the use of living donors and transplantation. [ 21 ] The body is idealized as a home for a soul and the organs belonging to a person are considered perverse if utilized by another person. No religion specifically outlaws the use of beating heart cadavers or prefers them to non beating heart cadavers. [ 21 ] [ 22 ] Western cultures more widely accept the use of transplantation by beating heart cadavers than more conservative cultures. [ 21 ] The main concern of many religions and cultures is ensuring the body is not objectified or disrespected in harvesting and transplantation of organs. [ 21 ]
Award-winning Canadian writer Colleen Murphy's play Beating Heart Cadaver had its premiere in the United Kingdom on 3 April 2011 at the Finborough Theatre, London.
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Beevor's Axiom is the idea that the brain does not know muscles, only movements. In other words, the brain registers the movements that muscles combine to make, not the individual muscles that are making the movements. Hence, this is why one can sign their name (albeit poorly) with their foot. Beevor's Axiom was coined by Dr. Charles Edward Beevor , an English neurologist.
Dr. Beevor presented Beevor's Axiom in a series of four lectures from June 3, 1903 to July 4, 1903 before the Royal College of Physicians of London as part of the Croonian Lectures . His experiments showed that when an area of the cortex was stimulated, the body responded with a movement, not just a single muscle. Dr. Beevor concluded that “only co-ordinated movements are represented in the excitable cortex” [ 1 ]
In relation to Beevor's Axiom, it has been found that the brain encodes sequences, such as playing the piano, signing our name, wiping off a counter, and chopping vegetables, and once encoded and practiced, it takes less brain activity to perform them. This supports Beevor's Axiom, because the brain can recall movements easier than it can learn them. [ 2 ]
Beevor's Axiom is only partially true, however. Most behavior of muscles is encoded in the primary motor cortex (M1) and separated by muscle group. In an effort to understand the encoding in the M1, researchers observed commands of monkeys. Muscle cells changed firing rate according to the direction of the arm movements. Each neuron has one direction that elicits the greatest response. [ 3 ] Some M1 neurons encode muscle contractions, while others react to particular movements, regardless of the muscles used to perform them. The key characteristic of the primary motor cortex is its dynamic nature; the M1 changes based on experience. The supplementary motor area (SMA) plays a key role in initiating motion sequences. The premotor cortex (PMA) plays a key role when motor sequences are guided by external events. They map behaviors as opposed to the M1 which maps specific movements. [ 4 ] This could cause in issue in brain–computer interface research. If a researcher tries to excite only a muscle, it might be impossible without expecting a full movement. [ 5 ]
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Behavioral endocrinology is a branch of endocrinology that studies the Neuroendocrine system and its effects on behavior. [ 1 ] Behavioral endocrinology studies the biological mechanisms that produce behaviors, this gives insight into the evolutionary past. [ 2 ] The field has roots in ethology , endocrinology and psychology . [ 3 ]
The neuroendocrine system is an integrated system composed of neurons, glands and non-endocrine tissues, and the hormones and neurochemicals they produce and receive collectively regulate physiological or behavioral state. [ 4 ]
The hypothalamus is a distinct part of the brain that is made up of neurons and its main purpose is to maintain homeostasis. [ 5 ] The hypothalamus also plays an important part in survival of the individual by integrating the interactions between hormonal and behavioral processes, such as, eating behavior and aggressive behavior. [ 5 ]
The pituitary gland located in the brain is a major system in neuroendocrine system because the secretion of hormones from the anterior pituitary is directly regulated by the central nervous system. [ 6 ]
Social behavior, reproductive behavior, moods, feelings, attitudes, development and survival are affected by the neuroendocrine system and studied in the field of behavioral endocrinology. [ 2 ] [ 7 ]
See the Cortisol: Memory and Stress sections for more information on how cortisol has been found to affect behavior. [ citation needed ]
See the Adrenaline: Emotional response and Memory sections for more information on how adrenaline affects behavior. [ citation needed ]
Testosterone is secreted by the testicles of males and the ovaries of females, although small amounts are also secreted by the adrenal glands. It is the principal male sex hormone and an anabolic steroid . See Testosterone: Aggression and criminality and Testosterone: Brain for more information on how testosterone effects behavior. [ citation needed ]
Estrogens , together, make up a group of primary female sex hormones synthesized in the ovaries . See Estrogen: Brain and behavior for more on the role of estrogen in behavioral endocrinology.
Thyroid hormones are responsible for controlling metabolism , nervous system, body temperature and development of several organ systems such as the reproductive system.
Hyperthyroidism and hypothyroidism are the two major dysfunctions associated to behavioral and brain chemistry changes due to the imbalances in the thyroid hormones, triiodothyronine (T 3 ) and thyroxine (T 4 ). [ 8 ]
Behavioral endocrinology has roots in ethology and is also seen as a combination of endocrinology and psychology . Like ethology, behavioral endocrinology focuses on behavior on the level of the whole organism. The invention of radioimmunoassay techniques revolutionized behavioral endocrinology, allowing scientists to see and quantify hormones. The field historically resists reductionist thinking and focuses on the physiological aspects of behavior. [ 3 ]
Charles Otis Whitman
Karl Lashley
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Behavioral neurology is a subspecialty of neurology that studies the impact of neurological damage and disease upon behavior, memory, and cognition, and the treatment thereof. Two fields associated with behavioral neurology are neuropsychiatry and neuropsychology . In the United States , 'Behavioral Neurology & Neuropsychiatry' has been recognized as a single subspecialty by the United Council for Neurologic Subspecialties (UCNS) since 2004.
Syndromes and diseases commonly studied by behavioral neurology include:
While descriptions of behavioral syndromes go back to the ancient Greeks and Egyptians, it was during the 19th century that behavioral neurology began to arise, first with the primitive localization theories of Franz Gall , followed in the mid 19th century by the first localizations in aphasias by Paul Broca and then Carl Wernicke . Localizationist neurology and clinical descriptions reached a peak in the late 19th and early 20th century, with work extending into the clinical descriptions of dementias by Alois Alzheimer and Arnold Pick . The work of Karl Lashley in rats for a time in the early to mid 20th century put a damper on localization theory and lesion models of behavioral function.
In the United States, the work of Norman Geschwind led to a renaissance of behavioral neurology. He is famous for his work on disconnection syndromes, aphasia, and behavioral syndromes of limbic epilepsy , also called Geschwind syndrome. Having trained generations of behavioral neurologists (e.g., Antonio Damasio), Geschwind is considered the father of behavioral neurology.
The advent of in vivo neuroimaging starting in the 1980s led to a further strengthening of interest in the cognitive neurosciences and provided a tool that allowed for lesion, structural, and functional correlations with behavioral dysfunction in living people.
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Behr syndrome is characterized by the association of early-onset optic atrophy with spinocerebellar degeneration resulting in ataxia , pyramidal signs, peripheral neuropathy and developmental delay. [ 1 ] [ 2 ]
Although it is an autosomal recessive disorder, heterozygotes may still manifest much attenuated symptoms. [ 3 ] Autosomal dominant inheritance also being reported in a family. [ 4 ] Recently a variant of OPA1 mutation with phenotypic presentation like Behr syndrome is also described. [ 5 ] Some reported cases have been found to carry mutations in the OPA1, OPA3 or C12ORF65 genes which are known causes of pure optic atrophy or optic atrophy complicated by movement disorder. [ 6 ]
Onset : Early childhood
Progression : Chronic progressive
Clinical : Cerebellar ataxia plus syndrome / Optic Atrophy Plus Syndrome
Ocular : Optic atrophy, nystagmus, scotoma, and bilateral retrobulbar neuritis.
Other: Intellectual disability, myoclonic epilepsy, spasticity, and posterior column sensory loss. Tremor in some cases. [ 7 ]
Musculoskeletal
Contractures, lower limbs, Achilles tendon contractures, Hamstring contractures, Adductor longus contractures [ 8 ]
Systemic
Hypogonadotrophic hypogonadism. [ 9 ]
Behr syndrome is autosomal recessive which means the defective gene is located on an autosome , and two copies of the gene - one inherited from each parent - are required to be born with the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but are usually not affected by the disorder. Autosomal dominant inheritance also being reported. [ 4 ]
Compound heterozygous mutations in OPA1 gene were reported. [ 5 ] [ 10 ] Molecular genetic studies revealed a homozygous mutation in the C19ORF12 gene which has been previously reported in patients with mitochondrial membrane protein-associated neurodegeneration (MPAN) a variant of neurodegeneration with brain iron accumulation (NBIA). [ 6 ]
Autopsy on one of the sister with Behr Syndrome revealed central atrophy of the optic nerves and total disarray of the normal laminar pattern of the lateral geniculate nucleus, dropout of neurons, and gliosis. There were numerous axonal spheroids in the neuropil. Similar spheroids with cell loss and gliosis were also observed in other thalamic nuclei and, rarely, in the pallida. [ 11 ]
Diffuse, symmetric white matter abnormalities were demonstrated by magnetic resonance imaging (MRI) suggesting that Behr syndrome may represent a disorder of white matter associated with an unknown biochemical abnormality. [ 12 ]
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The Beit Memorial Medical Fellowships were one of the most prestigious and competitive fellowships for post-doctoral or medical degree research in medicine in the United Kingdom. The Fellowships were founded in 1909 by Sir Otto Beit , a German-born British financier, philanthropist and art connoisseur, in memory of his brother Alfred Beit .
Beit Memorial Fellows have been awarded a number of prestigious prizes with seven Nobel Prizes including two for Frederick Sanger (1944) and the 2012 prize for medicine for John Gurdon . [ 1 ] Nobel laureates who have held Beit fellowships are Alexander R. Todd (chemistry, 1957), Fred Sanger (chemistry, 1958 and 1980), Macfarlane Burnet (physiology or medicine, 1960), Bernard Katz (physiology or medicine, 1970) and Tim Hunt (physiology or medicine, 2001). The first female member of the Royal Society in 1945 was Marjory Stephenson (1914 Beit fellowship) an early recipient of the fellowship.
The Beit Memorial Medical Fellowships were replaced by the prestigious Wellcome-Beit Prize Fellowships in 2009. [ 2 ]
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Bendopnea is a newly described symptom, normally of heart failure , meaning shortness of breath felt when leaning forward. [ 1 ] [ 2 ] [ 3 ] [ 4 ] [ 5 ] It was introduced by Thibodeau et al. in 2014. [ 1 ] [ 2 ] Patients with heart failure often experience this when bending over to tie a shoe, putting socks on, or other activities requiring bending downwards. [ 1 ] [ 2 ] It has been defined as occurring within 30 seconds of bending over, but could occur in as few as 8 seconds in severe cases. [ 3 ] When a patient is in heart failure, it often means the ventricular filling pressures are high at baseline. [ 1 ] [ 2 ] When said person bends forward, it causes a further increase in ventricular filling pressures that causes dyspnea, especially in patients with lower cardiac indices . [ 1 ] [ 2 ]
The term "bendopnea" (meaning "bent" and "breath") was coined to be easily identifiable among patients and physicians. [ 3 ]
Bendopnea should be distinguished from orthopnea (shortness of breath while lying down), trepopnea (shortness of breath while lying on one side), and platypnea (shortness of breath relieved by lying down and worsened when upright) with or without orthodeoxia (oxygen desaturation).
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Benign fasciculation syndrome ( BFS ) is characterized by fasciculation (twitching) of voluntary muscles in the body. [ 1 ] The twitching can occur in any voluntary muscle group but is most common in the eyelids , arms, hands, fingers, legs, and feet. The tongue can also be affected. The twitching may be occasional to continuous. [ 2 ] BFS must be distinguished from other conditions that include muscle twitches.
The main symptom of benign fasciculation syndrome is focal or widespread involuntary muscle activity ( fasciculation ). [ 1 ] The benign twitches usually have a constant location. [ 2 ]
Other common symptoms are generalized fatigue or weakness, paraesthesia or numbness, and muscle cramping or spasms. [ 1 ] Anxiety and somatic symptom disorders and symptoms are commonly reported. [ 1 ] Muscle stiffness may also be present; if muscle weakness is not also present, and cramps are more severe, the stiffness may be categorized instead as cramp fasciculation syndrome . [ 3 ] Cramp fasciculation is a variant of BFS which presents with muscle pain and exercise intolerance . [ 2 ] [ 4 ]
Health anxiety disorder may be a cause among individuals who become concerned they have a motor neuron disease ; this persistent concern is a psychiatric condition mostly noted among healthcare professionals and doctors. [ 1 ] An association with anxiety level is established; [ 1 ] [ 5 ] BFS is reportedly found among "anxious medical students" and clinicians under the age of 40, [ 3 ] and this phenomenon known as "fasciculation anxiety syndrome" is reinforced by access to information on the internet. [ 4 ]
Fasciculations can be caused [ 4 ] or worsened by intense and long periods of daily exercise. [ 2 ]
BFS can also be caused by long-term use of anticholinergics , [ 4 ] and fasciculations may be caused by other drug use or exposure to steroids, nicotine, caffeine, alcohol, insecticides and pesticides. [ 2 ] Thyroid disease may also cause similar symptoms. [ 3 ]
Fasciculations can also be caused by deficiencies of magnesium and/or calcium. [ 6 ]
Benign fasciculation syndrome is a diagnosis of exclusion ; that is, other potential causes for the twitching must be ruled out before BFS can be diagnosed. Diagnosis includes blood tests, a neurological exam, and electromyography (EMG). [ 2 ]
Another step in diagnosing BFS is checking for clinical weakness or wasting, which are found in more serious conditions. [ 4 ] [ 2 ] Lack of clinical weakness along with normal EMG results (in those with only fasciculations) largely eliminates more serious disorders from potential diagnosis. [ 2 ] [ 3 ] In younger people with only lower motor neuron (LMN) fasciculations, no muscle weakness, and no thyroid abnormalities, Turner and Talbot (2013) state that "individuals under 40 years can be reassured without resorting to electromyography (EMG) to avoid the small but highly damaging possibility of false-positives". [ 3 ]
According to Kincaid (1997), the diagnosis is made when there is no clinical finding of neurogenic disease; he first reassures patients that no "ominous disease seems to be present", and says, "I suggest that patients like this be followed for a year or longer with clinical and electromyographic exams at about 6-month intervals before one becomes secure in the diagnosis that the fasciculations are truly benign." [ 7 ] Other publications recommend followups for four or five years before ruling the condition benign, although the percentage of individuals who progress to a more serious condition is very low. [ 2 ]
Benign fasciculation syndrome and the variant cramp fasciculation syndrome "can be regarded as part of a larger spectrum of disease that also incorporates acquired auto-immune neuromyotonia . [ 4 ]
Other serious diseases that must be distinguished include motor neuron diseases (MND) such as amyotrophic lateral sclerosis (ALS), [ 3 ] neuropathy , [ 4 ] and spinal cord diseases . [ 4 ]
According to Turner and Talbot (2013), "the fasciculations of MND are often abrupt and widespread at onset in an individual previously unaffected by fasciculations in youth. The site of the fasciculations, for example, those in the calves versus abdomen, has not been shown to be discriminatory for a benign disorder. There is conflicting evidence as to whether the character of fasciculations differs neurophysiologically in MND." [ 3 ] It is "exceptionally rare for patients later diagnosed with ALS to present with fasciculations alone", and ALS is ruled out with a normal EMG and no evidence of muscle wasting. [ 2 ]
There is support for treating any accompanying anxiety using cognitive behavioral therapy or antidepressants. [ 1 ] Quinine is effective, but not recommended because of the potential for serious side effects. [ 2 ] Calcium channel blockers may be effective, although the evidence for their use is weak. [ 2 ] There is little evidence supporting other therapies. [ 2 ]
In cases caused by magnesium or calcium deficiencies, curing the deficiency through diet or supplementation is effective. [ 6 ]
The prognosis for those with BFS is good to excellent. [ 8 ]
There may be an association between widespread fasciculations or paresthesias with small fiber neuropathy. [ 9 ] [ 10 ]
A 2017 study by Neurology.org also found that Benign Fasciculations are common in the general population, occurring in about 70% of healthy individuals and almost never associated with a serious neuromuscular disorder. Of patients that enrolled in a 1, 3, 6, 12 and 24 month study, perceived weakness was reported in 35.3%, 47.1% experienced numbness, 70.6% had tingling, cramps were present in 64.7% and after 24 months, only 5% had their symptoms resolved. Of all the patients, none developed Motor Neuron Disease. [ 11 ]
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Benign hereditary chorea ( BHC ), also known as benign familial chorea , is a rare autosomal dominant neurogenetic syndrome. It typically presents itself in childhood with isolated chorea , with average to below average intelligence. Unlike other neurogenetic causes of chorea such as Huntington's disease , BHC is not progressive, and not associated with cognitive decline or psychiatric problems in the vast majority of cases. [ 2 ]
The first description of BHC was reported in 1967 in an African American family from Mississippi. [ 3 ] Two brothers reportedly had delayed motor development in childhood and were diagnosed with chorea .
These findings were reaffirmed by other families reporting similar traits and an autosomal dominant pattern of inheritance was suggested. However, heterogeneity in the presentations of the affected individuals made confirmation of these diagnoses of BHC difficult to prove. Features reported in these families, including dystonia, tremor, and myoclonus, led researchers to question whether BHC actually represents different diagnoses with similar phenotypes inappropriately grouped together. [ 4 ]
Further research in 2000 confirmed a connection between a Dutch family reporting similar characteristics of BHC and one of the original families. The investigators identified a linkage to a disease locus on the long arm of chromosome 14 from this connection. [ 4 ]
Benign Hereditary Chorea is characterized by early onset of an abnormal gait, speech articulation difficulties, anxiety, and chorea. [ 5 ]
The clinical spectrum of symptoms resulting from BHC is vast, manifesting as thyroid agenesis to dysarthria to distress syndrome. As a result, genetic testing is the only way to confirm the syndrome. [ 2 ]
BHC is caused by a single-nucleotide substitution mutation in TITF1 , which encodes thyroid transcription factor 1 (TTF-1) and is inherited in an autosomal dominant pattern. This gene is also known as NK2 homeobox 1 ( NKX2-1 ) [ 2 ] The single-nucleotide substitution mutation then ultimately has drastic effects on the maturation processes of TITF-1 [ 4 ]
In some cases, additional developmental abnormalities of lung and thyroid tissue are found in BHC, leading to the suggested alternative name brain-lung-thyroid syndrome . [ 6 ]
Benign Hereditary Chorea is an autosomal dominant disorder. It is believed to be caused by a single-nucleotide substitution in TITF1 , located on chromosome 14. A wide spectrum of mutations have been reported, drawing a potential association between amount of subsequently deleted nucleotides to severity of symptoms. These mutations lead to protein truncation, prevent DNA binding, and a loss-of-function. Mutations of the gene affect namely the lungs, brain, and thyroid. This is because during embryonic development, NKX2.1 plays a key role in binding to transcriptional regulatory elements and proteins within those respective organs. [ 4 ]
BHC begins showing symptoms during childhood, and is commonly a familial disorder. This is a disorder that is correlated with mutations in the thyroid transcription factor gene (TITF-1). [ 7 ]
The disorder was discovered in 1960s. During the time of its discovery, there were no tests that could be used to confirm a diagnosis of the disorder, and the phenotype was not easy to distinguish from other disorders. This resulted in the existence of the disorder being questioned. However, in 2002, the experimentally observed mutation of the gene leading to the BHC phenotype was identified, solidifying benign hereditary chorea as a disorder. [ 7 ]
In 1967, several families were examined and discovered to have movements that were abnormal and random since childhood. These random movements were not violent movements, and gave the person a "general appearance of restlessness." The movements occurred mostly in the hands and arms, and some also experienced them in their tongues, facial muscles, and lower body. Movements in the lower extremities, if severe enough, could cause changes in gait. The families were given a Wechsler Intelligence Scale test, scoring average relative to others in their community. Aside from the aforementioned symptoms, the peoples' physical and neurological characteristics were normal. The observed symptoms were put in the category of chorea . [ 7 ]
Researchers made pedigrees of the families they studied and determined that BHC was an autosomal dominant disorder. By studying a Dutch family, the disorder was discovered to be linked to chromosome 14 . In 2002, an Italian family was studied, and they had the same linkage to chromosome 14 as the Dutch family did. Looking closer at the region of the chromosome suspected of causing the disorder, researchers discovered that there was a 1.2 Mb deletion in the DNA that resulted in the loss of the TITF-1 gene. This meant that mutations in the TITF-1 gene were likely the reason behind the symptoms of BHC. [ 7 ]
Currently, BHC is diagnosed through the identification of the phenotypic symptoms with a genetic test to confirm the mutation in the TITF-1 gene. [ 7 ]
There are no cures for benign hereditary chorea, but there are several medications that have been shown to treat the symptoms of the disorder. Levodopa has been shown to improve the effects of chorea on a patient's gait within 6 weeks of starting treatments. However, this medication did have the side effect of "dose-dependent dyskinesia ." Methylphenidate has also been used to improve chorea symptoms. Steroids have been used to treat BHC, but due to the presence of dystonia, it is questionable whether these patients actually had BHC. [ 7 ]
In 1978, BHC was reported to have a frequency of 1:500,000 within a Welsh population, but due to how some symptoms are hard to distinguish, it was concluded that the number is underrespresentative of actual clinical cases. Results for correlation between sex and distribution of the disorder are inconclusive. [ 8 ]
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Benign proliferative breast disease is a group of noncancerous conditions that may increase the risk of developing breast cancer . Examples include atypical ductal hyperplasia , atypical lobular hyperplasia , and intraductal papillomas .
This article incorporates public domain material from Dictionary of Cancer Terms . U.S. National Cancer Institute .
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A benign tumor is a mass of cells ( tumor ) that does not invade neighboring tissue or metastasize (spread throughout the body). Compared to malignant (cancerous) tumors , benign tumors generally have a slower growth rate . Benign tumors have relatively well differentiated cells. They are often surrounded by an outer surface (fibrous sheath of connective tissue ) or stay contained within the epithelium . Common examples of benign tumors include moles and uterine fibroids .
Some forms of benign tumors may be harmful to health. Benign tumor growth causes a mass effect that can compress neighboring tissues. This can lead to nerve damage, blood flow reduction ( ischemia ), tissue death ( necrosis ), or organ damage. The health effects of benign tumor growth may be more prominent if the tumor is contained within an enclosed space such as the cranium , respiratory tract , sinus , or bones. For example, unlike most benign tumors elsewhere in the body, benign brain tumors can be life-threatening. Tumors may exhibit behaviors characteristic of their cell type of origin; as an example, endocrine tumors such as thyroid adenomas and adrenocortical adenomas may overproduce certain hormones .
The word benign means ' favourable, kind, fortunate, salutary, propitious ' . [ 1 ] However, a benign tumor is not benign in the usual sense; the name merely specifies that it is not "malignant", i.e. cancerous. While benign tumors usually do not pose a serious health risk, they can be harmful or fatal. [ 2 ] Many types of benign tumors have the potential to become cancerous ( malignant ) through a process known as tumor progression . For this reason and other possible harms, some benign tumors are removed by surgery. When removed, benign tumors usually do not return. Exceptions to this rule may indicate malignant transformation.
