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The Oral Health Foundation (formerly known as the British Dental Health Foundation) was formed in 1971 and is one of the world’s leading independent oral health charities (registered charity number 263198). [ 1 ] It is headquartered in the United Kingdom and aims to help the public improve their oral health and hygiene through a range of activities run under the name of the Oral Health Foundation. The current president of the Oral Health Foundation is Mhari Coxon, [ 2 ] [ 3 ] and the CEO is Dr Nigel Carter OBE. [ 4 ]
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https://en.wikipedia.org/wiki/British_Dental_Health_Foundation
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The British Heart Foundation ( BHF ) is a cardiovascular research charity in the United Kingdom. [ 5 ] It funds medical research related to heart and circulatory diseases and their risk factors, and runs influencing work aimed at shaping public policy and raising awareness. [ 5 ]
In 2021, a study conducted by YouGov ranked the British Heart Foundation as the top charity or organisation in the UK by per cent of adults who hold a positive opinion of the organisation. [ 6 ]
The British Heart Foundation was founded in 1961 by a group of medical professionals who were concerned about the increasing death rate from cardiovascular disease . They wanted to fund extra research into the causes, diagnosis, treatment, and prevention of heart and circulatory diseases. [ 7 ]
Dr Charmaine Griffiths has been the BHF's Chief Executive since February 2020, succeeding Simon Gillespie OBE.
Professor Bryan Williams OBE became the charity's first Chief Scientific and Medical Officer (CSMO) in December 2023, after Professor Sir Nilesh Samani stood down as Medical Director after more than 7 years in the role. [ 8 ]
The BHF's Board of Trustees is made up of up to 14 Trustees, and is a mix of medically-qualified and lay members: [ 9 ]
Karen A. Frank is the Chair of the Board of Trustees.
King Charles III has been the BHF's Patron since May 2024, succeeding Prince Philip, Duke of Edinburgh . [ 10 ]
The British Heart Foundation's main focus is to fund cardiovascular research, aiming to spend around £100 million a year funding scientists around the UK. They are currently funding over 1000 research projects. [ 11 ]
Since 2008 the BHF has been investing in Centres of Research Excellence. The eight current centres bring together scientists from a number of disciplines to work on research projects to beat heart and circulatory disease. [ 12 ] The current Centres of Research are:
In 2013 the BHF committed to funding three multi-institution Centres of Regenerative Medicine, investing £7.5 million over four years to fund scientists looking for new treatments for heart failure . [ 13 ]
The British Heart Foundation Clinical Research Collaborative was launched in 2019, hosted by the British Cardiovascular Society . [ 14 ] Designed to support the planning of high-quality national cardiovascular research, it brings together professional societies, research groups and patient and public involvement to better coordinate and prioritise research efforts. [ 14 ] It also launched a fund to support the development of clinical research in cardiovascular disease, providing grants from £5,000-20,000, and all topic ideas will be considered. [ 14 ]
Other patients and public activities include:
In 2020, The British Heart Foundation had a net income of just over £107m. [ 17 ] In the same year, the BHF spent over £93m on funding cardiovascular research. [ 18 ]
The charity announced, in June 2021, that it had joined forces with leading cardiovascular research funders around the world to form the Global Cardiovascular Research Funders Forum (GCRFF). [ 19 ] In addition to the British Heart Foundation, the Forum's members are:
In 2019, The British Heart Foundation launched the Big Beat Challenge, a global competition with a single award of £30m for the research team who proposed a transformational solution to any cardiovascular disease. [ 21 ] The Big Beat Challenge was open to applications from any country globally, and accepted proposals in any research area related to cardiovascular disease. Based on a panel of BHF research-funding committee members and an International Advisory panel, a shortlist was finalised in January 2020 to include a robotic heart, a 'Google map' of atherosclerosis, a project harnessing artificial intelligence (AI) and wearables to create a cardiovascular digital twin of a patient, and a genetic cure for inherited heart conditions. [ 22 ]
CureHeart, led by co-PIs Professor Hugh Christian Watkins and Professor Christine Seidman , which aims to find a cure for genetic cardiomyopathies, was announced as the winner of the Big Beat Challenge in July 2022. [ 23 ]
BHF fundraising events accounted for nearly £54m of income in 2019-20. [ 24 ]
The BHF won the bid to be named as the London Marathon charity partner for the 2022 raise, aiming to raise £3m through the partnership to invest in clinical research. [ 25 ]
The annual London to Brighton Bike Ride is a flagship fundraising event, with over 16,000 cyclists and raising over £2.8m. [ 26 ] The event was cancelled in 2020 and 2021, and was expected to return in 2022 with PureGym as the sponsor. [ 26 ] [ needs update ]
The BHF runs the largest network of charity shops in the UK, and generates income through online sales too. [ 27 ] As of 2021, they run around 730 shops which include over 160 furniture and electrical shops selling up to 85,000 items daily. [ 28 ] The BHF Retail division makes roughly £30 million every year. [ 29 ]
In June 2011, the British Heart Foundation was one of several health charities, alongside Cancer Research UK , the Alzheimer's Society and Parkinson's UK , targeted by animal rights pressure group Animal Aid , in a series of newspaper advertisements urging the public not to donate to the organizations under the pretence of funding experiments on animals. [ 32 ] [ 33 ] The pressure group argued that 100 dogs had died since 1988 during the experiments. [ 34 ] [ 35 ]
The BHF has responded to these criticisms by saying the charity only funds animal research after grant applications have gone through an independent peer review process and follows the three Rs principles when considering such grants. [ 36 ]
In 2016, the BHF was fined by the UK Information Commissioner's Office which ruled that the charity had breached data protection legislation by employing external bodies to analyse the financial status of supporters in order to appeal to them for further donations, a practice known as 'wealth screening'. [ 37 ] BBC News Online reported that, "Information Commissioner Elizabeth Denham said donors had not been informed of the charity's practices, and were therefore unable to consent or object to them." She suggested other charities could also be engaged in similar activities. [ 37 ]
The charity's chief executive stated that "The ICO's conclusions were 'wrong, disproportionate and inconsistent […] We find the decision surprising, as earlier this year in June the ICO praised our data handling. Our trustees will therefore consider whether it's in the interests of our supporters and beneficiaries to challenge this decision." [ 37 ]
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The British Journal of Cancer ( BJC ) is a twice-monthly professional medical journal published by Springer Nature .
The BJC provides a forum for clinicians and scientists to communicate original research findings that have relevance to understanding the etiology of cancer and to improving patient treatment and survival. Once accepted, papers are published in print and online.
Full research papers are published under six broad headings:
The journal was founded in 1947 by the then British Empire Cancer Campaign (later named Cancer Research Campaign), [ 1 ] one of the research charities which later merged to form Cancer Research UK . Cancer Research Campaign began partnering with Nature as publisher of the journal in the 1980s, but retained ownership and editorial control. In 2021, after the charity experienced a fall in charitable income during the COVID-19 pandemic , Cancer Research UK sold the journal to Springer Nature. [ 2 ]
According to the Journal Citation Reports , the journal received an impact factor of 9.0, [ 3 ] ranking it 39th journals in the category of Oncology . [ 4 ] SJR ranked BJC as 30th journal in cancer research with H-index 224. [ 5 ]
BJC is a top cited general cancer journal committed to publishing cutting edge discovery, translational and clinical cancer research. [ 6 ] The journal is indexed in:
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https://en.wikipedia.org/wiki/British_Journal_of_Cancer
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BJS is a peer-reviewed surgical journal featuring high-quality research, education, and debate with a 2023 impact factor of 8.6 - current time to first decision is only 17 days for most submissions. A broad range of article types is available to suit most authors looking to submit in the following specialty areas:
Acute Care Surgery; Breast; Cardiothoracic Surgery; Education; Endocrine; Experimental Science; General; Hernia; HPB; Lower GI; Orthopaedics; Paediatric Surgery; Plastic Surgery; Transplantation; Trauma; Upper GI; Urology; Vascular
It has been published since 1913 and is currently published by Oxford University Press .
In 2021 they established their new education arm BJS Academy and in 2022 launched the new BJS Academy website to provide surgeons with learning materials.
This article about a surgery 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/British_Journal_of_Surgery
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The British Library Leyden Medical Dissertations Collection is a collection of medical dissertations submitted to Dutch universities at Amsterdam, Utrecht, Harlingen, and Leyden . It includes, in particular, a fine set of Leyden medical dissertations and disputations for the period 1593 to 1746. The collection is in 53 volumes, all bound in white vellum , with 20 to 75 documents in each volume. The collection was formed principally by Hans Sloane . [ 1 ]
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The British Neuropathological Society is a professional organisation dedicated to the science of neuropathology . It is one of several national societies composed of neuropathologists. These national groups are members of the International Society of Neuropathology (ISN) which was formed in May 1967, derived from a previous international group of neuropathologists formed in 1950.
The object of the Society is to further the study of neuropathology, to promote the exchange of scientific and professional information by means of regular meetings, lectures and publications, and to provide the opportunity for discussions between neuropathologists in Britain and 'overseas'. [ 1 ]
Godwin Greenfield is regarded [ 2 ] as the founding father of the British Neuropathological Society. His career had spanned the years during which neuropathology began to be recognised as a specialty, rather than as merely applied neurology or psychiatry , and he was one of the first to regard himself as a neuropathologist. [ citation needed ]
By the time he retired from Queen Square in 1949 the advent of the National Health Service had seen the establishment of neurosurgical centres throughout the country, many with neuropathologists already in post. In 1950 with a group of senior colleagues Greenfield started the Neuropathological Club, with 28 founder members. The Club served two useful purposes. It had an important educational function, allowing members of the different schools of neuropathology that had sprung up around the country the opportunity to get together to discuss problem cases, and it united those who had a major clinical commitment in neuropathology with those concerned principally with experimental work.
Two years later in 1952 the first International Congress of Neuropathology was held in Rome . This was not to everyone's approval: the neurologist Sir Francis Walshe commented with dismay that separate international meetings for neuropathologists and neurosurgeons tore “the seamless garment of neurology”.In 1962 the club had grown sufficiently for it to become more formal, and the name was changed to the British Neuropathological Society (BNS).1967 saw the founding of the International Society of Neuropathology, in which BNS members have played an active role, providing four of the Secretaries-General and two of the Presidents to date. [ citation needed ]
In 1975 the BNS launched Neuropathology and Applied Neurobiology, which has become one of the major neuropathology journals [ 3 ]
By the year 2000, when the British Neuropathological Society celebrated its 50th anniversary, there were more than 200 active members.
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https://en.wikipedia.org/wiki/British_Neuropathological_Society
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The British Society for Plant Pathology , or BSPP , is a UK -based organisation of British plant pathologists but accepts members from all countries. [ 1 ] It was founded in 1981 and publishes three scientific journals : Plant Pathology , [ 2 ] Molecular Plant Pathology [ 3 ] and New Disease Reports . [ 4 ] The BSPP has links to the International Society for Plant Pathology . [ 1 ]
The organisation gives an annual award for the best student paper published in one of society's journals. The P. H. Gregory prize is awarded to the best presenter of an oral paper at the annual presidential meeting.
Like other organisations of its type it arranges conferences and also awards various scholarships and fellowships .
The Federation of British Plant Pathologists was founded in 1966 and became the independent British Society for Plant Pathology in 1981. [ 5 ]
This article about a biology organization is a stub . You can help Wikipedia by expanding it .
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The British Society for Restorative Dentistry was founded in 1968 and promotes standards in the dental profession through conferences, meetings and scientific literature . The society provides a forum for members to debate current issues in Restorative Dentistry and especially in Prosthodontics .
The conference calendar includes two scientific meetings a year (Spring and Autumn). [ 1 ] The society is affiliated to the European Journal of Prosthodontics and Restorative Dentistry , and has also published policy documents on ‘Guidelines for Crown and Bridge’ and ‘A Strategy for Planning Restorative Care’. [ 2 ]
The British Society for Restorative Dentistry (BSRD) award prizes to clinicians and researchers in three broad domains; audits, research and clinical cases. [ 3 ]
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The British Society of Periodontology is a society of periodontologists (i.e. Dental Care Professionals who specialize in treating gum diseases) in the United Kingdom. It was founded in 1949 and its aim is to "promote the art and science of periodontology ". Its activities include advisory publications for professionals and the public, educational workshops, society meetings and awards for research.
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The British Stammering Association ( BSA ), trading as Stamma (styled 'STAMMA') since 2019, [ 3 ] is a national membership organisation in the United Kingdom for adults and children who stammer , their friends and families, speech and language therapists and other professionals. It became a charity in 1978 and is based in London. The mission of the charity is to support anyone who stammers in the UK and tackle the stigma, ignorance and discrimination that people who stammer face so that they can live their lives in full and with dignity. [ 3 ] It describes stammering as a neurological condition and estimates that up to 3% of adults in the UK have a stammer. [ 4 ] [ 5 ]
The association's chief executive, since June 2018, is Jane Powell. [ 1 ] The interim chair, since 2022, is Paul Fix.
The organisation's president was Brian Dodsworth, who died in 2021. [ 6 ]
Stamma's patrons are: [ 7 ] broadcaster and former MP Ed Balls , former Scotland international rugby captain Kelly Brown , author Jonty Claypole , Dame Margaret Drabble DBE, [ 8 ] former MP and MSP John McAllion , [ 9 ] David Mitchell , author of Black Swan Green , [ 10 ] [ 11 ] [ 12 ] actor, rapper and podcaster Scroobius Pip , [ 13 ] Arwel Richards , [ 14 ] novelist, poet, playwright and presenter Owen Sheers , [ 15 ] Jon Smith and Baroness Whitaker . [ 16 ] [ 17 ]
Previous patrons have included Nicholas Parsons CBE [ 18 ] and Jonathan Miller , [ 19 ] both now deceased.
The British Stammering Association is a member of the European League of Stuttering Associations [ 20 ] and the International Stuttering Association . [ 21 ] At its World Congress in Brazil, the International Fluency Association awarded the IFA Consumer Award of Distinction 2009 to the British Stammering Association.
The association had a Scottish branch, BSA Scotland, which was founded in 2004 and is now closed. It was a focus for Scottish campaigns, events and support services as well as to engage with the Scottish Parliament . [ 22 ]
The association operates a helpline , webchat and email support service, and offers information leaflets for parents of children under 5, primary and secondary school children, young adults and adults who stammer and teachers. It can also signpost callers to their local NHS Speech and Language Therapy Service. Those who stammer can also use the helpline to practise phone conversations or share how they are feeling. [ citation needed ]
Between 2004 and 2005 the association published a research journal , Stammering Research , [ 23 ] which was edited by Professor Peter Howell of University College London . [ 24 ] In 2010 the association produced research showing that children with signs of stammering are more likely to overcome the problem if they receive help before they reach school age.
The Association produces a variety of information resources. [ 25 ]
The British Stammering Association published a magazine, Speaking Out , [ 26 ] which ended in 2014. The spring 2011 issue included an article in which BSA member Richard Oerton recalled his own experiences with King George VI 's speech therapist Lionel Logue who is featured in the film The King's Speech . [ 27 ] An interview with Neil Swain, voice coach for the film, was published in the summer 2011 issue. [ 28 ] The spring/summer 2012 issue included an interview with the actor Charles Edwards , who played George VI in the West End stage version of the film. [ 29 ]
The association has campaigned for several years to eradicate misleading advertising claims made by stammering treatment providers. Some claim, for example, that they can " cure " stammering − but it is not possible to "cure" a stammer, in the accepted medical sense of the word. [ 30 ] Accordingly, the BSA believes such claims not only give false hope to those who stammer − but also give people who do not stammer the false impression that stammering can easily be rectified. Respectable healthcare companies carry out independent trials on large numbers of people, over long periods of time, before claiming any benefit for their products or services. The campaign has been conducted by, firstly, encouraging treatment providers who are making doubtful claims to provide supporting data and, if they cannot do so, to moderate those claims; and, secondly, in cases where the treatment provider has not co-operated, the association has reported their advertisements to the UK Advertising Standards Authority (ASA), [ 31 ] who have investigated the claims and, if they prove to be unsupportable, have instructed them to remove the offending advertisement and amend any future claims. As from 1 March 2011, the ASA, and thus the association, have also been able to act against misleading claims made in editorial copy on websites. [ 32 ] Following a complaint by the association, on 13 July 2011 the Advertising Standards Authority issued an adjudication against a website which said: "Discover how to stop stuttering with stammering cure that works". [ 33 ]
BSA's then chief executive Norbert Lieckfeldt, who has described stammering as "the hidden disability ", [ 34 ] said the charity had received calls from members who said people were asking them about their stammer for the first time, because of The King's Speech . The film had created a "good opportunity" for people to talk about stammering. He said: "Suddenly it has become a thing that can be talked about, which is very important for us...For those people who are engaged in conversations about it, their situation will have changed for the better." [ 35 ] [ 36 ]
The association criticised comedian Lenny Henry for his opening sketch for the 2011 Comic Relief , during which he spoofed the film and grew impatient with Colin Firth 's portrayal of King George VI as he stammered over his speech. [ 37 ]
In 2007 the association's then chair, Leys Geddes, strongly protested to the YouTube website about their classifying, as comedy, videos showing people struggling to speak, including three which he said appeared to be "malicious and stereotypical". [ 38 ] [ 39 ] YouTube replied that the videos did not violate its terms of use. Geddes has now posted his own video on YouTube, arguing for greater understanding for those who stammer. Speaking in support of the association's stance, Labour MP Kate Hoey said: "For many people, particularly youngsters, stammering is not a joke – we need to ensure that help and support is given as early as possible and, most of all, we need to educate the public to understand the impact it has on people for the whole of their lives". [ 38 ]
In May 2012, the association criticised a headline and story on the front page of The Sun mocking newly appointed England football manager Roy Hodgson 's rhotacism . [ 40 ]
Commenting on the media coverage of Ed Balls' stumbling over his response in the House of Commons on 5 December 2012 to the Autumn Statement by Chancellor of the Exchequer George Osborne , Norbert Lieckfeldt said: "The experience of a lifetime of stammering gives an edge to a personality, something to rub against, and I'd prefer that over smooth glibness any day. This is also the advice we at the British Stammering Association would give to anyone who stammers who is considering a career in politics". [ 4 ]
Under the new leadership of Jane Powell, the charity launched a major new campaign, Stamma, in 2019 which aimed to give the public an insight into what it means to stammer, dispel stereotypes and encourage people to take stammering seriously. To coincide with International Stammering Awareness Day on 22 October 2019 a nationwide advertising campaign was launched, with Stamma being promoted on outdoor advertising spaces across the UK.