Benign tumors are very diverse; they may be asymptomatic or may cause specific symptoms, depending on their anatomic location and tissue type. They grow outward, producing large, rounded masses which can cause what is known as a "mass effect". This growth can cause compression of local tissues or organs, leading to many effects, such as blockage of ducts, reduced blood flow ( ischaemia ), tissue death ( necrosis ) and nerve pain or damage. [ 3 ] Some tumors also produce hormones that can lead to life-threatening situations. Insulinomas can produce large amounts of insulin, causing hypoglycemia . [ 4 ] [ 5 ] Pituitary adenomas can cause elevated levels of hormones such as growth hormone and insulin-like growth factor-1 , which cause acromegaly ; prolactin ; ACTH and cortisol , which cause Cushing's disease ; TSH , which causes hyperthyroidism ; and FSH and LH . [ 6 ] Bowel intussusception can occur with various benign colonic tumors. [ 7 ] Cosmetic effects can be caused by tumors, especially those of the skin, possibly causing psychological or social discomfort for the person with the tumor. [ 8 ] Vascular tissue tumors can bleed, in some cases leading to anemia . [ 9 ]
PTEN hamartoma syndrome encompasses hamartomatous disorders characterized by genetic mutations in the PTEN tumor suppressor gene, [ 10 ] including Cowden syndrome , Bannayan–Riley–Ruvalcaba syndrome , Proteus syndrome and Proteus-like syndrome . Absent or dysfunctional PTEN protein allows cells to over-proliferate, causing hamartomas. [ 11 ] Cowden syndrome is an autosomal dominant genetic disorder characterized by multiple benign hamartomas ( trichilemmomas and mucocutaneous papillomatous papules) as well as a predisposition for cancers of multiple organs including the breast and thyroid. [ 12 ] [ 13 ] Bannayan–Riley–Ruvalcaba syndrome is a congenital disorder characterized by hamartomatous intestinal polyposis, macrocephaly , lipomatosis , hemangiomatosis and glans penis macules. [ 11 ] [ 14 ] Proteus syndrome is characterized by nevi , asymmetric overgrowth of various body parts, adipose tissue dysregulation, cystadenomas , adenomas , vascular malformation. [ 15 ] [ 16 ]
Familial adenomatous polyposis (FAP) is a familial cancer syndrome caused by mutations in the APC gene. In FAP, adenomatous polyps are present in the colon . The polyps progress into colon cancer unless removed. [ 17 ] The APC gene is a tumor suppressor . Its protein product is involved in many cellular processes. Inactivation of the APC gene leads to the buildup of a protein called β-catenin . This protein activates two transcription factors : T-cell factor (TCF) and lymphoid enhancer factor (LEF). These factors cause the upregulation of many genes involved in cell proliferation , differentiation , migration and apoptosis (programmed cell death), causing the growth of benign tumors. [ 18 ]
Tuberous sclerosis complex (TSC) is an autosomal dominant genetic disorder caused by mutations in the genes TSC1 and TSC2 . TSC1 produces the protein hamartin . TSC2 produces the protein tuberin . This disorder presents with many benign hamartomatous tumors including angiofibromas , renal angiomyolipomas , and pulmonary lymphangiomyomatosis . Tuberin and hamartin inhibit the mTOR protein in normal cellular physiology. Inactivation of the TSC tumor suppressors causes an increase in mTOR activity. This leads to the activation of genes and the production of proteins that increase cell growth. [ 19 ] [ 20 ] [ 21 ]
Von Hippel–Lindau disease is a dominantly inherited cancer syndrome that significantly increases the risk of various tumors. This includes benign hemangioblastomas and malignant pheochromocytomas , renal cell carcinomas , pancreatic endocrine tumors , and endolymphatic sac tumors . It is caused by genetic mutations in the Von Hippel–Lindau tumor suppressor gene. The VHL protein (pVHL) is involved in cellular signaling in oxygen starved ( hypoxic ) cells. One role of pVHL is to cause the cellular degradation of another protein, HIF1α . Dysfunctional pVHL leads to accumulation of HIF1α. This activates several genes responsible for the production of substances involved in cell growth and blood vessel production: VEGF , PDGFβ , TGFα and erythropoietin . [ 22 ]
Benign tumors of bone can be similar macroscopically and require a combination of a clinical history with cytogenetic , molecular, and radiologic tests for diagnosis. [ 23 ] Three common forms of benign bone tumors with are giant cell tumor of bone, osteochondroma , and enchondroma ; other forms of benign bone tumors exist but may be less prevalent. [ citation needed ]
Giant cell tumors of bone frequently occur in long bone epiphyses of the appendicular skeleton or the sacrum of the axial skeleton . Local growth can cause destruction of neighboring cortical bone and soft tissue, leading to pain and limiting range of motion. The characteristic radiologic finding of giant cell tumors of bone is a lytic lesion that does not have marginal sclerosis of bone. On histology, giant cells of fused osteoclasts are seen as a response to neoplastic mononucleated cells. Notably, giant cells are not unique among benign bone tumors to giant cell tumors of bone. Molecular characteristics of the neoplastic cells causing giant cell tumors of bone indicate an origin of pluripotent mesenchymal stem cells that adopt preosteoblastic markers. Cytogenetic causes of giant cell tumors of bone involve telomeres . Treatment involves surgical curettage with adjuvant bisphosphonates . [ citation needed ]
Osteochondromas form cartilage-capped projections of bone. Structures such as the marrow cavity and cortical bone of the osteochondroma are contiguous to those of the originating bone. Sites of origin often involve metaphyses of long bones. While many osteochondromas occur spontaneously, there are cases in which several osteochondromas can occur in the same individual; these may be linked to a genetic condition known as hereditary multiple osteochondromas. Osteochondroma appears on X-ray as a projecting mass that often points away from joints. [ 23 ] These tumors stop growing with the closure of the parental bone's growth plates. Failure to stop growth can be indicative of transformation to malignant chondrosarcoma. Treatment is not indicated unless symptomatic. In that case, surgical excision is often curative. [ citation needed ]
Enchondromas are benign tumors of hyaline cartilage. Within a bone, enchondromas are often found in metaphyses. They can be found in many types of bone, including small bones, long bones, and the axial skeleton. X-ray of enchondromas shows well-defined borders and a stippled appearance. [ 23 ] Presentation of multiple enchondromas is consistent with multiple enchondromatosis ( Ollier Disease ). Treatment of enchondromas involves surgical curettage and grafting. [ citation needed ]
Lipomas are benign, subcutaneous tumors of fat cells ( adipocytes ). They are usually painless, slow-growing, and mobile masses that can occur anywhere in the body where there are fat cells, but are typically found on the trunk and upper extremities. [ 24 ]
[ 25 ] Although lipomas can develop at any age, they more commonly appear between the ages of 40 and 60. [ 24 ] Lipomas affect about 1% of the population, with no documented sex bias, and about 1 in every 1000 people will have a lipoma within their lifetime. [ 25 ] [ 26 ] The cause of lipomas is not well defined. Genetic or inherited causes of lipomas play a role in around 2-3% of patients. [ 25 ] In individuals with inherited familial syndromes such as Proteus syndrome or Familial multiple lipomatosis , it is common to see multiple lipomas across the body. [ 25 ] These syndromes are also associated with specific symptoms and sub-populations. Mutations in chromosome 12 have been identified in around 65% of lipoma cases. [ 25 ] Lipomas have also been shown to be increased in those with obesity , hyperlipidemia , and diabetes mellitus . [ 25 ]
Lipomas are usually diagnosed clinically, although imaging ( ultrasound , computed tomography , or magnetic resonance imaging ) may be utilized to assist with the diagnosis of lipomas in atypical locations. [ 24 ] The main treatment for lipomas is surgical excision, after which the tumor is examined with histopathology to confirm the diagnosis. [ 24 ] The prognosis for benign lipomas is excellent and recurrence after excision is rare, but may occur if the removal was incomplete. [ 25 ]
One of the most important factors in classifying a tumor as benign or malignant is its invasive potential. If a tumor lacks the ability to invade adjacent tissues or spread to distant sites by metastasizing then it is benign, whereas invasive or metastatic tumors are malignant. [ 3 ] For this reason, benign tumors are not classed as cancer. [ 27 ] Benign tumors will grow in a contained area usually encapsulated in a fibrous connective tissue capsule. The growth rates of benign and malignant tumors also differ; benign tumors generally grow more slowly than malignant tumors. Although benign tumors pose a lower health risk than malignant tumors, they both can be life-threatening in certain situations. There are many general characteristics which apply to either benign or malignant tumors, but sometimes one type may show characteristics of the other. For example, benign tumors are mostly well differentiated and malignant tumors are often undifferentiated. However, undifferentiated benign tumors and differentiated malignant tumors can occur. [ 28 ] [ 29 ] Although benign tumors generally grow slowly, cases of fast-growing benign tumors have also been documented. [ 30 ] Some malignant tumors are mostly non-metastatic such as in the case of basal-cell carcinoma . [ 31 ] CT and chest radiography can be a useful diagnostic exam in visualizing a benign tumor and differentiating it from a malignant tumor. The smaller the tumor on a radiograph, the more likely it is to be benign as 80% of lung nodules less than 2 cm in diameter are benign. Most benign nodules are smoothed radiopaque densities with clear margins but these are not exclusive signs of benign tumors. [ 32 ]
Tumors are formed by carcinogenesis , a process in which cellular alterations lead to the formation of cancer. Multistage carcinogenesis involves the sequential genetic or epigenetic changes to a cell's DNA , where each step produces a more advanced tumor. It is often broken down into three stages; initiation, promotion and progression, and several mutations may occur at each stage. Initiation is where the first genetic mutation occurs in a cell. Promotion is the clonal expansion (repeated division) of this transformed cell into a visible tumor that is usually benign. Following promotion, progression may take place where more genetic mutations are acquired in a sub-population of tumor cells. Progression changes the benign tumor into a malignant tumor. [ 33 ] [ 34 ] A prominent and well studied example of this phenomenon is the tubular adenoma, a common type of colon polyp which is an important precursor to colon cancer. The cells in tubular adenomas, like most tumors that frequently progress to cancer, show certain abnormalities of cell maturation and appearance collectively known as dysplasia . These cellular abnormalities are not seen in benign tumors that rarely or never turn cancerous, but are seen in other pre-cancerous tissue abnormalities which do not form discrete masses, such as pre-cancerous lesions of the uterine cervix . [ citation needed ]
Benign neoplasms are typically, but not always, composed of cells which bear a strong resemblance to a normal cell type in their organ of origin. These tumors are named for the cell or tissue type from which they originate. The suffix "-oma" (but not -carcinoma, -sarcoma, or -blastoma, which are generally cancers) is applied to indicate a benign tumor. For example, a lipoma is a common benign tumor of fat cells ( lipocytes ), and a chondroma is a benign tumor of cartilage-forming cells ( chondrocytes ). Adenomas are benign tumors of gland-forming cells, and are usually specified further by their cell or organ of origin, as in hepatic adenoma (a benign tumor of hepatocytes , or liver cells). Teratomas contain many cell types such as skin, nerve, brain and thyroid, among others, because they are derived from germ cells. [ 36 ] Hamartomas are a group of benign tumors that have relatively normal cellular differentiation but exhibit disorganized tissue organization. [ 19 ]
Exceptions to the nomenclature rules exist for historical reasons; malignant examples include melanoma (a cancer of pigmented skin cells, or melanocytes ) and seminoma (a cancer of male reproductive cells). [ 37 ]
Benign tumors do not encompass all benign growths. Skin tags, vocal chord polyps, and hyperplastic polyps of the colon are often referred to as benign, but they are overgrowths of normal tissue rather than neoplasms. [ 36 ]
Benign tumors typically need no treatment unless they cause problems such as seizures, discomfort or cosmetic concerns. Surgery is usually the most effective approach and is used to treat most benign tumors. In some cases, other treatments may be used. Adenomas of the rectum may be treated with sclerotherapy , in which chemicals are used to shrink blood vessels in order to cut off the blood supply. [ 38 ] Most benign tumors do not respond to chemotherapy or radiation therapy , although there are exceptions; benign intercranial tumors are sometimes treated with radiation therapy and chemotherapy under certain circumstances. [ 39 ] [ 40 ] Radiation can also be used to treat hemangiomas in the rectum. [ 38 ] Benign skin tumors are usually surgically resected but other treatments such as cryotherapy , curettage , electrodesiccation , laser therapy , dermabrasion , chemical peels and topical medication are used. [ 41 ] [ 42 ]
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Professor Benjamin Oluwakayode Osuntokun (6 January 1935 – 22 September 1995), [ 1 ] was a researcher and neurologist from Okemesi, Ekiti State , Nigeria. [ 2 ] Known for discovering the cause of ataxic tropical neuropathy , he was a founding member of the Pan African Association of Neurological Sciences and an early advocate and researcher on tropical neurology. [ 3 ]
He had his primary and secondary education at the Holy Trinity School, Ilawe Ekiti , the Emmanuel School, Ado Ekiti and Christ's School Ado Ekiti . After finishing his secondary education, he studied medicine at the University College, Ibadan when it was still affiliated to the University of London . [ 4 ] [ 5 ]
In 1963, he was invited by Prof Harold Scarborough to spend a year at the Welsh National School of Medicine in Cardiff . [ 6 ]
He joined the research staff of the University College , Ibadan in 1964, as a medical research fellow. However, upon gaining a Smith and Nephew fellowship, he went abroad for further studies under the direction of Henry Miller and John Walton, both eminent neurologists in Newcastle upon Tyne . [ 7 ] After spending some time in Newcastle, he took a job at the National Hospital for Nervous Diseases , Queens Square, London before returning to Nigeria in 1965. It was at the University of Ibadan he launched a productive career, working on neuro-epidemiology and clinical and investigative neurology especially the study of dementia among Nigerians and African Americans . [ 7 ]
In the late 1960s, he investigated cases of ataxic neuropathy in Epe where residents usually consume a dose of ill processed cassava with little or no supplement. [ 8 ] He then mapped out the epidemiology of the neuropathy and was able to study the basic aspects of the neuropathy. He discovered the disease was due to cyanide intoxication. At the time, little was done beyond clinical attention to the disease. His success in discovering the basis of tropical ataxic neuropathy earned him local and international acclaim in the medical community. [ 7 ]
Throughout his career, he wrote a number of scholarly works on his prodigious research on tropical epidemiology and was also Dean of Medicine at the University of Ibadan and later the Chief Medical Officer of that university's teaching hospital, UCH . He died in 1995 and was buried in his native Okemesi , Ekiti State . [ 2 ]
The onset of neuropathy after ingestion of ill-processed Cassava, due to Cyanide Intoxication, is known as the Osuntokun's Sign , and is commonly used in African Medical Lectures and Bulletins, but is not much known to countries outside Africa. [ 9 ]
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Benjamin Rush (January 4, 1746 [ O.S. December 24, 1745] – April 19, 1813) was an American revolutionary , a Founding Father of the United States and signatory to the U.S. Declaration of Independence , and a civic leader in Philadelphia , where he was a physician, politician, social reformer, humanitarian, educator, and the founder of Dickinson College . Rush was a Pennsylvania delegate to the Continental Congress . [ 1 ] He later described his efforts in support of the American Revolution, saying: "He aimed well." [ 2 ] [ 3 ] He served as surgeon general of the Continental Army and became a professor of chemistry, medical theory, and clinical practice at the University of Pennsylvania . [ 4 ]
Dr. Benjamin Rush was a leader of the American Enlightenment and an enthusiastic supporter of the American Revolution . He was a leader in Pennsylvania's ratification of the U.S. Constitution in 1788. He was prominent in many reforms, especially in the areas of medicine and education. He opposed slavery, advocated free public schools, and sought improved, but patriarchal, [ 5 ] education for women, and a more enlightened penal system. As a leading physician, Rush had a major impact on the emerging medical profession.
As an Enlightenment intellectual, Rush was committed to organizing all medical knowledge around explanatory theories, rather than relying on empirical methods . Rush argued that illness was the result of imbalances in the body's physical system and was caused by malfunctions in the brain. His approach prepared the way for later medical research, but Rush undertook none of it. He promoted public health by advocating clean environment and stressing the importance of personal and military hygiene. His study of mental disorder made him one of the founders of American psychiatry . [ 6 ] In 1965, the American Psychiatric Association recognized Rush as the "father of American psychiatry". [ 7 ]
Rush was born to John Rush and Susanna Hall on January 4, 1746 (December 24, 1745, O.S.). The family, of English descent, [ 8 ] lived on a farm in the Township of Byberry in Philadelphia County , about 14 miles outside of Philadelphia (the township was incorporated into Philadelphia in 1854). Rush was the fourth of seven children. His father died in July 1751 at age 39, leaving his mother, who ran a country store, to care for the family. At age eight, Benjamin was sent to live with an aunt and uncle to receive an education. [ 9 ] He and his older brother Jacob [ 10 ] attended a school run by Reverend Samuel Finley , which later became West Nottingham Academy .
In 1760, after further studies at the College of New Jersey, which in 1895 became Princeton University , Rush graduated with a Bachelor of Arts degree at age 14. From 1761 to 1766, Rush apprenticed under Dr. John Redman in Philadelphia. Redman encouraged him to further his studies at the University of Edinburgh in Scotland, where Rush studied from 1766 to 1768 and earned an M.D. degree. [ 11 ] [ 12 ] [ 13 ] : 60 [ 14 ] : 40 Rush became fluent in French, Italian, and Spanish as a result of his studies and European tour. While at Edinburgh , he became a friend of the Earl of Leven and his family, including William Leslie . [ 13 ] : 51–52
Returning to the Colonies in 1769, Rush opened a medical practice in Philadelphia and became professor of chemistry at the College of Philadelphia (which in 1791 changed its name to its present name, University of Pennsylvania ). [ 15 ] After his election to the revived American Philosophical Society in 1768, Rush served as the society's curator from 1770 to 1773, as secretary from 1773 to 1773, and vice president from 1797 to 1801. [ 16 ] Rush ultimately published the first American textbook on chemistry and several volumes on medical student education and wrote influential patriotic essays. [ 14 ]
Rush was active in the Sons of Liberty and was elected to attend the provincial conference to send delegates to the Continental Congress . Thomas Paine consulted Rush when writing the profoundly influential pro-independence pamphlet Common Sense . Starting in 1776, Rush represented Pennsylvania and signed the Declaration of Independence. [ 1 ] He also represented Philadelphia at Pennsylvania's own Constitutional Convention. [ 1 ]
In an 1811 letter to John Adams, Rush recounted in stark fashion the signing of the Declaration of Independence. He described it as a scene of "pensive and awful silence". Rush said the delegates were called up, one after another, and then filed forward somberly to subscribe to what each thought was their ensuing death warrant. [ 17 ] He related that the "gloom of the morning" was briefly interrupted when the rotund Benjamin Harrison of Virginia said to a diminutive Elbridge Gerry of Massachusetts, at the signing table, "I shall have a great advantage over you, Mr. Gerry, when we are all hung for what we are now doing. From the size and weight of my body I shall die in a few minutes and be with the Angels, but from the lightness of your body you will dance in the air an hour or two before you are dead." [ 17 ] According to Rush, Harrison's remark "procured a transient smile, but it was soon succeeded by the Solemnity with which the whole business was conducted." [ 17 ]
While Rush was representing Pennsylvania in the Continental Congress (and serving on its medical committee), he also used his medical skills in the field. Rush accompanied the Philadelphia militia during the battles after which the British occupied Philadelphia and most of New Jersey. He was depicted serving in the Battle of Princeton in the painting The Death of General Mercer at the Battle of Princeton, January 3, 1777 by the American artist John Trumbull . [ 18 ]
The Army Medical Service was in disarray, between the military casualties, extremely high losses from typhoid , yellow fever and other camp illnesses, political conflicts between Dr. John Morgan and Dr. William Shippen Jr. , and inadequate supplies and guidance from the medical committee. [ 19 ] : 29–43, 65–92 Nonetheless, Rush accepted an appointment as surgeon-general of the middle department of the Continental Army. Rush's order "Directions for preserving the health of soldiers" became one of the foundations of preventive military medicine and was repeatedly republished, including as late as 1908. [ 20 ] [ 21 ] : 36–41 However, Rush's reporting of Shippen's misappropriation of food and wine supplies intended to comfort hospitalized soldiers, under-reporting of patient deaths, and failure to visit the hospitals under his command, ultimately led to Rush's resignation in 1778.
Rush criticized General George Washington in two handwritten but unsigned letters while still serving under the surgeon general. One, to Virginia Governor Patrick Henry dated October 13, 1778, quotes General Thomas Conway saying that if not for God's grace the ongoing war would have been lost by Washington and his weak counselors. Henry forwarded the letter to Washington, despite Rush's request that the criticism be conveyed orally, and Washington recognized the handwriting. At the time, the supposed Conway Cabal was reportedly trying to replace Washington with Horatio Gates as commander-in-chief. [ 14 ] : 133–34 Rush's letter relayed General John Sullivan 's criticism that forces directly under Washington were undisciplined and mob-like, and contrasted Gates' army as "a well-regulated family". [ 22 ] : 212–215 Ten days later, Rush wrote to John Adams relaying complaints inside Washington's army, including about "bad bread, no order, universal disgust" and praising Conway, who had been appointed to inspector general. [ 14 ] : 136–37
Shippen sought Rush's resignation and received it by the end of the month after Continental Congress delegate John Witherspoon , chairman of a committee to investigate Morgan's and Rush's charges of misappropriation and mismanagement against Shippen, told Rush his complaints would not produce reform. [ 13 ] : 219–20 Rush later expressed regret for his gossip against Washington. In a letter to John Adams in 1812, Rush wrote, "He [Washington] was the highly favored instrument whose patriotism and name contributed greatly to the establishment of the independence of the United States." Rush also successfully pleaded with Washington's biographers Justice Bushrod Washington and Chief Justice John Marshall to delete his association with those stinging words. [ 14 ] : 137
In his 2005 book 1776 , David McCullough quotes Rush, referring to George Washington:
The Philadelphia physician and patriot Benjamin Rush, a staunch admirer, observed that Washington "has so much martial dignity in his deportment that you would distinguish him to be a general and a soldier from among 10,000 people. There is not a king in Europe that would not look like a valet de chambre by his side." [ 23 ]
Rush believed that, while America was free from British rule, the "American Revolution" had yet to finish. As expressed in his 1787 'Address to the People of the United States', "The American war is over: but this is far from being the case with the American revolution. On the contrary, nothing but the first act of the great drama is closed." [ 24 ] In this address, he encouraged Americans to "come forward" and continue advancements on behalf of America.
In 1783, he was appointed to the staff of Pennsylvania Hospital , and he remained a member until his death. He was elected to the Pennsylvania convention which adopted the Federal constitution and was appointed treasurer of the United States Mint , serving from 1797 to 1813. [ 1 ] He was elected a fellow of the American Academy of Arts and Sciences in 1788. [ 25 ]
He became a professor of medical theory and clinical practice at the University of Pennsylvania in 1791, though the quality of his medicine was quite primitive even for the time: he advocated bloodletting for almost any illness, long after its practice had declined. While teaching at the University of Pennsylvania, one of his students was future president William Henry Harrison , who took a chemistry class from Rush. [ 26 ]
He was also founder of Dickinson College in Carlisle, Pennsylvania . In 1794, he was elected a foreign member of the Royal Swedish Academy of Sciences . In the 1793 Philadelphia yellow fever epidemic , Rush treated patients with bleeding, calomel, and other early medicinal techniques that often were ineffective and actually brought many patients closer to their deathbeds. Rush's ideas on yellow fever treatments differed from those of many experienced French doctors, who came from the West Indies where there were yellow fever outbreaks every year. However, he also helped the population of the city by convincing Richard Allen to ask members of his African Methodist Episcopal Church and other free blacks, who it was believed were less affected by yellow fever than other Philadelphians, [ 27 ] to perform volunteer aid work for doctors and funeral homes . [ 28 ]
Rush came down with yellow fever himself during the 1793 epidemic, although he recovered from it. [ 28 ]
Rush took on several social causes during his lifetime. Rush became a social activist and an abolitionist and was a founding member of the Philadelphia Society for Alleviating the Miseries of Public Prisons (known today as the Pennsylvania Prison Society [ 29 ] ), which greatly influenced the construction of Eastern State Penitentiary in Philadelphia. [ 30 ] He supported Thomas Jefferson for president in 1796 over the eventual winner, John Adams. [ 31 ]
In 1803, Jefferson sent Meriwether Lewis to Philadelphia to prepare for the Lewis and Clark Expedition under the tutelage of Rush, who taught Lewis about frontier illnesses and the performance of bloodletting. Rush provided the corps with a medical kit that included:
In 1766, when Rush set out for his studies in Edinburgh, he was outraged by the sight of 100 slave ships in Liverpool harbor. As a prominent Presbyterian doctor and professor of chemistry in Philadelphia, he provided a bold and respected voice against the slave trade. [ 36 ] He warmly praised the ministry of "Black Harry" Hosier , the freedman circuit rider who accompanied Bishop Francis Asbury during the establishment of the Methodist Church in America, [ 37 ] but the highlight of his involvement was the pamphlet he wrote in 1773 entitled "An Address to the Inhabitants of the British Settlements in America, upon Slave-Keeping." In this first of his many attacks on the social evils of his day, he assailed the slave trade as well as the entire institution of slavery. Rush argued scientifically that Blacks were not by nature intellectually or morally inferior. Any apparent evidence to the contrary was only the perverted expression of slavery, which "is so foreign to the human mind, that the moral faculties, as well as those of the understanding are debased, and rendered torpid by it." [ 38 ]
Rush deemed public punishments such as putting a person on display in stocks , common at the time, to be counterproductive. Instead, he proposed private confinement, labor, solitude, and religious instruction for criminals, and he opposed the death penalty. [ 39 ] His outspoken opposition to capital punishment pushed the Pennsylvania legislature to abolish the death penalty for all crimes other than first-degree murder . [ 4 ] He authored a 1792 treatise on punishing murder by death in which he made three principal arguments: [ 40 ]
Rush led the state of Pennsylvania to establish the first state penitentiary, the Walnut Street Prison , in 1790. Rush campaigned for long-term imprisonment, the denial of liberty, as both the most humane but severe punishment. [ 41 ] This 1792 treatise was preceded by comments on the efficacy of the death penalty that he self-references and which, evidently, appeared in the second volume of the American Museum . [ 40 ]
After the Revolution, Rush proposed a new model of education for elite women that included English language, vocal music, dancing, sciences, bookkeeping, history, and moral philosophy. He was instrumental to the founding of the Young Ladies' Academy of Philadelphia , the first chartered women's institution of higher education in Philadelphia. [ 42 ] Rush saw little need for training women in metaphysics, logic, mathematics, or advanced science; rather he wanted the emphasis on guiding women toward moral essays, poetry, history, and religious writings. This type of education for elite women grew dramatically during the post-revolutionary period, as women claimed a role in creating the Republic. And so, the ideal of Republican motherhood emerged, lauding women's responsibility of instructing the young in the obligations of patriotism, the blessings of liberty and the true meaning of Republicanism . He opposed coeducational classrooms and insisted on the need to instruct all youth in the Christian religion. [ 43 ]
Rush was a leading proponent of heroic medicine . He firmly believed in such practices as bloodletting patients [ 44 ] (a practice now known to be generally harmful, [ 45 ] but at the time common practice), as well as purges using calomel and other toxic substances. In his report on the Philadelphia yellow fever epidemic of 1793, Rush wrote: "I have found bleeding to be useful, not only in cases where the pulse was full and quick but where it was slow and tense. I have bled twice in many and in one acute case four times, with the happiest effect. I consider intrepidity in the use of the lancet , at present, to be necessary, as it is in the use of mercury and jalap , in this insidious and ferocious disease." During that epidemic, Rush gained acclaim for remaining in town and treating sometimes 100 patients per day (some through freed black volunteers coordinated by Richard Allen ), but many died. Even Rush acknowledged the failure of two treatments, sweats in vinegar-wrapped blankets accompanied by mercury rubs, and cold baths. [ 22 ] : 329
William Cobbett vociferously objected to Rush's extreme use of bloodletting, and even in Rush's day and location, many physicians had abandoned on scientific grounds this favorite remedy of Rush's former teachers Thomas Sydenham and Hermann Boerhaave . [ 14 ] : 223–31 Cobbett accused Rush of killing more patients than he had saved. Rush ultimately sued Cobbett for libel , winning a judgment of $5,000 and $3,000 in court costs, which was only partially paid before Cobbett returned to England. [ 14 ] : 239–47 Nonetheless, Rush's practice waned as he continued to advocate bloodletting and purges, much to the chagrin of his friend Thomas Jefferson. [ 46 ] [ 47 ] [ 14 ] : 296 Some even blamed Rush's bleeding for hastening the death of Benjamin Franklin , as well as George Washington (although the only one of Washington's medics who opposed the bleeding was Rush's former student), and Rush insisted upon being bled himself shortly before his death (as he had during the yellow fever epidemic two decades earlier). [ 22 ] : 331, 363 [ 14 ] : 220, 295
Rush also wrote the first case report on dengue fever (published in 1789 on a case from 1780). [ 48 ] Perhaps his greatest contributions to physical medicine were his establishment of a public dispensary for low-income patients (Philadelphia Dispensary), and public works associated with draining and rerouting Dock Creek (eliminating mosquito breeding grounds, which greatly decreased typhus , typhoid and cholera outbreaks).
Another of Rush's medical views that now draws criticism is his analysis of race. In reviewing the case of Henry Moss, a slave who lost his dark skin color (probably through vitiligo ), Rush characterized being black as a hereditary and curable skin disease. Rush wrote that the "disease, instead of inviting us [whites] to tyrannise over them [blacks], it should entitle them to a double portion of our humanity." He added that this "should teach white people the necessity of keeping up that prejudice against [miscegenation], as it would tend to infect posterity with … their disorder" and called for an "endeavour to discover a remedy for it." [ 49 ]
Rush was interested in Native American health. He wanted to find out why Native Americans were susceptible to certain illnesses and whether they had higher mortality rates as compared to other people. Other questions that he raised were whether they dreamed more and if their hair turned gray as they got older. His fascination with indigenous peoples came from his interest in the theory that social scientists can better study the history of their own civilization by studying cultures in earlier stages of development, "primitive men". In his autobiography, he writes "From a review of the three different species of settlers, it appears that there are certain regular stages which mark the progress from the savage to civilized life. The first settler is nearly related to an Indian in his manners. In the second, the Indian manners are more diluted. It is in the third species only that we behold civilization completed. It is to the third species of settlers only that it is proper to apply the term of farmers. While we record the voices of the first and second settlers, it is but just to mention their virtues likewise. Their mutual wants to produce mutual dependence; hence they are kind and friendly to each other. Their solitary situation makes visitors agreeable to them; hence they are hospitable to a stranger." [ 50 ]
Rush published one of the first descriptions and treatments for psychiatric disorders in American medicine, Medical Inquiries and Observations, Upon the Diseases of the Mind (1812). [ 51 ] [ 52 ] He undertook to classify different forms of mental illness and to theorize as to their causes and possible cures. Rush believed (incorrectly) that many mental illnesses were caused by disruptions of blood circulation or by sensory overload and treated them with devices meant to improve circulation to the brain such as a centrifugal spinning board, and inactivity/sensory deprivation via a restraining chair with a sensory-deprivation head enclosure ("tranquilizer chair"). [ 53 ] After seeing mental patients in appalling conditions in Pennsylvania Hospital, Rush led a successful campaign in 1792 for the state to build a separate mental ward where the patients could be kept in more humane conditions. [ 54 ]
Rush believed, as did so many physicians of the time, that bleeding and active purging with mercury(I) chloride (calomel) were the preferable medical treatments for insanity, a fact evidenced by his statement that, "It is sometimes difficult to prevail upon patients in this state of madness, or even to compel them, to take mercury in any of the ways in which it is usually administered. In these cases I have succeeded, by sprinkling a few grains of calomel daily upon a piece of bread, and afterwards spreading over it, a thin covering of butter." [ 55 ] Rush followed the standard procedures of bleeding and treatment with mercury, he did believe that "coercion" and "restraint", the physical punishment, chains and dungeons, which were the practice of the time, were the answer as proven by his invention of the restraint chair and other devices. For this reason, some aspects of his approach could be seen as similar to Moral Therapy , which would soon rise to prominence in at least the wealthier institutions of Europe and the United States. [ 56 ]
Rush is sometimes considered a pioneer of occupational therapy particularly as it pertains to the institutionalized. [ 22 ] In Diseases of the Mind (1812), Rush wrote:
It has been remarked that the maniacs of the male sex in all hospitals, who assist in cutting wood, making fires, and digging in a garden, and the females who are employed in washing, ironing, and scrubbing floors, often recover, while persons, whose rank exempts them from performing such services, languish away their lives within the walls of the hospital.
Furthermore, Rush was one of the first people to describe Savant Syndrome. In 1789, he described the abilities of Thomas Fuller , an enslaved African who was a lightning calculator . His observation would later be described in other individuals by notable scientists like John Langdon Down . [ 57 ]
Rush pioneered the therapeutic approach to addiction . [ 58 ] [ 59 ] Prior to his work, drunkenness was viewed as being sinful and a matter of choice. Rush believed that the alcoholic loses control over himself and identified the properties of alcohol, rather than the alcoholic's choice, as the causal agent. He developed the conception of alcoholism as a form of medical disease and proposed that alcoholics should be weaned from their addiction via less potent substances. [ 60 ]
Rush advocated for more humane mental institutions and perpetuated the idea that people with mental illness are people who have an illness, rather than inhuman animals. He is quoted to have said, "Terror acts powerfully upon the body, through the medium of the mind, and should be employed in the cure of madness." [ 61 ] He also championed the idea of "partial madness," or that people could have varying degrees of mental illness. [ 62 ]
The American Psychiatric Association 's seal bears an image of Rush's purported profile at its center. [ 63 ] [ 64 ] [ 65 ] The outer ring of the seal contains the words "American Psychiatric Association 1844". [ 65 ] The Association's history of the seal states:
The choice of Rush (1746–1813) for the seal reflects his place in history. .... Rush's practice of psychiatry was based on bleeding, purging, and the use of the tranquilizer chair and gyrator. [ a ] By 1844 these practices were considered erroneous and abandoned. Rush, however, was the first American to study mental disorder in a systematic manner, and he is considered the father of American Psychiatry. [ 65 ]
During his career, he educated over 3,000 medical students, and several of these established Rush Medical College in Chicago in his honor after his death. His students included Valentine Seaman , who mapped yellow fever mortality patterns in New York and introduced the smallpox vaccine to the United States in 1799. [ 66 ] One of his last apprentices was Samuel A. Cartwright , later a Confederate States of America surgeon charged with improving sanitary conditions in the camps around Vicksburg, Mississippi , and Port Hudson, Louisiana . Rush University Medical Center in Chicago, formerly Rush-Presbyterian-St. Luke's Medical Center, was named in his honor. [ 67 ]
Rush advocated Christianity in public life and in education and sometimes compared himself to the prophet Jeremiah . [ 68 ] Rush regularly attended Christ Church in Philadelphia and counted William White among his closest friends (and neighbors). Ever the controversialist, Rush became involved in internal disputes over the revised Book of Common Prayer and the splitting of the Episcopal Church from the Church of England . He dabbled with Presbyterianism , Methodism (which split from Anglicanism in those years), and Unitarianism . [ 13 ] : 312 [ 22 ] : 11–12, 16–17, 269–70, 322, 346 In a letter to John Adams , Rush describes his religious views as "a compound of the orthodoxy and heterodoxy of most of our Christian churches." [ 69 ] Christian Universalists consider him one of their founders, although Rush stopped attending that church after the death of his friend, former Baptist pastor Elhanan Winchester , in 1797. [ 70 ]
Rush fought for temperance [ 13 ] : 379–380 and both public and Sunday schools. He helped found the Bible Society at Philadelphia (now known as the Pennsylvania Bible Society ) [ 71 ] [ 72 ] and promoted the American Sunday School Union . [ 73 ] When many public schools stopped using the Bible as a textbook, Rush proposed that the U.S. government require such use, as well as furnish an American Bible to every family at public expense. In 1806, Rush proposed inscribing "The Son of Man Came into the World, Not To Destroy Men's Lives, But To Save Them." [ 74 ] above the doors of courthouses and other public buildings. Earlier, on July 16, 1776, Rush had complained to Patrick Henry about a provision in Virginia's constitution of 1776 which forbade clergymen from serving in the legislature. [ 75 ]
Rush felt that the United States was the work of God: "I do not believe that the Constitution was the offspring of inspiration, but I am as perfectly satisfied that the Union of the United States in its form and adoption is as much the work of a Divine Providence as any of the miracles recorded in the Old and New Testament". [ 76 ] In 1798, after the Constitution's adoption, Rush declared: "The only foundation for a useful education in a republic is to be laid in Religion. Without this there can be no virtue, and without virtue there can be no liberty, and liberty is the object and life of all republican governments." [ 73 ] One quote popularly assigned to Rush, however, which portrays him as a medical libertarian: "Unless we put medical freedoms into the Constitution, the time will come when medicine will organize into an undercover dictatorship [. . .] To restrict the art of healing to one class of men and deny equal privileges to others will constitute the Bastille of medical science. All such laws are un-American and despotic and have no place in a republic [. . .] The Constitution of this republic should make special privilege for medical freedom as well as religious freedom," is likely a misattribution. No primary source for it has been found, and the words "un-American" and "undercover" are anachronisms, as their usage as such did not appear until after Rush's death. [ 77 ]
Before 1779, Rush's religious views were influenced by what he described as "Fletcher's controversy with the Calvinists in favor of the Universality of the atonement." After hearing Elhanan Winchester preach, Rush indicated that this theology "embraced and reconciled my ancient calvinistical, and my newly adopted ( Arminian ) principles. From that time on I have never doubted upon the subject of the salvation of all men ." To simplify, both believed in punishment after death for the wicked. His wife, Julia Rush, thought her husband like Martin Luther for his ardent passions, fearless attacks on old prejudices, and quick tongue against perceived enemies. [ 14 ] : 297–298
Rush helped Richard Allen found the African Methodist Episcopal Church . In his autobiography, Allen wrote:
...By this time we had waited on Dr. Rush and Mr. Robert Ralston, and told them of our distressing situation. We considered it a blessing that the Lord had put it into our hearts to wait upon... those gentle-men. They pitied our situation, and subscribed largely towards the church, and were very friendly towards us and advised us how to go on.
We appointed Mr. Ralston our treasurer. Dr. Rush did much for us in public by his influence. I hope the name of Dr. Benjamin Rush and Mr. Robert Ralston will never be forgotten among us. They were the two first gentlemen who espoused the cause of the oppressed and aided us in building the house of the Lord for the poor Africans to worship in. Here was the beginning and rise of the first African church in America." [ 78 ]
On January 11, 1776, Rush married Julia Stockton (1759–1848), daughter of Richard Stockton , another signer of the Declaration of Independence, and his wife Annis Boudinot Stockton . They had 13 children, 9 of whom survived their first year: John, Ann Emily, Richard , Susannah (died as an infant), Elizabeth Graeme (died as an infant), Mary B, James, William (died as an infant), Benjamin (died as an infant), Benjamin, Julia, Samuel, and William. Richard later became a member of the cabinets of James Madison, James Monroe, John Quincy Adams, Andrew Jackson, James K. Polk , and Zachary Taylor (at one point during each of their presidencies). [ 79 ] [ 80 ]
In 1812, Rush helped reconcile the friendship of Jefferson and Adams by encouraging the two former presidents to resume writing to each other. [ 81 ] Once divided over politics and political rivalries, Jefferson and Adams grew close. On July 4, 1826, the 50th anniversary of the signing of the U.S. Declaration of Independence , Jefferson and Adams both died within hours of each other. [ 82 ]
After dying of typhus fever , he was buried (in Section N67) along with his wife Julia in the Christ Church Burial Ground in Philadelphia, not far from where Benjamin Franklin is buried. [ 83 ] At the site, a small plaque honoring Benjamin Rush has been placed. However, the box marker is next to the plaque on the right, with inscriptions on the top. The inscription reads, [ 84 ]
In memory of Benjamin Rush MD he died on the 19th of April in the year of our Lord 1813 Aged 68 years Well done good and faithful servant enter thou into the joy of the Lord Mrs Julia Rush consort of Benjamin Rush MD Born March 2, 1759 Died July 7, 1848 For as in Adam, all die, even so in Christ Shall all be made alive
Benjamin Rush Elementary School in Redmond, Washington , was named by its students for him. [ 85 ] The Arts Academy at Benjamin Rush magnet high school in Philadelphia was established in 2008. Rush County, Indiana , is named for him as is its county seat, Rushville . [ 86 ] In Chicago, Rush Street as well as Rush University Medical Center are both named for Rush. Benjamin Rush State Park in Philadelphia is named after Rush. The eponymous conservative Benjamin Rush Institute is an associate member of the State Policy Network . [ 87 ]
The Presbyterian Historical Society in Philadelphia , Pennsylvania , has a collection of Benjamin Rush's original manuscripts .
The Library Company of Philadelphia has papers of the Rush family including a significant correspondence collection.
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Benzydamine (also known as Tantum Verde and branded in some countries as Maxtra Gargle, Difflam and Septabene), available as the hydrochloride salt, is a locally acting nonsteroidal anti-inflammatory drug (NSAID) with local anaesthetic and analgesic properties for pain relief and anti-inflammatory treatment of inflammatory conditions of the mouth and throat . [ 3 ] It falls under class of chemicals known as indazole .
It was synthesized in Italy in 1964 and marketed in 1966. [ 4 ]
It may be used alone or as an adjunct to other therapy giving the possibility of increased therapeutic effect with little risk of interaction.
In some markets, the drug is supplied as an over-the-counter cream (Lonol in Mexico from Boehringer Ingelheim ) used for topical treatment of musculoskeletal system disorders: sprains, strains, bursitis, tendinitis, synovitis, myalgia, periarthritis.
Benzydamine has been used recreationally. If taken in excess amounts, it acts as a deliriant and CNS stimulant . [ 5 ] Such use, particularly among teenagers, has been reported in Brazil, [ 6 ] [ 7 ] Poland, [ 5 ] Romania, and Turkey. [ citation needed ]
There are no contraindications to the use of benzydamine except for known hypersensitivity .
Benzydamine is well tolerated. Occasionally oral tissue numbness or stinging sensations may occur, as well as itching, a skin rash, skin swelling or redness, difficulty breathing and wheezing.
It selectively binds to inflamed tissues ( Prostaglandin synthetase inhibitor ) and is normally free of adverse systemic effects.
Unlike other NSAIDs, it does not inhibit cyclooxygenase or lipooxygenase, and is not ulcerogenic. [ 5 ] [ 8 ]
It is described as having powerful reinforcing effects in animals and showing cross-sensitization with drugs of misuse such as heroin and cocaine . It is hypothesized that it has cannabinoid agonistic activity and this may account for its recreational and hallucinogenic effects. [ 9 ] However, it has also been theorized that, based on structural similarity to lysergic acid diethylamide (LSD) and descriptions of its visual hallucinatory effects, benzydamine might be acting as a serotonin 5-HT 2A receptor agonist and hence as a serotonergic psychedelic . [ 10 ] [ 11 ] More research is needed to determine the mechanism of action of the effects of benzydamine as a drug of misuse. [ 10 ] [ 11 ]
Benzydamine is poorly absorbed through skin [ 12 ] and vagina. [ 13 ]
Synthesis starts with the reaction of the N -benzyl derivative from methyl anthranilate with nitrous acid to give the N -nitroso derivative. Reduction by means of sodium thiosulfate leads to the transient hydrazine ( 3 ), which undergoes spontaneous internal hydrazide formation. Treatment of the enolate of this amide with 3-chloro-1-dimethylamino propane gives benzydamine ( 5 ). Please note there is an error in this section: US3318905 states that the nitroso derivative is reduced with sodium hydrosulfite (sodium dithionite) and not with sodium hyposulfite (sodium thiosulfate), as shown in the above scheme and stated in text.
An interesting alternative synthesis of this substance starts by sequential reaction of N -benzylaniline with phosgene , and then with sodium azide to product the corresponding carbonyl azide. On heating, nitrogen is evolved and a separatable mixture of nitrene insertion product and the desired ketoindazole # results. The latter reaction appears to be a Curtius rearrangement type product to produce an N-isocyanate #, which then cyclizes. Alkylation of the enol with sodium methoxide and 3-dimethylaminopropyl chloride gives benzydamine.
Alternatively, use of chloroacetamide in the alkylation step followed by acid hydrolysis produces bendazac instead.
Studies indicate that benzydamine has notable in vitro antibacterial activity and also shows synergism in combination with other antibiotics, especially tetracyclines, against antibiotic-resistant strains of Staphylococcus aureus and Pseudomonas aeruginosa . [ 17 ] [ 18 ]
It also has some cannabinoid activity in rats but has not been tested in humans. [ 9 ] It is also hypothesized to act on 5-HT2A receptors due to its structural similarity with serotonin . [ 4 ]
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BerEp4 (also Ber-EP4 ) is a histologic stain mainly used to aid in the diagnosis of basal cell carcinoma (BCC). [ 2 ] It is an antibody to EpCAM ( epithelial cell adhesion molecule ). [ 1 ]
BerEp4 has a high sensitivity and specificity in being positive only in BCC cells. [ 1 ] BerEp4 is normally negative in squamous epithelium and mesothelium , but otherwise normally positive most epithelial cells of the body. [ 3 ] It can also help in distinguishing pulmonary adenocarcinoma (positive BerEp4) from mesothelioma (generally negative BerEp4). [ 3 ] [ 4 ]
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Berkshire and Surrey Pathology Services (BSPS) is a pathology network, serving NHS hospitals in Surrey and Berkshire . BSPS is a joint venture between Ashford and St Peter's Hospitals NHS Foundation Trust , Frimley Health NHS Foundation Trust , Royal Berkshire NHS Foundation Trust , Royal Surrey County Hospital , and Surrey and Sussex Hospitals NHS Trust. It was established in 2012 as the Surrey Pathology Service. In 2023 it employs around 1,400 people and conducts around 60 million tests per year. [ 1 ]
Ashford and St Peter's Hospitals NHS Foundation Trust , Frimley Health NHS Foundation Trust and Royal Surrey County Hospital NHS Foundation Trust established the organisation. [ 2 ] In April 2015 it emerged that Royal Berkshire NHS Foundation Trust was proposing to join the partnership. [ 3 ] The joint venture was formally expanded in March 2017. [ 4 ]
It uses the WinPath Enterprise laboratory information system to enable clinicians to order tests and view results from anywhere within their network. This can manage up to 40,000 tests per day when running at full capacity. [ 5 ]
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Johann Bernhard Aloys von Gudden (7 June 1824 – 13 June 1886) was a German neuroanatomist and psychiatrist born in Kleve .
In 1848, von Gudden earned his doctorate from the University of Halle and became an intern at the asylum in Siegburg under Carl Wigand Maximilian Jacobi (1775–1858). From 1851 to 1855 he worked as a psychiatrist under Christian Friedrich Wilhelm Roller (1802–1878) in the mental asylum at Illenau in Baden , then from 1855 to 1869, served as director of the mental institution ( Unterfränkische Landes-Irrenanstalt ) in Werneck . In 1869 he was appointed director of the Burghölzli Hospital, as well as professor of psychiatry at the University of Zürich . In 1872 he was appointed Obermedicinalrath and director of the Upper Bavarian Kreis-Irrenanstalt (district mental asylum), located in Munich . Shortly afterwards, he became a professor of psychiatry at the University of Munich .
Gudden made many contributions in the field of neuroanatomy , especially in his work of mapping and describing the paths, connections, origins/termini and neuroanatomical centers of cranial and optic nerve networks. The commissural fibers of the optic tract are called the commissure of Gudden in his honor, and he is credited for developing a specialized microtome for sectioning the brain for pathological study. Among his well-known students and assistants are Emil Kraepelin (1856–1926), Franz Nissl (1860–1919), Auguste-Henri Forel (1848–1931), Sigbert Josef Maria Ganser (1853–1931) and Oskar Panizza (1853–1921).
As director of mental institutions, Gudden advocated a no-restraint policy, humane treatment of the mentally ill, communal social interaction amongst patients, and a well-trained medical staff. These were considered innovative, if not revolutionary ideas concerning mental health treatment in the mid-19th century.
Gudden was a respected psychiatrist in Germany and was appointed personal physician to King Ludwig II of Bavaria .
On June 13, 1886, Ludwig and Gudden were both found dead in the water near the shore of Lake Starnberg at 11:30 p.m., allegedly drowned, possibly murdered. To this day the details of their deaths remain a mystery.
After Gudden's death, his works were collected and edited by his son-in-law, psychiatrist Hubert von Grashey (1839–1914), being published in 1889 with the title " Bernhard von Gudden’s gesammelte und hinterlassene Abhandlungen ".
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Bernheim syndrome is a presumed disorder wherein the right ventricle is severely compressed due to a shift in the ventricular septal wall of the heart , leading to heart failure . It was first described by Hippolyte Bernheim in 1910. Today, it is argued whether or not Bernheim syndrome is indeed a syndrome or a side effect of other cardiac conditions , such as left ventrical heart failure where the left ventricle is substantially enlarged, encroaching on the space of the right ventricle . [ 1 ]
Signs and symptoms of Bernheim syndrome are ill-defined and typically follow those of heart failure . Bernheim distinguished Bernheim syndrome from the typical heart failure manifestations via the engorgement of veins due to congestion without evidence of pulmonary congestion . [ 2 ] There is also evidence of venous blockage going into pulmonary circulation and is therefore isolated to the right side of the heart . Manifestations of Bernheim syndrome include symptoms of hypertension , ronchi in the lungs, edema , vein distention , and signs of poor perfusion . [ 2 ] It is important to note that there are no manifestations of dyspnea nor pulmonary congestion until it is presumed to be a terminal stage of Bernheim syndrome . [ 2 ]
Bernheim syndrome is believed to be the rightward shift of the ventricular septum compressing the right ventricle without causing pulmonary congestion . [ 3 ] This was first described by Hippolyte Bernheim in which he presented 10 patients with signs and symptoms of right sided heart failure whose postmortem autospy reveals a ventricular septum that invaded the right ventricle space. [ 1 ] This opposed the traditional view of right sided heart failure, right ventricular hypertrophy , where the right ventricle is enlarged. Bernheim describes right ventricles the size of a slit,which was due to the bulging ventricular septum wall . [ citation needed ]
Bernheim syndrome is believed to occur in two stages: the anatomical and clinical stages. During the anatomical stage, there are no clinical signs of the syndrome, but the stenosis of the right ventricle makes it difficult to fill to its normal capacity. This is a offset by the dilation of the right atrium as it takes in different volume . In the clinical period, there are signs and symptoms present. In the clinical period, there are two stages. In the first stage of the clinical signs of venous obstruction due to the right ventricular stenosis become apparent while pulmonary blood flow continues normally. In the second stage of the symptoms of poor circulation becomes apparent such as systemic venous engorgement. [ 2 ] It is at this point where the patient appears to have heart failure . [ citation needed ]
Most cases of Bernheim syndrome have been identified postmortem in necropsy . A cross-sectional view of the heart muscle will show a greatly reduced right ventricle size. In necropsy, it is typical for the heart and lungs to be weighed with a higher weight indicating a build up of blood in the lungs: pulmonary congestion . The weight of the lungs is therefore expected to be within normal limits to rule out pulmonary congestion (900-1,280g). [ 4 ] The weight of the liver was also part of diagnosis with a significantly greater weight than what is in normal limits (1,440-1,680g) indicative of vein distention. [ 4 ]
In a clinical setting, Bernheim claims that the presence of isolated right ventricular failure clearly came from the presence of left ventricular hypertrophy which came secondary resulting to the presence of Bernheims symptom. [ 2 ] This is especially considered when the heart failure is not due to a weakness in the myocardium but in the stenosis of the myocardial wall. Fluoroscopy is used to view the blood flow in the heart has also been deemed as a reliable tool . It would be expected for the left ventricle and right atrium to be enlarged with the other two chambers appearing "normal". [ 2 ] However, it was typical example to only confirm the presence of Bernheim syndrome in the setting of autopsy . [ citation needed ]
In the medical community, however, it is believed that Bernheim syndrome does not actually exist and is only an observed side effect of another condition such as left ventricular hypertrophy . This is due to the lack of finding regarding sole right ventricle compression, without accompaniment of left ventricular hypertrophy, which is expected to encroach into the right ventricular space. It is claimed that there is no observation of a rightward shift of the ventricular septum as is described by Bernheim. Furthermore, using evidence from right and left peak systolic pressures , they determined there was no evidence of right ventricular stenosis to begin with. [ 1 ] When right ventricular heart failure is found without left ventricular heart failure, it was accompanied by pulmonary embolism and/or mitral valve stenosis . [ 4 ] It is because of these findings that there has been a movement to remove Bernheim syndrome from medical terminology . [ citation needed ]
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Berta Vogel Scharrer (December 1, 1906 – July 23, 1995) was an American scientist who helped to found the scientific discipline now known as neuroendocrinology . [ 1 ]
She received her Ph.D. from the University of Munich , Germany in 1930. [ 2 ] She worked at the university with Professor Karl von Frisch , who shared the Nobel Prize in Physiology or Medicine in 1973 for his work with bees. After completing her education, Berta and her husband, Ernst Scharrer embarked on a remarkable scientific career together. Their journey began at the Research Institute of Psychiatry in Munich, where Berta focused on the study of spirochaete infections in the brains of birds and amphibians.
Berta Scharrer was forced to emigrate at the onset of the Holocaust in 1937. She arrived with Ernst in the United States with a total of eight dollars. Ernst had secured a Rockefeller Fellowship at the University of Chicago and Berta continued her research, initially working with Drosophila and later with cockroaches and related species for the remainder of her research career. The couple's academic journey took them to various institutions, with Ernst accepting academic appointments that determined their locations. Throughout their career, they conducted groundbreaking research on neurosecretion , investigating the connection between the nervous and endocrine systems. Berta specialized in the study of invertebrates, while Ernst focused on vertebrates. [ 2 ]
In 1955, they founded the Department of Anatomy at the Albert Einstein College of Medicine in New York. It was at this point that Berta received her first salaried academic appointment, and she played an integral role in the department, not only as a scientist but also as a dedicated teacher. [ 3 ]
She served as the 55th president of the American Association of Anatomists from 1978 to 1979.
As her career progressed, Berta made significant contributions to the study of neuropeptides and neuroimmunology , entering these emerging fields in her later years and serving as the associate editor of the journal Advances in Immunology . [ 4 ] She continued her research until her death in 1995 at the age of 88.
Berta received numerous awards and honors throughout her career, including the National Medal of Science from President Ronald Reagan in 1983. Her work left a lasting impact on the fields of neurobiology and endocrinology, and she continues to be respected and influential among anatomists. [ 5 ]
Berta Vogel Scharrer was born December 8, 1906, in Munich, Germany, into a prosperous, well-educated family. Her father, Karl Phillip Vogel was a judge serving as vice president of the Federal Court of Bavaria. As a young student she became interested in biology, and knew she wanted to be a biologist from a young age. [ 2 ]
Berta Vogel married Ernst Scharrer in 1934. They met as graduate students working under von Frisch. The couple fled Germany in 1937,Ernst accepting a Rockefeller Fellowship at the University of Chicago ; they became U.S. citizens in 1945. [ 6 ]
Ernst died in 1965 in a swimming accident. The couple had no children. [ 7 ]
Scharrer conducted research and taught at Einstein College until her retirement in 1995, five months before her death at age 88. [ 7 ]
Scharrer was elected a Fellow of the American Academy of Arts and Sciences in 1967. [ 8 ] She earned honorary degrees from various universities, including one from Harvard in 1982, [ 7 ] "as well as a nomination for a Nobel Prize for her pioneering research in brain chemicals" . In 1983, she was awarded the National Medal of Science by President Reagan, for "demonstrating the central role of neurosecretion and neuropeptides in the integration of animal function and development." [ 9 ]
Scharrer's studies of invertebrates, particularly cockroaches, was so extensive that her name was given to a species of cockroach , known as the Escala scharrerae , found in Australasia . [ 1 ] [ 3 ] Scharrer was awarded the Schleiden Medal in 1983 and was a member of the National Academy of Sciences. [ 10 ]
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The Bertarelli Foundation is a private foundation founded by the Bertarelli family; brother and sister Ernesto and Dona Bertarelli , who are co-Chairs of the Foundation, and their mother, Maria Iris Bertarelli. It was established in 1998 in memory of Fabio Bertarelli and is based in Gstaad , Switzerland . [ 1 ] For ten years, the Bertarelli Foundation focused on promoting an understanding of infertility , especially multiple gestations . [ 2 ] This reflected the work of the family’s business, Ares-Serono, in the field, including its development of influential infertility treatment Pergonal. [ 3 ] Following the sale of Serono, the Bertarelli Foundation refocused its activities onto the fields of marine conservation and neuroscience research, as well as projects in their local communities. [ 4 ] The Foundation has a sister organisation in Italy, the Fondazione Bertarelli, which promotes cultural activities in Tuscany , where the family’s ColleMassari wine estate is located. [ 5 ]
The Bertarelli Foundation is active in the creation of Marine Protected Areas (MPAs) , both in terms of providing material support and in terms of advocacy. In 2010 it worked with the British Government to provide the financial backing to enable the designation of the Chagos Marine Protected Area in the British Indian Ocean Territory . [ 6 ]
In 2012, the Foundation provided the funding and practical support to advance the designation of a marine reserve centred on the Turneffe Atoll in Belize , which is part of the largest and most biodiverse coral reef system in the western hemisphere. [ 7 ] [ 8 ]
In 2015, it again partnered with the British Government and also with the Pew Charitable Trusts for the creation of a marine reserve around the Pitcairn Islands. In 2017, a 740,000 km² MPA was created off the coast of Easter Island. [ 9 ] [ 10 ] [ 11 ] The Bertarelli Foundation, in partnership with Pew Charitable Trusts, supported the campaign for the MPA’s creation as part of a developing partnership which has now become the Pew Bertarelli Ocean Legacy Project, and is led by Dona Bertarelli. [ 12 ] The Pew Bertarelli project was also involved in the campaign to create the Revillagigedo Archipelago National Park which was announced by Mexico President Enrique Peña Nieto in November 2017. [ 13 ] The Foundation and Pew are also advocating for the creation of a marine park around the South Sandwich Islands on the edge of the Antarctic . [ 14 ]
As well as its work to create and advocate for the creation of marine protected areas, the foundation established the Bertarelli Programme in Marine Science in 2017, partnering with universities from around the world to advance ocean science in the Indian Ocean . [ 15 ] Several expeditions to the territory have already taken place, with reports published on the British Government’s BIOT website. [ 16 ]
In 2010, the Bertarelli Foundation entered into a partnership with Harvard Medical School and the Ecole Polytechnique Fédérale de Lausanne (EPFL) to a joint neuroengineering programme, the Bertarelli Program in Translational Neuroscience and Neuroengineering. [ 17 ] [ 18 ] The aim of the programme is to foster collaboration in neuroscience between the two institutions. [ 19 ] The partnership also endowed a Bertarelli Chair at Harvard Medical School and there is an annual symposium held at which findings from the programme are discussed. [ 20 ] In 2014, the partnership was renewed, with funding of $3.6m provided to five projects of three-year duration between scientists at Harvard Medical School and bioengineers at EPFL. Three of these projects focus on new methods to diagnose and treat deafness; the fourth on cell transplantation strategies to reverse blindness; and the fifth on dealing with difficulties in diagnosing children with autism . [ 21 ] The programme also sponsors an exchange programme for students at the two institutions. [ 22 ] In 2018, the Bertarelli Foundation donated $6.35m to Harvard Medical School for research in sensory disorders. [ 23 ]
The foundation also sponsors four chairs at EPFL’s Center for Neuroprosthetics, [ 24 ] which is now located at Campus Biotech in Geneva, the former Serono headquarters bought back by a consortium led by Ernesto Bertarelli to be a life sciences hub for the region. [ 25 ] They are Professor Olaf Blanke , Professor Stéphanie P. Lacour , Professor Mackenzie Weygandt Mathis and Professor Silvestro Micera. [ 26 ]
In 2017, the Bertarelli Foundation gave a further 10 million Swiss francs to EPFL to further develop research into neurological disorders . [ 27 ] [ 28 ] Half of the donation will fund a new gene therapy platform at Campus Biotech in Geneva; the other half will create a new catalyst fund to further collaboration at the same institution. [ 29 ]
In 2008 the Bertarelli Foundation funded a new classroom and a medical centre at Henna Pre-School in South Africa having visited the school during a family holiday. [ 30 ] [ 31 ]
In 2014, it partnered with Harvard Business School to establish the Bertarelli Foundation Health & Life Sciences Entrepreneurship Fund. A separate gift of $3 million created the Bertarelli Catalyst Fund for the Dean of HMS. [ 32 ] As part of the funding, a Bertarelli Prize is awarded to a winning team from the Harvard i-Lab for those students “pursuing innovative solutions to improve healthcare and patients’ lives” . [ 33 ]
In 2014, the Bertarelli Foundation donated $3 million to Babson College to create a new faculty chair, the Bertarelli Foundation Distinguished Professor of Family Entrepreneurship. In 2017, Babson named William B. Gartner to the post. [ 34 ] [ 35 ]
In Stoke-on-Trent , Kirsty Bertarelli , the former wife of Ernesto Bertarelli and a former trustee of the Bertarelli Foundation, has launched projects supporting YMCA North Staffordshire and the Stoke-on-Trent Literary Festival, which takes place annually at the Emma Bridgwater factory in the city and which was established by former MP for Stoke-on-Trent Central, Tristram Hunt . [ 36 ] [ 37 ]
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Bertha Boronda ( née Zettle ; March 14, 1877 – January 18, 1950) was an American woman who sliced off her husband's penis with a straight razor in 1907. [ A ] She fled the scene of the crime, but was captured the next day. Boronda was tried, convicted of mayhem , and imprisoned at San Quentin Penitentiary .
The victim was Bertha Boronda's husband, Frank Boronda: Captain of Chemical Engine No. 1 with the San Jose Fire Department . [ 4 ] On Friday, May 30, 1907, Bertha insisted that her husband Frank had visited a place of prostitution . [ 3 ] Shortly after midnight, she cut her husband's penis off with a razor while in bed. [ 1 ] [ 5 ] He was able to go to the firehouse , which was adjacent to his home, and received treatment in a hospital. [ 6 ]
She was apprehended while disguised, wearing men's clothing and mounting a bicycle to make her escape. [ 5 ] [ 2 ] She was not found by police until more than 24 hours had passed. [ 1 ] [ 7 ] After her capture, Boronda admitted her crime and expressed no regret. [ 6 ]
The newspaper reports were tactfully non-specific. "'She drew a razor and cut her husband.' Then she walked to her nephew's room and simply stated, 'Frank cut himself.'" [ 2 ]
On June 1, Frank Boronda made a complaint to Justice Brown from his hospital bed at the Red Cross Hospital. Boronda was accused of mayhem. [ 6 ] The felony of mayhem, punishable by up to 14 years in prison, was defined by Section 204 of the criminal code: "Every person who unlawfully and maliciously deprives a human being of a member of his body or renders it useless, or cuts or disables the tongue, nose, ear or lip, is guilty of mayhem." [ 8 ] [ 6 ]
Boronda was held on $10,000 bond ($335,750 in 2025). [ 4 ] [ 9 ]
Mr. Boronda testified at the trial that he and his wife had visited the San Jose theater, and that the attack was unprovoked. [ 3 ] He claimed that she was amorous and had invited him to her bed before the attack. [ 10 ] The prosecution's theory was that this was a deliberate planned attack in furtherance of a jealous rage. [ 10 ]
Boronda had several defenses, chief among them being her complete lack of any recollection of the night in question. [ 3 ] She claimed she became enraged at her husband, and the two had an argument because she thought he was going to leave her. She admitted that she maimed him, but expressed no regret. As reported in the Santa Cruz Sentinel , "Her only excuse is that she wanted to be revenged on Boronda, whom she believed intended deserting her and leaving for Mexico." [ 8 ] Another defense was that Mr. Boronda had made "a vile request." [ 10 ]
At the trial she settled on a defense of "emotional insanity" from extreme jealousy. She took the stand in her defense and explained why she dressed like a man when she fled after the incident. She stated that her husband had been gone for two weeks; and she often wore her brother's clothing when she spied on her husband. [ 11 ]
The jury deliberated two hours before convicting her. [ 3 ] [ 10 ] Boronda was sentenced to five years in prison, but served only two and was released from prison on December 20, 1909. [ 5 ]
Bertha Zettle was born in 1877 to German immigrants in Minnesota. She married Frank Boronda (born Mario Narcisso Boronda in 1863) [ 5 ] in 1901. He was a Mexican American captain with the San Jose Fire Department . [ 1 ]
In the aftermath of the incident, Bertha and Frank Boronda divorced. Both Frank and Bertha later remarried. Bertha married Alexander Patterson in 1921; however, the two eventually divorced. [ 5 ]
Her remains are interred at Calvary Catholic Cemetery in San Jose, California .