Launched on 9 May 2013 with a reception in the House of Commons hosted by The Rt Hon Ed Balls (who was then an MP), [ 41 ] the Employers Stammering Network, an initiative of the BSA and employers, aims to create a culture where people who stammer can achieve their full potential. [ 42 ] In 2018, leading members with their own active networks included the Civil Service , [ 43 ] the Defence Stammering Network and EY (formerly known as Ernst & Young) . [ 44 ] As the initiative matured, the Employers Stammering Network was in contact as of 2018 [update] with supporters in some 150 organisations and over 50 change-makers in a range of work settings. [ 45 ]
The " Find The Right Words " campaign was created by VMLY&R for Stamma, and launched in October 2020. It highlights the problems caused by negative language used in relation to stammering and asks people to change perceptions of those who stammer. [ 46 ]
Articles on the English-language Wikipedia featuring famous or notable people who stammer or stammered were reviewed, and edited by members of Stamma to correct information that failed to adhere to a neutral point of view.
The campaign includes digital advertising and a social media activity, and a video narrated by one of the charity's patrons, Scroobius Pip , who said:
Imagine you're 15 and you stammer. You love Ed Sheeran and Emily Blunt. Not that long ago you were amazed by Lewis Carroll's stories. But according to articles and stories online, these people are "plagued" by a "terrible impediment" which they had to "get rid of". When all they did was stammer. A physical condition that few of us stop to think about, yet 1 in 100 people have it. So we worked together with the community at Wikipedia and carefully rewrote every bit of language that spoke of it in a damaging or false way. There shouldn't be shame in having a stammer, whether you're 15 or 65. It's how we talk.
Early in June 2021, Stamma investigated instances where, when the word "stammering" was typed into certain Apple devices, the "woozy face" emoji was suggested, causing offence to many in the stammering community. The woozy face emoji, with a wavy mouth and a closed eye, was added to Apple's roster in 2018 and is supposed to depict being drunk, dazed, infatuated, or tired and emotional.
Stamma logged a complaint with Apple on 16 June and asked for a response, pointing out that stammering can be seen as a disability under the Equality Act 2010 , as for many people it can severely impair day-to-day functions and for adults is lifelong. As such, the linkage between stammering and the woozy face emoji could constitute harassment under the Equalities Act.
Stamma issued a press release in which its CEO, Jane Powell, stated: "This is demeaning and damaging. Stammering is how some people talk. Treating it as a joke is stigmatising. It can leave people embarrassed about how they sound, bullied and ashamed which can affect their mental health, careers and relationships."
It was picked up by the Metro newspaper in the UK, as well as by platforms which covered Apple internationally. Stamma were contacted by supporters around the world and worked with the International Stuttering Association and VivaVoce Assoziatione in Italy, plotting a coordinated international campaign, with a petition on change.org .
On 2 July 2021, Stamma received word that Apple had released iOS update 14.7, which stopped the woozy face emoji from appearing when typing the word stammering. Stamma are still [ when? ] waiting for a formal response from Apple.
Stamma started a campaign, "No Diversity Without Disfluency", in October 2021 to get more people who stammer on TV, radio and film. They set up a change.org petition at www.stamma.org/petition which to date has received over 20,000 signatures. It is currently working with stammering associations in the US and Australia to adopt the campaign in their territories. The campaign was picked up by Ofcom , who said, "We applaud the work to raise awareness of stammering and encourage broadcasters to take notice". [ citation needed ]
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The Broadbent inverted sign is a clinical sign in which pulsation is seen on the postero-lateral wall of the left side of the chest in time with cardiac systole . This was originally thought to be due to an aneurysm of the left atrium , but is now known to be more commonly associated with left ventricular hypertrophy . [ 1 ] The sign is named after Sir William Broadbent . [ 2 ]
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Broadbent sign is a clinical sign in which the 11th and 12th ribs are indrawn during systolic phase of a heartbeat, with narrowing of the intercostal space posteriorly, which is seen in case adhesive pericarditis due to pericardial adhesions to the diaphragm . [ 1 ]
During diseased status of adhesive pericarditis, the pericardium of the heart may adhere not only to the central tendon of diaphragm , but also to a large area of muscular portion of diaphragm as well as anterior chest wall. Thus when the heart contracts, the adhesion portion may be dragged inward and downward (if the main contraction force is toward central tendon of diaphragm). [ 2 ] Besides, absent palpable apical impulse can also be detected in the case of adhesive pericarditis.
The sign is named after Walter Broadbent , and was published in his first paper in 1895, although it may have been inspired by his father, Sir William Broadbent . [ 3 ]
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Broca's fissure is a medical and scientific term for a sulcus occurring in the area of the brain known as Broca's area . [ 1 ] Broca's area contains the motor speech area and controls movements of tongue, lips and vocal cords.
Broca's fissure produces the typical effects of a lesion in Broca's area (i.e., expressive aphasia ).
Some individuals afflicted with Broca's fissure are aided by speech entrainment(SE) . [ 2 ]
Sufferers of Broca's fissure have an inability to understand the processes of syntax and word order. For example, a sufferer is unable to distinguish between the chef burned the noodles and the noodles burned the chef . In many circumstances, sufferers are able to use inference about the world to determine the most likely option. The difficulty is not in the meaning of the individual words- most sufferers still know the definitions of words like chef and noodles , but with the relationships between those words. [ 3 ]
Broca's aphasics typically have slow and hard to understand speech, stringing together individual nouns and adjectives with very few function words and little pluralization. This is also one of the major differences between Wernicke's aphasia and Broca's aphasia. Those with Wernicke's aphasia typically speak in full sentences with semi-coherent contents that may not be relevant to the topic.
For example, a person with Broca's aphasia may say "Boy... down.. taking... cookie", while a person with Wernicke's aphasia describing the same scene may say "Mother is away working her work out of here, but when she's looking in the other part. One their small tile into their time here." [ 3 ]
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The Broermann Medical Innovation Award is an international prize to honor groundbreaking medical science and healthcare innovation achievements. Established in 2024 and endowed with €1 million, it recognizes individuals or teams whose work has or has the potential to advance medical research and patient care significantly.. [ 1 ] The award ceremony will be held yearly in the state chancellery of Hesse in Wiesbaden. [ 2 ]
The award was established by Dr. Bernard Broermann , a German lawyer, businessman, and founder of the Asklepios Kliniken Clinics Group, who passed away [ 3 ] in 2024. He wanted to reward scientists who help humanity through medical innovation with recognition, money, and prestige as part of his will [ 4 ]
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https://en.wikipedia.org/wiki/Broermann_Medical_Innovation_Award
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Bromism is the syndrome which results from the long-term consumption of bromine , usually through bromine-based sedatives such as potassium bromide and lithium bromide . Bromism was once a very common disorder, being responsible for 5 to 10% of psychiatric hospital admissions, but is now uncommon since bromide was withdrawn from clinical use in many countries and was severely restricted in others.
High levels of bromide chronically impair the membrane of neurons, which progressively impairs neuronal transmission, leading to toxicity, known as bromism. Bromide has an elimination half-life of 9 to 12 days, which can lead to excessive accumulation. Doses of 0.5 to 1 gram per day of bromide can lead to bromism. Historically, the therapeutic dose of bromide is about 3 to 5 grams of bromide, thus explaining why chronic toxicity (bromism) was once so common. While significant and sometimes serious disturbances occur to neurologic, psychiatric, dermatological, and gastrointestinal functions, death is rare from bromism. [ 1 ]
Bromism is caused by a neurotoxic effect on the brain which results in somnolence , psychosis , seizures , and delirium . [ 2 ] Bromism has also been caused by excessive consumption of soda that contains brominated vegetable oil , leading to headache , fatigue , ataxia , memory loss , and potentially inability to walk as observed in one case. [ 3 ]
Bromism is diagnosed by checking the serum chloride level, electrolytes, glucose, blood urea nitrogen and creatinine , as well as symptoms such as psychosis . Bromine is also radiopaque , so an abdominal X-ray may also help in the diagnosis. [ 1 ]
There are no specific antidotes or protocols for bromide poisoning of the body. Increased intake of regular salt and water, which increases the flow of the related chloride ion through the body, is one way of flushing out the bromide. Furosemide may help aid urinary excretion in individuals with renal impairment or where bromide toxicity is severe. [ 1 ] In one case, hemodialysis was used to reduce bromide's half-life to 1.38h, dramatically improving the patient's condition. [ 3 ]
Iodine deficiency is also linked to weaker (less detectable) forms of bromism. [ citation needed ] Iodine and bromine are closely related to each other in behavior (and location on the periodic table) and high levels of bromine will displace iodine in tissues and blood when there is an opportunity to do so. Supplementary intake of iodine should be preceded by a salt loading protocol, or consumption of dietary sulfur beforehand. [ citation needed ]
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https://en.wikipedia.org/wiki/Bromism
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Brostallicin is a chemical compound being studied in the treatment of cancer . It is an alkylating agent that binds DNA. [ 1 ]
This article incorporates public domain material from Dictionary of Cancer Terms . U.S. National Cancer Institute .
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Brown atrophy of the heart is atrophy of the heart muscle (or myocardium ) commonly found in the elderly. [ 1 ] [ 2 ] It is described as brown because fibers become pigmented by intracellular deposits (mostly around the cell nucleus ) of lipofuscin , [ 1 ] a type of lipochrome granule .
It has no known effect on function, [ 1 ] [ 2 ] and is described as being expected or normal in aging. [ 2 ]
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Bruce B. Lerman is a cardiologist . He is the Hilda Altschul Master Professor of Medicine at Weill Cornell Medical College , and was chief of the Division of Cardiology and director of the Cardiac Electrophysiology Laboratory at Weill Cornell Medicine and the New York Presbyterian Hospital .
Lerman received a BA at Clark University in 1972, an MD medical degree from Loyola University - Stritch School of Medicine in 1977, was an intern and medical resident in internal medicine at Northwestern University , and completed a fellowship in cardiovascular disease at the Johns Hopkins School of Medicine . [ 1 ] [ 2 ] [ 3 ] He trained in cardiac electrophysiology at the Perelman School of Medicine at the University of Pennsylvania . [ 2 ]
Lerman is a cardiologist in New York City, with specialties in adult congenital heart disease and cardiac electrophysiology . [ 1 ]
Lerman is the Hilda Altschul Master Professor of Medicine at Weill Cornell Medical College , and chief of the Division of Cardiology and director of the Cardiac Electrophysiology Laboratory at Weill Cornell Medicine and the New York Presbyterian Hospital . [ 2 ] [ 3 ] [ 4 ] [ 5 ] [ 6 ] [ 7 ]
He has focused in his research on clarifying the electrophysiologic mechanisms of the nucleoside adenosine , current-based defibrillation , and determining the role of mechanoelectrical feedback as a stimulus for causing malignant ventricular arrhythmias . [ 2 ] He has been issued 4 patents . [ 2 ] Lerman has focused in his clinical work on the diagnosis and treatment by ablation of complicated atrial and ventricular arrhythmias , and treating life-threatening arrhythmias with implantable devices. [ 2 ]
Lerman received the Established Investigator Award from the American Heart Association , and had received a number of grants from the National Institutes of Health . [ 2 ] He is on the editorial boards of a number of medical and scientific journals, including Circulation and Heart Rhythm . [ 2 ]
Lerman has written or co-written over 200 medical articles, 60 book chapters, and two books. [ 8 ] [ 2 ]
Among his publications are: [ 9 ]
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https://en.wikipedia.org/wiki/Bruce_Lerman
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The Brunelli Procedure [ 1 ] is a surgical procedure that can be used to correct instability in the wrist . [ 2 ] Instability in the wrist can be caused by a torn Scapholunate ligament . The Brunelli Procedure does not fix the torn ligament. A hole is drilled through the Scaphoid bone and a part of a tendon taken from the patient is put through this hole and attached to the nearby bones. The procedure usually results in reduced movement of the wrist. Instability in the wrist can, over time, lead to wrist osteoarthritis .
This surgery article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/Brunelli_procedure
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Bruns apraxia , or frontal ataxia , is a gait apraxia [ 1 ] found in patients with bilateral frontal lobe disorders . It is characterised by an inability to initiate the process of walking, despite the power and coordination of the legs being normal when tested in the seated or lying position. The gait is broad-based with short steps with a tendency to fall backwards. It was originally described in patients with frontal lobe tumours , but is now more commonly seen in patients with cerebrovascular disease . [ 2 ]
It is named after Ludwig Bruns . [ 3 ] [ 4 ]
Unlike ataxias of cerebellar origin, Bruns apraxia exhibits many frontal lobe ataxia characteristics, with some or all present.
Often patients with frontal lobe ataxia may experience minute cognitive changes that accompany the gait disturbances, such as frontal dementia and presentation of frontal release signs ( Plantar reflex ). Urinary incontinence may also be present. [ 5 ] [ 6 ] Bruns apraxia can be distinguished from Parkinsonian ataxia and cerebellar ataxia in a number of ways. Patients typically afflicted with Parkinsonian ataxia typically have irregular arm swing, a symptom not typically present in frontal ataxia. Walking stride in cerebellar ataxia varies dramatically, accompanied by erratic foot placement and sudden, uncontrolled lurching, not generally characteristic of Bruns apraxia. [ 7 ]
Frontal lobe ataxia is often associated with damage to the frontopontocerebellar tract (Arnold's bundle) that connects the frontal lobe to the cerebellum. This pathway normally sends information from the cortical regions to the cerebellum, particularly information used to initiate planned movement. [ 8 ] Many neurologists describe frontal lobe ataxia as really an apraxia , in which voluntary control of initiating movement is greatly hindered, but normal movement is present when elicited involuntarily or reflexively. [ 9 ] This indicates that cerebellar function is intact and that the presented symptoms of Bruns apraxia are due to damage located within frontal lobe regions and pathways leading from there to the cerebellum. [ 10 ]
Diagnosis consists of a variety of tests, including but not limited to: [ citation needed ]
Treatment consists of physical rehabilitation programs designed to improve overall function, increase strength and improve balance. The ultimate goal is to increase the patient's degree of independence, thus improving the patient's quality of life. Exercise typically begins with simple movements, gradually transitioning into more complex actions. Various aspects of treatment are assessed based on the individual patient's condition, utilizing many assessment tools: [ citation needed ]
Various scales are also utilized
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https://en.wikipedia.org/wiki/Bruns_apraxia
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The buccal branches of the facial nerve (infraorbital branches), are of larger size than the rest of the branches, pass horizontally forward to be distributed below the orbit and around the mouth .
The superficial branches run beneath the skin and above the superficial muscles of the face, which they supply: some are distributed to the procerus , joining at the medial angle of the orbit with the infratrochlear and nasociliary branches of the ophthalmic .
The deep branches pass beneath the zygomaticus and the quadratus labii superioris , supplying them and forming an infraorbital plexus with the infraorbital branch of the maxillary nerve . These branches also supply the small muscles of the nose .
The lower deep branches supply the buccinator and orbicularis oris , and join with filaments of the buccinator branch of the mandibular nerve .
The facial nerve innervates the muscles of facial expression. The buccal branch supplies these muscles
• Puff up cheeks (buccinator)
i. Tap with finger over each cheek to detect ease of air expulsion on the affected side
• Smile and show teeth (orbicularis oris)
This article incorporates text in the public domain from page 905 of the 20th edition of Gray's Anatomy (1918)
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https://en.wikipedia.org/wiki/Buccal_branches_of_the_facial_nerve
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The buccal object/SLOB rule is a method used to determine the relative position of two objects in the oral cavity using projectional dental radiography.
In 1909, Charles A. Clark described a radiographic procedure for localizing impacted teeth to determining their relative antero-posterior position. [ 1 ] If the two teeth (or, by extension, any two objects, such as a tooth and a foreign object) are located in front of one another relative to the x-ray beam, they will appear superimposed on one another on a dental radiograph, but it will be impossible to know which one is in front of the other. To determine which is in front and which is behind, Clark proposed his SLOB rule , as a complicated set of three radiographs, but which can be simplified as follows using just two:
The video below shows a 5 minute illustration describing SLOB rule in dentistry
https://www.youtube.com/embed/AzjvFPlZtZg
In 1952, Richards amended this rule using only 2 radiographs, [ 2 ] [ 3 ] asserting that the object positioned more buccally will move more relative to the object positioned more palatally or lingually.
As a generalization, but not specifically stated as part of Richards' buccal object rule, the more buccal an object is (i.e. the closer it is to the x-ray source) the more it will move in the second radiograph when repositioning the x-ray source.
At the University of Alabama School of Dentistry , this rule is referred to as the BAMA rule : b uccal a lways m oves a way.