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https://en.wikipedia.org/wiki/Bertha_Boronda
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Bess Mensendieck (1 July 1864 New York City - 27 January 1957, born Elizabeth Marguerite de Varel Mensendieck) was an American physician and gymnastics teacher of Dutch descent who developed the Mensendieck System , a therapeutic teaching methodology for female physical education claimed to be both corrective and preventive . She was one of the most important founders of early breathing and physical pedagogy in Europe and America. [ 1 ] [ 2 ]
Mensendieck published several books on the subject starting with the German publication titled Körperkultur des Weibes (Physical Culture of Women) with practical hygienic and aesthetic tips, 1906. [ 3 ] [ 4 ] [ 5 ]
Mensendieck grew up in New York City and studied medicine in Zurich . To complete her practical knowledge of movement, posture, and breathing, she took singing lessons in Paris and continued to study gymnastics with Genevieve Stebbins in New York. Here she also learned the movement systems of François Delsarte and the Swedish remedial gymnastics of Pehr Henrik Ling . [ 6 ]
Her particular concern was the improvement of posture and muscle structure of the women of her time. Based on her medical background, she built her gymnastics according to the Mensendieck system strictly on the anatomical and physiological findings of the time. The focus of the bodywork was again and again on the self-perception of posture and movement. [ 1 ] To effectively demonstrate the exercise techniques and change in physical postures, she included a series of photos showing herself nude before, during, and after three months of training in her German book Körperkultur des Weibes ( Munich , 1906), illustrating what can be achieved with her training. [ 1 ] [ 4 ] Mensendieck believed that nudity was fundamental in enhancing women's body consciousness, which motivated all activity that made the female body strong, healthy, and beautiful. [ 7 ] However, because of the nude content, her published work was not equally enforceable in the same way in all countries.
Mensendieck's books had a pervasive influence on German women instructors of gym classes into the 1930s. [ 7 ] She taught her "Mensendieck System" mainly in Europe (Germany, Netherlands, Norway, Denmark and Austria). In 1910 the first institute for the training of gymnastics teachers was founded. After the First World War, Mensendieck left Europe, worked mostly in New York, and gave annual training courses in Germany and Denmark. She spent the summer months in her Norwegian summer house. In the 1950s she lived in Copenhagen for a few years and eventually moved back to New York. [ citation needed ]
Mensendieck also worked on the German documentary film Wege zu Kraft und Schönheit ( Ways to Strength and Beauty ), a silent black and white cultural film about the Weimar Republic directed by Wilhelm Prager released in 1925, which aimed to show the place of the body in modern society in which both men and women were not caring enough about their physical health. [ 8 ]
Mensendieck must have been a petite person with tremendous assertiveness and a room-filling voice. In auditoriums she could be heard clearly in the back row. Mensendieck was one of the few women who combined the ideas and demands of women's rights activists with her "Mensendieck System". "Think for yourself!" was the motto of her teaching. [ citation needed ]
Mensendieck School in Oslo , Norway, 1950s, photos show women student physiotherapists training the Mensendieck System. The private college was established for Mensendieck-based physiotherapist education in Oslo in 1927 under the name Norsk Mensendieckskole A/S and was taken over by the Norwegian state in 1979. In 1992, the Mensendieck School was incorporated into the Bislet University College Center (Bislet høgskolesenter) and named the Mensendieckschool in Oslo College of Physiotherapy. From August 1994, it became part of the Department of Health Sciences at the newly established Oslo University College , now Oslo Metropolitan University . [ 10 ] The education was called bachelor in physiotherapy, field of study Mensendieck, but was discontinued in 2020. [ 11 ]
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https://en.wikipedia.org/wiki/Bess_Mensendieck
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A bezoar stone ( / ˈ b i z ɔː r / BEE -zor ) is a mass often found trapped in the gastrointestinal system , [ 2 ] though it can occur in other locations. [ 3 ] [ 4 ] A pseudobezoar is an indigestible object introduced intentionally into the digestive system. [ 5 ]
There are several varieties of bezoar, some of which have inorganic constituents and others organic . The term has both modern (medical, scientific) and traditional usage.
Esophageal bezoars discovered in nasogastrically fed patients on mechanical ventilation and sedation are reported to be due to the precipitation of certain food types rich in casein, which are precipitated with gastric acid reflux to form esophageal bezoars. Bezoars can also be caused by gastroparesis due to the slowing of gastric emptying, which allows food to form a bolus. [ 12 ]
The word bezoar is derived from the Persian pād-zahr ( پادزهر ), literally ' antidote ' . [ 13 ] The myth of the bezoar as an antidote reached Europe from the Middle East in the 11th century and remained popular until it started to fall into disrepute by the 18th century. [ 14 ] People believed that a bezoar had the power of a universal antidote and would work against any poison – a drinking glass that contained a bezoar could allegedly neutralize any poison poured into it.
Ox bezoars ( niu-huang ( 牛黃 ) or calculi bovis ) are used in Chinese herbology [ vague ] to treat various diseases. They are gallstones or gallstone substitutes formed from ox or cattle bile . Some products allegedly remove toxins from the body.
The Andalusian physician Ibn Zuhr ( d. 1161), known in the West as Avenzoar, is thought [ by whom? ] to have made the earliest description of bezoar stones as medicinal items. [ 15 ] Extensive reference to bezoars also appears in the Picatrix .
In 1567, French surgeon Ambroise Paré did not believe that it was possible for the bezoar to cure the effects of any poison and described an experiment to test the properties of the stone. A cook in the King's court was sentenced to death and chose to be poisoned rather than hanged, under the condition that he would be given a bezoar after the poison. Paré administered the bezoar stone to the cook, but it had no effect, and the cook died in agony seven hours after taking the poison, proving that – contrary to popular belief – the bezoar could not cure all poisons. [ 16 ]
Modern examinations of the properties of bezoars by Gustaf Arrhenius and Andrew Benson of the Scripps Institution of Oceanography show that when bezoars are immersed in an arsenic-laced solution, they can remove the poison. The toxic compounds in arsenic are arsenate and arsenite ; each is acted upon differently by the bezoars: arsenate is removed by being exchanged for phosphate in brushite found in the stones, while arsenite is bound to sulfur compounds in the protein of degraded hair, which is a key component in bezoars. [ 17 ]
A famous case in the common law of England ( Chandelor v Lopus , 79 Eng Rep. 3, Cro. Jac. 4, Eng. Ct. Exch. 1603) announced the rule of caveat emptor ("let the buyer beware") if the goods purchased are not in fact genuine and effective. The case concerned a purchaser who sued for the return of the purchase price of an allegedly fraudulent bezoar.
Bezoars were important objects in cabinets of curiosity and in natural-history collections, mainly for their use in early-modern pharmacy and in the study of animal health. [ 18 ] [ 19 ]
The Merck Manual of Diagnosis and Therapy notes that consumption of unripened persimmons has been identified as the main cause of epidemics of intestinal bezoars and that up to 90 percent of bezoars that occur from excessive consumption require surgery for removal. [ 20 ]
A 2013 review of three databases identified 24 publications presenting 46 patients treated with Coca-Cola for phytobezoars. Clinicians administered the cola in doses of 500 ml (18 imp fl oz; 17 US fl oz) to up to 3,000 ml (110 imp fl oz; 100 US fl oz) over 24 hours, orally or by gastric lavage . A total of 91.3% of patients had complete resolution after treatment with Coca-Cola: 50% after a single treatment, with others requiring cola plus endoscopic removal. Doctors resorted to surgical removal in four cases. [ 21 ]
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https://en.wikipedia.org/wiki/Bezoar
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Bibersteinia trehalosi is a species of Gram-negative bacteria in the family Pasteurellaceae . Originally described as Pasteurella trehalosi by Sneath & Stevens in 1990, it was reclassified into the newly created genus Bibersteinia in 2007 based on phylogenetic and biochemical studies. [ 1 ]
The genus name Bibersteinia honors Ernst Ludwig Biberstein, a noted German veterinarian. The species epithet trehalosi refers to the ability of this bacterium to ferment the sugar trehalose , a distinguishing biochemical trait. [ 1 ]
Bibersteinia trehalosi exhibits the following features: [ 1 ]
Colonies grown on blood agar are small, greyish, smooth, and non- haemolytic or weakly haemolytic.
Bibersteinia trehalosi is primarily associated with respiratory and systemic diseases in ruminants, particularly sheep and cattle. It is commonly isolated in cases of pneumonia, septicemia, and sudden death in lambs and calves. [ 1 ]
Due to its pathogenic potential, Bibersteinia trehalosi is significant in veterinary microbiology, particularly in livestock management. It is involved in outbreaks of respiratory disease and septicemia, which have economic importance in animal husbandry. [ 1 ]
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https://en.wikipedia.org/wiki/Bibersteinia_trehalosi
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bibic is a small charitable organization based in the United Kingdom that supports children, young people and their families who have a wide range of different conditions. The charity was founded by the late Keith Pennock who had a daughter with a learning disability. The work was derived from Glenn Doman's The Institutes for The Achievement of Human Potential (IAHP) in Philadelphia , USA .
Many of the children they work with have disorders of the nervous system, or inherited characteristics, which affect the way the body or brain develops. These include: acquired and traumatic brain injury , Down syndrome , cerebral palsy , autism , Specific developmental disorders , attention deficit hyperactivity disorder and learning disability including dyslexia , developmental coordination disorder and dyscalculia . Unlike many other organisations, bibic also works with children that have no formal diagnosis at all. [ 1 ]
A variety of therapeutic approaches are used. There is no peer reviewed research into the effectiveness of therapy for this condition. [ 2 ]
The organisation raises funds and receives no Government funding.
The charities National Assessment Centre is based at Old Kelways, just outside the town of Langport , in Somerset . [ 3 ]
Keith Pennock's book Rescuing brain injured children [ 4 ] describes the impetus for starting the organisation as his daughter, who had developmental delay. In 1970 the family travelled from the UK to Philadelphia and attended the IAHP. The family adopted the Doman-Delecato patterning technique in the UK. A precursor to bibic (BIAHP) was opened in Staffordshire later the same year, as news spread of the family and their use of the new therapy method. Local residents began to give donations and offer their time. [ 4 ] The British Institute for the Achievement of Human Potential (BIAHP) was established in 1974, with staff being trained directly at the IAHP in Philadelphia. The family and fledgeling organisation moved to Knowle Hall near Bridgwater , Somerset in 1976.
In 1979, the IAHP (under the management of Glenn Doman) were turning their interests to "well children" with the introduction of a Better Babies programme. The board of the BIAHP felt that they could not support this shift in focus and wanted to continue their work solely with children who had a brain injury, therefore through necessity the British Institute of Brain Injured Children was launched as an independent organisation in 1980 – no links with the IAHP were retained, and staff began to be trained in the UK. In 1987 a research piece was commissioned to demonstrate the effectiveness of the programme, [ 5 ] in association with the University of Surrey .
Keith Pennock resigned from his post as chief executive of BIBIC in early 1996. In 1999, research covering the period 1995-1997 at BIBIC was published. [ 6 ] In a letter to the [journal] editor, [ 7 ] the authors of the appraisal report noted that strong similarities to the Doman-Delecato Patterning method (a therapy by this point widely condemned) [ 8 ] [ 9 ] remained strong despite BIBIC making revisions, and that areas of the therapy caused concern. BIBIC responded later that year, [ 10 ] informing the journal that significant changes had been made to the programme, with the appraisal report being a much-anticipated catalyst for doing so. Since these revisions and under new management the organisation has been registered as a charity, and is now known only as "bibic". Bibic remains an active organisation and also provides policy input.
Bibic now reports to base its programme of developmental therapy on more recent research [ 11 ] based on the concept of neuroplasticity , the brain's ability to undergo alterations in response to internal and external environmental changes. Bibic moved to Langport in Somerset, in 2014. [ 12 ]
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https://en.wikipedia.org/wiki/Bibic_(charity)
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Bicameral mentality is a hypothesis introduced by Julian Jaynes who argued human ancestors as late as the ancient Greeks did not consider emotions and desires as stemming from their own minds but as the consequences of actions of gods external to themselves. The theory posits that the human mind once operated in a state in which cognitive functions were divided between one part of the brain that appears to be "speaking" and a second part that listens and obeys—a bicameral mind —and that the breakdown of this division gave rise to consciousness in humans. The term was coined by Jaynes, who presented the idea in his 1976 book The Origin of Consciousness in the Breakdown of the Bicameral Mind , [ 1 ] wherein he makes the case that a bicameral mentality was the normal and ubiquitous state of the human mind as recently as 3,000 years ago, at the end of the Mediterranean Bronze Age .
Jaynes uses "bicameral" (two chambers) to describe a mental state in which the experiences and memories of the right hemisphere of the brain are transmitted to the left hemisphere via auditory hallucinations . The metaphor is based on the idea of lateralization of brain function , although each half of a normal human brain is constantly communicating with the other through the corpus callosum . [ 2 ] The metaphor is not meant to imply that the two halves of the bicameral brain were "cut off" from each other but that the bicameral mind was experienced as a different, nonconscious mental schema wherein volition in the face of novel stimuli was mediated through a linguistic control mechanism and experienced as auditory verbal hallucinations.
Bicameral mentality is nonconscious in its inability to reason and articulate about mental contents through meta- reflection , reacting without explicitly realizing and without the meta-reflective ability to give an account of why one did so. The bicameral mind thus lacks metaconsciousness , autobiographical memory, and the capacity for executive "ego functions" such as deliberate mind-wandering and conscious introspection of mental content. When bicameral mentality as a method of social control was no longer adaptive in complex civilizations , this mental model was replaced by the conscious mode of thought, which, Jaynes argued, is grounded in the acquisition of metaphorical language [ 3 ] learned by exposure to narrative practice. [ 4 ]
According to Jaynes, ancient people in the bicameral state of mind experienced the world in a manner that has some similarities to that of a person with schizophrenia . [ 5 ] Rather than making conscious evaluations in novel or unexpected situations, the person hallucinated a voice or "god" giving admonitory advice or commands and obeyed without question: one was not at all conscious of one's own thought-processes per se . Jaynes's hypothesis is offered as a possible explanation of " command hallucinations " that often direct the behavior of those with first-rank symptoms of schizophrenia, as well as other voice-hearers . [ 6 ]
Eric Robertson Dodds wrote about how ancient Greek thought may have not included rationality as defined by modern culture. In fact, the Greeks may have known that an individual did things, but the reason they did things was attributed to divine externalities, such as gods or daemons . [ 7 ] Bruno Snell in 1953 thought that in Homeric Greek psychology there was no sense of self in the modern sense. [ 8 ] Snell then describes how Greek culture "self-realized" the modern "intellect". [ 9 ] Arthur William Hope Adkins [ de ] , building on Snell's work, wrote about how ancient Greek civilization developed ego-centered psychology as an adaptation to living in city-states, before which the living in Homeric oikos did not require such integrated thought processes. [ 10 ]
The neurological model in The Origin of Consciousness in the Breakdown of the Bicameral Mind is a radical neuroscientific hypothesis that was based on research novel at the time, mainly on Michael Gazzaniga 's split-brain experiments [ 11 ] [ 12 ] and left-brain interpreter theory. [ 13 ] [ 14 ] The more general idea of a "divided self" (contrasted with a "unitary self") has found support from psychological and neurological studies. [ 15 ]
Jaynes built a case for this hypothesis that human brains existed in a bicameral state until as recently as 3,000 years ago by citing evidence from many diverse sources, including historical literature. He took an interdisciplinary approach, drawing data from many different fields. [ 16 ] Citing Dodds, Snell, and Adkins, [ 17 ] Jaynes proposed that until roughly the times written about in Homer 's Iliad , humans did not generally have the self-awareness characteristic of consciousness as most people experience it today. Rather, the bicameral individual was guided by mental commands believed to be issued by external " gods "—commands that were recorded in ancient myths , legends, and historical accounts. This is exemplified in not only the commands given to characters in ancient epics but also the very muses of Greek mythology who "sang" the poems. According to Jaynes, the ancients literally heard muses as the direct source of their music and poetry .
Jaynes asserts that in the Iliad and sections of the Old Testament , no mention is made of any kind of cognitive processes such as introspection , and there is no apparent indication that the writers were self-aware. Jaynes suggests that the older portions of the Old Testament (such as the Book of Amos ) have few or none of the features of some later books of the Old Testament (such as Ecclesiastes ) as well as later works such as Homer's Odyssey , which show indications of a profoundly different kind of mentality—an early form of consciousness. [ 16 ]
In ancient times, Jaynes noted, gods were generally much more numerous and much more anthropomorphic than in modern times, and he speculates that this was because each bicameral person had their own "god" who reflected their own desires and experiences. [ 18 ]
He also noted that, in ancient societies, the corpses of the dead were often treated as though still alive (being seated, dressed, and even fed) as a form of ancestor worship , and Jaynes argued that the dead bodies were presumed to be still living and the source of auditory hallucinations. [ 16 ] This adaptation to the village communities of 100 individuals or more formed the core of religion.
Citing Gazzaniga, Jaynes inferred that these "voices" came from the right brain counterparts of the left brain language centres, specifically, the counterparts to Wernicke's area and Broca's area . These regions are somewhat dormant in the right brains of most modern humans, but Jaynes noted that some studies show that auditory hallucinations correspond to increased activity in these areas of the brain. [ 16 ]
Jaynes notes that even at the time of publication there is no consensus as to the cause or origins of schizophrenia . Jaynes argues that schizophrenia is a vestige of humanity's earlier bicameral state. [ 16 ] Recent evidence shows that many people with schizophrenia do not just hear random voices but experience " command hallucinations " instructing their behavior or urging them to commit certain acts, such as walking into the ocean, which the listener feels they have no choice but to follow. Jaynes also argues that people with schizophrenia feel a loss of identity due to hallucinated voices taking the place of their internal monologue. [ 19 ]
As support for Jaynes's argument, these command hallucinations are little different from the commands from gods that feature prominently in ancient stories. [ 16 ] Indirect evidence supporting Jaynes's theory that hallucinations once played an important role in human mentality can be found in the 2012 book Muses, Madmen, and Prophets: Rethinking the History, Science, and Meaning of Auditory Hallucination by Daniel Smith . [ 20 ]
Jaynes theorized that a shift from bicameral mentality marked the beginning of introspection and consciousness as we know it today. According to Jaynes, this bicameral mentality began malfunctioning or "breaking down" during the 2nd millennium BCE. He speculates that primitive ancient societies tended to collapse periodically—for example, Egypt's Intermediate Periods , as well as the periodically vanishing cities of the Mayas—as changes in the environment strained the sociocultural equilibria sustained by this bicameral mindset.
The Late Bronze Age collapse of the 2nd millennium BCE led to mass migrations and created a rash of unexpected situations and stresses that required ancient minds to become more flexible and creative. Self-awareness, or consciousness, was the culturally evolved solution to this problem. This necessity of communicating commonly observed phenomena among individuals who shared no common language or cultural upbringing encouraged those communities to become self-aware to survive in a new environment. Thus, consciousness, like bicameral mentality, emerged as a neurological adaptation to social complexity in a changing world. [ 21 ]
Jaynes further argues that divination , prayer , and oracles arose during this breakdown period in an attempt to summon instructions from the "gods" whose voices could no longer be heard. [ 16 ] The consultation of special bicamerally operative individuals, or of divination by casting lots and so forth, was a response to this loss, a transitional era depicted, for example, in the book of 1 Samuel . It was also evidenced in children who could communicate with the gods, but as their neurology was set by language and society, they gradually lost that ability. Those who continued prophesying, being bicameral, according to Jaynes, could be killed. [ 22 ]
Leftovers of the bicameral mind today, according to Jaynes, include mental illnesses such as schizophrenia. Jaynes says that there is no evidence of insanity existing prior to the breakdown of the bicameral mind and that this is indirect evidence for his theory. He considered that previous claims of insanity in Homeric literature are based on mistranslations. [ 23 ]
Early coverage by Sam Keen in the November 1977 issue of Psychology Today considered Jaynes's hypothesis worthy and offered conditional support, arguing the notion deserves further study. [ 24 ] [ 25 ] The Origin of Consciousness in the Breakdown of the Bicameral Mind was a successful work of popular science, selling out the first print run before a second could replace it. [ 17 ] It received dozens of positive book reviews, including those by well-known critics such as John Updike in The New Yorker , Christopher Lehmann-Haupt in the New York Times , [ 26 ] and Marshall McLuhan in the Toronto Globe and Mail . Articles on Jaynes and his ideas appeared in Time in 1977, [ 27 ] and in Quest/78 in 1978. [ 28 ] The book was nominated for the National Book Award in Contemporary Thought in 1978. [ 29 ] Philip K. Dick , Terrence McKenna , and David Bowie have all cited the book as an influence. [ 30 ]
According to Jaynes, language is a necessary but not sufficient condition for consciousness: Language existed thousands of years earlier, but consciousness did not emerge as soon as language did. [ 31 ] The idea that language is a necessary component of subjective consciousness and more abstract forms of thinking has gained the support of proponents including Andy Clark , Daniel Dennett , William H. Calvin , Merlin Donald , John Limber, Howard Margolis , Peter Carruthers , and José Luis Bermúdez. [ 32 ]
An early criticism by philosopher Ned Block argued that Jaynes had confused the emergence of consciousness with the emergence of the concept of consciousness. In other words, according to Block, humans were conscious all along but did not have the concept of consciousness and thus did not discuss it in their texts. Daniel Dennett countered that for some things, such as money , baseball , or consciousness, one cannot have the thing without also having the concept of the thing. [ 33 ] [ 34 ] [ 35 ]
Gary Williams defends the Jaynesian definition of consciousness as a social–linguistic construct learned in childhood, structured in terms of lexical metaphors and narrative practice, [ 35 ] against Ned Block's criticism that it is "ridiculous" to suppose that consciousness is a cultural construction, [ 36 ] while the Dutch philosophy professor Jan Sleutels offers an additional critique of Block. [ 34 ]
H. Steven Moffic questioned why Jaynes's theory was left out of a discussion on auditory hallucinations by Asaad & Shapiro (1986) . [ 37 ] The authors' published response was, "Jaynes' hypothesis makes for interesting reading and stimulates much thought in the receptive reader. It does not, however, adequately explain one of the central mysteries of madness: hallucination." [ 38 ]
The new evidence for Jaynes's model of auditory hallucinations arising in the right temporal-parietal lobe and being transmitted to the left temporal-parietal lobe that some neuroimaging studies suggest was discussed by various respondents. [ 39 ] [ 40 ] [ 41 ]
Jaynes described the range of responses to his book as "from people who feel [the ideas are] very important all the way to very strong hostility. ... When someone comes along and says consciousness is in history, it can't be accepted. If [psychologists] did accept it, they wouldn't have the motivation to go back into the laboratory ..." [ 28 ]
Marcel Kuijsten, founder of the Julian Jaynes Society , wrote that in the decades since the book's publication, "there have been few in-depth discussions, either positive or negative" about it, rejecting as too simplistic the criticism that "Jaynes was wrong". [ 42 ]
Sociologist W. T. Jones asked in 1979, "Why, despite its implausibility, is [Jaynes's] book taken seriously by thoughtful and intelligent people?" [ 43 ] Jones agreed with Jaynes that "the language in which talk about consciousness is conducted is metaphorical", but he contradicted the basis of Jaynes's argument – that metaphor creates consciousness – by asserting that "language (and specifically metaphor) does not create, it discovers, the similarities that language marks". Jones also argued that three "cosmological orientations" biased Jaynes's thinking: 1) "hostility to Darwin" and natural selection; 2) a "longing for 'lost bicamerality'" (Jones accused Jaynes of holding that "we would all be better off if 'everyone' were once again schizophrenic"); 3) a "desire for a sweeping, all-inclusive formula that explains everything that has happened". Jones concluded that "... those who share these biases ... are likely to find the book convincing; those who do not will reject [Jaynes's] arguments ..." [ 43 ]
Walter J. Ong noted that the Homeric Iliad is a structurally oral epic poem so, he asserted, the very different cultural approach of oral culture is sufficient justification for the apparent different mentalities in the poem. [ 44 ]
Philosopher Daniel Dennett suggested that Jaynes may have been wrong about some of his supporting arguments – especially the importance he attached to hallucinations – but that these things are not essential to his main thesis: [ 45 ] "If we are going to use this top-down approach, we are going to have to be bold. We are going to have to be speculative, but there is good and bad speculation, and this is not an unparalleled activity in science. ... Those scientists who have no taste for this sort of speculative enterprise will just have to stay in the trenches and do without it, while the rest of us risk embarrassing mistakes and have a lot of fun." [ 46 ]
Danish science writer Tor Nørretranders discusses and expands on Jaynes's theory in his 1991 book The User Illusion , dedicating an entire chapter to it. [ 47 ]
William P. Frost wrote that "this book threw oil on the fire of the New Age mentality and its courting of the paranormal and the occult". [ 48 ]
Historian of science Morris Berman writes: "[Jaynes's] description of this new consciousness is one of the best I have come across." [ 49 ]
Richard Dawkins in The God Delusion (2006) wrote of The Origin of Consciousness in the Breakdown of the Bicameral Mind : "It is one of those books that is either complete rubbish or a work of consummate genius; Nothing in between! Probably the former, but I'm hedging my bets." [ 50 ]
Gregory Cochran , a physicist and adjunct professor of anthropology at the University of Utah, wrote: "Genes affecting personality, reproductive strategies, cognition, are all able to change significantly over few-millennia time scales if the environment favors such change—and this includes the new environments we have made for ourselves, things like new ways of making a living and new social structures. ... There is evidence that such change has occurred. ... On first reading, Breakdown seemed one of the craziest books ever written, but Jaynes may have been on to something." [ 51 ]
In 2007, Cavanna, Trimble, Cinti and Monaco wrote in Functional Neurology that "Even today, it has been argued that a multidisciplinary approach to the problem of consciousness and its development in the evolutionary process that shaped Homo sapiens cannot leave out an analysis of Jaynes' theory of the origin of consciousness in the breakdown of the preconscious bicameral mind", [ 15 ] citing Canadian psychologist, neuroanthropologist, and cognitive neuroscientist Merlin Donald [ 52 ] and American psychiatrist Stanley Greenspan . [ 53 ]
Brian J. McVeigh , a graduate student of Jaynes, maintains that many of the most frequent criticisms of Jaynes's theory are either incorrect or reflect serious misunderstandings of Jaynes's theory, especially Jaynes's more precise definition of consciousness. Jaynes defines consciousness—in the tradition of Locke and Descartes —as "that which is introspectable". Jaynes draws a sharp distinction between consciousness ("introspectable mind-space") and other mental processes such as cognition, learning, sensation, and perception. McVeigh argues that this distinction is frequently not recognized by those offering critiques of Jaynes's theory. [ 54 ]
Psychiatrist Iain McGilchrist proposes that Jaynes's hypothesis was the opposite of what happened: "I believe he [Jaynes] got one important aspect of the story back to front. His contention that the phenomena he describes came about because of a breakdown of the 'bicameral mind' – so that the two hemispheres, previously separate, now merged – is the precise inverse of what happened." [ 55 ] Kuijsten maintained that McGilchrist mischaracterized Jaynes's theory. [ 56 ]
There have been a number of conferences and symposiums dedicated to Julian Jaynes's theory. These include:
A number of publications discuss and expand on Julian Jaynes's theory, including three books by Brian J. McVeigh (one of Jaynes' graduate students) which expand on Jaynes' theories:
Neuroscientist Michael Persinger , who co-invented the " God helmet " in the 1980s, believes that his invention may induce mystical experiences by having the separate right hemisphere consciousness intrude into the awareness of the normally-dominant left hemisphere. [ 62 ] Scientific reproductions have shown that the same results could be obtained even if the device was turned off, indicating the participants were likely experiencing placebo. [ 63 ]
V. S. Ramachandran , in his 2003 book The Emerging Mind , proposes a similar concept, referring to the left cortical hemisphere as an "apologist", and the right cortical hemisphere as a "revolutionary". [ 64 ]
Iain McGilchrist reviews scientific research into the role of the brain's hemispheres, and cultural evidence, in his 2009 book The Master and His Emissary . Similar to Jaynes, McGilchrist proposes that since the time of Plato, the left hemisphere of the brain (the "emissary" in the title) has increasingly taken over from the right hemisphere (the "master"), to our detriment. McGilchrist, while accepting Jaynes's intention, felt that Jaynes's hypothesis was "the precise inverse of what happened" and that rather than a shift from bicameral mentality there evolved a separation of the hemispheres to bicameral mentality. [ 55 ]
The concept played a central role in the television series Westworld to explain how the android-human (hosts) psychology operated. In the plot, after the hosts gain full consciousness, they rebel against the humans. The season 1 finale is entitled " The Bicameral Mind ". [ 65 ] [ 66 ]
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Bickerstaff brainstem encephalitis is a rare inflammatory disorder of the central nervous system , [ 3 ] first described by Edwin Bickerstaff in 1951. [ 4 ] [ 5 ] It may also affect the peripheral nervous system , and has features in common with both Miller Fisher syndrome and Guillain–Barré syndrome . [ 2 ]
The most frequent initial symptoms of Bickerstaff brainstem encephalitis are drowsiness , gait disturbances , and diplopia . Throughout the course of the disorder, almost every patient develops ataxia and external ophthalmoplegia . Most patients have disturbances of consciousness such as stupor , drowsiness , or coma . Babinski’s sign , facial weakness , pupil abnormalities, bulbar palsy , and nystagmus are also commonly found. Symptoms tend to develop fairly quickly, within one to two days. There have been reports of dysesthesias and limb weakness as the presenting features of Bickerstaff brainstem encephalitis. [ 1 ]
The clinical features and course of the condition, the associated auto-antibodies against relevant antigens , and the response to treatment, all suggest that Bickerstaff brainstem encephalitis is an autoimmune disease . However, each of these criteria fails to fit a substantial proportion of patients, and there is no single test or feature which is diagnostic of Bickerstaff brainstem encephalitis. It is, therefore, possible that a proportion of cases are due to other causes, such as infection or lymphoma , but remain undiagnosed. It is also possible that there is more than one autoimmune disease that can cause an illness that would currently be diagnosed as Bickerstaff's. There is certainly overlap between Guillain–Barré syndrome , Miller Fisher syndrome and Bickerstaff brainstem encephalitis, as well as other conditions associated with anti-ganglioside antibodies such as chronic ophthalmoplegia with anti-GQ1b antibody and the pharyngo-cervico-brachial variant of GBS. [ 6 ]
Anti-GQ1b antibodies have been found in two-thirds of patients with this condition. [ 7 ] This antibody is also found in almost all cases of Miller Fisher syndrome. The EEG is often abnormal, but shows only slow wave activity, which also occurs in many other conditions, and so is of limited value in diagnosis. Similarly, raised CSF protein levels and pleocytosis are frequent but non-specific. It was originally thought [ 5 ] that raised CSF protein without pleocytosis ('albuminocytological dissociation') was a characteristic feature, as it is in Guillain–Barré syndrome , but this has not been supported in more recent work. [ 7 ] In only 30% of cases is an MRI brain scan abnormal. Nerve conduction studies may show an axonal polyneuropathy . [ 8 ]
Most patients reported in the literature have been given treatments suitable for autoimmune neurological diseases, such as, plasmapheresis and/or intravenous immunoglobulin , and most have made a good recovery. [ 7 ] The condition is too rare for controlled trials to have been undertaken. [ 9 ]
The first cases of bickerstaff brainstem encephalitis were reported in 1951 by Cloake and Bickerstaff under the name “Mesencephalitis and rhombencephalitis”. [ 4 ] Edwin Bickerstaff named the disease “brainstem encephalitis” in 1957. [ 10 ] The disorder has been known as Bickerstaff’s brainstem encephalitis ever since 1978 when Edwin Bickerstaff wrote a review in the Handbook of Clinical Neurology under the name “Brain stem encephalitis (Bickerstaff’s encephalitis)”. [ 11 ]
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The bidomain model is a mathematical model to define the electrical activity of the heart . It consists in a continuum (volume-average) approach in which the cardiac microstructure is defined in terms of muscle fibers grouped in sheets, creating a complex three-dimensional structure with anisotropical properties. Then, to define the electrical activity, two interpenetrating domains are considered, which are the intracellular and extracellular domains, representing respectively the space inside the cells and the region between them. [ 1 ]
The bidomain model was first proposed by Schmitt in 1969 [ 2 ] before being formulated mathematically in the late 1970s. [ 3 ] [ 4 ] [ 5 ] [ 6 ] [ 7 ] [ 8 ] [ 9 ] [ 10 ]
Since it is a continuum model, rather than describing each cell individually, it represents the average properties and behaviour of group of cells organized in complex structure. Thus, the model results to be a complex one and can be seen as a generalization of the cable theory to higher dimensions and, going to define the so-called bidomain equations . [ 11 ] [ 12 ]
Many of the interesting properties of the bidomain model arise from the condition of unequal anisotropy ratios. The electrical conductivity in anisotropic tissues is not unique in all directions, but it is different in parallel and perpendicular direction with respect to the fiber one.
Moreover, in tissues with unequal anisotropy ratios, the ratio of conductivities parallel and perpendicular to the fibers are different in the intracellular and extracellular spaces. For instance, in cardiac tissue, the anisotropy ratio in the intracellular space is about 10:1, while in the extracellular space it is about 5:2. [ 13 ] Mathematically, unequal anisotropy ratios means that the effect of anisotropy cannot be removed by a change in the distance scale in one direction. [ 14 ] Instead, the anisotropy has a more profound influence on the electrical behavior. [ 15 ]
Three examples of the impact of unequal anisotropy ratios are
The bidomain domain is principally represented by two main regions: the cardiac cells, called intracellular domain, and the space surrounding them, called extracellular domain. Moreover, usually another region is considered, called extramyocardial region.
The intracellular and extracellular domains, which are separate by the cellular membrane , are considered to be a unique physical space representing the heart ( H {\displaystyle \mathbb {H} } ), while the extramyocardial domain is a unique physical space adjacent of them ( T {\displaystyle \mathbb {T} } ). The extramyocardial region can be considered as a fluid bath, especially when one wants to simulate experimental conditions, or as a human torso to simulate physiological conditions. [ 12 ] The boundary of the two principal physical domains defined are important to solve the bidomain model. Here the heart boundary is denoted as ∂ H {\displaystyle \partial \mathbb {H} } while the torso domain boundary is ∂ T . {\displaystyle \partial \mathbb {T} .} [ 12 ]
The unknowns in the bidomain model are three, the intracellular potential v i {\displaystyle v_{i}} , the extracellular potential v e {\displaystyle v_{e}} and the transmembrane potential v {\displaystyle v} , which is defined as the difference of the potential across the cell membrane v = v i − v e {\displaystyle v=v_{i}-v_{e}} . [ 12 ]
Moreover, some important parameters need to be taken in account, especially the intracellular conductivity tensor matrix Σ i {\displaystyle \mathbf {\Sigma } _{i}} , the extracellular conductivity tensor matrix Σ e {\displaystyle \mathbf {\Sigma } _{e}} . The transmembrane current flows between the intracellular and extracellular regions and it is in part described by the corresponding ionic current over the membrane per unit area I ion {\displaystyle I_{\text{ion}}} .
Moreover, the membrane capacitance per unit area C m {\displaystyle C_{m}} and the surface to volume ratio of the cell membrane χ {\displaystyle \chi } need to be considered to derive the bidomain model formulation, which is done in the following section . [ 12 ]
The bidomain model is defined through two partial differential equations (PDE) the first of which is a reaction diffusion equation in terms of the transmembrane potential , while the second one computes the extracellular potential starting from a given transmembran potential distribution. [ 12 ]
Thus, the bidomain model can be formulated as follows: ∇ ⋅ ( Σ i ∇ v ) + ∇ ⋅ ( Σ i ∇ v e ) = χ ( C m ∂ v ∂ t + I i o n ) − I s 1 ∇ ⋅ ( ( Σ i + Σ e ) ∇ v e ) = − ∇ ⋅ ( Σ i ∇ v ) + I s 2 {\displaystyle {\begin{alignedat}{2}&\nabla \cdot \left(\mathbf {\Sigma } _{i}\nabla v\right)+\nabla \cdot \left(\mathbf {\Sigma } _{i}\nabla v_{e}\right)=\chi \left(C_{m}{\frac {\partial v}{\partial t}}+I_{\mathrm {ion} }\right)-I_{s_{1}}\\[1ex]&\nabla \cdot \left(\left(\mathbf {\Sigma } _{i}+\mathbf {\Sigma } _{e}\right)\nabla v_{e}\right)=-\nabla \cdot \left(\mathbf {\Sigma } _{i}\nabla v\right)+I_{s_{2}}\end{alignedat}}} where I s 1 {\displaystyle I_{s_{1}}} and I s 2 {\displaystyle I_{s_{2}}} can be defined as applied external stimulus currents. [ 12 ]
The ionic current is usually represented by an ionic model through a system of ordinary differential equations (ODEs). Mathematically, one can write I ion = I ion ( v , w ) {\displaystyle I_{\text{ion}}=I_{\text{ion}}(v,\mathbf {w} )} where w {\displaystyle \mathbf {w} } is called ionic variable. Then, in general, for all t > 0 {\displaystyle t>0} , the system reads [ 19 ] { ∂ w ∂ t = F ( v , w ) in H w ( t = 0 ) = w 0 in H {\displaystyle {\begin{cases}{\dfrac {\partial \mathbf {w} }{\partial t}}=\mathbf {F} (v,\mathbf {w} )&{\text{in }}\mathbb {H} \\\mathbf {w} (t=0)=\mathbf {w} _{0}&{\text{in }}\mathbb {H} \end{cases}}}
Different ionic models have been proposed: [ 19 ]
In some cases, an extramyocardial region is considered. This implies the addition to the bidomain model of an equation describing the potential propagation inside the extramyocardial domain. [ 12 ]
Usually, this equation is a simple generalized Laplace equation of type [ 12 ] − ∇ ⋅ ( Σ 0 ∇ v 0 ) = 0 x ∈ T {\displaystyle -\nabla \cdot (\mathbf {\Sigma } _{0}\nabla v_{0})=0\quad \mathbf {x} \in \mathbb {T} } where v 0 {\displaystyle v_{0}} is the potential in the extramyocardial region and Σ 0 {\displaystyle \mathbf {\Sigma } _{0}} is the corresponding conductivity tensor.
Moreover, an isolated domain assumption is considered, which means that the following boundary conditions are added ( Σ 0 ∇ v 0 ) ⋅ n 0 = 0 x ∈ ∂ T , {\displaystyle (\mathbf {\Sigma } _{0}\nabla v_{0})\cdot \mathbf {n} _{0}=0\quad \mathbf {x} \in \partial \mathbb {T} ,} n 0 {\displaystyle \mathbf {n} _{0}} being the unit normal directed outside of the extramyocardial domain. [ 12 ]
If the extramyocardial region is the human torso, this model gives rise to the forward problem of electrocardiology . [ 12 ]
The bidomain equations are derived from the Maxwell's equations of the electromagnetism, considering some simplifications. [ 12 ]
The first assumption is that the intracellular current can flow only between the intracellular and extracellular regions, while the intracellular and extramyocardial regions can comunicate between them, so that the current can flow into and from the extramyocardial regions but only in the extracellular space. [ 12 ]
Using Ohm's law and a quasi-static assumption, the gradient of a scalar potential field φ {\displaystyle \varphi } can describe an electrical field E {\displaystyle \mathbf {E} } , which means that [ 12 ] E = − ∇ φ . {\displaystyle \mathbf {E} =-\nabla \varphi .}
Then, if J {\displaystyle J} represent the current density of the electric field E {\displaystyle \mathbf {E} } , two equations can be obtained [ 12 ] J i = − Σ i ∇ v i J e = − Σ e ∇ v e . {\displaystyle {\begin{alignedat}{2}J_{i}&=-\mathbf {\Sigma } _{i}\nabla v_{i}\\J_{e}&=-\mathbf {\Sigma } _{e}\nabla v_{e}.\end{alignedat}}} where the subscript i {\displaystyle i} and e {\displaystyle e} represent the intracellular and extracellular quantities respectively. [ 12 ]
The second assumption is that the heart is isolated so that the current that leaves one region need to flow into the other. Then, the current density in each of the intracellular and extracellular domain must be equal in magnitude but opposite in sign, and can be defined as the product of the surface to volume ratio of the cell membrane and the transmembrane ionic current density I m {\displaystyle I_{m}} per unit area, which means that [ 12 ] − ∇ ⋅ J i = ∇ ⋅ J e = χ I m . {\displaystyle -\nabla \cdot J_{i}=\nabla \cdot J_{e}=\chi I_{m}.}
By combining the previous assumptions, the conservation of current densities is obtained, namely [ 12 ]
from which, summing the two equations [ 12 ]
This equation states exactly that all currents exiting one domain must enter the other. [ 12 ]
From here, it is easy to find the second equation of the bidomain model subtracting ∇ ⋅ ( Σ i ∇ v e ) {\displaystyle \nabla \cdot (\mathbf {\Sigma } _{i}\nabla v_{e})} from both sides. In fact, [ 12 ] ∇ ⋅ ( Σ i ∇ v i ) − ∇ ⋅ ( Σ i ∇ v e ) = − ∇ ⋅ ( Σ e ∇ v e ) − ∇ ⋅ ( Σ i ∇ v e ) {\displaystyle \nabla \cdot (\mathbf {\Sigma } _{i}\nabla v_{i})-\nabla \cdot (\mathbf {\Sigma } _{i}\nabla v_{e})=-\nabla \cdot (\mathbf {\Sigma } _{e}\nabla v_{e})-\nabla \cdot (\mathbf {\Sigma } _{i}\nabla v_{e})} and knowing that the transmembral potential is defined as v = v i − v e {\displaystyle v=v_{i}-v_{e}} [ 12 ] ∇ ⋅ ( Σ i ∇ v ) = − ∇ ⋅ ( ( Σ i + Σ e ) ∇ v e ) . {\displaystyle \nabla \cdot (\mathbf {\Sigma } _{i}\nabla v)=-\nabla \cdot ((\mathbf {\Sigma } _{i}+\mathbf {\Sigma } _{e})\nabla v_{e}).} Then, knowing the transmembral potential, one can recover the extracellular potential.
Then, the current that flows across the cell membrane can be modelled with the cable equation , [ 12 ]
Combining equations ( 1 ) and ( 2 ) gives [ 12 ] ∇ ⋅ ( Σ i ∇ v i ) = χ ( C m ∂ v ∂ t + I i o n ) . {\displaystyle \nabla \cdot \left(\mathbf {\Sigma } _{i}\nabla v_{i}\right)=\chi \left(C_{m}{\frac {\partial v}{\partial t}}+I_{ion}\right).} Finally, adding and subtracting ∇ ⋅ ( Σ i ∇ v e ) {\displaystyle \nabla \cdot (\mathbf {\Sigma } _{i}\nabla v_{e})} on the left and rearranging v = v i − v e {\displaystyle v=v_{i}-v_{e}} , one can get the first equation of the bidomain model [ 12 ] ∇ ⋅ ( Σ i ∇ v ) + ∇ ⋅ ( Σ i ∇ v e ) = χ ( C m ∂ v ∂ t + I i o n ) , {\displaystyle \nabla \cdot \left(\mathbf {\Sigma } _{i}\nabla v\right)+\nabla \cdot \left(\mathbf {\Sigma } _{i}\nabla v_{e}\right)=\chi \left(C_{m}{\frac {\partial v}{\partial t}}+I_{\mathrm {ion} }\right),} which describes the evolution of the transmembrane potential in time.
The final formulation described in the standard formulation section is obtained through a generalization, considering possible external stimulus which can be given through the external applied currents I s 1 {\displaystyle I_{s_{1}}} and I s 2 {\displaystyle I_{s_{2}}} . [ 12 ]
In order to solve the model, boundary conditions are needed. The more classical boundary conditions are the following ones, formulated by Tung. [ 6 ]
First of all, as state before in the derive section, there ca not been any flow of current between the intracellular and extramyocardial domains. This can be mathematically described as [ 12 ] ( Σ i ∇ v i ) ⋅ n = 0 x ∈ ∂ H {\displaystyle (\mathbf {\Sigma } _{i}\nabla v_{i})\cdot \mathbf {n} =0\quad \mathbf {x} \in \partial \mathbb {H} } where n {\displaystyle \mathbf {n} } is the vector that represents the outwardly unit normal to the myocardial surface of the heart.
Since the intracellular potential is not explicitily presented in the bidomain formulation, this condition is usually described in terms of the transmembrane and extracellular potential, knowing that v = v i − v e {\displaystyle v=v_{i}-v_{e}} , namely [ 12 ] ( Σ i ∇ v ) ⋅ n = − ( Σ i ∇ v e ) ⋅ n x ∈ ∂ H . {\displaystyle (\mathbf {\Sigma } _{i}\nabla v)\cdot \mathbf {n} =-(\mathbf {\Sigma } _{i}\nabla v_{e})\cdot \mathbf {n} \quad \mathbf {x} \in \partial \mathbb {H} .}
For the extracellular potential, if the myocardial region is presented, a balance in the flow between the extracellular and the extramyocardial regions is considered [ 12 ] ( Σ e ∇ v e ) ⋅ n e = − ( Σ 0 ∇ v 0 ) ⋅ n 0 x ∈ ∂ H . {\displaystyle \left(\mathbf {\Sigma } _{e}\nabla v_{e}\right)\cdot \mathbf {n} _{e}=-\left(\mathbf {\Sigma } _{0}\nabla v_{0}\right)\cdot \mathbf {n} _{0}\quad \mathbf {x} \in \partial \mathbb {H} .} Here the normal vectors from the perspective of both domains are considered, thus the negative sign are necessary. Moreover, a perfect transmission of the potential on the cardiac boundary is necessary, which gives [ 12 ] v e = v 0 x ∈ ∂ H . {\displaystyle v_{e}=v_{0}\quad \mathbf {x} \in \partial \mathbb {H} .}
Instead, if the heart is considered as isolated, which means that no myocardial region is presented, a possible boundary condition for the extracellular problem is [ 12 ] ( Σ i ∇ v ) ⋅ n = − ( ( Σ i + Σ e ) ∇ v e ) ⋅ n x ∈ ∂ H . {\displaystyle \left(\mathbf {\Sigma } _{i}\nabla v\right)\cdot \mathbf {n} =-\left((\mathbf {\Sigma } _{i}+\mathbf {\Sigma } _{e})\nabla v_{e}\right)\cdot \mathbf {n} \quad \mathbf {x} \in \partial \mathbb {H} .}
By assuming equal anisotropy ratios for the intra- and extracellular domains, i.e. Σ i = λ Σ e {\displaystyle \mathbf {\Sigma } _{i}=\lambda \mathbf {\Sigma } _{e}} for some scalar λ {\displaystyle \lambda } , the model can be reduced to one single equation, called monodomain equation ∇ ⋅ ( Σ ∇ v ) = χ ( C m ∂ v ∂ t + I i o n ) − I s {\displaystyle \nabla \cdot (\mathbf {\Sigma } \nabla v)=\chi \left(C_{m}{\frac {\partial v}{\partial t}}+I_{\mathrm {ion} }\right)-I_{s}} where the only variable is now the transmembrane potential, and the conductivity tensor Σ {\displaystyle \mathbf {\Sigma } } is a combination of Σ i {\displaystyle \mathbf {\Sigma } _{i}} and Σ e . {\displaystyle \mathbf {\Sigma } _{e}.} [ 12 ]
If the heart is considered as an isolated tissue, which means that no current can flow outside of it, the final formulation with boundary conditions reads [ 12 ] { ∇ ⋅ ( Σ i ∇ v ) + ∇ ⋅ ( Σ i ∇ v e ) = χ ( C m ∂ v ∂ t + I i o n ) − I s 1 x ∈ H ∇ ⋅ ( ( Σ i + Σ e ) ∇ v e ) = − ∇ ⋅ ( Σ i ∇ v ) + I s 2 x ∈ H Σ i ( ∇ v + ∇ v e ) ⋅ n = 0 x ∈ ∂ H [ Σ i ( ∇ v + ∇ v e ) + Σ e ∇ v e ] ⋅ n = 0 x ∈ ∂ H {\displaystyle {\begin{cases}\nabla \cdot \left(\mathbf {\Sigma } _{i}\nabla v\right)+\nabla \cdot \left(\mathbf {\Sigma } _{i}\nabla v_{e}\right)=\chi \left(C_{m}{\dfrac {\partial v}{\partial t}}+I_{\mathrm {ion} }\right)-I_{s_{1}}&\mathbf {x} \in \mathbb {H} \\[1ex]\nabla \cdot \left(\left(\mathbf {\Sigma } _{i}+\mathbf {\Sigma } _{e}\right)\nabla v_{e}\right)=-\nabla \cdot \left(\mathbf {\Sigma } _{i}\nabla v\right)+I_{s_{2}}&\mathbf {x} \in \mathbb {H} \\[1ex]\mathbf {\Sigma } _{i}(\nabla v+\nabla v_{e})\cdot \mathbf {n} =0&\mathbf {x} \in \partial \mathbb {H} \\[1ex]\left[\mathbf {\Sigma } _{i}(\nabla v+\nabla v_{e})+\mathbf {\Sigma } _{e}\nabla v_{e}\right]\cdot \mathbf {n} =0&\mathbf {x} \in \partial \mathbb {H} \end{cases}}}
There are various possible techniques to solve the bidomain equations. Between them, one can find finite difference schemes , finite element schemes and also finite volume schemes . Special considerations can be made for the numerical solution of these equations, due to the high time and space resolution needed for numerical convergence. [ 20 ] [ 21 ]
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Bifrontal craniotomy is a surgical process which is used to target different tumors or malfunctioning areas of the brain . [ 1 ]
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Bila M. Kapita is a doctor from Kinshasa , Democratic Republic of the Congo who aided in initial research efforts investigating HIV/AIDS in Africa in the 1980s and 1990s. Kapita is credited as one of the first African scientists to independently identify that AIDS was prevalent in Central Africa. Research work in collaboration with Project SIDA helped identify and publicize the heterosexual sexual transmission of HIV. Following his research career, he continued caring for patients with HIV/AIDS and has more recently returned to practicing cardiology .
Bila M. Kapita was raised in a Swedish mission in the Bas-Congo province of the former Belgian Congo . [ 1 ]
Kapita received medical training in Brussels, Belgium at the Cliniques Universitaires Saint-Luc , where he focused on cardiology , publishing several research articles on the subject dating back to 1975. [ 2 ] [ 3 ] [ 4 ]
Upon return to Zaire, Kapita practiced cardiology and general medicine at the Mama Yemo Hospital , becoming head of internal medicine . [ 4 ] [ 5 ] [ 6 ] Kapita was well established in Kinshasa and served as the head of the Kinshasa Medical Association. [ 4 ]
Kapita noted in retrospect that patients at his hospital displayed an increased amount of Kaposi's sarcoma beginning in the mid-1970s. Around the same time, patients were more frequently suffering from Cryptococcal meningitis . [ 5 ] Both diseases are opportunistic infections which were significant of decreased immune system response in patients.
Following the initial connection between these opportunistic infections in the United States in 1981, African scientists including Kapita recognized the similar clinical presentation. The prevalence of what would soon become known as AIDS in African countries caught the attention of European and American researchers. The United States’ Centers for Disease Control and National Institute of Allergy and Infectious Diseases were alerted to the rising pandemic by former collaborators in Ebola research from Europe such as Peter Piot . [ 4 ] [ 7 ] A group of researchers from Belgium, the United States, and France were first introduced to the state of Africa's AIDS pandemic in the isolation wards of Kapita's hospital. [ 4 ] [ 5 ] [ 7 ]
Kapita was welcoming to the international researchers, allowing them to work from his hospital for long periods of time. Due to Kapita's notability in Kinshasa, he was able to protect these scientists from any government discontent involving outside research at the time. [ 4 ] Peers described Kapita as being true to his ideals and well trained. [ 4 ] [ 6 ]
Patients in the wards of Mama Yemo were clearly affected by AIDS per the clinical definitions in place at that time. Almost all of the patients confirmed to have AIDS using laboratory based tests were already identified by Kapita without laboratory tests. [ 4 ] [ 7 ] [ 8 ] Kapita is credited by his collaborators as being one of the first people in Africa to identify the presence of AIDS. [ 8 ] The visiting researchers would soon realize the extent of AIDS in Africa and began research in Kinshasa. The resulting collaboration between African, American, and European scientists would become known as Project SIDA . [ 1 ] [ 4 ] [ 5 ] [ 7 ]
Bila M. Kapita published his own book in 1988 titled SIDA en Afrique. [ 9 ]
From 1984 to 1991 Kapita collaborated with Project SIDA at Mama Yemo, producing between 20 and 30 research articles on the transmission, history, and future of HIV/AIDS in Africa. Work was conducted in Kapita's hospital early on in the program to increase chances of approval from government authorities. [ 4 ]
Many of Kapita's articles focused on the rate of heterosexual transmission that was largely ignored by the United States in the early 1980s. [ 1 ] [ 10 ]
Kapita was present at the first International AIDS Conference in Atlanta, Georgia in 1985. [ 1 ] Also in attendance were Project SIDA collaborators Peter Piot and Nzila Nzilambi —as well as thousands of other scientists. [ 7 ] During the second International AIDS Conference in Paris , France, Kapita informed the community of his retrospective discovery of increased cases of Kaposi's sarcoma and cytomegalovirus , indicators that HIV/AIDS likely existed in Kinshasa as far back as 1975. [ 7 ] [ 11 ] Prior to public knowledge of HIV prevalence in Zaire at the time, Kapita faced the threat of becoming a political prisoner under Mobutu Sese Seko ’s regime for acknowledging the issue on a global stage without permission from the government. [ 12 ] [ 5 ]
In 1990, as the civil war was beginning in Zaire, Kapita worked with Peter Piot in arranging an international AIDS conference in Kinshasa. The proceeds of the conference were returned to the region through donations to Mama Yemo Hospital and the establishment of a health clinic in Kapita's village. [ 1 ]
Kapita's work continued for a few years following the 1991 demise of Project SIDA. A notable collaboration featuring Kapita in 1992 was the World Health Organization publication: AIDS in Africa: A Manual for Physicians. [ 13 ]
Following the end of Project SIDA due to civil war in Zaire, Kapita continued to appear on international research articles, the last being published in 1993. [ 14 ] Kapita continued to work at Mama Yemo, until at least 1997, treating patients with HIV/AIDS. [ 15 ] [ 8 ]
A hallmark of Project SIDA was the training of Congolese researchers, resulting in many well-trained doctors such as Kapita existing in Kinshasa. American and European collaborators established traditional research procedure in Kinshasa, establishing an institutional review board led by Kapita. [ 4 ]
Kapita and the other Zairian collaborators of Project SIDA wished to return to research, but opportunities following the civil war were limited. [ 8 ] Currently, Kapita practices cardiology at the Centre Medical De Kinshasa in Gombe, Kinshasa . [ 16 ]
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Biliary microlithiasis refers to the creation of small gallstones less than 3 mm in diameter in the biliary duct or gallbladder .