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https://en.wikipedia.org/wiki/Buccal_object_rule
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The Bueno-Orovio–Cherry–Fenton model , also simply called Bueno-Orovio model , is a minimal ionic model for human ventricular cells . [ 1 ] It belongs to the category of phenomenological models , because of its characteristic of describing the electrophysiological behaviour of cardiac muscle cells without taking into account in a detailed way the underlying physiology and the specific mechanisms occurring inside the cells. [ 2 ] [ 3 ]
This mathematical model reproduces both single cell and important tissue -level properties, accounting for physiological action potential development and conduction velocity estimations. [ 1 ] It also provides specific parameters choices, derived from parameter-fitting algorithms of the MATLAB Optimization Toolbox , for the modeling of epicardial, endocardial and myd-myocardial tissues. [ 1 ] In this way it is possible to match the action potential morphologies, observed from experimental data, in the three different regions of the human ventricles. [ 1 ] The Bueno-Orovio–Cherry–Fenton model is also able to describe reentrant and spiral wave dynamics, which occurs for instance during tachycardia or other types of arrhythmias . [ 1 ]
From the mathematical perspective, it consists of a system of four differential equations . [ 1 ] One PDE , similar to the monodomain model , for an adimensional version of the transmembrane potential , and three ODEs that define the evolution of the so-called gating variables , i.e. probability density functions whose aim is to model the fraction of open ion channels across a cell membrane . [ 1 ] [ 4 ] [ 2 ]
The system of four differential equations reads as follows: [ 1 ]
where Ω {\displaystyle \Omega } is the spatial domain and T {\displaystyle T} is the final time. The initial conditions are u 0 = 0 {\displaystyle u_{0}=0} , v 0 = 1 {\displaystyle v_{0}=1} , w 0 = 1 {\displaystyle w_{0}=1} , s 0 = 0 {\displaystyle s_{0}=0} . [ 1 ]
H ( x − x 0 ) {\displaystyle H(x-x_{0})} refers to the Heaviside function centered in x 0 {\displaystyle x_{0}} . The adimensional transmembrane potential u {\displaystyle u} can be rescaled in mV by means of the affine transformation V m V = 85.7 u − 84 {\displaystyle V_{mV}=85.7u-84} . [ 1 ] v {\displaystyle v} , w {\displaystyle w} and s {\displaystyle s} refer to gating variables, where in particular s {\displaystyle s} can be also used as an indication of intracellular calcium C a i 2 + {\displaystyle {{Ca}_{i}}^{2+}} concentration (given in the adimensional range [0, 1] instead of molar concentration ). [ 5 ]
All the above-mentioned ionic density currents are partially adimensional and are expressed in 1 seconds {\displaystyle {\dfrac {1}{\text{seconds}}}} . [ 1 ]
Different parameters sets, as shown in Table 1, can be used to reproduce the action potential development of epicardial, endocardial and mid-myocardial human ventricular cells. There are some constants of the model, which are not located in Table 1, that can be deduced with the following formulas: [ 1 ]
where the temporal constants, i.e. τ v − , τ w − , τ s o , τ s , τ o {\displaystyle \tau _{v}^{-},\tau _{w}^{-},\tau _{so},\tau _{s},\tau _{o}} are expressed in seconds, whereas v ∞ {\displaystyle v_{\infty }} and w ∞ {\displaystyle w_{\infty }} are adimensional. [ 1 ]
The diffusion coefficient D {\displaystyle D} results in a value of 1.171 ± 0.221 cm 2 seconds {\displaystyle 1.171\pm 0.221{\dfrac {{\text{cm}}^{2}}{\text{seconds}}}} , which comes from experimental tests on human ventricular tissues. [ 1 ]
In order to trigger the action potential development in a certain position of the domain Ω {\displaystyle \Omega } , a forcing term J app ( x , t ) {\displaystyle J_{\text{app}}({\boldsymbol {x}},t)} , which represents an externally applied density current, is usually added at the right hand side of the PDE and acts for a short time interval only. [ 5 ]
Assume that z {\displaystyle {\boldsymbol {z}}} refers to the vector containing all the gating variables, i.e. z = [ v , w , s ] T {\displaystyle {\boldsymbol {z}}=[v,w,s]^{T}} , and F : R 4 → R 3 {\displaystyle {\boldsymbol {F}}:\mathbb {R} ^{4}\rightarrow \mathbb {R} ^{3}} contains the corresponding three right hand sides of the ionic model. The Bueno-Orovio–Cherry–Fenton model can be rewritten in the compact form: [ 6 ]
Let p ∈ U = H 1 ( Ω ) {\displaystyle p\in U=H^{1}(\Omega )} and q ∈ W = [ L 2 ( Ω ) ] 3 {\displaystyle {\boldsymbol {q}}\in {\boldsymbol {W}}=[L^{2}(\Omega )]^{3}} be two generic test functions. [ 6 ]
To obtain the weak formulation : [ 6 ]
Finally the weak formulation reads:
There are several methods to discretize in space this system of equations, such as the finite element method (FEM) or isogeometric analysis (IGA). [ 7 ] [ 8 ] [ 5 ] [ 6 ]
Time discretization can be performed in several ways as well, such as using a backward differentiation formula (BDF) of order σ {\displaystyle \sigma } or a Runge–Kutta method (RK). [ 7 ] [ 5 ]
Let T h {\displaystyle {\mathcal {T}}_{h}} be a tessellation of the computational domain Ω {\displaystyle \Omega } by means of a certain type of elements (such as tetrahedrons or hexahedra ), with h {\displaystyle h} representing a chosen measure of the size of a single element K ∈ T h {\displaystyle K\in {\mathcal {T}}_{h}} .
Consider the set P r ( K ) {\displaystyle \mathbb {P} ^{r}(K)} of polynomials with degree smaller or equal than r {\displaystyle r} over an element K {\displaystyle K} . Define X h r = { f ∈ C 0 ( Ω ¯ ) : f | K ∈ P r ( K ) ∀ K ∈ T h } {\displaystyle {\mathcal {X}}_{h}^{r}=\{f\in C^{0}({\bar {\Omega }}):f|_{K}\in \mathbb {P} ^{r}(K)\,\,\forall K\in {\mathcal {T}}_{h}\}} as the finite dimensional space, whose dimension is N h = dim ( X h r ) {\displaystyle N_{h}=\dim({\mathcal {X}}_{h}^{r})} .
The set of basis functions of X h r {\displaystyle {\mathcal {X}}_{h}^{r}} is referred to as { ϕ i } i = 1 N h {\displaystyle \{\phi _{i}\}_{i=1}^{N_{h}}} . [ 5 ]
The semidiscretized formulation of the first equation of the model reads: find u h = u h ( t ) = ∑ j = 1 N h u ¯ j ( t ) ϕ j {\displaystyle u_{h}=u_{h}(t)=\sum _{j=1}^{N_{h}}{\bar {u}}_{j}(t)\phi _{j}} projection of the solution u ( t ) {\displaystyle u(t)} on X h r {\displaystyle {\mathcal {X}}_{h}^{r}} , ∀ t ∈ ( 0 , T ) {\displaystyle \forall t\in (0,T)} , such that [ 5 ]
with u h ( 0 ) = ∑ j = 1 N h ( ∫ Ω u 0 ϕ j d Ω ) ϕ j {\displaystyle u_{h}(0)=\sum _{j=1}^{N_{h}}\left(\int _{\Omega }u_{0}\phi _{j}\,d\Omega \right)\phi _{j}} , z h = z h ( t ) = [ v h ( t ) , w h ( t ) , s h ( t ) ] T {\displaystyle {\boldsymbol {z}}_{h}={\boldsymbol {z}}_{h}(t)=[v_{h}(t),w_{h}(t),s_{h}(t)]^{T}} semidiscretized version of the three gating variables, and J ion ( u h , z h ) = J f i ( u h , z h ) + J s o ( u h , z h ) + J s i ( u h , z h ) {\displaystyle J_{\text{ion}}(u_{h},{\boldsymbol {z}}_{h})=J_{fi}(u_{h},{\boldsymbol {z}}_{h})+J_{so}(u_{h},{\boldsymbol {z}}_{h})+J_{si}(u_{h},{\boldsymbol {z}}_{h})} is the total ionic density current. [ 5 ]
The space discretized version of the first equation can be rewritten as a system of non-linear ODEs by setting U h ( t ) = { u ¯ j ( t ) } j = 1 N h {\displaystyle {\boldsymbol {U}}_{h}(t)=\{{\bar {u}}_{j}(t)\}_{j=1}^{N_{h}}} and Z h ( t ) = { z ¯ j ( t ) } j = 1 N h {\displaystyle {\boldsymbol {Z}}_{h}(t)=\{{\bar {\boldsymbol {z}}}_{j}(t)\}_{j=1}^{N_{h}}} : [ 5 ]
where M i j = ∫ Ω ϕ j ϕ i d Ω {\displaystyle \mathbb {M} _{ij}=\int _{\Omega }\phi _{j}\phi _{i}\,d\Omega } , K i j = ∫ Ω D ∇ ϕ j ⋅ ∇ ϕ i d Ω {\displaystyle \mathbb {K} _{ij}=\int _{\Omega }D\nabla \phi _{j}\cdot \nabla \phi _{i}\,d\Omega } and ( J ion ( U h ( t ) , z h ( t ) ) ) i = ∫ Ω J ion ( u h , z h ) ϕ i d Ω {\displaystyle \left({\boldsymbol {J}}_{\text{ion}}({\boldsymbol {U}}_{h}(t),{\boldsymbol {z}}_{h}(t))\right)_{i}=\int _{\Omega }J_{\text{ion}}(u_{h},{\boldsymbol {z}}_{h})\phi _{i}\,d\Omega } . [ 5 ]
The non-linear term J ion ( U h ( t ) , Z h ( t ) ) {\displaystyle {\boldsymbol {J}}_{\text{ion}}({\boldsymbol {U}}_{h}(t),{\boldsymbol {Z}}_{h}(t))} can be treated in different ways, such as using state variable interpolation (SVI) or ionic currents interpolation (ICI). [ 9 ] [ 10 ] In the framework of SVI, by denoting with { x s K } s = 1 N q {\displaystyle \{{\boldsymbol {x}}_{s}^{K}\}_{s=1}^{N_{q}}} and { ω s K } s = 1 N q {\displaystyle \{\omega _{s}^{K}\}_{s=1}^{N_{q}}} the quadrature nodes and weights of a generic element of the mesh K ∈ T h {\displaystyle K\in {\mathcal {T}}_{h}} , both u h {\displaystyle u_{h}} and z h {\displaystyle {\boldsymbol {z}}_{h}} are evaluated at the quadrature nodes: [ 5 ]
The equations for the three gating variables, which are ODEs, are directly solved in all the degrees of freedom (DOF) of the tessellation T h {\displaystyle {\mathcal {T}}_{h}} separately, leading to the following semidiscrete form: [ 5 ]
With reference to the time interval ( 0 , T ] {\displaystyle (0,T]} , let Δ t = T N {\displaystyle \Delta t={\dfrac {T}{N}}} be the chosen time step, with N {\displaystyle N} number of subintervals. A uniform partition in time [ t 0 = 0 , t 1 = Δ t , … , t k , … , t N − 1 , t N = T ] {\displaystyle [t_{0}=0,t_{1}=\Delta t,\ldots ,t_{k},\ldots ,t_{N-1},t_{N}=T]} is finally obtained. [ 7 ]
At this stage, the full discretization of the Bueno-Orovio ionic model can be performed both in a monolithic and segregated fashion. [ 11 ] With respect to the first methodology (the monolithic one), at time t = t k {\displaystyle t=t^{k}} , the full problem is entirely solved in one step in order to get ( U h k + 1 , Z h k + 1 ) {\displaystyle ({\boldsymbol {U}}_{h}^{k+1},{\boldsymbol {Z}}_{h}^{k+1})} by means of either Newton method or Fixed-point iterations : [ 11 ]
where U ext , h k {\displaystyle {\boldsymbol {U}}_{{\text{ext}},h}^{k}} and Z ext , h k {\displaystyle {\boldsymbol {Z}}_{{\text{ext}},h}^{k}} are extrapolations of transmembrane potential and gating variables at previous timesteps with respect to t k + 1 {\displaystyle t^{k+1}} , considering as many time instants as the order σ {\displaystyle \sigma } of the BDF scheme. α {\displaystyle \alpha } is a coefficient which depends on the BDF order σ {\displaystyle \sigma } . [ 11 ]
If a segregated method is employed, the equation for the evolution in time of the transmembrane potential and the ones of the gating variables are numerically solved separately: [ 11 ]
Another possible segregated scheme would be the one in which U h k + 1 {\displaystyle {\boldsymbol {U}}_{h}^{k+1}} is calculated first, and then it is used in the equations for Z h k + 1 {\displaystyle {\boldsymbol {Z}}_{h}^{k+1}} . [ 11 ]
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https://en.wikipedia.org/wiki/Bueno-Orovio–Cherry–Fenton_model
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Bulbar palsy refers to a range of different signs and symptoms linked to impairment of function of the glossopharyngeal nerve (CN IX), the vagus nerve (CN X), the accessory nerve (CN XI), and the hypoglossal nerve (CN XII). It is caused by a lower motor neuron lesion in the medulla oblongata , or from lesions to these nerves outside the brainstem , and also botulism . This may be caused by any of a number of genetic, vascular, degenerative, inflammatory, and other underlying conditions. It can be differentiated from pseudobulbar palsy . When there is airway obstruction , intubation is used.
In addition, there may be lower motor neuron lesions of the limbs.
The ocular muscles are spared and this differentiates it from myasthenia gravis .
Bulbar palsy involves problems with function of the glossopharyngeal nerve (CN IX), the vagus nerve (CN X), the accessory nerve (CN XI), and the hypoglossal nerve (CN XII). [ 1 ] These all emerge from pathways in the medulla oblongata . [ 1 ] A lower motor neuron lesion can impair their function. [ 5 ] [ 1 ]
In contrast, pseudobulbar palsy is a clinical syndrome similar to bulbar palsy but in which the damage is located in upper motor neurons of the corticobulbar tracts in the mid-pons (i.e., in the cranial nerves IX-XII), that is the nerve cells coming down from the cerebral cortex innervating the motor nuclei in the medulla. This is usually caused by stroke .
In patients with airway obstruction due to bulbar palsy, intubation may be used. [ 2 ] This can be tracheal intubation or supraglottal intubation. [ 2 ]
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https://en.wikipedia.org/wiki/Bulbar_palsy
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A bulldog forceps , clamp or serrefine is a type of forceps which is used in surgery . It has serrated jaws and a spring action so that it will grip and hold sutures , tissues or vessels. The spring may be weak or the jaws sheathed in a soft material so that the item being gripped is not crushed too severely.
Forceps of this general type were designed by particular surgeons including Johann Dieffenbach and Robert Liston . [ 1 ] [ 2 ]
This article related to medical equipment is a stub . You can help Wikipedia by expanding it .
This surgery article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/Bulldog_forceps
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The Bundeswehr Institute of Microbiology (IMB, military abbreviation InstMikroBioBw) in Munich is the German Armed Forces' scientific competence center in the field of medical defense against biological warfare agents and other dangerous pathogens or biotoxins . The institute provides procedures and methods for the rapid and unambiguous identification and verification of allegations of the use of biological warfare agents, conducts specialized training, and participates in the development of medical biodefense concepts and strategies.
The institute was established in 1966 as the Microbiology Laboratory Group at the Medical Corps School of the Bundeswehr (now: Bundeswehr Medical Academy ) in Munich. In 1984, today's Bundeswehr Institute of Microbiology was officially founded as an independent military unit. It has been stationed in the Ernst-von-Bergmann barracks in the north of Munich ever since.
In response to the September 11 attacks in 2001, the German Council of Science and Humanities recommended that the Bundeswehr Institute of Microbiology be developed into a national military competence center for biodefense. [ 1 ]
The institute provides medical diagnostics for biological warfare agents and naturally occurring infectious agents of military importance for all members of the Bundeswehr. These services include infectious agents of biological risk groups 3 and 4 and are also available to civilian healthcare facilities. In September 2012, the Central Diagnostic Department (ZBD) of the Institute was flexibly accredited by the German Accreditation Body according to ISO 15189 .
In August 2002, along with the Bundeswehr Institute of Radiobiology and the Bundeswehr Institute of Pharmacology and Toxicology, the institute became an independent entity under the Central Medical Service of the Bundeswehr and was placed under the supervision of the Bundeswehr Medical Office. Since 2012, all three institutes have once again been under the military command of the Medical Academy, but now as independent military units at battalion level.
Since 2010, the institute, together with the Technical University of Munich , the Ludwig Maximilian University of Munich , and the Helmholtz Zentrum München , forms the partner site in Munich of the German Center for Infection Research (DZIF). In February 2013, the cooperation with the Institute of Microbiology, Immunology, and Hygiene and the Institute of Virology of the TU Munich began. In 2016, a cooperation agreement was signed with the University of Stuttgart-Hohenheim . [ 2 ]
Since 2009, the Medical Biodefense Conference [ 3 ] has been organized in the format of an international conference. [ 4 ]
The Bundeswehr Institute for Microbiology has been leading the development of a modular and rapidly deployable mobile laboratory system for the German Armed Forces since 2007. The institute's mobile lab systems are crafted to deliver a prompt response to sudden disease outbreaks, featuring adaptable configurations and cutting-edge biosafety measures. [ 5 ] The incorporation of a collapsible glove box with sturdy polycarbonate walls [ 6 ] ensures a secure working environment for handling highly infectious samples. Leveraging diagnostic technologies like qPCR, ELISA , and NGS , the system aims for expeditious turnaround times in sample analysis. With minimal infrastructure requirements, it can be rapidly deployed worldwide and utilized across diverse environments. Following initial deployments in the Balkans, the mobile laboratory seamlessly integrated into the European Mobile Lab Project (EMLab) from 2013. Remarkably, these systems played a pivotal role during the 2014 Ebola outbreak in West Africa and are now acknowledged as a global technical standard for diagnostic field operations in combating disease outbreaks. [ 7 ]
The Bundeswehr Institute of Microbiology reached a significant milestone during the COVID-19 pandemic . [ 8 ] On January 27, 2020, researchers at the institute diagnosed the first cases of illness caused by the SARS-CoV-2 virus in Germany, marking a pivotal early detection in the laboratory. [ 9 ] Notably, the institute successfully cultured the virus in cell cultures, achieving a feat previously only accomplished by Australian researchers outside of China. [1] Furthermore, the research group sequenced the genome of SARS-CoV-2, providing comprehensive insights beyond the partial information available from Chinese online transmissions. The institute offered the initial description of the replication of SARS-CoV-2 in the nasal and throat cavity and the excretion of the virus in the stool. [ 10 ]
On May 19, 2022, amidst the largest outbreak of mpox in Europe to date, the Bundeswehr Institute of Microbiology confirmed the first case of mpox in Germany. [ 11 ]
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https://en.wikipedia.org/wiki/Bundeswehr_Institute_of_Microbiology
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A bundle branch block is a partial or complete interruption in the flow of electrical impulses in either of the bundle branches of the heart's electrical system . [ 1 ]
The heart's electrical activity begins in the sinoatrial node (the heart's natural pacemaker ), which is situated on the upper right atrium . The impulse travels next through the left and right atria and summates at the atrioventricular node . From the AV node the electrical impulse travels down the bundle of His and divides into the right and left bundle branches . The right bundle branch contains one fascicle . The left bundle branch subdivides into two fascicles: the left anterior fascicle , and the left posterior fascicle . Other sources divide the left bundle branch into three fascicles: the left anterior, the left posterior, and the left septal fascicle. The thicker left posterior fascicle bifurcates, with one fascicle being in the septal aspect. Ultimately, the fascicles divide into millions of Purkinje fibres , which in turn interdigitate with individual cardiac myocytes, allowing for rapid, coordinated, and synchronous physiologic depolarization of the ventricles. [ citation needed ]
When a bundle branch or fascicle becomes injured (by underlying heart disease , myocardial infarction , or cardiac surgery), it may cease to conduct electrical impulses appropriately. This results in altered pathways for ventricular depolarization. Since the electrical impulse can no longer use the preferred pathway across the bundle branch, it may move instead through muscle fibers in a way that both slows the electrical movement and changes the directional propagation of the impulses. As a result, there is a loss of ventricular synchrony, ventricular depolarization is prolonged, and there may be a corresponding drop in cardiac output. When heart failure is present, a specialized pacemaker may be used to resynchronize the ventricles. In theory a pacemaker like this will shorten the QRS interval, thus bringing the timing of contraction of the left and right ventricles closer together and slightly increasing the ejection fraction . [ citation needed ]
A bundle branch block can be diagnosed when the duration of the QRS complex on the ECG exceeds 120 ms. A right bundle branch block typically causes prolongation of the last part of the QRS complex and may shift the heart's electrical axis slightly to the right. The ECG will show a terminal R wave in lead V1 and a slurred S wave in lead I.
Left bundle branch block widens the entire QRS, and in most cases shifts the heart's electrical axis to the left. The ECG will show a QS or rS complex in lead V1 and a monophasic R wave in lead I. Another normal finding with bundle branch block is appropriate T wave discordance. In other words, the T wave will be deflected opposite the terminal deflection of the QRS complex.
Bundle branch block, especially left bundle branch block, can lead to cardiac dyssynchrony. The simultaneous occurrence of left and right bundle branch block leads to total AV block.
Depending on the anatomical location of the defect which leads to a bundle branch block, the blocks are further classified into:
The left bundle branch block can be further sub classified into:
Other classifications of bundle branch blocks are;
A simple way to quickly differentiate between the two types is to note the deflection of the QRS complex in the V1 lead. A (V1) QRS segment deflected down indicates left bundle branch block, while a deflection up indicates right bundle branch block. In both types, the QRS is wide (> 0.12 seconds).