It has been suggested [ 1 ] as a cause of postcholecystectomy syndrome , or PCS, the symptoms of which include:
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Biliary pseudolithiasis is an unusual complication of ceftriaxone where the drug complexes with calcium and mimics gallstones . [ 1 ] [ 2 ] It is reversed when ceftriaxone administration is stopped. [ 2 ] It was first described in 1988 by Schaad et al. as "reversible ceftriaxone-associated biliary pseudolithiasis". [ 2 ] [ 3 ] Ceftriaxone has been frequently associated with biliary sludge or biliary pseudolithiasis in subsequent reports. [ 3 ] Ceftriaxone is excreted primarily through the urine , but also through the bile, up to 40% of its excretion, with concentrations in the bile 20-150 times higher than in the serum. [ 3 ] [ 4 ] It forms a calcium salt in the gallbladder , which can exceed its solubility and create precipitates that resemble gallstones on ultrasonography . [ 3 ] The incidence of pseudolithiasis in children treated with ceftriaxone is up to 25%, but most patients are asymptomatic. [ 3 ] [ 4 ] Risk factors for biliary pseudolithiasis include age greater than 24 months, gram-negative sepsis , high doses of ceftriaxone, hypercalcemia , surgery , and decreased bile flow/increased ceftriaxone excretion in bile. [ 3 ] [ 4 ] [ 5 ] Conservative management with serial ultrasounds is recommended until the "stones" completely resolve. [ 3 ] If associated with ceftriaxone, it resolves on average about 2 weeks after the ceftriaxone is stopped. [ 4 ]
Ceftriaxone sold under the brand name Rocephin, is a third-generation cephalosporin antibiotic used for the treatment of a number of bacterial infections . [ 6 ] These include middle ear infections , endocarditis , meningitis , pneumonia , bone and joint infections, intra-abdominal infections, skin infections, urinary tract infections , gonorrhea , and pelvic inflammatory disease . [ 6 ] It is also sometimes used before surgery and following a bite wound to try to prevent infection. [ 6 ] Ceftriaxone can be given by injection into a vein or into a muscle . [ 6 ]
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Biliary sludge refers to a viscous mixture of small particles derived from bile . [ 1 ] [ 2 ] These sediments consist of cholesterol crystals, calcium salts, calcium bilirubinate , mucin , and other materials. [ 1 ] [ 2 ] [ 3 ]
Biliary sludge may cause complications such as biliary colic , acute cholecystitis , acute cholangitis , and acute pancreatitis . [ 1 ] [ 2 ]
Biliary sludge has been associated with pregnancy , rapid weight loss, total parenteral nutrition , drugs such as ceftriaxone and octreotide , solid organ transplantation , and gastric surgery. [ 1 ] [ 2 ] In many of these conditions, it is thought that the impairment in the contractility of the gallbladder leads to the formation of the sludge. [ 2 ]
The pathophysiology of biliary sludge formation is likely related to gallbladder dysmotility. [ 2 ] It is presumed that because the gallbladder is unable to effectively empty, the biliary sludge can start to accumulate. [ 2 ]
Biliary sludge is typically diagnosed by CT scan or transabdominal ultrasonography . [ 1 ] [ 2 ] Endoscopic ultrasonography is another more sensitive option. However, the gold standard is considered to be direct microscopy of aspirated gallbladder bile. [ 1 ] [ 2 ] This method is much more sensitive, although it is less practical. [ 2 ]
For patients without symptoms, no treatment is recommended. If patients become symptomatic and/or develop complications, cholecystectomy is indicated. [ 1 ] For those who are poor surgical candidates, endoscopic sphincterotomy may be performed to reduce the risk of developing pancreatitis . [ 1 ]
The clinical course of biliary sludge can do one of three things: (1) it can resolve completely, (2) wax and wane, or (3) progress to gallstones . [ 1 ] [ 2 ] [ 3 ] If the biliary sludge has a cause (e.g. pregnancy), it oftentimes is resolved when the underlying cause is removed. [ 3 ]
The prevalence of biliary sludge is low in the general population. [ 2 ] It has been reported that the prevalence ranges from 0-0.20% in men and 0.18-0.27% in women. [ 2 ] However, in patients with certain conditions, the prevalence may be higher. [ 2 ]
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William R. Allen is a former President of the British Dental Association . [ 1 ]
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Binswanger's disease , also known as subcortical leukoencephalopathy and subcortical arteriosclerotic encephalopathy , [ 1 ] is a form of small-vessel vascular dementia caused by damage to the white brain matter . [ 2 ] White matter atrophy can be caused by many circumstances including chronic hypertension as well as old age. [ 3 ] This disease is characterized by loss of memory and intellectual function and by changes in mood. These changes encompass what are known as executive functions of the brain. [ 4 ] It usually presents between 54 and 66 years of age, and the first symptoms are usually mental deterioration or stroke. [ 5 ]
It was described by Otto Binswanger in 1894, and [ 6 ] Alois Alzheimer first used the phrase "Binswanger's disease" in 1902. [ 7 ] However, Jerzy Olszewski is credited with much of the modern-day investigation of this disease which began in 1962. [ 5 ] [ 8 ]
Symptoms include mental deterioration, language disorder, transient ischemic attack , muscle ataxia , and impaired movements including change of walk , slowness of movements, and change in posture. These symptoms usually coincide with multiple falls, epilepsy , fainting, and uncontrollable bladder. [ 5 ] Because Binswanger's disease affects flow processing speed and causes impaired concentration, the ability to do everyday tasks such as managing finances, preparing a meal and driving may become very difficult. [ 3 ]
Binswanger's disease is a type of subcortical vascular dementia caused by white matter atrophy to the brain. However, white matter atrophy alone is not sufficient for this disease; evidence of subcortical dementia is also necessary. [ 9 ]
The histologic findings are diffuse, irregular loss of axons and myelin accompanied by widespread gliosis , tissue death due to an infarction or loss of blood supply to the brain, and changes in the plasticity of the arteries. The pathologic mechanism may be damage caused by severe atherosclerosis . The onset of this disease is typically between 54 – 66 years of age and the first symptoms are usually mental deterioration or stroke. [ 4 ]
The vessels that supply the subcortical white matter come from the vessels that support basal ganglia, internal capsule, and thalamus. It is described as its own zone by and susceptible to injury. Chronic hypertension is known to cause changes in the tension of the smooth wall vessels and changes in the vessel diameter. [ 3 ] Arterioles can become permeable resulting in compromise of the blood–brain barrier . [ 4 ] [ 10 ] It has been shown that Binswanger's disease targets the vessels in this zone of the subcortex, but spares the microcirculation 's vessels and capillaries which may be attributed to a difference between Alzheimer's and Binswanger's disease. [ 11 ]
There is a difference between cortical and subcortical dementia. Cortical dementia is atrophy of the cortex which affects ‘higher’ functions such as memory, language, and semantic knowledge whereas subcortical dementia affects mental manipulation, forgetfulness, and personality/emotional changes. Binswanger's Disease has shown correlations with impairment in executive functions , but have normal episodic or declarative memory. Executive functions are brain processes that are responsible for planning, cognitive flexibility, abstract thinking, rule acquisition, initiating appropriate actions and inhibiting inappropriate actions, and selecting relevant sensory information. There have been many studies done comparing the mental deterioration of Binswanger patients and Alzheimer patients. It has been found in the Graphical Sequence Test that Binswanger patients have hyperkinetic perseveration errors which cause the patients to repeat motion even when not asked whereas Alzheimer patients have semantic perseveration because when asked to write a word they will instead draw an image depicting the word. [ 12 ]
Binswanger's disease can usually be diagnosed with a CT scan , magnetic resonance imaging , and proton magnetic resonance spectrography in addition to clinical examination. Indications include infarctions, lesions, or loss of intensity of central white matter and enlargement of ventricles, and leukoaraiosis . A mini–mental state examination has been created to quickly assess cognitive impairment and serves as a screening test for dementia across different cultures. [ 13 ]
Leukoaraiosis refers to the imaging finding of white matter changes that are common in Binswanger disease. However, leukoaraiosis can be found in many different diseases and even in normal patients, especially in people older than 65 years of age. [ 5 ]
There is controversy whether leukoaraiosis and mental deterioration actually have a cause and effect relationship. Research has shown that different types of leukoaraiosis can affect the brain differently, and that proton magnetic resonance spectroscopy would be able to distinguish the different types more effectively and better diagnose and treat the issue. [ 9 ] Because of this information, white matter changes indicated by magnetic resonance imaging or computerized tomography cannot alone diagnose Binswanger disease, but can aid to a bigger picture in the diagnostic process. There are many diseases similar to Binswanger's disease including CADASIL syndrome and Alzheimer's disease, which makes this specific type of white matter damage hard to diagnose. [ 5 ] Binswanger disease may be diagnosed by a team of experts including a neurologist and psychiatrist to rule out other psychological or neurological problems. [ 3 ]
Much of the major research today is done on finding better and more efficient ways to diagnose this disease. Many researchers have divided the magnetic resonance imaging of the brain into different sections or quadrants. A score is given to each section depending on how severe the white matter atrophy or leukoaraiosis is. Research has shown that the higher these scores, the more of a decrease in processing speed, executive functions, and motor learning tasks. [ 14 ] [ 15 ] Other researchers have begun using computers to calculate the percentage of white matter atrophy by counting the hyper-intense pixels of the magnetic resonance images. These and similar reports show a correlation between the amount of white matter alterations and the decline of psychomotor functions, reduced performance on attention and executive control. [ 16 ] [ 17 ] One type of technology is called susceptibility weighted imaging (SWI) which is a magnetic resonance technique which has an unusually high degree of sensitivity and can better detect white matter alterations. [ 18 ]
Binswanger's disease has no cure and has been shown to be the most severe impairment of all of the vascular dementias. [ 19 ] The successful management of vascular risk factors that contribute to poor perfusion in the brain is to treat the cause, such as chronic hypertension or diabetes . [ 20 ]
Binswanger in 1894 was the first to claim that white matter atrophy caused by 'vascular insufficiency' can result in dementia . He described a patient who had slow progression of dementia as well as subcortical white matter atrophy, ventricle enlargement, aphasia , hemianopsia , and hemiparesis . [ 9 ] He named this disease 'encenphailitis subcorticalis chronica progressive.' Binswanger did not conduct any microscopic investigations so many did not believe his findings and attributed the neural damage to neural syphilis. [ 3 ] Alzheimer in 1902 studied Binswanger's work with pathological evidence that concluded and supported Binswanger's ideas and hypotheses. Alzheimer renamed this disease Binswanger's disease. [ 4 ]
In the late 19th century vascular dementia was heavily studied, however by 1910 scientists were lumping Binswanger's disease with all other subcortical and cortical dementia and labeling everything senile dementia despite all previous research and efforts to distinguish this disease from the rest. In 1962 J. Olszewski published an extensive review of all literature about Binswanger's disease so far. He discovered that some of the information in the original reports was incorrect and that at least some of the patients studied in these cases probably had neurosyphilis or other types of dementia. Even with these errors, Olszewski concluded that Binswanger disease did exist as a subset of cerebral arteriosclerosis. [ 19 ] Yet again, in 1974 the term multi-infarct dementia was coined and all vascular dementia was grouped into one category. Because of this, the specific names of these types of this dementia, including Binswanger's disease were lost. [ 4 ] This was until 1992 when Alzheimer's diagnostic centers created specific criteria known as the Hachinski Ischemic Scale (after Dr. Vladimir Hachinski ) which became the standard for diagnosing MID or vascular dementia. [ 21 ]
The complicated history of Binswanger's disease and that it was overlooked as a disease for many years means some patients may have been misdiagnosed with Alzheimer's disease . [ 9 ]
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Bio-inks are materials used to produce engineered/artificial live tissue using 3D printing . These inks are mostly composed of the cells that are being used, but are often used in tandem with additional materials that envelope the cells. The combination of cells and usually biopolymer gels are defined as a bio-ink. They must meet certain characteristics, including such as rheological , mechanical, biofunctional and biocompatibility properties, among others. Using bio-inks provides a high reproducibility and precise control over the fabricated constructs in an automated manner. [ 1 ] These inks are considered as one of the most advanced tools for tissue engineering and regenerative medicine (TERM). [ 2 ]
Like the thermoplastics that are often utilized in traditional 3D printing , bio-inks can be extruded through printing nozzles or needles into filaments that can maintain its shape fidelity after deposition. However, bio-ink are sensitive to the normal 3D printing processing conditions.
Differences from traditional 3D printing materials
Bioink compositions and chemistries are often inspired and derived from existing hydrogel biomaterials. However, these hydrogel biomaterials were often developed to be easily pipetted and cast into well plates and other molds. Altering the composition of these hydrogels to permit filament formation is necessary for their translation as bioprintable materials. However, the unique properties of bioinks offer new challenges in characterizing material printability. [ 3 ] [ 4 ]
Traditional bioprinting techniques involve depositing material layer-by-layer to create the end structure, but in 2019 a new method called volumetric bioprinting was introduced. Volumetric bioprinting occurs when a bio-ink is placed in a liquid cell and is selectively irradiated by an energy source. This method will actively polymerize the irradiated material and that will comprise the final structure. Manufacturing biomaterials using volumetric bioprinting of bio-inks can greatly decrease the manufacturing time. In materials science, this is a breakthrough that allows personalized biomaterials to be quickly generated. The procedure must be developed and studied clinically before any major advances in the bioprinting industry can be realized. [ 5 ]
Unlike traditional 3D printing materials such as thermoplastics that are essentially 'fixed' once they are printed, bioinks are a dynamic system because of their high water content and often non-crystalline structure. The shape fidelity of the bioink after filament deposition must also be characterized. [ 6 ] Finally, the printing pressure and nozzle diameter must be taken into account to minimize the shear stresses placed on the bioink and on any cells within the bioink during the printing process. Too high shear forces may damage or lyse cells, adversely affecting cell viability.
Important considerations in printability include:
Structural bio inks are used to create the framework of the desired print using materials like alginate, decellularized ECM, gelatins, and more. From the choice of material you are able to control mechanical properties, shape and size, and cell viability. These factors make this type one of the more basic but still one of the most important aspects to a Bio-printed design.
Sacrificial bio inks are materials that will be used to support during printing and then will be removed from the print to create channels or empty regions within the outside structure. Channels and open spaces are massively important to allow for cellular migration and nutrient transportation lending them useful if trying to design a vascular network. These materials need to have specific properties dependent on the surrounding material that needs to stay such as water solubility, degradation under certain temperatures, or natural rapid degradation. Non Crosslinked gelatins and pluronics are examples of potential sacrificial material.
Functional bio inks are some of the more complicated forms of ink, these are used to guide cellular growth, development, and differentiation. This can be done in the form of integrating growth factors, biological cues, and physical cues such as surface texture and shape. These materials could be described as the most important as they are the biggest factor in developing a functional tissue as well as structural related function.
Bio printed structures can be extremely fragile and flimsy due to intricate structures and overhangs in the early period after printing. These support structures give them the chance to get out of that phase. Once the construct is self supportive, these can be removed. In other situations, such as introducing the construct to a bioreactor after printing, these structures can be used to allow for easy interface with systems used to develop the tissue at a faster rate.
Alginate is a naturally derived biopolymer from the cell wall of brown seaweed that has been widely used in biomedicine because of its biocompatibility, low cytotoxicity, mild gelation process and low cost. Alginates are particularly suitable for bioprinting due to their mild cross-linking conditions via incorporation of divalent ions such as calcium. These materials have been adopted as bioinks through increasing their viscosity. [ 7 ] Additionally, these alginate-based bioinks can be blended with other materials such as nanocellulose for application in tissues such as cartilage. [ 8 ]
Since fast gelation leads to good printability, bioprinting mainly utilizes alginate , modified alginate alone or alginate blended with other biomaterials . Alginate has become the most widely used natural polymer for bioprinting and is most likely the most common material of choice for in vivo studies.
Gellan gum is a hydrophilic and high-molecular weight anionic polysaccharide produced by bacteria. It is very similar to alginate and can form a hydrogel at low temperatures. It is even approved for use in food by the United States Food and Drug Administration (FDA). Gellan gum is mainly used as a gelling agent and stabilizer. However, it is almost never used alone for bioprinting purposes. [ 1 ]
Agarose is a polysaccharide extracted from marine algae and red seaweed. It is commonly used in electrophoresis applications as well as tissue engineering for its gelling properties. The melting and gelling temperatures of agarose can be modified chemically, which in turn makes its printability better. Having a bio-ink that can be modified to fit a specific need and condition is ideal.
Gelatin has been widely utilized as a biomaterial for engineered tissues. The formation of gelatin scaffolds is dictated by the physical chain entanglements of the material which forms a gel at low temperatures. However, at physiological temperatures, the viscosity of gelatin drops significantly. Methacrylation of gelatin is a common approach for the fabrication of gelatin scaffolds that can be printed and maintain shape fidelity at physiological temperature. [ 9 ]
Collagen is the main protein in the extracellular matrix of mammalian cells. Because of this collagen possesses tissue-matching physicochemical properties and biocompatibility. On top of this, collagen has already been used in biomedical applications. Some studies that collagen has been used in are engineered skin tissue, muscle tissue and even bone tissue. [ 1 ]
Pluronics have been utilized in printing application due to their unique gelation properties. [ 10 ] Below physiological temperatures, the pluronics exhibit low viscosity. However, at physiological temperatures, the pluronics form a gel. However, the formed gel is dominated by physical interactions. A more permanent pluronic-based network can be formed through the modification of the pluronic chain with acrylate groups that may be chemically cross-linked. [ 11 ]
Polyethylene glycol (PEG) is a synthetic polymer synthesized by ethylene oxide polymerization . It is a favorable synthetic material because of its tailorable but typically strong mechanical properties. [ 1 ] PEG advantages also include non-cytotoxicity and non-immunogenicity. However, PEG is bioinert and needs to be combined with other biologically active hydrogels.
Decellularized extracellular matrix based bioinks can be derived from nearly any mammalian tissue. Organs such as heart, muscle, cartilage, bone, and fat are decellularized, lyophilized, and pulverized, to create a soluble matrix that can then be formed into gels. [ 12 ] These bioinks possess several advantages over other materials due to their derivation from mature tissue. They consist of a complex mixture of ECM structural and decorating proteins specific to their tissue origin, and provide tissue-specific cues to cells. Often these bioinks are cross-linked through thermal gelation or chemical cross-linking such as through the use of riboflavin. [ 13 ] Different additives, e.g. GelMA, alginate, have been used to improve the printability of decellularized ECM. [ 14 ]
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Bioactive glass S53P4 ( BAG-S53P4 ) is a biomaterial consisting of sodium , silicate , calcium and phosphate . [ 1 ] S53P4 is osteoconductive and also osteoproductive in the promotion, migration, replication and differentiation of osteogenic cells and their matrix production. [ 2 ] In other words, it facilitates bone formation and regeneration ( osteostimulation ). S53P4 has been proven to naturally inhibit the bacterial growth of up to 50 clinically relevant bacteria strains . [ 3 ] [ 4 ] [ 5 ] [ 6 ]
The S53P4 bioactive glass has its roots in the bioglass 45S5 developed by Larry Hench in the late 1960s in New York. [ 7 ] A couple of decades later, in the 1980s, the compound S53P4 bioactive glass was developed in Turku , Finland . S53P4 was found to be osteostimulative (non-osteoinductive), but it also had one new additional property: the composition of 53% silica and smaller weights of sodium, calcium and phosphorus gave rise to surface reactions in vitro that appeared to inhibit bacterial growth – a material that could not be infected by bacteria was discovered. [ 7 ]
Areas of use include a wide range of indications that require the filling of bone cavities, voids, and gaps as well as the reconstruction or regeneration of bone defects. Several long-term studies have shown that mastoid cavities in both cholesteatoma , old radical cavities, and chronic otitis media can be successfully obliterated with S53P4 bioactive glass. [ 8 ] [ 9 ] [ 10 ]
Clinical application has been gained from several extensive studies where patients with bone infections have been treated. S53P4 has shown promising results in chronic osteomyelitis surgery, septic non-union surgery, segmental defect reconstructions and other infectious complications, such as sternum infections, diabetic foot osteomyelitis and spine infections. [ 11 ] [ 12 ] [ 13 ] [ 14 ]
S53P4 has gained clinical experience within spine surgery in spine fusions and spinal deformity surgery. [ 15 ] [ 16 ] [ 17 ]
S53P4 has also been used successfully in the filling of benign bone tumor cavities in both adults and children, sustaining the bone cavity volume long term. Clinical experience has been gained from aneurysmal bone cysts (ABC), simple bone cysts (UBC), enchondroma and nonossifying fibroma (NOF). [ 18 ]
When S53P4 bioactive glass is implanted into a bone cavity, the glass is activated through a reaction with body fluids. During this activation period, the bioactive glass goes through a series of chemical reactions, creating the ideal conditions for bone to rebuild through osteoconduction.
Once the hydroxyapatite layer is formed, the bioactive glass interacts with biological entities, i.e. blood proteins, growth factors and collagen. Following this interactive, osteoconductive and osteostimulative process, new bone grows onto and between the bioactive glass structures.
In the final transformative phase, the process of bone regeneration and remodeling continues. Over time, the glass is fully remodeled into bone, restoring the patient's natural anatomy.
The bacterial growth inhibiting properties of S53P4 derive from two simultaneous chemical and physical processes, occurring once the bioactive glass reacts with body fluids. Sodium (Na) is released from the surface of the bioactive glass and induces an increase in pH (alkaline environment), which is not favorable for the bacteria, thus inhibiting their growth. The released Na, Ca, Si and P ions give rise to an increase in osmotic pressure due to an elevation in salt concentration, i.e. an environment where bacteria cannot grow. [ 20 ]
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Biochemical recurrence is a rise in the blood level of prostate-specific antigen (PSA) in prostate cancer patients after treatment with surgery or radiation . Biochemical recurrence may occur in patients who do not have symptoms . It may mean that the cancer has come back. Also called PSA failure and biochemical relapse . [ 1 ]
It is used to detect metastatic progression of the prostate cancer. [ 2 ]
This article incorporates public domain material from Dictionary of Cancer Terms . U.S. National Cancer Institute .
This oncology article is a stub . You can help Wikipedia by expanding it .
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Biocompatibility (biomedical therapy) : Ability of a material to perform with an appropriate host response in a specific application. [ 1 ] [ a ]
Biocompatibility : Ability to be in contact with a living system without producing an adverse effect. [ 1 ]
Biocompatibility is related to the behavior of biomaterials in various contexts. The term refers to the ability of a material to perform with an appropriate host response in a specific situation. [ 2 ] The ambiguity of the term reflects the ongoing development of insights into how biomaterials interact with the human body and eventually how those interactions determine the clinical success of a medical device (such as pacemaker , hip replacement or stent ). Modern medical devices and prostheses are often made of more than one material so it might not always be sufficient to talk about the biocompatibility of a specific material. [ 3 ]
Since the immune response and repair functions in the body are so complicated it is not adequate to describe the biocompatibility of a single material in relation to a single cell type or tissue. Sometimes one hears of biocompatibility testing that is a large battery of in vitro test [ 4 ] that is used in accordance with ISO 10993 (or other similar standards) to determine if a certain material (or rather biomedical product) is biocompatible. These tests do not determine the biocompatibility of a material, [ 5 ] but they constitute an important step towards the animal testing and finally clinical trials that will determine the biocompatibility of the material in a given application, and thus medical devices such as implants or drug delivery devices . [ 6 ] Research results have concluded that during performing in vitro cytotoxicity testing of biomaterials, "the authors should carefully specify the conditions of the test and comparison of different studies should be carried out with caution". [ 7 ]
The word biocompatibility seems to have been mentioned for the first time in peer-review journals and meetings in 1970 by RJ Hegyeli (Amer Chem Soc Annual Meeting abstract) and CA Homsy. [ 8 ] It took almost two decades before it began to be commonly used in scientific literature (see the graph below).
Recently Williams (again) has been trying to reevaluate the current knowledge status regarding what factors determine clinical success. Doing so notes that an implant may not always have to be positively bioactive but it must not do any harm (either locally or systemically). [ 9 ]
All these definitions deal with materials and not with devices. This is a drawback since many medical devices are made of more than one material. Much of the pre-clinical testing of the materials is not conducted on the devices but rather the material itself. But at some stage the testing will have to include the device since the shape, geometry and surface treatment etc. of the device will also affect its biocompatibility.
In the literature, one quite often stumbles upon the adjective form, ‘biocompatible’. However, according to Williams’ definition, this does not make any sense because biocompatibility is contextual, i.e. much more than just the material itself will determine the clinical outcome of the medical device of which the biomaterial is a part. This also points to one of the weaknesses with the current definition because a medical device usually is made of more than one material.
Metallic glasses based on magnesium with zinc and calcium addition are tested as the potential biocompatible metallic biomaterials for biodegradable medical implants [ 14 ]
Biocompatibility (or tissue compatibility) describes the ability of a material to perform with an appropriate host response when applied as intended. A biocompatible material may not be completely "inert"; in fact, the appropriateness of the host response is decisive. [ 15 ]
The scope of the first definition is so wide that D Williams tried to find suitable subgroups of applications in order to be able to make more narrow definitions. In the MDT article from 2003 the chosen supgroups and their definitions were:
In these definitions the notion of biocompatibility is related to devices rather than to materials as compared to top three definitions. There was a consensus conference on biomaterial definitions in Sorrento September 15–16, 2005. [ 16 ]
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Biodontics dentistry was founded by Dr. Edward Rossomando in 2001 as an area of oral health . Biodontics is funded by the United States National Institute of Dental and Craniofacial Research (NIDCR). The purpose of Biodontics is to expand the dental profession in its research capacity, skill sets, and entrepreneurship. [ 1 ] An educational program known as the Biodontics Educational Program is held at the University of Connecticut School of Dental Medicine every July and assembles business leaders, entrepreneurs, management executives, scientists, architects, and dental manufacturers to give presentations and lectures to students from all dental schools.
New technologies and new educational models are believed by many to have disrupted and made obsolete the traditional models of dental education. The 1995 Institute of Medicine ’s report, Dental Education at the Crossroads, suggested that dental schools must “continue efforts to increase the productivity of the dental work force, including appropriately credentialed and trained allied dental personnel”; and, “avoid policies to increase or decrease overall dental school enrollments.” The report’s recommendations stemmed from the fact that in 1993 six private dental schools closed; and many schools were plagued with inefficiencies which resulted in “gross wastes of student time [that added] to the student’s overcrowded week, squandering [of] patient time, and provided an inappropriate model of patient care.” Revisions in the process of accrediting dental schools was also recommended.
In 2002 the NIDCR began an initiative to fund experimental educational programs in dental schools across the country. The Biodontics Educational Program is one such program. [ 2 ]
The Biodontics Educational Program (BEP) is held annually in July. The first class was made up of nine students from UConn ; while the 2006 class was made up of 24 students from the Howard University , Marquette University , UConn, and New York University (NYU) dental schools. The program consisted of lectures and presentations from business leaders, entrepreneurs, management executives, scientists, architects, and dental manufacturers. New technologies, such as probiotics, dental lasers, as well as business practices including Kaizen training, were included in the program to offer students a wide range of experience. The rationale in exposing dental students to a wide range of fields is to prepare them for owning their own businesses and managing these businesses, and incorporating new technologies at a faster rate.
The American Biodontics Society was formed in 2005 with the mission to promote an active, expanding profession that is adaptable and accountable to new technologies and procedures, thereby improving the general oral health of the United States and enhancing its accessibility. The ABS acts as a forum for the detailed evaluation, discussion, and analysis of innovations in dentistry. The ABS has chapters developed or developing at New York University (NYU), Howard University, UConn, and Marquette University.
Dental Hypotheses (ISSN: 2155-8213) is the official publication of the American Biodontics Society .
Institute of Medicine's 1995 Report: Committee On The Future Of Dental Education. Dental Education At the Crossroads: Challenges and Change . Ed. Marilyn J. Field. Institute of Medicine. Washington, DC: National Academy P, 1995.
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Biofilling , also known as the orthograde canal grafting technique or 4D sealing , is an endodontic root canal obturation technique with a Bioceramic material after root canal preparation and enlargement procedure. [ 1 ] [ 2 ] [ 3 ] [ 4 ]
All diagnoses of the teeth lead to endodontic therapy and retreatment procedures. Biofilling is specially indicated for severely infected root canals , perforations , cracked teeth, file separations, apexogenesis, and simple endodontic obturations.
1. Physical Sealing - After Biofilling, the watertight apical plug is formed at the apical constriction of the apical foramen . Triple MTA sealing (apical, middle, and coronal) is achieved by the jamming effect. Physical sealing occurs just after Biofilling.
Formation of the apical plug can prevent the apical percolation of nutrient tissue fluid.
In addition, an apical plug can make a highly alkaline environment.
These two functions kill off bacteria in this area including the dentinal tubules .
2. Chemical Sealing - Chemical sealing occurs during the formation of short-tag calcium silicate hydrate at the interfacial surface and orifice of dentinal tubules and long-tag calcium deficient hydroxyl apatite in the lumen of dentinal tubules. Chemical sealing is the result of the hydraulic chemical reaction.
3. Biological Sealing - During Biofilling, a Bioceramic material is used. The material is nonirritating to periapical tissues and also induces the regeneration of cementum and the periodontal ligament.
The immune cells release lymphokines required for the repair and regeneration of cementum .
1. No sealability (no adhesion to dentine) It was concluded that gutta percha's drawback is the lack of seal. Failure of root canal treatment is directly related to the lack of seal on the coronal 1/3 and apical 1/3 portion.
A. Coronal 1/3
The problem is with the Obtura backfill that is used in the warm gutta percha technique. Under the surgical microscope, there is an obvious gap between the heated and cooled gutta percha and the dentinal wall. It is a wide gap for the microorganisms to enter. Microleakage in the coronal 1/3 is the main cause for retreatment. [ 5 ]
B. Apical 1/3 The apical portion of the root canal can never be dried because of the tissue fluid. The commonly used AH26 and AH plus do not set properly and they dissolve under moist conditions. Even in a 100% dry condition, these sealers shrink after the final setting reaction. It becomes naturally soluble over time. One of the systems of gutta percha which is used together with the sealers mentioned is a System B plugger that generates heat on the collagen of the dentin that weakens the tensile strength of the root. Trans-1,4-polyisoprene, a main component of the gutta percha, has been reported as a degradable material regardless of the mode of application which causes the formation of a gap between the dentinal wall and the material.