Some people with bundle branch blocks are born with this condition. Many others acquire it as a consequence of heart disease. People with bundle branch blocks may still be quite active, and may have nothing more remarkable than an abnormal appearance to their ECG. However, when bundle blocks are complex and diffuse in the bundle systems, or are associated with additional and significant ventricular muscle damage, they may be a sign of serious underlying heart disease. In more severe cases, a pacemaker may be required to restore an optimal electrical supply to the heart muscle. [ citation needed ]
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The bundle of His ( BH ) [ 1 ] : 58 or His bundle ( HB ) [ 1 ] : 232 ( / h ɪ s / "hiss" [ 2 ] ) is a collection of heart muscle cells specialized for electrical conduction . As part of the electrical conduction system of the heart , it transmits the electrical impulses from the atrioventricular node (located between the atria and the ventricles ) to the point of the apex of the fascicular branches via the bundle branches . The fascicular branches then lead to the Purkinje fibers , which provide electrical conduction to the ventricles, causing the cardiac muscle of the ventricles to contract at a paced interval.
The bundle of His is an important part of the electrical conduction system of the heart , as it transmits impulses from the atrioventricular node, located at the anterior-inferior end of the interatrial septum , to the ventricles of the heart. The bundle of His branches into the left and the right bundle branches , which run along the interventricular septum . The left bundle branch further divides into the left anterior fascicle and the left posterior fascicle . These bundles and fascicles give rise to thin filaments known as Purkinje fibers . These fibers distribute the impulse to the ventricular muscle. The ventricular conduction system comprises the bundle branches and the Purkinje networks. It takes about 0.03–0.04 seconds for the impulse to travel from the bundle of His to the ventricular muscle .
Disorders affecting the cardiomyocytes that make up the electrical conduction system of the heart are called heart blocks . Heart blocks are separated into different categories based on the location of the cellular damage. Damage to any of the conducting cells in or below the bundle of His is collectively referred to as "infra-Hisian blocks". To be specific, blocks that occur in the right or left bundle branches are called " bundle branch blocks ", and those that occur in either the left anterior or the left posterior fascicles are called "fascicular blocks", or "hemiblocks". The conditions in which both the right bundle branch and either the left anterior fascicle or the left posterior fascicle are blocked are collectively referred to as bifascicular blocks , and the condition in which the right bundle branch, the left anterior fascicle, and the left posterior fascicle are blocked is called trifascicular block . Infra-hisian blocks limit the heart's ability to coordinate the activities of the atria and ventricles, which usually results in a decrease in its efficiency in pumping blood.
A 2000 study found that direct His bundle pacing is more effective in producing synchronized ventricular contraction—and therefore in improving cardiac function—than apical pacing. [ 3 ]
These specialized muscle fibers in the heart were named after the Swiss cardiologist Wilhelm His Jr. , who discovered them in 1893. [ 4 ] [ 5 ]
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The Burns Archive is the world’s largest private collection of early medical photography and historic photographs , housing over one million photographs. While it primarily contains images related to medical practises, it is also famous for photographs depicting 'the darker side of life'. [ 1 ] Other themes prevalent throughout the collection involve death, crime, racism, and war. [ 2 ] [ 3 ]
Known as one of the world’s most important repositories of early medical history, [ 2 ] images of “the darker side of life” make up the collection: [ 4 ] anatomical and medical oddities , memorial and post-mortem photography , and original historic photographs depicting death, disease, disaster, crime, racism, revolution, riots, and war. [ 4 ] The collection traces the history of photography , from its beginnings in 1839 to the 1950s, and includes hundreds of thousands of Daguerreotypes , ambrotypes , tintypes , [ 5 ] carte de visites , and hand-colored photographs. [ 6 ] The Burns Archive actively acquires, donates, researches, lectures, exhibits, consults, [ 7 ] and shares its rare and unusual [ 8 ] photographs and expertise worldwide.
The Archive’s medical collection houses photographs in the categories of pioneers and innovators, operative scenes, therapy and treatments, disease and pathology, medical specialties, interesting cases and medical curiosities, hospitals and wards, nursing, alternative practitioners, anatomy and education, laboratories and doctors’ offices, medicine and war, and more. [ 9 ] Many of these collected pictures allowed the medical community of the era to share knowledge and define pathology. [ 10 ] The Archive's historical collection ranges from categories of death and memorial, war and conflict, and crime and punishment, to occupations and industry, social and cultural history, photographic history, Judaica, Egyptology, ethnology, folk, and African American history. [ 5 ] [ 9 ] The collection has been featured in over 100 exhibitions [ 11 ] at museums and galleries worldwide, including New York’s Metropolitan Museum of Art and Paris' Musée d'Orsay , [ 12 ] and has donated thousands of images to institutions, including The Smithsonian Institution , the Museum of Modern Art , and the J. Paul Getty Museum . [ 13 ]
Having written over 1,100 articles and over 40 books, the Burns Archive has published photographic historic texts [ 14 ] ranging from Victorian era funeral portraits to early oncology . [ 15 ] Dr. Burns authored Sleeping Beauty: Memorial Photography In America , and Forgotten Marriage: The Painted Tintype & The Decorative Frame, 1860–1910, A Lost Chapter in American Portraiture , which both received the American Photographic Historical Society's award for the best publication of their kind, an honor never before bestowed on one author. [ 16 ] Sleeping Beauty (disambiguation) was praised by Pulitzer Prize winning author, John Updike , in the American Heritage (magazine) article he wrote on the book. [ 17 ] Burns Archive Creative Director, Elizabeth A. Burns, co-authored various books with Dr. Burns, including Sleeping Beauty II: Grief, Bereavement & the Family, American and European Traditions , as well as Geisha: A Photographic History, 1872–1912 , and Stiffs, Skulls, and Skeletons , released in 2014 from Schiffer Publishing . [ 18 ] [ 19 ]
Images from the Burns Archive have been a major source for various documentaries ( Ken Burns , the History channel , PBS American Experience ), television series ( NBC ’s Hannibal , HBO ’s Autopsy , Travel Channel ’s Mysteries at the Museum , Cinemax 's The Knick ), and feature films ( The Silence of the Lambs , Gangs of New York , The Others ), and has inspired artists from Joel Peter Witkin to makeup artists for Jacob's Ladder . [ 20 ] [ 21 ]
Stanley B. Burns MD, Elizabeth A. Burns, and The Burns Archive, serve as the medical, historical and technical advisers for Steven Soderbergh ’s period medical Cinemax series, The Knick , starring Clive Owen . [ 21 ] The Knick looks at the professional and personal lives of Dr. John W. Thackery (played by Owen) and the staff at New York's Knickerbocker Hospital during the early part of the twentieth century. The Archive was instrumental in the recreation of turn-of-the-century medicine, [ 21 ] as Dr. Burns worked closely with production and the actors to make the hospital scenes realistic and authentic to the period. [ 22 ] [ 23 ] Dr. Burns provided immersive tutorials in the world of early-20th-century surgery, complete with hands-on practice. [ 24 ] The Archive's extensive photographic record of medical history served as comprehensive resources for procedures [ 25 ] and became important references for everything from the antiseptic atomizers in the operating theater to an early X-ray machine, to the prosthetic worn by a recurring character. [ 26 ]
In 2020 the Harvey Cushing/John Hay Whitney Medical Library at Yale acquired 15,400 photographs from The Burns Archive. [ 27 ] [ 28 ] The photographs are now held in the Stanley B. Burns, M.D., historic medical photography collection .
Dr. Stanley B. Burns, the Archive’s Founder, is a New York City ophthalmologist who acquired his first medical photograph in 1975 and established the Burns Archive in 1977. [ 18 ] The Archive began receiving recognition in 1978, when a selection of its 19th and 20th century photographs were featured in the Time Life Encyclopedia of Collectibles entry on photographs. [ 29 ] The Archive was called “one of the world’s most important repositories of early medical history” by The New York Times , [ 30 ] “the world’s greatest collection of early medical photography” by New York (magazine) , “one of the six most important collections in the world” by Aperture (magazine) , “one of America’s Top 100 Collectors” by Art and Antiques Magazine , and “the most important privately held photo archive in the world” by New York’s The Village Voice . [ 20 ]
The Burns Archive, through Burns Archive Press and other publishers, has published over 40 books in 40 years, including: [ 15 ] [ 31 ]
The Burns Archive has contributed images, as well as consulting and advisory services to various feature films, including: [ 32 ]
The Burns Archive has contributed images, as well as consulting and advisory services, to various documentaries and television series, including: [ 32 ]
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Burst suppression is an electroencephalography (EEG) pattern that is characterized by periods of high-voltage electrical activity alternating with periods of no activity in the brain. The pattern is found in patients with inactivated brain states, such as from general anesthesia , coma , or hypothermia . [ 1 ] This pattern can be physiological, as during early development, or pathological, as in diseases such as Ohtahara syndrome . [ 2 ]
The burst suppression pattern was first observed by Derbyshire et al. while studying effects of anesthetics on feline cerebral cortices in 1936, where the researchers noticed mixed slow and fast electrical activity with decreasing amplitude as anesthesia deepened. [ 3 ] In 1948, Swank and Watson coined the term "burst-suppression pattern" to describe the alternation of spikes and flatlines in electrical activity in deep anesthesia. [ 4 ] It wasn't until after the early 1960s that the burst suppression pattern began being used in medical settings; it had been primarily observed in animal studies and psychosurgeries . [ 5 ]
A paper published in 2023 showed that burst suppression and epilepsy may share the same ephaptic coupling mechanism. [ 6 ] When inhibitory control is sufficiently low, as in the case of certain general anesthetics such as sevoflurane (due to a decrease in the firing of interneurons [ 7 ] ), electric fields are able to recruit neighboring cells to fire synchronously, in a burst suppression pattern. This same mechanism also underlies epileptic bursts, but the magnitude of bursts is comparatively weaker in burst suppression, as the neuronal network still retains partial inhibitory control under the effects of anesthesia.
The pseudo-rhythmic pattern of burst suppression is dictated by extracellular calcium depletion and the ability of neurons to restore the concentration. [ 4 ] Bursts are accompanied by depletion of extracellular cortical calcium ions to levels that inhibit synaptic transmission , which leads to suppression periods. [ 4 ] During suppression, neuronal pumps restore the calcium ion concentrations to normal levels, thus causing the cortex to be subject to the process again. [ 4 ] As the brain becomes more inactive, burst periods become shorter and suppression periods become longer. [ 8 ] The shortening of bursts and lengthening of suppression is caused by the central nervous system's inability to properly regulate calcium levels due to increased blood–brain permeability . [ 8 ]
At the cellular level, hyperpolarization of the membrane potential of cortical neurons reliably precedes any overt electroencephalographic activity of burst suppression. [ 9 ] This hyperpolarization, which has been attributed to an increase in neuronal membrane potassium conductance, [ 9 ] has been hypothesized to play a major role in the induction of burst suppression, supported by the induction of burst suppression through the application of a direct acting GABA A agonist , muscimol . [ 5 ] In contrast, inhibition is diminished when burst suppression is induced through the use of isoflurane . [ 10 ] Another theory is that alterations in brain metabolism regulate activity dependent slow modulation of ATP -gated potassium channel conductance which induces burst suppression. [ 1 ] However, modulating inhibitory activity alone may not be sufficient for burst suppression, and modulation in excitatory synaptic efficiency, stemming from the depletion and subsequent recovery of interstitial calcium levels, could contribute to the induction of burst suppression. [ 5 ]
Burst episodes are associated with excitatory activity in cortical neurons. [ 11 ] Suppression is caused by the absence of synaptic activity of cortical neurons; however, some thalamocortical neurons exhibit oscillations in the delta frequency range during these periods. [ 9 ] The burst suppression pattern varies with the brain anesthetic concentration when pharmacologically inducing coma. [ 12 ] Level of suppression is adjustable by decreasing or increasing anesthetic infusion rate, thus adjusting the level of inactivation. [ 13 ]
While burst suppression has typically been viewed as a homogeneous brain state, recent studies have shown that bursts and suppressions can occur in specific regions while other regions are unaffected. [ 14 ] The fact that the burst suppression pattern persists after a patient undergoes cortical deafferentation indicates that burst suppression represents an intrinsic dynamic mode of cortex. [ 5 ] Even when a burst appears to be homogeneous across the brain, the timing of the bursts in different regions may differ. [ 14 ]
Burst suppression patterns can be classified through comparisons of burst duration and inter-burst intervals, maximum peak to peak voltage, and the ratio of power in high versus low frequencies. (Akrawi et al., 1996) [ 15 ] Burst suppression with identical bursts suggests a deterministic process of burst generation, whereas other burst suppression patterns depend on stochastic processes . [ 2 ] Burst suppression with identical bursts is a distinct pathological EEG pattern that is typical in diffuse cerebral ischemia and is associated with poor outcomes in comatose patients after cardiac arrest. [ 2 ]
Bursts are identifiable on EEG readings by their high amplitude (75-250μV), typically short period of 1–10 seconds, and have frequency ranges of 0–4 Hz ( δ ) and 4–7 Hz ( θ ). [ 16 ] Suppression episodes are identifiable by their low amplitude (< 5μV) and typically long period (> 10s). [ 16 ]
EEG recordings of burst-suppression pattern differ between adults and neonates because of diverse pattern fluctuations found in the EEG of neonates. [ 16 ] These fluctuations, along with sudden changes in synchronous neuron firing, are caused by development of the newborn's brain. [ 16 ] Burst suppression patterns also occur spontaneously during neonatal development, rather than as a characteristic of inactivated brains as in adults. [ 12 ]
In order to quantify the burst suppression pattern, the EEG signal must be subject to segmentation. [ 17 ] The first segmentation used a fixed voltage-threshold, and various methods for segmentation or burst detection have developed in time domain, [ 12 ] frequency (Fourier) domain, and both. [ 18 ] These processes separates burst and suppression episodes based on EEG features such as entropies, non-linear-energy-operator, voltage variance, or adaptation of constant false alarm rate (CFAR) algorithm, [ 19 ] etc. When the features represent distinguishable patterns of burst and suppression, a fixed threshold using ROC-curve or machine learning methods [ 18 ] are used for segmentation.
Quantifying the burst suppression pattern allows for calculation of the burst suppression ratio (BSR) by assigning binary values of 0 to bursts and 1 to suppression episodes. [ 17 ] Thus, a burst suppression ratio of 1 is associated with a state of the brain that shows no electrical activity, while a ratio of 0 indicates that the brain is active. The burst suppression ratio measures the amount of time within an interval spent in the suppressed state. [ 12 ] This ratio increases as the brain becomes increasingly inactive until the brain's EEG signal flatlines , represented by a burst suppression ratio equal to 1. [ 20 ] Because of the direct relationship between burst suppression ratio and brain inactivity, the ratio is an indicator of suppression intensity. [ 12 ]
Using the same binary assignments to the burst suppression pattern, another measure of the depth of burst suppression, the burst suppression probability (BSP), can be determined. [ 12 ] Mathematically, the instantaneous probability of being suppressed, is
BSR = (Total time of suppression/epoch length) × 100%. [ 20 ] where x i is the brain's suppression state at time i Δ, with Δ representing intervals for analysis, and ranges across all real numbers. [ 17 ]
Because the burst suppression pattern is characteristic of inactivated brains, the pattern can be used as a marker for the level of coma a patient is in, with persistence of the pattern commonly associated with poor prognosis. [ 17 ] Note, however, that there is evidence linking sedation-induced burst suppression with positive outcomes in patients recovering from coma following traumatic brain injury, suggesting a neuroprotective effect. [ 21 ] When inducing coma to protect the brain post trauma, the pattern assists in maintaining the necessary level of coma so that no further damage occurs to the brain. [ 13 ] The pattern is also used to test the ability of anesthetic arousal agents to induce emergence from comas. [ 17 ] The burst suppression pattern can also be used to track ascent into and descent out of hypothermia through observing changes in the pattern. [ 17 ]
Monitoring the burst suppression ratio aids medical personnel in adjusting suppression intensity for therapeutic purposes; however, medical personnel currently rely on visually monitoring the EEG and arbitrarily assessing the depth of burst suppression. [ 12 ] Not only is the evaluation of the EEG signal for burst suppression done manually, but also the infusion rate of anesthetic to adjust suppression intensity. [ 13 ] The introduction of machines makes maintaining proper levels of inactivity more precise through the use of algorithms. This is done through the use of measures such as burst suppression probability [ 12 ] for real-time tracking of burst suppression or brain–machine interfaces to automate maintaining proper levels of inactivity. [ 13 ]
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Gluteoplasty (from Greek : gloutós γλουτός , 'rump' + plastos πλαστός , 'shaped, formed, moulded') denotes the plastic surgery and the liposuction procedures for the correction of congenital , traumatic , and acquired defects/deformities of the buttocks and the anatomy of the gluteal region; and for the aesthetic enhancement (by augmentation or by reduction) of the contour of the buttocks . [ 1 ]
The procedures for buttock augmentation and buttock repair include the surgical emplacement of a gluteal implant (buttock prosthesis); liposculpture (fat transfer and liposuction ); and body contouring (surgery, liposculpture, and Sculptra injections) to resolve the patient's particular concern or deformity of the gluteal region.
The functional purpose of the buttocks musculature is to establish a stable gait (balanced walk) for the person who requires the surgical correction of either a defect or a deformity of the gluteal region; therefore, the restoration of anatomic functionality is the therapeutic consideration that determines which gluteoplasty procedure will effectively correct the damaged muscles of the buttocks. The applicable techniques for surgical and correction include the surgical emplacement of gluteal implants; autologous tissue-flaps ; the excision (cutting and removal) of damaged tissues; lipoinjection augmentation; and liposuction reduction—to resolve the defect or deformity caused by a traumatic injury ( blunt , penetrating , blast ) to the buttocks muscles ( gluteus maximus , gluteus medius , gluteus minimus ), and any deformation of the anatomic contour of the buttocks. Likewise, the corrective techniques apply to resolving the sagging skin of the body, and the muscle and bone deformities presented by the formerly obese patient, after a massive weight loss (MWL) bariatric surgery procedure; and for resolving congenital defects and congenital deformities of the gluteal region. [ 2 ]
Anatomically, the mass of each buttock principally comprises two muscles—the gluteus maximus muscle and the gluteus medius muscle —which are covered by a layer of adipose body fat . The upper aspects of the buttocks end at the iliac crest (the upper edges of the wings of the ilium , and the upper lateral margins of the greater pelvis ), and the lower aspects of the buttocks end at the horizontal gluteal crease , where the buttocks anatomy joins the rear, upper portion of the thighs. The gluteus maximus muscle has two points of insertion: (i) the one-third superior portion of the (coarse line) linea aspera of the thigh bone ( femur ), and (ii) the superior portion of the iliotibial tract (a long, fibrous reinforcement of the deep fascia lata of the thigh). The left and the right gluteus maximus muscles (the butt cheeks) are vertically divided by the intergluteal cleft (the butt-crack) which contains the anus . [ 2 ]
The gluteus maximus muscle is a large and very thick muscle (6–7 cm) located on the sacrum , which is the large, triangular bone located at the base of the vertebral column , and at the upper- and back-part of the pelvic cavity , where it is inserted (like a wedge) between the two hip bones . The upper part of the sacrum is connected to the final lumbar vertebra (L5), and to the bottom of the coccyx (tailbone). At its origin, the gluteus maximus muscle extends to include parts of the iliac bone , the sacrum, the coccyx, the sacrosciatic ligament, and the tuberosity of the ischium . [ 3 ]
Like every pelvic-area muscle, the gluteus maximus muscle originates from the pelvis; nonetheless, it is the sole pelvic muscle not inserted to the trochanter (head of the femur), and is approximately aligned to the femur and the fascia lata (the deep fascia of the thigh); the tissues of the gluteus maximus muscle cover only the rear, lateral face of the trochanter, and there form a bursa (purse) that faces the interior of the thigh . [ 4 ]
The motor innervation of the gluteus maximus muscle is performed by the inferior gluteal nerve (a branch nerve of the sacral plexus ) and extends from the pelvis to the gluteal region, then traverses the greater sciatic foramen (opening) from behind and to the middle to then join the sciatic nerve . The inferior gluteal nerve divides into three collateral branches: (i) the gluteus branch , (ii) the perineal branch , and (iii) the femoral branch . The first ramification—the gluteus branch—is a branch nerve that is very close to the emergence of the inferior gluteal nerve to the area, next to the inferior border of the pyramidalis muscle . [ 5 ]
In surgical and body contouring praxis, the plastic surgeon creates the implant-pocket —either for the gluteal prosthesis or for the injections of autologous fat—by undermining the gluteus maximus muscle with a dissection technique that avoids the sacrum , the sacrotuberous ligament , and the tuberosity of the ischium ; which, if accidentally cut, might isolate the posterior (back) portion of the muscle and lead to denervation, the loss of nerve function and of innervation. [ 4 ] [ 6 ]
The superior gluteal artery , the inferior gluteal artery , the superior gluteal veins , and the inferior gluteal veins irrigate the gluteus maximus muscle with arterial and venous blood. The vascularization, the entrance of the blood vessels to the muscle tissues, occurs at the anterior (front) face of the muscle, very close to the sacrum . As the arteries and the veins enter the mass of the gluteal muscle, they divide into narrower blood-vessel ramifications (configured like the horizontal branches of a tree), most of which travel parallel to the muscle fibres. [ 7 ]
In surgical and body contouring praxis, the plastic surgeon effects the implant-pocket undermining of the gluteus maximus muscle by carefully separating the muscle fibres to avoid severing the pertinent blood vessels, which would interfere with the blood irrigation of the muscle tissue. Therefore, to create an implant-pocket, either for a gluteal prosthesis or for lipoinjection, a low-angle muscle-dissection is performed in order to avoid the risk of severing any major branch— superior or inferior —of the gluteal artery, which travels very close to the sacrum and to the sacrotuberous ligament . [ 4 ]
While the resolution of the defects and deformities of the gluteal region can be realized surgically, the assessment of the degree of severity of the injury organizes treatment therapies into three types: (i) buttocks augmentation, (ii) buttocks reduction, and (iii) contour irregularity treatments that combine surgery and liposculpture ( liposuction and fat-injection). [ 2 ]
The augmentation of the buttocks is realized with a gluteal implant , which is emplaced under each gluteus maximus muscle ; the insertion of the buttock prosthesis is through a midline incision (5–8-cm-wide) over the tailbone ( coccyx ). Augmentation with a gluteal implant is the method most effective for enlarging the buttocks of a patient whose body possesses few stores of excess adipose fat in the lower portion of the trunk, the buttocks and thighs , the anatomic regions where the human body usually stores excess body fat. Post-operatively, because of the cutting (incising) into the flesh of the tailbone muscles, the full healing of the augmented tissues can be approximately 6–8 months, in the course of which the gluteal-muscle tissues relax, and the settled buttocks prostheses are integrated to the gluteal region. [ 8 ] The implantation procedure can be performed upon a patient who is either sedated or anaesthetized , either under general anaesthesia or under local anaesthesia . The usual operating-room time for a buttocks augmentation procedure is approximately two hours. The procedure can be managed either as an overnight in-patient treatment or as a hospital outpatient treatment. Given the nature of the surgical incisions to the gluteus maximus muscles, the therapeutic management of post-surgical pain (at the surgical-wound sites) and normal tissue-healing usually require a four to six-week convalescence, after which the patient resumes their normal-life activities. [ 2 ]
The augmentation and contouring of the buttocks with autologous fat transfer (lipoinjection) therapy is realized with the excess adipose-fat tissue harvested from the abdomen , flanks, and thighs of the patient. In 1987 Dr. Eduardo Krulig, a Venezuelan plastic surgeon, described the technique, using the name "lipoinjection" for the first time, mentioning the regions of the body where the technique is useful. [ 9 ] The gentle liposuction applied to harvest the autologous fat minimally disturbs the local tissues, especially the connective-tissue layer between the skin and the immediate subcutaneous muscle tissues. Then, the harvested fat is injected to the pertinent body area of the gluteal region, through a fine-gauge cannula inserted through a small surgical incision, which produces a short and narrow scar . Lipoinjection contouring and augmentation with the patient's own body fat avoids the possibility of tissue rejection, and is physically less invasive than buttocks-implant surgery. Therefore, depending upon the health of the patient, the convalescence period allows them to resume daily, normal-life activities at two days post-operative, and the full spectrum of physical activity at two weeks post-operative. Furthermore, the liposuction harvesting of the patient's excess body fat improves the aesthetic appearance of the body fat donor-sites. [ 10 ] Nonetheless, physiologically , the human body's normal, health-management chemistry does resorb (break down and eliminate) some of the injected adipose-fat tissue, and so might diminish the augmentation. According to the degree of diminishment of the volume and contour caused by the fat-resorption, the patient might require additional sessions of fat-transfer therapy to achieve the desired size, shape, and contour of the buttocks. [ 2 ]
In common parlance, lipoinjection into the buttocks for aesthetic purposes is often called a "Brazilian butt lift" (BBL). [ 11 ] This name is suggested to originate from the Brazilian surgeon Ivo Pitanguy , who pioneered the surgery in the 1960s. The popularity of the surgery significantly increased during the 2010s as a result of social media trends. [ 12 ]
The augmentation of the buttocks, by rearranging and enhancing the pertinent muscle and fat tissues of the gluteal region, is realized with a combined gluteoplasty procedure of surgery (subcutaneous dermal-fat flaps ) and liposculpture (fat-suction, fat-injection). Therapeutically, such a combined correction-and-enhancement procedure is a realistic and feasible lower-body-lift treatment for the patient who has undergone massive weight loss (MWL) in the course of resolving obesity with bariatric surgery . [ 13 ] [ 14 ] In the case of the patient who presents under-projected, flat buttocks ( gluteal hypoplasia ), and a degree of gluteal-muscle ptosis (prolapsation, falling forward), wherein neither gluteal-implant surgery nor lipoinjection would be adequate to restoring the natural anatomic contour of the gluteal region, the application of a combined treatment of autologous dermal-fat flap surgery and lipoinjection can achieve the required functional correction and aesthetic contour. [ 2 ]
The methods for reducing the size of the buttocks include the varieties of liposuction , such as lipectomy (with and without ultrasonic enhancement) to reduce excess body fat, and superficial liposculpture , to reshape, refine, and re-establish the natural contour of the body. The usual buttocks-reduction treatment is lipectomy with applied tumescence and anaesthesia , wherein the body fat is harvested by aspiration (suction) through a small-gauge cannula (2–4 mm) that is inserted through a small incision, either to the intergluteal sulcus (the butt-crack), or to the upper area of the gluteus maximus muscle proper. [ 2 ]
Ultrasonically assisted liposuction can quickly remove a large volume of body fat for the correction of a notable occurrence of lipodystrophy , a deposit of adipose fat to the buttocks and related anatomic areas. The ultrasonic liposuction machine liquefies the excess fat tissue, and so more readily facilitates its removal with conventional suction-lipectomy. The quick fat-harvesting allowed by the ultrasonic lipectomy technique has eliminated the larger (long and wide) surgical incisions that once were required for removing a large volume of adipose tissue. Nonetheless, because of the sensitivity of the gluteal-region tissues, the skin of the pertinent donor-site is cooled in order to prevent ultrasonic heat damage caused by the liquefying and removal of the excess adipose fat. [ 2 ]
Reshaping the buttocks with liposculpture is performed with a small cannula (2 mm) specifically for contouring superficial body fat, the configuration of which (number of open ports) is determined by the type and the degree of gluteal correction to be realized. To sculpt rounded contours to square-shaped buttocks muscles, superficial liposculpture allows the plastic surgeon to control the injection-rate of the fat-volume. Moreover, superficial liposuction can be combined with other treatment methods for contouring the gluteal region to achieve the required functional, anatomic correction, and the aesthetic enhancement sought by the patient, such as reshaping the lateral area of the buttocks into an athletic form. [ 15 ] [ 16 ] The study Contouring the Gluteal Region with Tumescent Liposculpture (2011) indicated that effective, gluteal-region contouring is best achieved by tailoring the liposuction-reduction and the lipoinjection-augmentation techniques to the anatomic topography of the body areas to be corrected. [ 17 ] Furthermore, the study Contouring of the Gluteal Region in Women: Enhancement and Augmentation (2011) indicated that natural contours of the buttocks and the thighs are effectively achieved with a combined gluteoplasty of selective liposuction and lipoinjection, which reduces the need for aggressive surgical procedures, decreases the risk of medical complications, abbreviates wound-recovery-time, and lessens post-operative scarring. Combined with any buttocks-correction method, superficial liposculpture facilitates the treatment of contour irregularities, the surgical revision of scars, and the correction of gluteal-region contour depressions. [ 18 ]
To meet the functional requirements and the aesthetic expectations ( body image ) of the patient, the plastic surgeon establishes a realistic and feasible surgery plan by which to correct the anatomic contour deficiencies of the gluteal region. The surgeon and the patient determine the location of the surgical-wound scars , and determine the best operative position, to allow the proper exposure of the pertinent anatomy to be corrected. Because the surgical procedure requires the tumescence and anaesthesia of the gluteal-region area to be corrected, the physician and the anaesthesiologist determine the volumes of the anaesthetic and tumescent fluids to be administered to the patient during the procedure, and so avoid the risks of drugs overdose and toxicity. [ 2 ]
For a lipoinjection augmentation, the surgeon first dissects and prepares the augmentation-pocket to which will be injected the autologous fat-tissue. The surgical creation (muscle dissection) of the augmentation-pocket avoids the gluteal innervation ( superior gluteal nerve and inferior gluteal nerve ) and the vascular system ( venous and arterial ) of the gluteus maximus muscle . Afterwards, the surgeon sutures the dissection-incision and secures it with adhesive tape to ensure that the augmentation-pocket remains open, as dissected, ready to receive the injections of adipose fat. For the revision of scars, with surgery and injections of autologous fat, or with allopathic synthetic fillers, the surgeon applies subcuticular closures to the incision wounds, which then are bandaged. [ 2 ]
After completing the surgical corrections and the lipoinjection contouring of the pertinent area(s) of the gluteal region, the surgeon thoroughly examines the patient to ensure his or her general recovery from the operation, and examines each surgical incision to ascertain that it is correctly sutured and taped, in order to facilitate the uneventful healing of the gluteus-muscle tissues, without medical complications. The patient is advised to avoid exercise and strenuous physical activity until three weeks post-operative, how to properly care for surgical-incision wounds, and how to wear a compression garment that will keep in place the surgically corrected tissues, and so ensure their healing as a whole anatomic unit of the gluteal region. [ 2 ]
When a patient has undergone a surgical contouring of the buttocks with gluteal implants, the final, corrected body contour usually is observed at six months post-operative or at one year post-operative, depending upon the tissue-healing capabilities of the patient's body. The liposculpture patient usually requires approximately six months, and occasionally one year before producing the final, corrected body contour. For both procedures, at approximately one month post-operative, marked aesthetic improvement is noticeable in the corrected body areas, as is the elimination of the initial, post-operative weight gain caused by the body's retention of the infiltrated anaesthetic and tumescent fluids. The patient is advised to wear a compression garment to contain swelling and to immobilize the corrected tissues, so that they heal as one anatomic unit of the gluteal region. Moreover, throughout the convalescence, to facilitate shrinking the skin to the new, corrected body contour, and to resolve unevenness, wrinkles to the skin, and localized swelling, the continual application of massage and (occasional) ultrasound treatments can facilitate the diminishment of the post-operative conditions. [ 2 ]
Of the three general methods of gluteal augmentation procedures, including implants, flaps and fat graft, a 2019 systemic literature review with meta-analysis of 46 publications revealed fat graft with the least complication rate (7%) while implants associated with highest complication rate (31%). [ 19 ] The surgical and liposculpture contouring of the human body presents possible medical complications such as: the psychological—unmet body image expectations of aesthetic improvement; the physical—uneven contour, local and general; the physiologic—toxic reactions to the anaesthesic and the tumescent drugs; and the nervous— paresthesia , localized areas of perduring numbness in the corrected portion(s) of the gluteal region. [ 2 ] The medical complications possible to a surgical buttocks augmentation procedure, the submuscular emplacement of a gluteal implant, include infection , surgical-wound dehiscence that exposes the implant, revision surgery, rupture of the implant, seroma (a pocket of clear serous fluid), capsular contracture , asymmetry of the corrected area, shifting of the implant, surgical over-correction, injury to the sciatic nerve , and paresthesia (tingling skin). The medical complications possible to a liposculpture buttocks augmentation include the bodily resorption of some of the injected adipose fat, asymmetric contour of the corrected body area, an irregular contour to the body, seroma, abscess (pus enclosed by inflamed tissue), cellulitis (subcutaneous connective-tissue inflammation), and paresthesia. [ 2 ]
Like most medical procedures, buttock augmentation comes with risks, some of which can be life-threatening. A total of 413 Mexican plastic surgeons reported 64 deaths related to liposuction, with 13 deaths caused by gluteal lipoinjection. In Colombia, nine deaths were documented. Of the 13 deaths in Mexico, eight (61.6 percent) occurred during lipoinjection, whereas the remaining five (38.4 percent) occurred within the first 24 hours. In Colombia, six deaths (77.7 percent) occurred during surgery and three occurred (22.2 percent) immediately after surgery. [ 20 ] Secondary lymphoedema of the lower extremities has been reported as an unusual side effect of liquid silicone injection on the hips and buttock while thromboembolism, implant displacement and explosion have also been listed as some of the dangers. [ 21 ] [ 22 ]
In the surgical praxis of body contouring therapy, the patient's body-image expectations can be different from the contoured body that is the outcome of the performed surgical operation. Such unmet aesthetic expectations can be avoided at the pre-operative consultation stage, whereby, with informed consent, the physician and the patient jointly establish a realistic and feasible surgery plan to achieve a mutually satisfactory corrective outcome (functional and aesthetic) of the operation to the gluteal region, the buttock- and thigh-areas. [ 2 ]
Contour problems of the corrected gluteal region can be prevented with the operational use of small-gauge cannulas (ca. 2.0 mm) specifically for superficial liposuction; and with the application of cross-pattern harvesting of the excess body fat, to avoid removing too much adipose fat tissue, which might disfigure the contour of the patient's fat-donor area. The possible contour problems that might arise from ultrasonic liposuction are skin burns and hypertrophic scarring, which might occur if the fat-donor area skin is not cooled and protected during the fat harvest. To that end, the infusion of a tumescence-inducing solution to the fat-donor area(s) assists in cooling the patient's skin during the ultrasonic lipo-harvesting; likewise, the application of moist towels, a skin protector, and the constant cooling-fluid infiltration of the cannula in an integrated sheath. [ 2 ]
The infiltration of a solution of anaesthesia - and tumescence -inducing drugs can present medical complications such as a fluid overload of the tissues, the inadequate replacement of the infiltrated solution, and the partitioning (separation) of a single infiltration into several pools, which then are removed by suction lipectomy. Moreover, during anaesthesia, maintaining the patient's stable blood pressure can be difficult, which increases the possibility of bleeding, and the possibility that anaesthetic toxicity can occur if excessive doses are administered by infiltration; the symptoms are manifested as central nervous system (CNS) occurrences of drug-induced anxiety , apprehension, restlessness, nervousness, disorientation, confusion, dizziness, blurred vision, tremors, nausea , vomiting, shivering, and seizures; likewise, as manifestations of drowsiness, unconsciousness, respiratory depression, and respiratory arrest. Furthermore, the toxicity symptoms of a tumescence-inducing drug (e.g. epinephrine ) might cause such CNS symptoms, for which reason the operative application of a tumescent drug is limited throughout the operation. [ 2 ]
Post-operatively, local areas of numbness ( paresthesia ) might occur in the contoured portion(s) of the gluteal region, and might perdure for a long time after the surgery. Hence, the patient is advised to facilitate the re-sensitizing of the numb area(s) with applications of gentle massage, to prevent the development of a neuroma complication, and to alleviate pain. Nonetheless, depending upon the tissue-healing capabilities of the patient, he or she can recover in full at two years post-operative. [ 2 ]
The outcome of a buttocks-contouring procedure depends upon the specific defect or deformity. Depressed scars and deep morphological defects are difficult to correct because of the curvature of the buttocks as an anatomic unit, and because of the scar-contracting elements of the tissues across the gluteal curvature. In such a case, although the injection of (autologous or artificial) tissue fillers to correct the defect or the deformity might be impermanent, that injection usually will remedy the functional and aesthetic shortcoming(s) required by the patient and will thus serve the therapeutic purpose of gluteoplasty. [ 2 ]
In common parlance, "Brazilian butt lift" (BBL) is often used to describe lipoinjection into the buttocks for aesthetic purposes. [ 23 ] This name is suggested to originate from the Brazilian surgeon Ivo Pitanguy , who pioneered the surgery in the 1960s. The popularity of the surgery significantly increased during the 2010s as a result of social media trends. [ 24 ]
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Buttock cells are cells having a notched appearance that are found in certain malignancies, [ 1 ] such as non-Hodgkin's lymphoma (including follicular lymphoma ), [ 2 ] [ 3 ] mycosis fungoides , [ 4 ] and Sézary syndrome . [ 4 ] [ 5 ]
This oncology article is a stub . You can help Wikipedia by expanding it .
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α-Naphthyl butyrate esterase , also referred to as naphthyl butyrate esterase or butyrate esterase , is a histological stain specific for white blood cells of the monocytic proliferation line. [ 1 ]
This article related to pathology is a stub . You can help Wikipedia by expanding it .