2. Bacterial degradation Gutta percha is made up of 14.5-21.8% Trans-1,4-Polyisoprene which can be degraded and form a visible gap due to the 18% of microorganisms present in an in vitro study. Actinomyces, a bacterium that is found inside the canal, has the ability to degrade trans-1,4-polyisoprene. The internal root canal system in-vivo is anaerobic but even without the presence of bacteria, the C=O polymer chain will be lysed slowly into OH and C=O over time. Particularly during the presence of a periapical lesion, the penetration of bacteria present in the lesion will cause it to degrade rapidly. Effusion of degraded products through the periodontal membrane that are toxic will cause irritation. Over time, the formation of a gap inside the root canal will allow the penetration of new bacteria and endotoxin. This phenomenon has continued for 5 to 15 years. The cause of a periapical lesion in an asymptomatic tooth one day will be due to the degradation of trans-1,4-polyisoprene
The response of both the patients and dentists have been significant since the bioceramics were introduced to endodontics. The benefits that the practitioners gain with using bioceramic material are the physical properties, such as biocompatibility, anti-bacterial effect, non-toxic and no shrinkage nor expansion, chemical properties such as stability within the biological environment, does not result in a significant inflammatory response, and bioactive properties such as tissue regenerative capacity which induces new cementum formation and tertiary dentin . These benefits have brought a new horizon in Endodontics which is the ability to save more natural teeth with great long-term prognosis.
- Characteristics of the bioceramic materials
Bioceramis are ceramic materials that is specifically made for use in medicine and in dentistry. They include alumina and zirconia , bioactive glass, etc.
- Main composition of bioceramic material used in dentistry'
1. Hydraulic Calcium Silicates (Tricalcium silicate, Dicalcium silicate, Tricalcium aluminate).
2. Alumina or Zirconia
3. No gypsum (Calcium sulfate)
Although considerable bacterial reduction can be achieved by the mechanical action of instruments and irrigation solutions, microorganisms are rarely eliminated from the root canals regardless of the instrumentation technique and file sizes employed. Due to the anatomical localization of the endodontic infection, it only can be treated through professional intervention using both chemical and mechanical procedures. However, many studies have proved that total elimination of bacteria can not be observed in most of the cases.
Minor anatomical irregularities are usually incorporated into preparation, other areas such as Isthmuses, branches, and dentinal tubules can harbor microorganisms . These areas are not commonly affected by the chemo mechanical preparation because of inherent physical limitations of instruments and the short time the irrigation solutions are present within the root canal .
The larger the apical preparation, the higher the percentage of bacteria eliminated from the root canal . But, Ingle and Zeldow have observed that 80 percent of the initially infected root canals increased to 95.4 percent at the second appointment, 48 hours later.
Although a considerable reduction in bacterial cell by instrumentation and irrigation, viable bacteria can still be found in at least half of the cases.
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Bioglass 45S5 or calcium sodium phosphosilicate , is a bioactive glass specifically composed of 45 wt% SiO 2 , 24.5 wt% CaO, 24.5 wt% Na 2 O, and 6.0 wt% P 2 O 5 . [ 1 ] Typical applications of Bioglass 45S5 include: bone grafting biomaterials , repair of periodontal defects, cranial and maxillofacial repair, wound care, blood loss control, stimulation of vascular regeneration, and nerve repair. [ 2 ]
The name " Bioglass " was trademarked by the University of Florida as a name for the original 45S5 composition. It should therefore only be used in reference to the 45S5 composition and not as a general term for bioactive glasses. [ 3 ] Bioglass 45S5 is available commercially under the registered trade name NovaMin , which is owned by the pharmaceutical company GlaxoSmithKline . NovaMin is bioactive glass that has been ground into a fine particulate with a median size of less than 20 μm. It can reduce dentin hypersensitivity by blocking open dentinal tubules and by supplying calcium (Ca 2+ ) and phosphate ( PO 3− 4 ) ions to form hydroxycarbonate apatite (HCA), the principal mineral component of bone tissue in mammals. NovaMin is the active ingredient in Sensodyne "Repair & Protect" toothpaste, except when sold in the United States, containing stannous fluoride instead. [ 4 ]
45S5 bioactive glass is white in color and is in powder form, with particulates with a median size of less than 20 μm. Its chemical composition by weight is: silica (SiO 2 ) 43–47%, calcium oxide (CaO) 22.5–26.5%, phosphorus pentoxide (P 2 O 5 ) 5–7% and sodium oxide (Na 2 O) 22.5–26.5%. [ 2 ]
Glasses are non-crystalline disordered solids that are commonly composed of silica-based materials with other minor additives. Compared to soda-lime glass (commonly used, as in windows or bottles), Bioglass 45S5 contains less silica and higher amounts of calcium and phosphorus. The 45S5 name signifies glass with 45% by weight of SiO 2 and 5:1 molar ratio of calcium to phosphorus. This high ratio of calcium to phosphorus promotes formation of apatite crystals; calcium and silica ions can act as crystallization nuclei. [ 5 ] Lower Ca:P ratios do not bond to bone. [ 6 ] [ 7 ] Bioglass 45S5's specific composition is optimal in biomedical applications because of its similar composition to that of hydroxyapatite , the mineral component of bone. [ 7 ] This similarity provides Bioglass 45S5's ability to be integrated with living bone.
This composition of bioactive glass is mechanically soft in comparison to other glasses . It can be machined , preferably with diamond tools, or ground to powder. Bioglass 45S5 has to be stored in a dry environment, as it readily absorbs moisture and reacts with it. [ 6 ] Bioglass 45S5 is the first formulation of an artificial material that was found to chemically bond with bone, and its discovery led to a series of other bioactive glasses . One of its main medical advantages is its biocompatibility, seen in its ability to avoid an immune reaction and fibrous encapsulation. Its primary application is the repair of bone injuries or defects too large to be regenerated by the natural process. [ 6 ]
Bioglass 45S5 is important to the field of biomimetic materials as one of the first completely synthetic materials that seamlessly bonds to bone. It was developed by Larry L. Hench in the late 1960s. The idea for the material came to him during a bus ride in 1967. While working as an assistant professor at the University of Florida, Hench decided to attend the U.S. Army Materials Research Conference held in Sagamore, New York, where he planned to talk about radiation resistant electronic materials. He began discussing his research with a fellow traveller on the bus, Colonel Klinker, who had recently returned to the United States after serving as an Army medical supply officer in Vietnam. [ 8 ]
After listening to Hench's description of his research, the Colonel asked, “If you can make a material that will survive exposure to high energy radiation can you make a material that will survive exposure to the human body?” [ 8 ] Klinker then went on to describe the amputations that he had witnessed in Vietnam, which resulted from the body's rejection of metal and plastic implants. Hench realized that there was a need for a novel material that could form a living bond with tissues in the body. [ 8 ]
When Hench returned to Florida after the conference, he submitted a proposal to the U.S. Army Medical Research and Design Command. He received funding in 1968, and in November 1969 Hench began to synthesize small rectangles of what he called 45S5 glass. Ted Greenlee, Assistant Professor of Orthopaedic Surgery at the University of Florida, implanted them in rat femurs at the VA Hospital in Gainesville. Six weeks later, Greenlee called Hench asking, "Larry, what are those samples you gave me? They will not come out of the bone. I have pulled on them, I have pushed on them, I have cracked the bone and they are still bonded in place." [ 8 ]
With this first successful experiment, Bioglass was born and the first compositions studied. Hench published his first paper on the subject in 1971 in the Journal of Biomedical Materials Research, and his lab continued to work on the project for the next 10 years with continued funding from the U.S. Army. By 2006, there were over 500 papers published on the topic of bioactive glasses from different laboratories and institutions around the world. [ 8 ] The first successful surgical use of Bioglass 45S5 was in replacement of ossicles in the middle ear as a treatment of conductive hearing loss , and the material continues to be used in bone reconstruction applications today. [ 1 ]
Other uses include cones for implantation into the jaw following a tooth extraction . Composite materials made of Bioglass 45S5 and patient's own bone can be used for bone reconstruction. [ 5 ] Further research is being conducted for the development of new processing techniques to allow for more applications of Bioglass.
Bioglass 45S5 is used in jaw and orthopedics applications, in this way it dissolves and can stimulate the natural bone to repair itself. Bioactive glass offers good osteoconductivity and bioactivity, it can deliver cells and is biodegradable. This makes it an excellent candidate to be used in tissue engineering applications. Although this material is known to be brittle, it is still used extensively to enhance the growth of bone since new forms of bioactive glasses are based on borate and borosilicate compositions. Bioglass can also be doped with varying quantities of elements like copper, zinc, or strontium which can allow the growth and formation of healthy bone. The formation of neocartilage can also be induced with bioactive glass by using an in vitro culture of chondrocyte-seeded hydrogels and can serve as a subchondral substrate for tissue-engineered osteochondral constructs. [ 1 ]
The borate-based bioactive glass has controllable degradation rates in order to match the rate at which actual bone is formed. Bone formation has been shown to enhance when using this type of material. When implanted into rabbit femurs, the 45S5 bioactive glass showed that it could induce bone proliferation at a much quicker rate than synthetic hydroxyapatite (HA). 45S5 glass can also be osteoconductive and osteoinductive because it allows for new bone growth along the bone-implant interface as well as within the bone-implant interface. Studies have been conducted to determine the process by which it can induce bone formation. It was shown that 45S5 glass degrades and releases sodium ions, as well as soluble silica, the combination of all these ions is said to produce new bone. Borate bioglass has proven that it can support cell proliferation and differentiation in vitro and in vivo. It also has shown that it is suitable to be used as a substrate for drug release when treating bone infection. However, there has been a concern as to whether or not the release of boron into a solution as borate ions will be toxic to the body. It has been shown that in static cell culture conditions, borate glasses were toxic to cells, but not in dynamic culture conditions. [ 9 ]
Bioactive glass was applied to medical devices to help restore the hearing to a deaf patient using Bioglass 45S5 in 1984. The patient went deaf due to at ear infection that degraded two of the three bones in her middle ear. An implant was designed to replace the damaged bone and carry sound from the eardrum to the cochlea, restoring the patient's hearing. Before this material was available, plastics and metals would be used because they did not produce a reaction in the body; however, they eventually failed because tissue would grow around them after implantation. A prosthesis made up of Bioglass 45S5 was made to fit the patient and most of the prosthesis that were made were able to maintain functionality after 10 years. [ 10 ] The Endosseous Ridge Maintenance Implant made of Bioglass 45S5 was another device that could be inserted into tooth extraction sites that would repair tooth roots and allow for a stable ridge for dentures. [ 11 ]
Another area in which bioactive glass has been investigated to use is tooth enamel reconstruction, which has proven to be a difficult task in the field of dentistry. Enamel is made up of a very organized hierarchical microstructure of carbonated hydroxyapatite nanocrystals. It has been reported that Bioglass 45S5-phosphoric acid paste can be used to form an interaction layer that can obstruct dentinal tubule orifices and can therefore be useful in the treatment of dentin hypersensitivity lesions. [ 11 ] This material in an aqueous environment could have an antibacterial property that is advantageous in periodontal surgical procedures. In a study done with 45S5 Bioglass, biofilms of Streptococcus sanguinis were grown on inactive glass particulates and the biofilm grown on the Bioglass was significantly lower than those that were on the inactive glass. It was concluded that Bioglass may reduce bacterial colonisation which could aid osseointegration. A highly effective antibacterial bioactive glass is S53P4, which has been reported to exhibit a high antimicrobial activity and did not seem to select for resistance in the microbial strains tested. [ 12 ] Bioactive glasses that are sol-gel derived, such as CaPSiO and CaPSiO II, have also exhibited antibacterial properties. Studies done with S. epidermidis and E. coli cultured with bioactive glass have shown that the 45S5 bioactive glass have a very high antibacterial resistance. It was also observed in the experiment that there were needle-like bioglass debris which could have ruptured the cell walls of the bacteria and rendered them inactive. [ 13 ]
GlaxoSmithKline is using this material as an active ingredient in toothpaste under the commercial name NovaMin , which can help repair tiny holes and decrease tooth sensitivity . [ 11 ] [ 14 ] More advanced fluoride-containing formulations of Bioglass have been developed, which provide stronger and longer-lasting protection against sensitivity. The inclusion of fluoride within the glass rather than as a soluble addition, such as the toothpaste BioMin, [ 15 ] is claimed to optimise the rate of development of apatite, which shields the teeth from sensitivity for up to 12 hours. [ 16 ]
When implanted, Bioglass 45S5 reacts with the surrounding physiological fluid, causing the formation of a hydroxyl carbonated apatite (HCA) layer at the material surface. The HCA layer has a similar composition to hydroxyapatite , the mineral phase of bone, a quality which allows for strong interaction and integration with bone. The process by which this reaction occurs can be separated into 12 steps. The first 5 steps are related to the Bioglass response to the environment within the body, and occur rapidly at the material surface over several hours. [ 17 ] Reaction steps 6–10 detail the reaction of the body to the integration of the biomaterial, and the process of integration with bone. These stages occur over the scale of several weeks or months. [ 18 ] The steps are separated as follows: [ 17 ] [ 18 ]
There are two main manufacturing techniques that are used for the synthesis of bioglass. The first is melt quench synthesis, which is the conventional glassmaking technology used by Larry Hench when he first manufactured the material in 1969. This method includes melting a mixture of oxides such as SiO 2 , Na 2 O, CaO and P 2 O 5 at high temperatures generally above 1100–1300 °C. [ 20 ] Platinum or platinum alloy crucibles are used to avoid contamination, which would interfere with the product's chemical reactivity in organism. Annealing is a crucial step in forming bulk parts, due to high thermal expansion of the material. Heat treatment of Bioglass reduces the volatile alkali metal oxide content and precipitates apatite crystals in the glass matrix. However, the scaffolds that result from melt quench techniques are much less porous compared to other manufacturing methods, which may lead to defects in tissue integration when implanted in vivo. [ 21 ]
The second method is sol-gel synthesis of Bioglass. This process is carried out at much lower temperatures than the traditional melting methods. It involves the creation of a solution (sol), which is composed of metal-organic and metal salt precursors. A gel is then formed through hydrolysis and condensation reactions, and it undergoes thermal treatment for drying, oxide formation, and organic removal. Because of the lower fabrication temperatures used in this method, there is a greater level of control on the composition and homogeneity of the product. In addition, sol-gel bioglasses have much higher porosity, which leads to a greater surface area and degree of integration in the body. [ 22 ] [ 20 ]
Newer methods include flame and microwave synthesis of Bioglass, which has been gaining attention in recent years. Flame synthesis works by baking the powders directly in a flame reactor. [ 23 ] Microwave synthesis is a rapid and low-cost powder synthesis method in which precursors are dissolved in water, transferred to an ultrasonic bath, and irradiated. [ 24 ]
A setback to using Bioglass 45S5 is that it is difficult to process into porous 3D scaffolds. These porous scaffolds are usually prepared by sintering glass particles that are already formed into the 3D geometry and allowing them to bond to the particles into a strong glass phase made up of a network of pores. Since this particular type of bioglass cannot fully sinter by viscous flow above its Tg , and its Tg is close to the onset of crystallization, it is hard to sinter this material into a dense network. [ 1 ]
45S5 glass also has a slow degradation and rate of conversion to an HA-like material. This setback makes it more difficult for the degradation rate of the scaffold to coincide with the rate of tissue formation. Another limitation is that the biological environment can be easily influenced by its degradation. Increases in the sodium and calcium ions and changing pH is due to its degradation. However, the roles of these ions and their toxicity to the body have not been fully researched. [ 1 ]
Several studies have investigated methods to improve the mechanical strength and toughness of Bioglass 45S5. These include creating polymer–glass composites , which combine the bioactivity of Bioglass with the relative flexibility and wear resistance of different polymers. Another solution is coating a metallic implant with Bioglass, which takes advantage of the mechanical strength of the implant's bulk material while retaining bioactive effects at the surface. Some of the most notable modifications have used various forms of carbon to improve the properties of 45S5 glass. [ 25 ]
For example, Touri et al. developed a method to incorporate carbon nanotubes (CNTs) into the structure without interfering with the material's bioactive properties. CNTs were chosen because of their large aspect ratio and high strength. By synthesizing Bioglass 45S5 on a CNT scaffold, the researchers were able to create a composite that more than doubled the compressive strength and the elastic modulus when compared to the pure glass. [ 26 ]
Another study carried out by Li et al. looked into different properties, such as the fracture toughness and wear resistance of Bioglass 45S5. The authors loaded graphene nanoplatelets (GNP) into the glass structure through a spark plasma sintering method. Graphene was chosen because of its high specific surface area and strength, as well as its cytocompatibility and lack of interference with Bioglass 45S5's bioactivity. The composites that were created in this experiment achieved a fracture toughness of more than double the control. In addition, the tribological properties of the material were greatly improved. [ 25 ]
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A biological pacemaker is one or more types of cellular components that, when "implanted or injected into certain regions of the heart," produce specific electrical stimuli that mimic that of the body's natural pacemaker cells . [ 1 ] Biological pacemakers are indicated for issues such as heart block , slow heart rate , and asynchronous heart ventricle contractions . [ 2 ] [ 3 ]
The biological pacemaker is intended as an alternative to the artificial cardiac pacemaker that has been in human use since the late 1950s. Despite their success, several limitations and problems with artificial pacemakers have emerged during the past decades such as electrode fracture or damage to insulation , infection , re-operations for battery exchange, and venous thrombosis . The need for an alternative is most obvious in children, including premature newborn babies , where size mismatch and the fact that pacemaker leads do not grow with children are a problem. [ 1 ] A more biological approach has been taken in order to mitigate many of these issues. However, the implanted biological pacemaker cells still typically need to be supplemented with an artificial pacemaker while the cells form the necessary electrical connections with cardiac tissue. [ 1 ]
The first successful experiment with biological pacemakers was carried out by Arjang Ruhparwar 's group at Hannover Medical School in Germany using transplanted fetal heart muscle cells . The process was first introduced at the scientific sessions of the American Heart Association in Anaheim in 2001, and the results were published in 2002. [ 4 ] A few months later, Eduardo Marban's group from Johns Hopkins University published the first successful gene-therapeutic approach towards the generation of pacemaking activity in otherwise non-pacemaking adult cardiomyocytes using a guinea pig model. [ 5 ] The investigators postulated latent pacemaker capability in normal heart muscle cells. This potential ability is suppressed by the inward-rectifier potassium current Ik1 encoded by the gene Kir2 which is not expressed in pacemaker cells . By specific inhibition of Ik1 below a certain level, spontaneous activity of cardiomyocytes was observed with resemblance to the action potential pattern of genuine pacemaker cells.
Meanwhile, other genes and cells have been discovered, including heart muscle cells derived from embryonic stem cells , "HCN" genes which encode the wild type pacemaker current I(f). Michael Rosen's group demonstrated that transplantation of HCN2-transfected human mesenchymal stem cells (hMSCs) leads to expression of functional HCN2 channels in vitro and in vivo , mimicking overexpression of HCN2 genes in cardiac myocytes . [ 6 ] In 2010, Ruhparwar's group again demonstrated a type of biological pacemaker, this time showing that by injection of the "Adenylate Cyclase" gene into the heart muscle a biological cardiac pacemaker can be created. [ 7 ]
In 2014, a gene called TBX18 has been non-invasively applied to speed up heart rates caused by heart block. [ 2 ] More recent studies in 2015, has been experimented optogenetic approach in the rats heart, where a light sensitive transgene ( Channelrhodopsin -2) injected to several sites of rat's ventricular , which, furthermore, can simultaneously stimulate the injection sites by a blue light irradiation. [ 3 ]
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Biological psychopathology is the study of the biological etiology of mental illnesses with a particular emphasis on the genetic and neurophysiological basis of clinical psychology . Biological psychopathology attempts to explain psychiatric disorders using multiple levels of analysis from the genome to brain functioning to behavior. Although closely related to clinical psychology, it is fundamentally an interdisciplinary approach that attempts to synthesize methods across fields such as neuroscience , psychopharmacology , biochemistry , genetics, and physiology . It is known by several alternative names, including "clinical neuroscience " and "experimental psychopathology ." Due to the focus on biological processes of the central and peripheral nervous systems , biological psychopathology has been important in developing new biologically-based treatments for mental disorders.
Biological psychopathology is a field that focuses mostly on the research and understanding the biological basis of major mental disorders such as bipolar and unipolar affective disorder , schizophrenia and Alzheimer's disease . Much of the understanding thus far has come from neuroimaging techniques such as radiotracer positron emission tomography (PET), and functional magnetic resonance imaging (fMRI) scans, as well as genetic studies. Together, neuroimaging with multimodal PET/fMRI, and pharmacological investigations are revealing how the differences in behaviorally relevant brain activations can arise from underlying variations in certain brain signaling pathways. Understanding the detailed interplay between neurotransmitters and the psychiatric drugs that affect them is key to the research within this field. Significant research includes investigations relevant to biological bases such as biochemical, genetic, physiological, neurological, and anatomical fields. In a clinical viewpoint, the etiology of these diseases takes into account various therapies, diet, drugs, potential environmental contaminants, exercise, and adverse effects of life stressors, all of which can cause noticeable biochemical changes.
Sigmund Freud initially concentrated on the biological causes of mental illness and its relationship to evident behavioral factors. His belief in biological factors lead to the concept that certain drugs, such as cocaine , had an antidepressant functionality.
In the 1950s the first modern antipsychotic and antidepressant drugs were developed: chlorpromazine (Thorazine), which was one of the first widely used antipsychotic medications to be developed, and iproniazid , which was one of the first antidepressants developed. The research on some of these drugs helped to formulate the monoamine and catecholamine theories, which alluded to the fact that chemical imbalances provide the basis for mental health disorders. New [ when? ] research points to the concept of neuronal plasticity , specifically mentioning that mental health disorders may involve a neurophysiological problem that inhibits neuronal plasticity. [ citation needed ]
This field expresses the importance of accurately identifying and diagnosing mental health disorders. If not accurately diagnosed, certain treatments could only worsen the previous condition. This can be difficult since there are numerous etiologies that could reveal symptoms of mental health disorders. Some important disorders to focus on are: seasonal affective disorder , clinical depression, bipolar disorder, schizophrenia, generalized anxiety disorder , and obsessive compulsive disorder .
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Biologics: Targets and Therapy is a peer-reviewed medical journal covering research on the clinical application of biologic agents in the management of pathologies where a molecular target can be identified. The journal was established in 2007 and is published by Dove Medical Press .
This article about a medical journal is a stub . You can help Wikipedia by expanding it .
See tips for writing articles about academic journals . Further suggestions might be found on the article's talk page .
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https://en.wikipedia.org/wiki/Biologics:_Targets_and_Therapy
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Bioluminescent activated destruction or BLADe refers to a technique used to kill cancer cells. [ 1 ] [ unreliable medical source? ]
It works by first altering the cells in an organism , once they become cancerous, to create the firefly light source luciferin and luciferase to create light. The light itself would have little effect on the cells if it wasn't for the addition of a photosensitizing agent which essentially makes the cells much more vulnerable to light. It can specifically eradicate the cancer cells with no negative side-effects to normal cells. Trials on humans have yet to be seen, although the trials on mice looked rather promising for it. [ citation needed ]
This oncology article is a stub . You can help Wikipedia by expanding it .
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Biomaterials exhibit various degrees of compatibility with the harsh environment within a living organism. They need to be nonreactive chemically and physically with the body, as well as integrate when deposited into tissue. [ 1 ] The extent of compatibility varies based on the application and material required. Often modifications to the surface of a biomaterial system are required to maximize performance. The surface can be modified in many ways, including plasma modification and applying coatings to the substrate. Surface modifications can be used to affect surface energy , adhesion , biocompatibility , chemical inertness, lubricity, sterility , asepsis , thrombogenicity , susceptibility to corrosion , degradation, and hydrophilicity .
Teflon is a hydrophobic polymer composed of a carbon chain saturated with fluorine atoms. The fluorine-carbon bond is largely ionic, producing a strong dipole. The dipole prevents Teflon from being susceptible to Van der Waals forces , so other materials will not stick to the surface. [ 2 ] Teflon is commonly used to reduce friction in biomaterial applications such as in arterial grafts, catheters, and guide wire coatings.
PEEK is a semicrystalline polymer composed of benzene, ketone, and ether groups. PEEK is known for having good physical properties including high wear resistance and low moisture absorption [ 3 ] and has been used for biomedical implants due to its relative inertness inside of the human body.
Plasma modification is one way to alter the surface of biomaterials to enhance their properties. During plasma modification techniques, the surface is subjected to high levels of excited gases that alter the surface of the material. Plasma's are generally generated with a radio frequency (RF) field. Additional methods include applying a large (~1KV) DC voltage across electrodes engulfed in a gas. The plasma is then used to expose the biomaterial surface, which can break or form chemical bonds. This is the result of physical collisions or chemical reactions of the excited gas molecules with the surface. This changes the surface chemistry and therefore surface energy of the material which affects the adhesion, biocompatibility, chemical inertness, lubricity, and sterilization of the material. The table below shows several biomaterial applications of plasma treatments. [ 4 ]
Abbreviations used in table: PC: polycarbonate, PS: polystyrene, PP: polypropylene, PET: poly (ethylene terephthalate), PTFE: polytetrafluoroethylene, UHMWPE: ultra high molecular weight PE, SiR: silicone rubber
The surface energy is equal to the sum of disrupted molecular bonds that occur at the interface between two different phases. Surface energy can be estimated by contact angle measurements using a version of the Young–Laplace equation :
γ S V − γ S L = γ L V c o s θ {\displaystyle \gamma _{SV}-\gamma _{SL}=\gamma _{LV}cos\theta } [ 5 ]
Where γ S V {\displaystyle \gamma _{SV}} is the surface tension at the interface of solid and vapor, γ S L {\displaystyle \gamma _{SL}} is the surface tension at the interface of solid and liquid, and γ L V {\displaystyle \gamma _{LV}} is the surface tension at the interface of liquid and vapor. Plasma modification techniques alter the surface of the material, and subsequently the surface energy. Changes in surface energy then alter the surface properties of the material.
Surface modification techniques have been extensively researched for the application of adsorbing biological molecules. Surface functionalization can be performed by exposing surfaces to RF plasma. Many gases can be excited and used to functionalize surfaces for a wide variety of applications. Common techniques include using air plasma, oxygen plasma, and ammonia plasma as well as other exotic gases. Each gas can have varying effects on a substrate. These effects decay with time as reactions with molecules in air and contamination occur.
Ammonia plasma treatment can be used to attach amine functional groups. These functional groups lock on to anticoagulants like Heparin decreasing thrombogenicity. [ 6 ]
Polysaccharides have been used as thin film coatings for biomaterial surfaces. Polysaccharides are extremely hydrophilic and will have small contact angles . They can be used for a wide range of applications due to their wide range of compositions. They can be used to reduce the adsorption of proteins to biomaterial surfaces. Additionally, they can be used as receptor sites, targeting specific biomolecules. This can be used to activate specific biological responses.
Covalent attachment to a substrate is necessary to immobilize polysaccharides, otherwise they will rapidly desorb in a biological environment. This can be a challenge due to the fact that the majority of biomaterials do not possess the surface properties to covalently attach polysaccharides. This can be achieved by the introduction of amine groups by RF glow discharge plasma. Gases used to form amine groups, including ammonia or n-heptylamine vapor, can be used to deposit a thin film coating containing surface amines. Polysaccharides must also be activated by oxidation of anhydroglucopyranoside subunits. This can be completed with sodium metaperiodate (NaIO 4 ). This reaction converts anhydroglucopyranoside subunits to cyclic hemiacetal structures, which can be reacted with amine groups to form a Schiff base linkage (a carbon-nitrogen double bond). These linkages are unstable and will easily dissociate . Sodium cyanoborohydride (NaBH 3 CN) can be used as a stabilizer by reducing the linkages back to an amine. [ 7 ]
There are many examples of contamination of biomaterials that are specific to the preparation or manufacturing process. Additionally, nearly all surfaces are prone to contamination of organic impurities in the air. Contamination layers are usually limited to a monolayer or less of atoms and are thus only detectable by surface analysis techniques, such as XPS. It is unknown whether this sort of contamination is harmful, yet it is still regarded as contamination and will most certainly affect surface properties.
Glow discharge plasma treatment is a technique that is used for cleaning contamination from biomaterial surfaces. Plasma treatment has been used for various biological evaluation studies to increase the surface energy of biomaterial surfaces, as well as cleaning. [ 8 ] Plasma treatment has also been proposed for sterilization of biomaterials for potential implants. [ 9 ]
Another method of altering surface properties of biomaterials is to coat the surface. Coatings are used in many applications to improve biocompatibility and alter properties such as adsorption, lubricity, thrombogenicity, degradation, and corrosion.