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Bypass surgery refers to a class of surgery involving rerouting a tubular body part. [ 1 ]
Types include:
This surgery article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/Bypass_surgery
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Bálint's syndrome is an uncommon and incompletely understood triad of severe neuropsychological impairments: inability to perceive the visual field as a whole ( simultanagnosia ), difficulty in fixating the eyes ( oculomotor apraxia ), and inability to move the hand to a specific object by using vision ( optic ataxia ). [ 1 ] It was named in 1909 for the Austro-Hungarian neurologist and psychiatrist Rezső Bálint who first identified it. [ 2 ] [ 3 ] [ 4 ]
Bálint's syndrome occurs most often with an acute onset as a consequence of two or more strokes at more or less the same place in each hemisphere. Therefore, it occurs rarely. The most frequent cause of complete Bálint's syndrome is said by some to be sudden and severe hypotension, resulting in bilateral borderzone infarction in the occipito-parietal region. [ 1 ] More rarely, cases of progressive Bálint's syndrome have been found in degenerative disorders such as Alzheimer's disease [ 5 ] [ 6 ] or certain other traumatic brain injuries at the border of the parietal and the occipital lobes of the brain.
Lack of awareness of this syndrome may lead to a misdiagnosis and resulting inappropriate or inadequate treatment. Therefore, clinicians should be familiar with Bálint's syndrome and its various etiologies. [ 7 ]
Bálint's syndrome symptoms can be quite debilitating since they impact visuospatial skills, visual scanning and attentional mechanisms. [ 8 ] Since it represents impairment of both visual and language functions, it is a significant disability that can affect the patient's safety—even in one's own home environment, and can render the person incapable of maintaining employment. [ 9 ] In many cases the complete trio of symptoms—inability to perceive the visual field as a whole (simultanagnosia), difficulty in fixating the eyes (oculomotor apraxia), and inability to move the hand to a specific object by using vision (optic ataxia)—may not be noticed until the patient is in rehabilitation. Therapists unfamiliar with Bálint's syndrome may misdiagnose a patient's inability to meet progress expectations in any of these symptom areas as simply indicating incapability of benefiting from further traditional therapy. The very nature of each Bálint symptom frustrates rehabilitation progress in each of the other symptoms. Much more research is needed to develop therapeutic protocols that address Bálint symptoms as a group since the disabilities are so intertwined. [ 10 ]
Simultanagnosia is the inability to perceive simultaneous events or objects in one's visual field. [ 11 ] People with Bálint's syndrome perceive the world erratically, as a series of single objects rather than seeing the wholeness of a scene. [ 12 ]
This spatial disorder of visual attention—the ability to identify local elements of a scene, but not the global whole—has been referred to as a constriction of the individual's global gestalt window—their visual "window" of attention. People fixate their eyes to specific images in social scenes because they are informative to the meaning of the scene. Any forthcoming recovery in simultanagnosia may be related to somehow expanding the restricted attentional window that characterizes this disorder. [ 13 ]
Simultanagnosia is a profound visual deficit. It impairs the ability to perceive multiple items in a visual display, while preserving the ability to recognize single objects. One study suggests that simultanagnosia may result from an extreme form of competition between objects which makes it difficult for attention to be disengaged from an object once it has been selected. [ 14 ] Patients with simultanagnosia have a restricted spatial window of visual attention and cannot see more than one object at a time. They see their world in a patchy, spotty manner. Therefore, they pick out a single object, or even components of an individual object, without being able to see the global "big picture." [ citation needed ]
A study which directly tested the relationship between the restriction of the attentional window in simultanagnosia compared with the vision of healthy participants with normal limits of visual processing confirmed the limitations of difficulties of patients with simultanagnosia. [ 15 ]
There is considerable evidence that a person's cortex is essentially divided into two functional streams: an occipital-parietal-frontal pathway that processes "where" information and an occipital-temporal-frontal pathway that provides "what" information to the individual. [ 16 ]
Bálint referred to this as "psychic paralysis of gaze"—the inability to voluntarily guide eye movements, changing to a new location of visual fixation. A major symptom of Oculomotor apraxia is that a person has no control over their eye movements, however, vertical eye movements are typically unaffected. For example, they often have difficulty moving their eyes in the desired direction. In other words, the saccades (rapid eye movements) are abnormal. Because of this, most patients with Oculomotor apraxia have to turn their heads in order to follow objects coming from their peripherals. [ 17 ]
Optic ataxia is the inability to guide the hand toward an object using visual information [ 18 ] where the inability cannot be explained by motor, somatosensory, visual field deficits or acuity deficits. Optic ataxia is seen in Bálint's syndrome where it is characterized by an impaired visual control of the direction of arm-reaching to a visual target, accompanied by defective hand orientation and grip formation. [ 19 ] It is considered a specific visuomotor disorder, independent of visual space misperception. [ citation needed ]
Optic ataxia is also known as misreaching or dysmetria (English: difficult to measure ), secondary to visual perceptual deficits. A patient with Bálint's syndrome likely has defective hand movements under visual guidance, despite normal limb strength. The patient is unable to grab an object while looking at the object, due to a discoordination of eye and hand movement. It is especially true with their contralesional hand. [ citation needed ]
Dysmetria refers to a lack of coordination of movement, typified by the undershoot or overshoot of intended position with the hand, arm, leg, or eye. It is sometimes described as an inability to judge distance or scale. [ 18 ]
As Bálint states, optic ataxia impaired his patient's daily activities, since, 'while cutting a slice of meat...which he held with a fork in his left hand, ...would search for it outside the plate with the knife in his right hand', or '...while lighting a cigarette he often lit the middle and not the end'. Bálint pointed out the systematic nature of this disorder, which was evident in the patient's behaviour when searching in space. 'Thus, when asked to grasp a presented object with his right hand, he would miss it regularly, and would find it only when his hand knocked against it. [ 19 ]
The reaching ability of the patient is also altered. It takes them longer to reach toward an object. Their ability to grasp an object is also impaired. The patient's performance is even more severely deteriorated when vision of either the hand or the target is prevented. [ 20 ]
The visual difficulties in Bálint's syndrome are usually due to damage to the parieto-occipital lobes on both sides of the brain. The parietal lobe is the middle area of the top part of the brain and the occipital lobe is the back part of the brain. (It usually does not affect the temporal lobes) [ citation needed ]
Lack of awareness of the syndrome may lead to misdiagnosis such as blindness, psychosis, or dementia. [ 1 ] Symptoms of Bálint's syndrome are most likely to be noticed first by optometrists or ophthalmologists during an eye check up, or therapists providing rehabilitation following brain lesions. However, due to the scarcity among practitioners of familiarity with the syndrome, the symptoms are often explained away incorrectly without being considered as a possibility and followed by medical confirmation of clinical and neuroradiological findings. [ 21 ] Any severe disturbance of space representation, spontaneously appearing following bilateral parietal damage, strongly suggests the presence of Bálint's syndrome and should be investigated as such. [ 22 ] One study reports that damage to the bilateral dorsal occipitoparietal regions appeared to be involved in Bálint's syndrome. [ 23 ]
Bálint's syndrome has been found in patients with bilateral damage to the posterior parietal cortex . The primary cause of the damage and the syndrome can originate from multiple strokes , Alzheimer's disease , intracranial tumors , or brain injury. Progressive multifocal leukoencephalopathy and Creutzfeldt–Jakob disease have also been found to cause this kind of damage. This syndrome is caused by damage to the posterior superior watershed areas, also known as the parietal - occipital vascular border zone (Brodmann's areas 19 and 7). [ 24 ]
Some telltale signs suggesting Bálint's syndrome following bilateral brain insults may include: [ citation needed ]
In terms of the specific rehabilitation of visuoperceptual disorders such as Bálint's syndrome, the literature is extremely sparse. [ 8 ] According to one study, rehabilitation training should focus on the improvement of visual scanning, the development of visually guided manual movements, and the improvement of the integration of visual elements. [ 10 ] Very few treatment strategies have been proposed, and some of those have been criticized as being poorly developed and evaluated. [ citation needed ]
Three approaches to rehabilitation of perceptual deficits, such as those seen in Bálint's syndrome, have been identified:
Symptoms of Bálint's syndrome were found in the case of a 29-year-old with migraines. In the aura before the migraine headache, she experienced an inability to see all of the objects in the visual field simultaneously; an inability to coordinate hand and eye movements; and an inability to look at an object on command. [ 27 ] Symptoms were not present before the onset of the migraine or after it passed. [ citation needed ]
A study of a patient with Corticobasal Ganglionic Degeneration (CBGD) also showed a development of Bálint's syndrome. As a result of CBGD, the patient developed an inability to move his eyes to specific visual objects in his peripheral fields. He also was unable to reach out and touch objects in his peripheral fields. An inability to recognize more than one item at a time was also experienced when presented with the Cookie Theft Picture from the Boston Diagnostic Aphasia Examination . [ 28 ]
A 58-year-old male presented with Bálint's syndrome secondary to severe traumatic brain injury 4-months post-injury onset. He had completed a comprehensive post-acute brain injury rehabilitation program. He received 6 months of rehabilitation services as an inpatient. A three-pronged approach included the implementation of (a) compensatory strategies, (b) remediation exercises and (c) transfer of learned skills in multiple environments and situations. Comprehensive neuropsychological and occupational therapy evaluations were performed at admission and at discharge. Neuropsychological test improvements were noted on tasks that assess visuospatial functioning, although most gains were noted for functional and physical abilities. [ 8 ]
A patient with congenital deafness exhibited partial Bálint's syndrome symptoms. This patient experienced an inability to perceive simultaneous events in her visual field. She was also unable to fixate and follow an object with her eyes. In addition, her ability to point at targets under visual guidance was impaired. [ 21 ]
Bálint's syndrome is rarely reported in children, but some recent studies provide evidence that cases do exist in children. A case involving a 10-year-old male child with Bálint's syndrome has been reported [ 29 ] Similar results were seen in a 7-year-old boy. In children this syndrome results in a variety of occupational difficulties, but most notably difficulties in schoolwork, especially reading. The investigators encourage more careful recognition of the syndrome to allow adequate rehabilitation and environmental adaptation. [ 30 ]
The validity of Bálint's syndrome has been questioned by some. [ by whom? ] The components in the syndrome's triad of defects (simultanagnosia, oculomotor apraxia, optic ataxia) each may represent a variety of combined defects.
Because Bálint's syndrome is not common and is difficult to assess with standard clinical tools, the literature is dominated by case reports and confounded by case selection bias, non-uniform application of operational definitions, inadequate study of basic vision, poor lesion localisation, and failure to distinguish between deficits in the acute and chronic phases of recovery. [ 12 ]
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Carbohydrate antigen 19-9 ( CA19-9 ), also known as sialyl-Lewis A , is a tetrasaccharide which is usually attached to O- glycans on the surface of cells. It is known to play a role in cell-to-cell recognition processes. It is also a tumor marker used primarily in the management of pancreatic cancer . [ 1 ]
CA19-9 is the sialylated form of Lewis antigen A . It is a tetrasaccharide with the sequence Neu5Acα2-3Galβ1-3[Fucα1-4]GlcNAcβ.
Guidelines from the American Society of Clinical Oncology discourage the use of CA19-9 as a screening test for cancer, particularly pancreatic cancer . The reason is that the test may be falsely normal ( false negative ) in many cases or abnormally elevated in people who have no cancer ( false positive ) in others. The main use of CA19-9 is therefore to see whether a pancreatic tumor is secreting it; if that is the case, then the levels should fall when the tumor is treated, and they may rise again if the disease recurs. [ 2 ] Therefore it is useful as a surrogate marker for relapse .
In people with pancreatic masses , CA19-9 can be useful in distinguishing between cancer and other diseases of the gland. [ 1 ] [ 3 ]
CA19-9 can be elevated in many types of gastrointestinal cancer, such as colorectal cancer , esophageal cancer and hepatocellular carcinoma . [ 1 ] Apart from cancer, elevated levels may occur in pancreatitis , cirrhosis , [ 1 ] and diseases of the bile ducts. [ 1 ] [ 3 ] It can also be elevated in people with obstruction of the bile ducts . [ 3 ]
In people who lack Lewis antigen A (a blood type antigen on red blood cells ), which is about 10% of the white population, CA19-9 is not produced by any cells, [ 3 ] even in those with large tumors. [ 2 ] This is because of a deficiency of a fucosyltransferase enzyme that is needed to produce Lewis antigen A . [ 2 ]
CA19-9 was discovered in the serum of patients with colon cancer and pancreatic cancer in 1981. [ 4 ] It was characterized shortly after, and it was found to be carried primarily by mucins . [ 5 ]
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CAD/CAM dentistry is a field of dentistry and prosthodontics using CAD/CAM ( computer-aided-design and computer-aided-manufacturing ) to improve the design and creation of dental restorations , [ 1 ] [ 2 ] especially dental prostheses , including crowns , crown lays, veneers , inlays and onlays, fixed dental prostheses ( bridges ), dental implant supported restorations, dentures ( removable or fixed ), and orthodontic appliances . CAD/CAM technology allows the delivery of a well-fitting, aesthetic, and a durable prostheses for the patient. [ 3 ] CAD/CAM complements earlier technologies used for these purposes by any combination of increasing the speed of design and creation; increasing the convenience or simplicity of the design, creation, and insertion processes; and making possible restorations and appliances that otherwise would have been infeasible. Other goals include reducing unit cost and making affordable restorations and appliances that otherwise would have been prohibitively expensive. However, to date, chairside CAD/CAM often involves extra time on the part of the dentist, and the fee is often at least two times higher than for conventional restorative treatments using lab services.
Like other CAD/CAM fields, CAD/CAM dentistry uses subtractive processes (such as CNC milling ) [ 4 ] and additive processes (such as 3D printing ) to produce physical instances from 3D models .
Some mentions of "CAD/CAM" and "milling technology" in dental technology have loosely treated those two terms as if they were interchangeable, largely because before the 2010s, most CAD/CAM-directed manufacturing was CNC cutting, not additive manufacturing, so CAD/CAM and CNC were usually coinstantiated; but whereas this loose/imprecise usage was once somewhat close to accurate, it no longer is, as the term "CAD/CAM" does not specify the method of production except that whatever method is used takes input from CAD/CAM, [ 5 ] and today additive and subtractive methods are both widely used.
Computer-aided design (CAD) and computer-aided manufacture (CAM) is a process where non-digital data is captured, converted into a digital format, edited as necessary, and subsequently converted back into a physical form with the exact dimensions and materials specified during the digital design process, usually by either 3D printing or milling . [ 6 ] This set of stages is known as a “digital workflow”. [ 7 ]
CAD/CAM may be used to provide a machine-led means of fabricating dental prostheses that are used to restore or replace teeth. This is an alternative to the traditional process of prosthesis fabrication using physical techniques, in which the dentist makes an impression of the site that is to be restored. This is then transported to the laboratory where a study model is made. On that model, an imitation of the final design is made using wax – known as a wax up – which represents the size and shape of the finished dental prosthesis. The wax is then encased in an investment mold, burned out and replaced with the desired material as part of lost wax casting . [ 8 ] CAD/CAM makes such procedures unnecessary for the impression is recorded digitally and the manufacture of the appliance is accompanied by additive ( 3D printing ) or subtractive ( milling ) means.
Examples of dental prostheses that can be manufactured using this system include: [ 8 ]
Although CAD/CAM dentistry was used in the mid-1980s, early efforts were considered a cumbersome novelty, requiring an inordinate amount of time to produce a viable product. This inefficiency prevented its use within dental offices and limited it to labside use (that is, used within dental laboratories ). As adjunctive techniques, software , and materials improved, the chairside use of CAD/CAM (use within dental offices/surgeries) increased. [ 9 ] For example, the commercialization of Cerec by Sirona made CAD/CAM available to dentists who formerly would not have had avenues for using it.
The first CAD/CAM system used in dentistry was produced in the 1970s by Professor François Duret [ 10 ] [ 11 ] and colleagues. The process contains a number of steps. Firstly, an optical impression of the intraoral abutment is obtained by scanning with an intra-oral digitizer. The digitized information is transferred to the monitor where a 3D graphic design is produced. The restoration can then be designed on the computer. The final restoration is then milled from a block. Professor Duret and colleagues subsequently developed the ‘sopha system’ however this was not widely used, perhaps lacking the accuracy, materials and computer capabilities required in dentistry. [ 12 ] The second generation of CADCAM attempted to develop this system further, but struggled to obtain occlusal morphology using an intra oral scanner, so prepared a stone model first before digitising the model.
Development of a various digitizers followed: a laser beam with a position sensitive detector sensor, a contact probe and a laser with a charged coupled device camera. Due to development of more sophisticated CAD/CAM systems both metal and ceramic restorations could be produced. [ 12 ]
Mormann and colleagues later developed a CADCAM system named CEREC, which they used to produce a type of dental restoration called an inlay. The inlay preparation is scanned using an intra-oral camera. A compact machine used chairside allowed design of the restoration from a ceramic block. [ 12 ] The major advantage of this system was the chair side approach allowing same-day restorations. [ 13 ] However, this technique was limited in that it couldn’t be used for contouring or occlusal patterns. The CEREC system is used widely across the world, and studies have shown long term clinical success. [ 12 ]
The Procera system was developed by Anderson and colleagues. They used CADCAM to develop composite veneers. The Procera system later developed as a processing centre connected to satellite digitisers worldwide to produce all ceramic frameworks. This system is used around the world today. [ 13 ]
Chairside CAD/CAM restoration typically creates and lutes(bonds) the prosthesis the same day. Conventional prostheses, such as crowns, have temporaries placed for one to several weeks while a dental laboratory or in-house dental lab produces the restoration. [ 14 ] The patient returns later to have the temporaries removed and the laboratory-made crown cemented or bonded in place. An in-house CAD/CAM system enables the dentist to create a finished inlay in as little as one hour. [ 15 ] CAD/CAM systems use an optical camera to take a virtual impression by creating a 3D image which is imported into a software program and results in a computer-generated cast on which the restoration is designed. [ 16 ]
Bonded veneer CAD/CAM restorations are more conservative in their preparation of the tooth. As bonding is more effective on tooth enamel than the underlying dentin , care is taken not to remove the enamel layer. Though one-day service is a benefit that is typically claimed by dentists offering chairside CAD/CAM services, the dentist's time is commonly doubled and the fee is therefore doubled.
All CAD/CAM systems consist of a computer aided design (CAD) and computer aided manufacture (CAM) stage and the key stages can broadly be summarised as the following:
For a single unit prosthesis, after decayed or broken areas of the tooth are corrected by the dentist, an optical impression is made of the prepared tooth and the surrounding teeth. These images are then turned into a digital model by proprietary software within which the prosthesis is created virtually. The software sends this data to a milling machine where the prosthesis is milled. Stains and glazes can be added to the surfaces of the milled ceramic crown or bridge to correct the otherwise monochromatic appearance of the restoration. The restoration is then adjusted in the patient’s mouth and luted or bonded in place.
Integrating optical scan data with cone beam computed tomography datasets within implantology software also enables surgical teams to digitally plan implant placement and fabricate a surgical guide for precise implementation of that plan. Combining CAD/CAM software with 3D images from a 3D imaging system means greater safety and security from any kind of intraoperative mistakes.
To design and manufacture a dental prosthesis , the physical space which it will replace within the mouth has to be converted into a digital format. To do this, a digital impression must be taken. This will convert the space into a digital image which must then be converted into a file extension that can be read by the CAD software system being used. [ 13 ]
Once in a digital form, the structures within the mouth will be displayed as a 3D image. Using CAD software, the size and shape of the restoration can be virtually altered, thus replacing the wax up stage present in the traditional approach. [ 12 ] [ 17 ]
Digital impressions are a means of recording the shape of a patient’s dental structures by using scanners. In CAD/CAM's infancy, desktop scanners were used which digitised study models or Dental impressions - indirect representations of the patient's dentition. [ 18 ] These devices are also known as extra oral scanners and can be contact or non-contact. [ 17 ]
Contact scanners use stylus profilometers that are placed against and run along the contours of an object. The contact of the stylus against the object is represented digitally as a set of co-ordinates ( point cloud ), which is analyzed by an onboard mathematical algorithm to build up a 3D image of the object (mesh). [ 7 ] [ 19 ]
Non-contact scanners capture the shape of dental structures by using optics, such as light-emitting diodes . Light is emitted from the scanner which hits the object and then reflects into an onboard sensor, usually a charge couple device (CCD) or a position sensing detector (PSD). [ 12 ] These reflections allow the scanner to build up a 3D image of the object as with contact scanners [ 7 ] Extraoral non-contact scanners can obtain this information by different means, namely: structured light, laser light and confocal microscopy. [ 17 ] Contact scanners are more accurate than non-contact scanners but are rarely used anymore because they are slow and their imaging is unnecessarily detailed, ten times what is required for the success of a dental prosthesis. [ 17 ]
Intra-oral scanners are a form of non-contact scanners that have grown in popularity due to their ability to digitize a patient’s dentition directly in the mouth, avoiding the need for either a physical impression or a plaster study model, as is the case with extraoral scanners. This allows the fabrication of dental prostheses to be a completely digital process from the very first stage. Older scanners require a contrast powder to be placed on all the structures which were to be scanned whereas newer products do not require such a step. [ 17 ]
Intra-oral scanners interpret reflected light to produce a 3D image representing the patient's teeth, using systems including: [ 20 ]
The file extension most recognised by CAD software is an STL file . This file type records and describes an object’s geometry as a series of connected triangles, the density of which, depends upon the “resolution and the mathematical algorithm that was used to create the data”. [ 17 ] Most available scanners will produce STL files however some produce proprietary file types that can only be interpreted by select CAD software. [ 17 ] [ 20 ]
CAD software visualises the digital impression captured by extra or intra oral scanners and provides numerous design tools. Popular software packages include Dental System, DentalCAD and CEREC. [ 17 ] Some of the most common ways in which the virtual dental prosthesis can be edited are as follows:
CAD/CAM is a rapidly evolving field, hence the materials in use are always changing. Materials that can be manufactured using CADCAM software currently include metals, porcelain, lithium disilicate, zirconia and resin materials. CAD/CAM restorations are milled from solid blocks of ceramic or composite-resin. If pre-sintered ceramic ingots are used, subsequent sintering to reduce porosity is required and the CAD-CAM technology needs to account for any casting shrinkage during this process. Glass-based restorations can also be manufactured using CAD-CAM. Similar to ceramics, milling of glass ingots occurs and molten glass infiltration is used to reduce porosity . [ 21 ] The advantage of materials manufactured by CADCAM is the consistency in quality of restoration when mass produced.
Metals such as CoCr and titanium can be manufactured using CADCAM software. Precious metals cannot be machined for a variety of reasons, including expense. Pre-sintered CoCr blocks are available, and requires sintering after to achieve the desired mechanical properties . This method replaces the more traditional lost-wax technique. [ 22 ]
The microstructure of feldspathic and leucite reinforced ceramics is a glassy matrix with crystalline loads. It has low flexural strength , very good optical properties and an advantageous bonding abilities. A major advantage is its good aesthetics, with a variety of shades available and high translucency. However, it is a fragile material and is susceptible to damage by occlusal forces. [ 22 ]
Lithium disilicate, zirconium oxide and lithium silicate ceramics also have a biphasic structure with crystalline particles dispersed in a glass matrix. They have a high flexural strength, good optical properties and ability to bond. It produces highly aesthetic restorations in a variety of shades is useful as well as its high mechanical strength. [ 22 ]
Zirconia has a polycrystalline structure. It has a high flexural strength. However, both its optical properties and ability to bond are weak. Its main advantage is its mechanical strength. [ 21 ] CAD-CAM processing means that polycrystalline zirconia can be utilised for copings and frameworks. Its superior mechanical properties means it can be used for long-span bridgework, cores can be produced in thinner layers and can be utilised in posterior fixed partial dentures . [ 21 ] However, the aesthetics of zirconia restorations are not as good as other types of ceramic.
Three resin materials are available: resin composite, PMMA, and Nano-ceramics. PMMA is made of polymethylmethacrylate polymers with no filler. However, resin composite is composed of inorganic filler in a resin matrix. Similarly, nano-ceramic is nanoparticles embedded in a resin matrix. All three materials have a weak flexural strength and disadvantageous optical properties. However, the ability to bond is very effective. An advantage of these materials is the ability to manufacture them quickly through fast milling, so are great to used for direct composite repairs. However, the aesthetic quality of these materials limit their utility. [ 21 ]
CAD/CAM has improved the quality of prostheses in dentistry and standardised the production process. It has increased productivity and the opportunity to work with new materials with a high level of accuracy. [ 5 ]
Though CAD/CAM is a major technological advancement, it is important that dentists' technique is suited to CAD/CAM milling. This includes: correct tooth preparation with a continuous preparation margin (which is recognisable to the scanner e.g. in the form of a chamfer); avoiding the use of shoulderless preparations and parallel walls and the use of rounded incisor and occlusal edges to prevent the concentration of tension. [ 5 ]
Crowns and bridges require a precise fit on tooth abutments or stumps. Fit accuracy varies according to the CAD/CAD system utilized and from user to user. Some systems are designed to attain higher standards of accuracy than others and some users are more skilled than others. As of 2014 [update] , 20 new systems were expected to become available by 2020. [ 23 ]
Further research is needed to evaluate CAD/CAM technology compared to the other attachment systems (such as ball, magnetic and telescopic systems), as an option for attaching overdentures to implants. [ 24 ]
The advantages CAD/CAM provides when compared with the traditional laboratory and chairside led techniques are that it 1) allows for use of materials otherwise unavailable in the laboratory; 2) provides cheaper alternatives when compared with conventional materials; 3) decreases labour cost and time for dental technicians and 4) standardises the quality of restorations. [ 8 ] [ 13 ]
Ceramic materials in particular, can be highly time-consuming to work with. To make a ceramic dental prosthesis by hand, the technician has to meticulously build up porcelain powder and sinter it onto the surface of a coping. With CAD/CAM, labour times are significantly reduced, with CAD systems with some reviews reporting that only 5–6 minutes of technician input is required to produce a dental prosthesis. [ 13 ] In this way, the cost of production is reduced because labour costs are lower. Furthermore, CAD/CAM systems mill prosthesis from blocks of material which are mass manufactured, again reducing costs for the dental offices and laboratories when compared with traditional techniques. [ 13 ] These blocks are made so that any internal porosities have been removed which are difficult to eliminate during conventional fabrication. [ 13 ]
CAD/CAM has also found great merit with regards to reducing the shrinkage which occurs when ceramics are heated during sintering – a process required to give the ceramic restoration adequate strength so it can be used successfully within the mouth. It is difficult to account for this phenomenon in a dental laboratory using traditional techniques. [ 13 ] CAM can reduce shrinkage by two different methods. The first is to produce a prosthesis just greater than the desired size. This means that on firing, the prosthesis will shrink to the original intended size. [ 13 ] The second is by milling the prosthesis from a block that has already been fully sintered, which eliminates shrinkage but causes increased wear on cutting tools because the block is stronger than when partially sintered. [ 13 ]
The advent of intraoral scanners affords additional advantages when compared with the traditional physical workflow, particularly for dentists. In the traditional method, dental impressions must be taken, and the materials used to facilitate this are vulnerable to distortion over time which can decrease the accuracy of the eventual dental prosthesis . These inaccuracies are compounded by subsequent steps such as the fabrication of study models based on the impressions. Intra-oral scanners rapidly digitise what they scan which removes the risk of distortion/damage to the date. [ 25 ] Furthermore, dental impressions are often discomforting for patients, particularly those who have a strong gag reflex due to the bulk of material needed to capture a patient’s entire dentition. [ 25 ] Intra-oral scanners reduce this element.
Intraoral scanning saves considerable time in post processing when compared with conventional dental impressions because the 3D model can be instantly emailed to a dental laboratory, whereas with the conventional technique, the impression must be disinfected and physically transported to the laboratory which is a longer process. [ 25 ]
Digital dentistry is growing at an accelerating rate, and CAD/CAM systems will continue to evolve and improve. [ 30 ] [ 31 ]
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https://en.wikipedia.org/wiki/CAD/CAM_dentistry
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CAMBRA is an acronym for Caries Management by Risk Assessment . It describes a preventative form of dentistry in which patients are categorized by their relative risk for developing dental caries , based on risk factors including diet, oral hygiene , fluoride regiment, and past oral health history. It also attempts to avoid expenses associated with restorative processes.
It is meant to be used as a guide rather than an identification system, meaning the health care provider makes the judgement. However, a few medical experts have created an article on PubMed Central arguing that there is little evidence supporting CAMBRA and its integration into dentistry as it currently stands.
The CAMBRA system was developed at University of California, San Francisco (UCSF) in the early 2000's. The name was coined in 2002, and the protocol was introduced in 2007. The CAMBRA system would periodically receive updates until 2021. [ 1 ] CAMBRA was created to be an evidence-based approach to the prevention, reversal, and treatment of dental caries in patients, with risk factor as a main focus. [ 2 ] The CAMBRA system aims to provide an in-depth assessment tool as a key element of the overall approach and take account of caries disease indicators, examples being socio-economic status, developmental problems, or the presence of lesions or dental restorations placed within the previous 3 years. However, the health care provider makes the judgement about the patient's risk and preventative measures based on the CAMBRA system. [ 2 ]
CAMBRA focuses on the disease process and taking into account all factors that contribute to the development of dental caries (attacking factors) and all factors that research has shown to be protective from dental caries (defense factors).
CAMBRA claims to recognize the following as attacking factors for caries:
CAMBRA claims to recognize the following as defense factors against caries:
Caries can be identified by the presence of white spots, decalcifications of the teeth, restorations, or plaque deposits. CAMBRA assigns patients to low, moderate, high, or extreme risk and offers two formats; one for patients aged 0-5 years, and one for 6 years onward.
An intended benefit of CAMBRA is that it is meant to force both the dental professional and the patient (or their caregiver) to consider all the factors relevant to the patient’s risk and disease state, shifting the focus away from the traditional restorative approach of cavitation and restoration toward the cause of the disease and the need to modify the causes. It also attempts to improve communication and understanding between everyone involved, such as the patient and the members of the dental team. [ 3 ] CAMBRA also attempts to "save patients thousands of dollars in dental bills over their lifetimes" by offering these preventative measures so that expensive actions can be avoided. [ 2 ]
A PubMed Central article published to the United States National Library of Medicine (NLM)'s website by several medical experts in Portugal examines the results of 3 studies uploaded to PubMed Central in 2015, 2018, and 2021. The studies were obtained through an electronic search of PubMed, Cochrane , Web of Science , Scopus , and Embase , and were the only ones included as they were the only clinical studies to use the CAMBRA method with a control group. None of the articles used the 2019 or 2021 versions of CAMBRA, but all articles are in favor of implementing CAMBRA. [ 1 ]
The opposing article uses the Revised Cochrane Risk-Of-Bias Tool For Randomized Trials (RoB 2) for the 2015 and 2018 articles. A few concerns were raised on the 2015 article about possible selection bias and the final judgement, believed to have deviated from what CAMBRA had intended. The 2015 study had the most significant statistical differences from non-CAMBRA tests of the three studies, but the results were compared to control/intervention instead of the baseline/follow-up actions. Using the Risk Of Bias In Non-Randomized Studies - of Interventions (ROBINS-I) for the 2021 article, they raised extreme concerns about confounding and selection bias in the study. [ 1 ]
The opposing article uses these possible biases and inconsistencies as evidence that CAMBRA is not effective, and would not be worth implementing into dentistry in its current state.
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https://en.wikipedia.org/wiki/CAMBRA
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CAPOX (also called XELOX [ 1 ] ) is a chemotherapy regimen consisting of capecitabine ( trade name Xeloda) combined with oxaliplatin . [ 2 ] [ 3 ]
Xelox regime operates in 3-week cycles, usually with 8 cycles in total; Xeloda is taken orally twice daily for two weeks, while oxaliplatin is administered by IV on the first day of the cycle; there is a one-week rest period before the next cycle.
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https://en.wikipedia.org/wiki/CAPOX
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CA: A Cancer Journal for Clinicians is a bimonthly peer-reviewed medical journal published for the American Cancer Society by Wiley-Blackwell . The journal was established in 1950 and covers aspects of cancer research on diagnosis , therapy , and prevention . [ 1 ] The editor-in-chief is Arif Kamal. [ 2 ]
The journal is abstracted and indexed in:
The following table provides an overview of the latest rankings of CA: A Cancer Journal for Clinicians across major scientific indexing databases, highlighting its top position in multiple subject areas.
According to the Journal Citation Reports , the journal has a 2022 impact factor of 254.7, ranking it first among all journals in the database. [ 4 ]
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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/CA_(journal)
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CA 15-3 , for Carcinoma Antigen 15-3, is a tumor marker for many types of cancer, most notably breast cancer . [ 1 ] [ 2 ] [ 3 ]
It is derived from MUC1 . [ 4 ] CA 15-3 and associated CA 27-29 are different epitopes on the same protein antigen product of the breast cancer-associated MUC1 gene.
Elevated CA15-3, in conjunction with alkaline phosphatase (ALP), was found to be associated with an increased chance of early recurrence in breast cancer . [ 5 ]
Both CA 15-3 and CA 27-29 may be elevated in patients with benign ovarian cysts, benign breast disease, and benign liver disease. Elevations may also be seen in cirrhosis, sarcoidosis and lupus.
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https://en.wikipedia.org/wiki/CA_15-3
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CA 242 is a tumor marker for sialylated Lewis carbohydrates associated with adenocarcinomas and e-selectin -mediated metastatic risk. [ 1 ] [ 2 ] [ 3 ] It is commonly tested along with CEA, CA19-9 , and CA242 for detecting pancreatic cancer . [ 4 ] The specificity of CA 242 is higher than similar markers. Current research dictates that diagnostic efficiency is highest when various tumor markers are tested for at once. [ 5 ]
CA 242 has been used clinically as a diagnostic biomarker for pancreatic, colorectal and other cancers. Since CA 242 is overexpressed in malignant tumors, it is within reason to assume that CA 242 could be a product of cancer cells. [ 6 ] A study was conducted where CA 242 serum levels were acquired from 34, 680 patients with 27 clinically defined diseases. The data acquired shows that patients with pancreatic cancer, cervical cancer and lymphoma had the highest levels of the CA 242 serum, which was followed by esophageal , colon and ovarian cancer . CA 242 can be shown to detect other types of cancer as shown.
The objective of this study was to compare different tumor markers and their diagnostic value. The tumor markers tested in this experiment were CA 19-9, CA 242 and CEA tumor markers. The data revealed that although each marker has its own level of specificity and corresponds to a cancer, all three markers together increase diagnostic value. [ 7 ]
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https://en.wikipedia.org/wiki/CA_242_(tumor_marker)
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CA 27.29 is a tumor marker for breast cancer . [ 1 ]
It is a form of glycoprotein MUC1 . [ 2 ]
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https://en.wikipedia.org/wiki/CA_27-29
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CBV refers to Cytoxan (cyclophosphamide) , BCNU (carmustine) , and VP-16 (etoposide) , three drugs in a chemotherapy regimen commonly given to lymphoma patients in conjunction with stem cell therapy. [ 1 ]
CBV is usually given in high doses to patients who have relapsed or who have refractory disease and cannot benefit from standard chemotherapy. Since a patient's bone marrow is virtually guaranteed not to survive a course of CBV, the receiving patient must receive a transplant ( allogeneic or autologous , depending on his or her condition) of stem cells (formerly referred to as a bone marrow transplant ) to replace the patient's own hemopoietic ("blood-forming") stem cells. [ 2 ]
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https://en.wikipedia.org/wiki/CBV_(chemotherapy)
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The CFTR inhibitory factor ( Cif ) is a protein virulence factor secreted by the Gram-negative bacteria Pseudomonas aeruginosa [ 1 ] and Acinetobacter nosocomialis . [ 2 ] Discovered at Dartmouth Medical School , Cif is able to alter the trafficking of select ABC transporters in eukaryotic epithelial cells , such as the cystic fibrosis transmembrane conductance regulator (CFTR), [ 1 ] and P-glycoprotein [ 3 ] by interfering with the host deubiquitinating machinery. [ 4 ] By promoting the ubiquitin -mediated degradation of CFTR, Cif is able to phenocopy cystic fibrosis at the cellular level. [ 1 ] [ 5 ] The cif gene is transcribed as part of a 3 gene operon , whose expression is negatively regulated by CifR, a TetR family repressor. [ 6 ]
Cif was first discovered by co-culturing P. aeruginosa with human airway epithelial cells and monitoring the resulting effect on chloride ion efflux across a polarized monolayer. After co-culture, the CFTR specific chloride ion efflux was found to be drastically reduced. [ 5 ] This was determined to be caused by reduced levels of CFTR at the apical surface of these cells. This effect was later found to be the result of a single secreted protein produced by P. aeruginosa , which was named the CFTR inhibitory factor for this initial phenotype . Cif is secreted by P. aeruginosa PA14 as soluble protein as well as packaged into outer membrane vesicles (OMV). [ 7 ] Cif is far more potent when applied in OMVs, likely due to efficiency of delivery. Purified, recombinant Cif protein can be applied to polarized monolayers of mammalian cells and promote the removal of CFTR [ 1 ] [ 8 ] and P-glycoprotein [ 3 ] from the apical membrane . Cif accomplishes this by interfering with the host deubiquitylation system. [ 4 ]
Cif is an epoxide hydrolase (EH) with unique substrate selectivity. [ 8 ] Cif is the first example of an EH serving as a virulence factor. Based on structural comparison, it appears that the enzyme utilizes a catalytic triad of residues Asp129, Glu153 and His297, with accessory residues His177 and Tyr239 coordinating the epoxide oxygen during ring opening. Cif is also the first example of an EH utilizing a His-Tyr pair to coordinate an epoxide substrate, rather than the canonical Tyr-Tyr pair. [ 9 ] In the proposed enzyme mechanism, Asp129 nucleophilically attacks a carbon of the epoxide moiety of a substrate, forming an ester linked enzyme-acyl intermediate. The preference for which carbon is attacked varies depending upon the substrate. In the second step of the reaction, a water molecule is activated by the charge-relay His297-Glu153 pair, and undergoes nucleophilic attack on the Cγ of Asp129. This hydrolyzes the ester group, liberating the hydrolysis product as a vicinal diol. [ 8 ]
Cif belongs to the α/β hydrolase family of proteins. Its structure was determined by X-ray crystallography and consists of the canonical α/β hydrolase fold with a cap domain, which it uses to constitutively homo-dimerize in solution. The active site is buried in the interior of the protein at the interface between the α/β hydrolase core and the cap. [ 8 ] [ 10 ]
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https://en.wikipedia.org/wiki/CFTR_inhibitory_factor
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The CHDI Foundation , Inc., is a United States –based non-profit biomedical foundation that aims to "rapidly discover and develop drugs that delay or slow the progression of Huntington's disease ", [ 4 ] a neurodegenerative genetic disorder that affects muscle coordination and leads to cognitive decline. [ 5 ]
CHDI's predecessor, the High Q Foundation, was established in 2002 by a group of private donors. [ 1 ] It was officially incorporated in New Jersey on October 17, 2003. [ 6 ] Originally, the High Q foundation aimed to identify targets for treatments, while CHDI – the 'Cure Huntington's Disease Initiative' – was a sister organization allied to the Hereditary Disease Foundation , that focused on developing drugs to hit those targets. [ 1 ] 'CHDI', which is officially no longer an abbreviation for anything, now refers to the foundation as a whole. [ 7 ]
In 2012 CHDI adopted a new logo, depicting a tree composed of interconnected circles. According to Simon Noble, CHDI's Director of Scientific Communication, the logo represents the groundedness of the Foundation, the hereditary nature of HD, the interconnectedness of biological pathways and the medicinal chemistry of drug development. [ 8 ]
CHDI collaborates with a large number of academic and commercial research groups worldwide. [ 1 ] [ 9 ] It operates through a "virtual" biotechnology model, funding third party research organizations as opposed to having a physical research infrastructure of its own. [ 10 ] Rather than supplying grants, CHDI enters into research contracts with its collaborators, and exerts a managerial role in addition to providing financial support. [ 1 ] In a 2007 Nature news feature, CHDI's then senior scientific advisor Allan Tobin stated, "Ninety-five per cent of science works on the principle that the best thing to do is to let good scientists follow their noses ... But this is a different attitude. We think we can direct the science." [ 1 ]
CHDI's annual spend is unknown, but it is the largest single funder of Huntington's disease research: according to a Nature news feature, it spent $50 million in 2006. [ 11 ] The identity of CHDI's donors is not public. [ 12 ]
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https://en.wikipedia.org/wiki/CHDI_Foundation
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CHIMES Society is an international academic collaboration whose objective is to establish new stroke treatments.