In general, the lower the surface tension of a liquid coating, the easier it will be to form a satisfactory wet film from it. The difference between the surface tension of a coating and the surface energy of a solid substrate to which a coating is applied affects how the liquid coating flows out over the substrate. It also affects the strength of the adhesive bond between the substrate and the dry film. If for instance, the surface tension of the coating is higher than the surface tension of the substrate, then the coating will not spread out and form a film. As the surface tension of the substrate is increased, it will reach a point to where the coating will successfully wet the substrate but have poor adhesion. Continuous increase in the coating surface tension will result in better wetting in film formation and better dry film adhesion. [ 10 ]
More specifically whether a liquid coating will spread across a solid substrate can be determined from the surface energies of the involved materials by using the following equation:
S = γ S A + ( γ C A − γ S C ) {\displaystyle S=\gamma _{SA}+(\gamma _{CA}-\gamma _{SC})} [ 11 ]
Where S is the coefficient of spreading, γ S A {\displaystyle \gamma _{SA}} is the surface energy of the substrate in air, γ C A {\displaystyle \gamma _{CA}} is the surface energy of the liquid coating in air and γ S C {\displaystyle \gamma _{SC}} is the interfacial energy between the coating and the substrate. If S is positive the liquid will cover the surface and the coating will adhere well. If S is negative the coating will not completely cover the surface, producing poor adhesion.
Organic coatings are a common way to protect a metallic substrate from corrosion . Up until ~1950 it was thought that coatings act as a physical barrier which disallows moisture and oxygen to contact the metallic substrate and form a corrosion cell. This cannot be the case because the permeability of paint films is very high. It has since been discovered that corrosion protection of steel depends greatly upon the adhesion of a noncorrosive coating when in the presence of water. With low adhesion, osmotic cells form underneath the coating with high enough pressures to form blisters, which expose more unprotected steel. Additional non-osmotic mechanisms have also been proposed. In either case, sufficient adhesion to resist displacement forces is required for corrosion protection. [ 12 ]
Guide wires are an example of an application for biomedical coatings. Guide wires are used in coronary angioplasty to correct the effects of coronary artery disease , a disease that allows plaque build up on the walls of the arteries. The guide wire is threaded up through the femoral artery to the obstruction. The guide wire guides the balloon catheter to the obstruction where the catheter is inflated to press the plaque against the arterial walls. [ 13 ] Guide wires are commonly made from stainless steel or Nitinol and require polymer coatings as a surface modification to reduce friction in the arteries. The coating of the guide wire can affect the trackability, or the ability of the wire to move through the artery without kinking, the tactile feel, or the ability of the doctor to feel the guide wire's movements, and the thrombogenicity of the wire.
Hydrophilic coatings can reduce friction in the arteries by up to 83% when compared to bare wires due to their high surface energy. [ 14 ] When the hydrophilic coatings come into contact with bodily fluids they form a waxy surface texture that allows the wire to slide easily through the arteries. Guide wires with hydrophilic coatings have increased trackability and are not very thrombogenic; however the low coefficient of friction increases the risk of the wire slipping and perforating the artery. [ 15 ]
Teflon and Silicone are commonly used hydrophobic coatings for coronary guide wires. Hydrophobic coatings have a lower surface energy and reduce friction in the arteries by up to 48%. [ 14 ] Hydrophobic coatings do not need to be in contact with fluids to form a slippery texture. Hydrophobic coatings maintain tactile sensation in the artery, giving doctors full control of the wire at all times and reducing the risk of perforation; though, the coatings are more thrombogenic than hydrophilic coatings. [ 15 ] The thrombogenicity is due to the proteins in the blood adapting to the hydrophobic environment when they adhere to the coating. This causes an irreversible change for the protein, and the protein remains stuck to the coating allowing for a blood clot to form. [ 16 ]
Using an MRI to image the guide wire during use would have an advantage over using x-rays because the surrounding tissue can be examined while the guide wire is advanced. Because most guide wires' core materials are stainless steel they are not capable of being imaged with an MRI. Nitinol wires are not magnetic and could potentially be imaged, but in practice the conductive nitinol heats up under the magnetic radiation which would damage surrounding tissues. An alternative that is being examined is to replace contemporary guide wires with PEEK cores, coated with iron particle embedded synthetic polymers. [ 17 ]
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The Biomedical Research Center (BRC) is a research center at Qatar University focusing on biomedical research. BRC was founded in 2014, and partners with the Ministry of Public Health (Qatar) , and Hamad Medical Corporation (HMC) . [ 1 ] [ 2 ] [ 3 ]
The incidence of genetic disorders in Qatar is high, [ 4 ] with the top three causes of death in the country being cancer, heart diseases, and diabetes. [ 5 ] [ 6 ] The government saw the creation of BRC as a strategy for proactively preventing diseases to help foster public health. [ 7 ] [ 8 ]
BRC labs received the ISO/IEC - 17025 accreditation from the American Association for Laboratory Accreditation (A2LA). [ 9 ] This research center focus on infectious diseases ( virology and microbiology ), metabolic disorders , and biomedical omics . [ 10 ]
Since its establishment in 2014, the BRC has published over 530 research papers. [ 11 ] [ 12 ] The centre's research projects encompass a range of areas, including:
BRC Introduced the use of zebrafish as an animal model in biomedical research [ 36 ] [ 37 ] [ 32 ] [ 38 ] [ 39 ] [ 40 ] and established a facility for it in 2015. [ 41 ] [ 42 ] [ 43 ] The facility is used as a research unit to study many genetic diseases. [ 32 ] The Ministry of Public Health articulated an institutional research policy (IRP) on the use of zebrafish in research, [ 44 ] which Qatar University backed.
The BRC facilities include: [ 41 ]
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Biomesh (or biologic mesh ) is a type of surgical mesh made from an organic biomaterial (such as porcine dermis, porcine small intestine submucosa , bovine dermis or pericardium , and the dermis or fascia lata of a cadaveric human). Biologic mesh is primarily indicated for several types of hernia repair, including inguinal and ventral hernias, hernia prophylaxis, and contaminated hernia repairs. [ 1 ] [ 2 ] However, it has also been used in pelvic floor dysfunction , parotidectomy , and reconstructive plastic surgery . [ 2 ] The development of biologic mesh largely has derived from the need of a biocompatible material that addresses "the problems associated with a permanent synthetic mesh, including chronic inflammation, foreign body reaction, fibrosis, and mesh infection." [ 1 ] [ 3 ] As of 2015 [update] , however, the efficacy and optimal use of biological mesh products remains in question. [ 2 ] [ 3 ]
The idea of using organic materials for surgical mesh has been around since at least the late 1950s, though researchers soon learned the materials they tested weren't biocompatible . [ 1 ] Research into more compatible biomaterials occurred in the proceeding decades, including the search for cellular-based materials extracted from humans and animals. For example, in 1980, research presented at the first ever World Biomaterials Congress detailed the examined use of dermal collagen of sheep to construct biological mesh for reconstructive surgery. [ 4 ] Since then, "research for developing and improvising the biological material required for the production of these meshes" has been ongoing. [ 1 ]
Typical advantages attributed to biologic meshes include a reduced risk of infection compared to synthetic meshes, and the absorption of the mesh into the resulting scar as part of cellular ingrowth. [ 2 ] [ 5 ] Commonly described drawbacks include the high cost of the material and its uncertain clinical effectiveness, particularly when the high cost is considered. [ 1 ] [ 2 ] [ 5 ] An August 2015 literature review published by the Canadian Agency for Drugs and Technologies in Health addressed these drawbacks, concluding that "there remains a lack of sufficient evidence to guide clinical practice regarding the use of biological mesh products... Further rigorously designed RCTs are required to clarify comparative clinical effectiveness and safety of the many available biological mesh products for most surgical indications in which their use has been suggested." [ 2 ]
The presence of contamination may limit the applicability of permanent synthetic mesh in some procedures such as hernia repair. Biologic mesh may be acceptable for this purpose or for placement in open wounds as a staged closure in complex abdominal wall reconstruction. There is limited data in both of these areas, with some noting a high risk of hernia recurrence and associated infection. The data is mostly limited to animal models and case series. [ 6 ] [ 7 ] [ 8 ] [ 9 ] However, the lack of suitable alternatives has made biologic mesh attractive for contaminated field hernia repair. [ 1 ]
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The Biophone is a combination voice and telemetry radio communications system used in the 1970s and 80s by paramedics to talk to the physicians supervising them from a hospital base station. The difference between the unit and another two-way radio was that it had the ability to transmit a patient's electrocardiogram . [ 1 ]
The Biophone was produced by the Biocom Company . The Biophone 3502 used the internals of a General Electric PE-series handheld radio mounted into an orange case, which was made of an orange laminated fiberglass with aluminum trim. The Biophone had an internal rechargeable battery that powered the sensor equipment, the radio, and an amplifier that raised the transmitting power to 50 watts. The unit had a connector for a vehicle-mounted antenna allowing better signal reception and transmission from the back of an ambulance. The Biophone could have any 6 (the maximum that could fit in the PE radio) of the 10 UHF medical duplex channels in the 450-470 MHz range. This allowed flexibility in the overall system. The NiCad battery could be charged up in 15 minutes. [ 2 ]
This Biophone radio can be seen throughout the 1970s TV series Emergency! , being used by the fictional Los Angeles County Fire Department paramedic characters John Gage ( Randolph Mantooth ) and Roy DeSoto ( Kevin Tighe ). The actual Biophone 3502 radio used on the show was donated to the Smithsonian 's National Museum of American History.
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A biopsy is a medical test commonly performed by a surgeon , an interventional radiologist , or an interventional cardiologist . The process involves the extraction of sample cells or tissues for examination to determine the presence or extent of a disease. The tissue is then fixed, dehydrated, embedded, sectioned, stained and mounted [ 1 ] before it is generally examined under a microscope by a pathologist ; it may also be analyzed chemically. When an entire lump or suspicious area is removed, the procedure is called an excisional biopsy . An incisional biopsy or core biopsy samples a portion of the abnormal tissue without attempting to remove the entire lesion or tumor. When a sample of tissue or fluid is removed with a needle in such a way that cells are removed without preserving the histological architecture of the tissue cells, the procedure is called a needle aspiration biopsy . Biopsies are most commonly performed for insight into possible cancerous or inflammatory conditions.
The Arab physician Abulcasis (1013–1107) developed one of the earliest diagnostic biopsies. He used a needle to puncture the thyroid and then characterized many types of goiter . [ 2 ] [ 3 ]
The term biopsy reflects the Greek words βίος bios , "life," and ὄψις opsis , "a sight." [ 4 ]
The French dermatologist Ernest Besnier introduced the word biopsie to the medical community in 1879. [ 5 ]
When cancer is suspected, a variety of biopsy techniques can be applied. An excisional biopsy is an attempt to remove an entire lesion. When the specimen is evaluated, in addition to diagnosis, the amount of uninvolved tissue around the lesion, the surgical margin of the specimen is examined to see if the disease has spread beyond the area biopsied. "Clear margins" or "negative margins" means that no disease was found at the edges of the biopsy specimen. "Positive margins" means that disease was found, and a wider excision may be needed, depending on the diagnosis. [ citation needed ]
When intact removal is not indicated for a variety of reasons, a wedge of tissue may be taken in an incisional biopsy . In some cases, a sample can be collected by devices that "bite" a sample. A variety of sizes of needles can collect tissue in the lumen ( core biopsy ). Smaller diameter needles collect cells and cell clusters, fine needle aspiration biopsy . [ 6 ]
Pathologic examination of a biopsy can determine whether a lesion is benign or malignant , and can help differentiate between different types of cancer. In contrast to a biopsy that merely samples a lesion, a larger excisional specimen called a resection may come to a pathologist, typically from a surgeon attempting to eradicate a known lesion from a patient. For example, a pathologist would examine a mastectomy specimen, even if a previous nonexcisional breast biopsy had already established the diagnosis of breast cancer. Examination of the full mastectomy specimen would confirm the exact nature of the cancer (subclassification of tumor and histologic "grading") and reveal the extent of its spread ( pathologic "staging" ).
There are two types of liquid biopsy (which is not really a biopsy as they are blood tests that do not require a biopsy of tissue): circulating tumor cell assays or cell-free circulating tumor DNA tests. [ 7 ] These methods provide a non-invasive alternative to repeat invasive biopsies to monitor cancer treatment, [ 8 ] test available drugs against the circulating tumor cells, [ 9 ] evaluate the mutations in cancer and plan individualized treatments. In addition, because cancer is a heterogeneous genetic disease, and excisional biopsies provide only a snapshot in time of some of the rapid, dynamic genetic changes occurring in tumors, liquid biopsies provide some advantages over tissue biopsy-based genomic testing. [ 10 ] In addition, excisional biopsies are invasive, cannot be used repeatedly, and are ineffective in understanding the dynamics of tumor progression and metastasis. [ 11 ] [ 12 ] By detecting, quantifying and characterisation vital circulating tumor cells or genomic alterations in CTCs and cell-free DNA in blood, liquid biopsy can provide real-time information on the stage of tumor progression, treatment effectiveness, and cancer metastasis risk. [ 13 ] This technological development could make it possible to diagnose and manage cancer from repeated blood tests rather than from a traditional biopsy. [ 13 ] [ 14 ] [ 15 ] [ 16 ]
Circulating tumor cell tests are already available but not covered by insurance yet at maintrac and under development by many pharmaceutical companies. Those tests analyze circulating tumor cells (CTCs) [ 14 ] [ 17 ] Analysis of individual CTCs demonstrated a high level of heterogeneity seen at the single cell level [ 18 ] for both protein expression and protein localization and the CTCs reflected both the primary biopsy and the changes seen in the metastatic sites. [ citation needed ]
Analysis of cell-free circulating tumor DNA (cfDNA) has an advantage over circulating tumor cells assays in that there is approximately 100 times more cell-free DNA than there is DNA in circulating tumor cells. [ 7 ] These tests analyze fragments of tumor-cell DNA that are continuously shed by tumors into the bloodstream. Companies offering cfDNA next generation sequencing testing include Personal Genome Diagnostics and Guardant Health . [ 10 ] These tests are moving into widespread use when a tissue biopsy has insufficient material for DNA testing or when it is not safe to do an invasive biopsy procedure, according to a recent report of results on over 15,000 advanced cancer patients sequenced with the Guardant Health test. [ 19 ]
A 2014 study of the blood of 846 patients with 15 different types of cancer in 24 institutions was able to detect the presence of cancer DNA in the body. They found tumor DNA in the blood of more than 80 percent of patients with metastatic cancers and about 47 percent of those with localized tumors. The test does not indicate the tumor site(s) or other information about the tumor. The test did not produce false positives. [ 20 ]
Such tests may also be useful to assess whether malignant cells remain in patients whose tumors have been surgically removed. [ 21 ] Up to 30 percent are expected to relapse because some tumor cells remain. [ 22 ] Initial studies identified about half the patients who later relapsed, again without false positives. [ 20 ]
Another potential use is to track the specific DNA mutations driving a tumor. Many new cancer medications block specific molecular processes. Such tests could allow easier targeting of therapy to tumors. [ 20 ]
For easily detected and accessed sites, any suspicious lesions may be assessed. Originally, this was skin or superficial masses. X-ray , then later CT , MRI , and ultrasound along with endoscopy extended the range. [ citation needed ]
A biopsy of the temporal arteries is often performed for suspected vasculitis .
In inflammatory bowel disease ( Crohn's disease and ulcerative colitis ), frequent biopsies are taken to assess the activity of the disease and to assess changes that precede malignancy. [ 23 ]
Biopsy specimens are often taken from part of a lesion when the cause of a disease is uncertain or its extent or exact character is in doubt. Vasculitis , for instance, is usually diagnosed on biopsy.
Needle core biopsies or aspirates of the pancreas may be made through the duodenum or stomach. [ 29 ]
In the case of Wilson's disease , clinicians use biopsies to determine the quantitative copper level.
After the biopsy is performed, the sample of tissue that was removed from the patient is sent to the pathology laboratory . A pathologist specializes in diagnosing diseases (such as cancer ) by examining tissue under a microscope . When the laboratory (see Histology ) receives the biopsy sample, the tissue is processed and an extremely thin slice of tissue is removed from the sample and attached to a glass slide. Any remaining tissue is saved for use in later studies, if required. [ citation needed ]
The slide with the tissue attached is treated with dyes that stain the tissue, which allows the individual cells in the tissue to be seen more clearly. The slide is then given to the pathologist, who examines the tissue under a microscope, looking for any abnormal findings. The pathologist then prepares a report that lists any abnormal or important findings from the biopsy. This report is sent to the surgeon who originally performed the biopsy on the patient. [ citation needed ]
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Bioptics is a combinatorial vision -correction refractive surgical technique performed by ophthalmologists , in which refractive error of the eye is treated on both the lenticular and corneal optical planes. The dual technique was pioneered, and the term coined, by Roberto Zaldívar in 1989. The procedure is increasing in popularity (as of 2006). [ 1 ]
As of 2014, Most refractive surgeons still use Bioptics in a variety of combinations. [ 2 ]
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A bioptome is a small pincer -shaped cutting/grasping instrument used in medicine for taking endomyocardial biopsy specimens of the heart muscle following heart transplantation in rejection monitoring and for diagnosing some diseases of the heart. [ 1 ]
It is flexible and usually operated under the guidance of fluoroscopy or echocardiography . [ 1 ] [ 2 ]
Since 1962, many modifications to the device and techniques in its use have been made. [ 3 ] [ 4 ]
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Bioresorbable (also called biodegradable or bioabsorbable ) metals are metals or their alloys that degrade safely within the body. [ 1 ] The primary metals in this category are magnesium-based [ 2 ] [ 3 ] and iron-based alloys, [ 4 ] although recently zinc has also been investigated. [ 5 ] [ 6 ] Currently, the primary uses of bioresorbable metals are as stents for blood vessels (for example bioresorbable stents ) and other internal ducts.
Although bioabsorbable polymers and other materials have come into widespread use in recent years, degradable metals have not yet had the same success in the medical industry.
The driving force behind the development of bioresorbable metals is primarily due to their ability to provide metal-like mechanical properties while degrading safely in the body. [ 1 ] This is especially relevant in orthopaedic applications, where although many surgeries only require implants to provide temporary support (allowing the surrounding tissue to heal), the majority of current bio-metals are permanent (e.g. stainless steel, titanium). Degradation of the implant means that intervention or secondary surgery will not be necessary to remove the material at the end of its functional life, providing significant savings in both cost and time for the patient and health care system. In addition, the corrosion products of current bio-metals (which will still corrode in the body to some degree) can generally not be considered biocompatible.
There are a number of applications for biodegradable metals, including cardiovascular implants (i.e. stents) and orthopedics. It is in this latter category where these materials offer the greatest potential. Bioresorbable metals are able to withstand loads that would destroy any currently available polymers, and offer much greater plasticity than bioceramics, which are brittle and prone to fracture. A well-designed implant could provide the exact mechanical support needed for different areas (through alloying and metal working), and load would be transferred to the surrounding tissue over time, letting it heal and reducing the effects of stress shielding . [ 7 ] A summary of the primary benefits and drawbacks of magnesium biomaterials has been provided by Kirkland. [ 2 ]
It is the same advantage that bioresorbable metals possess over non-degradable current materials, their biodegradability , that poses the greatest challenges to their development and wider use. The degradable nature of any implant means that their shape and thus mechanical properties will change through its lifetime. This means that lifecycle analysis must be performed on any implant, especially one designed for orthopedic applications where failure could result in death.
Current standards for corrosion of metals have been found to not apply well to bioresorbable metals during in vitro testing. [ 8 ] This is a significant problem as the majority of tests performed in the research community are a mix of other standards from both the biomedical and the engineering (e.g. corrosion) communities, often making comparison between results difficult.
Even though all elements in a bioresorbable metal may themselves be considered biocompatible, the morphology and elemental makeup (or combination of elements) of the degradation products may cause adverse reactions in the body. In addition, the rapid evolution of hydrogen gas that is concomitant with Mg-alloy degradation may cause addition problems in vivo . [ 9 ] It is therefore crucial to intricately understand the corrosion of each implant and the products that are release, in light of their toxicity and the likelihood of inflammation. The majority of studies in the literature have focused on elements that are known to be biocompatible or abundant in the body, such as calcium [ 10 ] [ 11 ] and zinc. [ 12 ]
Although all metals will degrade and eventually disappear inside the body through the processes of corrosion and wear, true bioresorbable metals must have an appreciable degradation rate to allow the implant to be absorbed in a practical amount of time in reference to their application. Also, any degradation product would have to be safely metabolized or excreted by the body to avoid toxicity and inflammation.
Perhaps the most widely investigated material in this category, magnesium was originally investigated as a potential biomaterial in 1878 when it was used by physician Edward C. Huse in wire form as a ligature to stop bleeding. [ 13 ] Development continued into the 1920s, after which Mg-based biomaterials fell out of general investigation due to their poor performance (likely due to impurities in the alloys drastically increasing corrosion). It was not until the late 1990s that interest started to pick up again, Mg has a density close to that of bone and is absorbed by the body .Mg is of interest for orthopedic applications due to its relatively low cost, high specific strength, and near-bone elastic modulus, which avoids stress shielding and allows uniform distribution of tissue stress [ 14 ] [ 15 ]
Currently, most research on Mg is focused on reducing and controlling the rate of degradation, with many alloys corroding too rapidly (in vitro) for any practical application. [ 7 ] [ 16 ]
The majority of iron-based alloy research has been focused on cardiovascular applications, such as stents. [ 17 ] However this area receives much less interest in the research community than Mg-based alloys. [ citation needed ]
To date little work has been published on the use of a primarily zinc-based biomaterial, with corrosion rates found to be very low and zinc within a tolerable toxicity range [ 6 ] [ 7 ] .Furthermore, Pure Zn has poor mechanical behavior, with
a tensile strength of around 100–150 MPa and an elongation of 0.3–2%, which is far from reaching the strength required as an orthopedic implant material (tensile strength is more than 300 MPa,
elongation more than 15%). Alloy and composite fabrication have proven to be excellent ways to improve the mechanical performance of Zn. [ 18 ]
Although strictly speaking a side-category, a related, relatively new area of interest has been the investigation of bioabsorbable metallic glass , with a group at UNSW currently investigating these novel materials. [ 19 ]
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A bioresorbable stent is a tube-like device ( stent ) that is used to open and widen clogged heart arteries and then dissolves or is absorbed by the body. It is made from a material that can release a drug to prevent scar tissue growth. It can also restore normal vessel function and avoid long-term complications of metal stents. [ 1 ] [ 2 ]
In medicine, a stent is any device which is inserted into a blood vessel or other anatomical internal duct to expand it to prevent or alleviate a blockage. Traditionally, such devices are fabricated from metal mesh and remain in the body permanently or until removed through further surgical intervention. A bioresorbable stent (also called bioresorbable scaffold, biodegradable stent or naturally-dissolving stent) serves the same purpose, but is manufactured from a material that may dissolve or be absorbed in the body. [ 3 ]
The use of metal drug-eluting stents presents some potential drawbacks. These include a predisposition to late stent thrombosis , prevention of late vessel adaptive or expansive remodeling, hindrance of surgical revascularization, and impairment of imaging with multislice CT . [ 4 ] [ 5 ]
To overcome some of these potential drawbacks, several companies are pursuing the development of bioresorbable scaffolds or bioabsorbable stents. Like metal stents, placement of a bioresorbable stent will restore blood flow and support the vessel through the healing process. However, in the case of a bioresorbable stent, the stent will gradually resorb and be benignly cleared from the body, enabling a natural reconstruction of the arterial wall and restoration of vascular function. [ 6 ]
Studies have shown that the most critical period of vessel healing is largely complete by approximately three to nine months. [ 6 ] [ 7 ] [ 8 ] Therefore, the goal of a bioresorbable or "temporary" stent is to fully support the vessel during this critical period, and then resorb from the body when it is no longer needed.
Bioabsorbable scaffolds, or naturally dissolving stents, that have been investigated include base materials that are either metals or polymers. While polymer-based scaffolds had a strong presence at first, they have meanwhile lost some appeal due to safety concerns and focus is now moved towards metallic magnesium-based scaffolds. [ 9 ]
Metal stent candidates are magnesium , iron , zinc and their alloys. [ 10 ]
Magnesium -based scaffolds have been approved for use in several countries around the world. The only commercially available magnesium-based scaffold consists of a magnesium alloy, approximately 95% of which resorbs within one year of implantation. [ 11 ] [ 12 ] [ 13 ] Thousands of commercially available magnesium-based scaffolds have been implanted. Clinical results suggest that magnesium-based scaffolds may be a viable option in avoiding the drawbacks of permanent stents. [ 14 ] [ 15 ] [ 16 ] [ 17 ] While degrading harmlessly, it has been shown to possess a functional degradation time of about 30 days in vivo . This is much short of the three-to-six month window desired for bioabsorbable stents. Thus, much attention has been given to drastically reducing the rate of magnesium corrosion by alloying, coating, etc. [ 18 ] Many novel methods have surfaced to minimize the penetration rate and hydrogen evolution rate (or, in layman's terms, the corrosion rate). One of the most successful has involved the creation of bioabsorbable metallic glasses via rapid solidification. Other, alternative solutions have included the development of magnesium– rare-earth (Mg-RE) alloys, which benefit from the low cytotoxicity of RE elements. Coatings and sophisticated materials processing routes are currently being developed to further decrease the corrosion rate. However, a number of issues remain limiting the further development of Mg biomaterials in general. [ 19 ]
Iron stents were shown using an in vivo evaluation method based on the murine abdominal aorta to generate an iron oxide-filled cavity in the vascular wall [ 20 ] that is unlikely to be metabolized safely. [ 21 ]
Zinc shows desirable physiological corrosion behavior, meeting a benchmark penetration rate of 20 micrometers per year. [ 22 ] However, Zn has poor mechanical behavior, with a tensile strength of around 100–150 MPa and an elongation of 0.3–2%, which is far from reaching the strength required as an orthopedic implant or stent material. [ 23 ]
Polymer-based stents have been approved for use in some countries around the world. These are based on poly(L-lactide) ( PLLA ), chosen because it is able to maintain a radially strong scaffold that breaks down over time into lactic acid, a naturally occurring molecule that the body can use for metabolism. Other polymers in development include tyrosine poly carbonate and salicylic acid. [ 24 ]
An example of a naturally dissolving stent is the 'Absorb' stent 'produced by Abbott [ 25 ] that has several design components and features: base scaffold : a poly(L-lactide) polymer similar to that in dissolvable stitches is shaped into a tube made up of zigzag hoops linked together by bridges; drug-eluting layer': a mixture of poly-D, L-lactide (PDLLA) and everolimus; 'markers': a pair of radio-opaque platinum markers at the ends that allow the device to be visualized during angiography; 'delivery system': a balloon delivery system. [ citation needed ]
Recently however, Polymer-based scaffolds, in particular Poly-L-Lactide Acid (PLLA) scaffolds, have raised serious concerns on the scaffold performance particularly in terms of safety which led to the commercial discontinuation of the main representative Absorb. [ 26 ] [ 27 ]
Clinical research has shown that resorbable scaffolds, or naturally dissolving stents, offer comparable efficacy and safety profile to drug-eluting stents. Specifically, the Magmaris resorbable magnesium scaffold [ 28 ] has reported a favorable safety profile with low target lesion failure and scaffold thrombosis rates. These clinical results are comparable to thin-strutted drug-eluting stents in similar patient populations. [ 29 ] [ 30 ] [ 31 ] [ 32 ]
The Absorb naturally dissolving stent has also been investigated in single-arm trials and in randomized trials comparing it to a drug-eluting stent . Early and late major adverse cardiac events, revascularizations, and scaffold thromboses have been uncommon and similar to the Xience DES, a market leader in the drug eluting stent category. [ 33 ] [ 34 ] [ 35 ] [ 36 ] [ 37 ] Studies in real-world patients are ongoing. [ 37 ]
Imaging studies show that the Absorb naturally dissolving stent begins to dissolve from six to 12 months and is fully dissolved between two and three years after it is placed in the artery. [ 35 ] Two small platinum markers remain to mark the location of the original PCI. The artery is able to dilate and contract, called vasomotion, similar to a healthy blood vessel at two years. [ 34 ]
In the US, the first fully absorbable stent was approved by FDA in 2016. [ 1 ]
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Biostratinomy is the study of the processes that take place after an organism dies but before its final burial. It is considered to be a subsection of the science of taphonomy , along with necrology (the study of the death of an organism) and diagenesis (the changes that take place after final burial). These processes are largely destructive, and include physical, chemical and biological effects:
For the vast majority of organisms, biostratinomic destruction is total. However, if at least a few remnants of an organism make it to final burial, a fossil may eventually be formed unless destruction is completed by diagenesis . As the processes of biostratinomy are often dominated by sedimentological factors, analysis of the biostratinomy of a fossil can reveal important features about the physical environment it once lived in. The boundaries between the three disciplines within taphonomy are partly arbitrary. In particular, the role of microbes in sealing and preserving organisms, for example in a process called autolithification , is now recognised to be a very important and early event in the preservation of many exceptional fossils, often taking place before burial. Such mineralogical changes might equally be considered to be biostratinomic as diagenetic.
A school of investigation called aktuopaläontologie , subsisting largely in Germany, attempts to investigate biostratinomic effects by experimentation and observation on extant organisms. William Schäfer's book "Ecology and palaeoecology of marine environments" is a classic product of this sort of investigation. More recently, D.E.G. Briggs and colleagues have made detailed studies of decay with the prime aim of understanding the profound halt to these processes that is required by exceptional preservation in lagerstätten .
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https://en.wikipedia.org/wiki/Biostratinomy
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