CHIMES is a Singaporean non-profit society founded by a group of key opinion leaders in stroke, Southeast Asia regional experts, and clinicians interested in implementing a research project on Traditional Chinese Medicine efficacy on stroke recovery.
CHIMES society has received a grant in 2007 from Singapore National Medical Research Council which has allowed the initiation of a double-blind, randomized, placebo-controlled clinical trial in October 2007. The trial includes 1,100 patients and aims at measuring the efficacy of NeuroAid in reducing neurological deficit and improving functional outcome in patients with cerebral infarction . [ 1 ]
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https://en.wikipedia.org/wiki/CHIMES_Society
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During the manhunt for Osama bin Laden , the CIA ran a covert operation utilizing a fake hepatitis vaccine program in Pakistan to illicitly collect blood samples to confirm the presence of bin Laden or his family. [ 1 ] The CIA recruited physician Shakil Afridi to administer hepatitis vaccines, and used the collected DNA to compare with the DNA of bin Laden's sister, who died in Boston in 2010. [ 1 ]
The program was successful in locating Osama bin Laden but resulted in negative fallout. It led to the arrest of a participating physician, Shakil Afridi , and was widely ridiculed as undermining public health . [ 2 ] [ 3 ] The program is credited with increasing vaccine hesitancy in Pakistan [ 4 ] [ 5 ] [ 6 ] [ 7 ] and a rise in violence against healthcare workers for being perceived as spies. [ 8 ] The rise in vaccine hesitancy following the program led to the re-emergence of polio in Pakistan, with Pakistan having by far the largest number of polio cases in the world by 2014. [ 8 ]
In September of 2012, after working for 30 years in Pakistan, Save the Children was expelled. [ 9 ]
In 2011, the program was condemned by Doctors without Borders . [ 9 ] In February 2012, the program was condemned by the non-governmental organization InterAction . [ 9 ] On January 6, 2013, the deans of twelve American schools of public health sent a letter to Obama condemning the program. [ 10 ] [ 9 ]
On May 16, 2014, Lisa Monaco responded that vaccine programs would be excluded from espionage : [ 11 ] [ 12 ]
I wanted to inform you that the Director of the Central Intelligence Agency (CIA) directed in August 2013 that the agency make no operational use of vaccination programs, which includes vaccination workers. Similarly, the Agency will not seek to obtain or exploit DNA or other genetic material acquired through such programs. This CIA policy applies worldwide and to U.S. and non-U.S. persons alike.
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https://en.wikipedia.org/wiki/CIA_fake_vaccination_campaign_in_Pakistan
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Cyclophosphamide Methotrexate Fluorouracil (CMF) is a commonly used regimen of breast cancer chemotherapy that combines three anti-cancer agents: cyclophosphamide , methotrexate , and 5-fluorouracil (5-FU). [ 1 ]
While it is no longer considered the most efficient all-around chemotherapy , it retains a great importance in the treatment of elderly patients with luminal cancers and may become important for the treatment of estrogen receptor negative androgen receptor positive luminal ( GATA3 expressing) breast cancer.
The regimen was designed in order to mimic the highly successful regimen developed to treat Hodgkin's lymphoma . [ 2 ]
The treatment is administered over a four-week cycle. On days 1 and 8 methotrexate and 5-FU are given as injections. Cyclophosphamide may be also administered intravenously in conjunction with these drugs, or may be taken as an oral tablet, taken once each day for the first 14 days of each cycle. [ 3 ]
Side effects of CMF treatment include: [ 3 ]
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https://en.wikipedia.org/wiki/CMF_(chemotherapy)
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The CNIB Chanchlani Global Vision Research Award is an annual global research award that promotes research to explore the causes of blindness and vision loss, as well as potential cures, treatments and preventions. The award of $25,000 is given to vision scientists around the world who have made a major, original contribution for advancement in above said fields. [ 1 ]
The award was established in 2011 by Vasu and wife Jaya Chanchlani in collaboration with CNIB (Canadian National Institute for the Blind), the Toronto Netralya Lions Club and the Toronto Doctors Lions Club. The $500,000 endowment established with Mr. Chanchlani’s significant financial support, the awards promotes research of vision science and vision rehabilitation . [ 2 ]
Dr Molday is Professor of Biochemistry & Molecular Biology and Ophthalmology & Visual Sciences, University of British Columbia
Dr Ambati is Professor and Vice-Chair for Research of Ophthalmology and Founding Director of the Center for Advanced Vision Science at the University of Virginia .
Taylor is Melbourne Laureate Professor at the University of Melbourne and Chair of Indigenous Eye Health, where he was formerly Professor of Ophthalmology and department head and is founder of the Centre for Eye Research Australia. He is the Vice President of the International Agency for the Prevention of Blindness and Treasurer of the International Council of Ophthalmology.
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https://en.wikipedia.org/wiki/CNIB_Chanchlani_Global_Vision_Research_Award
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CNS metastasis is the spread and proliferation of cancer cells from their original tumour to form secondary tumours in portions of the central nervous system . [ 1 ]
The process of tumour cells invading distant tissue is complex and obscure, but modern technology has permitted an enhanced detection of metastasis . Currently, the diagnosis of central nervous system, or CNS, metastasis involves high-scale imaging to produce high-definition images of internal organs for analysis. This aids doctors and clinicians in prescribing suitable therapeutic methods, though there is yet to be a perfect treatment or preventative measure.
CNS metastasis is the spread and proliferation of cancer cells from their original tumour to form secondary tumours in portions of the CNS. [ 1 ] Typically, this progression initiates when tumour cells separate from the primary tumour and insert into the bloodstream or the lymph system via intravasation . [ 2 ] Intravasation into the circulatory system allows the tumour cells to travel and colonise distant sites such as the brain , a major structure of the CNS, forming a secondary brain tumour. [ 2 ] However, CNS metastasis only occurs when genetically unstable cancers can adapt to foreign tissue native to the CNS environments, but dissimilar from the original tumour. [ 3 ] Subsequently, metastasised cells assume new genomic phenotypes , while dropping unfavourable characteristics, once cells disassociate from the primary lesion . [ 4 ] This is particularly crucial for the formation of CNS metastasis, as the tumour cells require characteristics favourable for the disruption of the blood-brain barrier , allowing them to transverse. [ 5 ] [ 6 ]
Recent evidence demonstrates that the dissemination of cells from the primary tumour is not sequential but consists of overlapping processes and routes. [ 4 ] This includes the tumour cells invading and colluding with tissue stroma while adapting to evade immune surveillance by suppressive inhibition of regular cellular anti-tumourigenic properties. [ 4 ] These cancerous cells modulate the foreign tissue environment while evolving to adapt to therapeutic intervention. [ 4 ]
Any systemic tumour can progress towards CNS metastasis. [ 7 ] Up to 30% of adult cancer cases harbour CNS metastasis, although this statistic is reportedly underdiagnosed because of the fallibility of medical diagnostic methods. [ 7 ] Clinically, the majority of diagnosed CNS metastasis are derived from well-known primary tumours, while still, about 5-10% are from unknown sources. [ 8 ] Since most cancers can progress towards CNS metastasis despite multimodal treatments, it is a significant risk for patients with systemic cancer.
Metastasis occurrence indicates stage 4 cancer progression and carries a poor prognosis . [ 7 ] Cancer usually causes numerous and varying symptoms at this stage depending on the underlying cancer and metastasis location. [ 7 ] Importantly for diagnosis, a symptomatic primary lesion is localised through either surgery or radiation . [ 7 ] Notably, CNS metastasis may occur in the brain , spinal cord , leptomeninges , epidural space , or even the dura singly or in combination. [ 7 ] Patients are often asymptomatic with several neurological manifestations depending on tumour size and location. [ 9 ] Clinically, CNS metastasis is known to cause haemorrhage or obstruction in the cranial portion of the CNS leading to hydrocephalus . [ 9 ]
Additionally, metastatic lesions are usually discrete within the brain and appear as spherical masses that displace the brain parenchyma rather than invading the tissues. [ 10 ] Generally, other symptoms include cystic degeneration, necrosis , as well as CNS haemorrhage commonly within the brain. [ 10 ] These conditions lead to the long-term degradation of neurocognition , speech , coordination, and behaviour, altering the quality of life of patients. [ 1 ]
Since CNS metastasis is the pathway of the natural progression of primary cancers, hence, main risk factors include modifiers of cancer risk. These modifiers include the accumulation of genetic , epigenetic , and environmental factors resulting in chromosomal and genomic aberrations and instability. [ 11 ] Research has demonstrated that 80-90% of malignant tumours are caused by external environmental factors such as carcinogens . [ 11 ]
Clinically, research evidence demonstrated that the primary tumours that have the greatest association with brain metastasis consist of lung , breast , melanoma , and colon cancers . [ 1 ] [ 5 ] Despite the knowledge of sources, there is a lack of understanding regarding why these sources have increased predilection , nor an understanding of the mechanism difference behind each metastasis process. [ 1 ]
CNS metastases can be diagnosed through various imaging approaches and clinical manifestations. These techniques allow doctors to detect abnormalities and identify the location and extent of the metastatic spread. [ 12 ]
CNS metastases are diagnosed through imaging techniques that produce detailed images of the inside of the body, including parts such as the bones, organs, muscles, and nerves. [ 13 ] Magnetic resonance imaging (MRI) and computed tomography (CT) are two representative imaging procedures for this purpose. [ 12 ]
MRI scans use strong magnetic fields and radio waves to create an image, while CT scans use X-rays . MRI scans produce more detailed images of bodily structures, particularly soft tissues including the brain, [ 13 ] and are better at detecting CNS metastases than CT scans. However, CT scans are sometimes used for the initial imaging modality due to their lower cost and efficiency in screening for multiple conditions. [ 14 ]
When a lesion is suspected of having CNS metastases and its primary site is unknown, additional imaging and biopsies maybe necessary for an accurate diagnosis. [ 14 ] These procedures allow medical practitioners to examine and evaluate the histology , or micro-anatomy, of the suspected tissue. [ 15 ]
Biopsies involve surgical removal of the suspected tissue but can be invasive. They warrant a thorough evaluation of their necessity and the patient’s capability to withstand the side effects .
A less intrusive alternative imaging technique is magnetic resonance spectroscopy (MRS) , which is used to determine the chemical compositions of cells. However, it is not as reliable as biopsies. [ 12 ]
These techniques are also relevant if a singular metastasis site is inadequate to explain the patient symptoms . In this case, additional screenings would be warranted to locate the other lesions and the tumour source. With this information, doctors aim to determine the metastasis lineage and accurately identify the underlying cancer. Modern clinical screening allows the detection of numerous serum levels of circulating tumour cells . However, a disproportionate amount of metastasis is still undetectable, causing under-diagnosis. [ 4 ]
The best treatment approach for patients depends on a comprehensive assessment of several factors, including the primary cancer type , tumour location, prognosis , and patient preference, among others. Some of the main treatment methods are surgery , radiotherapy , chemotherapy , immunotherapy , and other system-targeting therapies . [ 14 ]
The typical treatment pathway is receiving surgical resection to remove the CNS metastases, then undergo postoperative radiotherapy. [ 14 ] Radiation therapy can be delivered through stereotactic radiosurgery (SRS) , whole-brain radiotherapy (WBRT) , or a combination of the two. In SRS, a high dose of radiation is delivered to the tumour site while sparing the surrounding healthy tissues. This is particularly useful for small CNS metastases. WBRT is, as the name suggests, delivered to the entire brain, and is preferred in cases with a risk of developing metastases or having multiple metastases. [ 15 ]
Other methods of management are mostly in the form of drugs . These medications can be employed to target specific systems in patients, or the cancer cells themselves. The wide variety of available drugs have varying impacts and side effects on a per-patient basis. [ 14 ] One of the most popular examples of drug-based management is immunotherapy, which bolsters the patient’s immune system to fight cancer. Since this process is less intrusive and more varied than traditional chemotherapy or surgery, it is preferred for patients with lower tolerability , such as the elderly. [ 16 ]
If cancer recurs or progresses , the therapeutic methods are adjusted, and varying combinations of all available options are explored. Coping with successive disease progression can be challenging due to the taxing side effects, which can take a physical and mental toll on patients . Consequently, the prognosis for further attempts may not be as promising as it was initially. [ 17 ]
Diagnostic techniques for CNS metastasis are a major area of ongoing research, as detecting metastatic lesions early is crucial for timely treatment and better patient outcomes. [ 14 ]
One promising field is the use of biomarkers - proteins, genes, or other molecules associated with a specific condition. These are used to indicate normal or abnormal conditions of the body. [ 18 ] Early research suggests screening for biomarkers could facilitate easier diagnosis and have predictive applications. [ 19 ] Biomarkers need to be uniquely representative of CNS metastasis. Otherwise, there could be high incidences of false-positive results, rendering the method less precise. [ 18 ]
Another rising approach is chimeric antigen receptor (CAR) T cells . [ 14 ] This is a type of immunotherapy that involves engineering a patient’s T cells , a type of white blood cell , to identify and attack cancerous cells. [ 18 ]
Both methods require a better understanding of the molecular determinants of CNS metastasis. Knowing these biomolecular factors could also lead to the development of preventative methods , a heavily underdeveloped area in CNS metastasis. [ 20 ]
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https://en.wikipedia.org/wiki/CNS_metastasis
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During the early days of the COVID-19 pandemic , the disease and virus were sometimes called "coronavirus", "novel coronavirus", " Wuhan coronavirus", or "Wuhan pneumonia". [ 1 ] [ 2 ] [ 3 ] [ 4 ] [ 5 ]
In January 2020, the World Health Organization (WHO) tentatively named it "2019-nCoV", short for "2019 Novel Coronavirus", or "2019 Novel Coronavirus Acute Respiratory Disease". This naming was based on the organization's 2015 guidelines for naming novel viruses and diseases, avoiding the use of geographic locations (such as Wuhan ), in part to prevent social stigma. [ 6 ] [ 7 ] [ 8 ] A similar structure has also been used by the AP when referring to virus variants, for example, referring to it as the "Delta variant" rather than the "South African variant". [ 9 ] [ 10 ]
On 11 February 2020, the WHO named the disease COVID-19 (short for coronavirus disease 2019). That same day, the International Committee on Taxonomy of Viruses (ICTV) formally announced it had named the causative virus as SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) based upon its genetic similarity to the 2003 SARS-CoV . The separation between the disease and the causative virus is based on the same nomenclature policies that separate AIDS and the virus which causes it, HIV . [ 11 ]
WHO Director General Tedros Adhanom Ghebreyesus explained that CO stands for coronavirus, VI for virus, and D stands for disease, while 19 stands for the year, 2019, that the outbreak was first detected. [ 11 ] [ 12 ] As such, there has never been a "COVID-1" or any other "COVID-" series disease with a number below 19. [ 13 ]
From January to March 2020, US President Donald Trump repeatedly described the virus as the "Chinese virus". [ 14 ] In March 2020, the president claimed to have abandoned the term, telling Fox News "we shouldn't make any more of a big deal out of it". [ 15 ] On March 18 and 19, 2020, Trump twice defended using the term "Chinese virus" amid instances of bigotry against Asians in the United States . [ 16 ] Trump referred to it as "the China Virus" at least as late as January 2021. [ 17 ]
This description was also used by members of the Spanish far-right political party Vox , especially by its leader Santiago Abascal in March 2020. [ 18 ]
The Epoch Times has reportedly funded right-wing groups promoting the use of the term "CCP virus" to lay blame on the Chinese Communist Party (CCP) for the pandemic. [ 19 ] [ 20 ] Chinese-born New Zealand sculptor Chen Weiming created a 20-foot statue in Liberty Sculpture Park in Yermo, California , depicting Chinese leader and CCP general secretary Xi Jinping with spike proteins as his hair, naming it "CCP virus". [ 21 ]
Stylization of the term has varied since the virus's and disease's discovery. The World Health Organization (WHO) stylizes the disease as COVID-19 with all letters capitalized and many other organizations have followed their lead. [ 11 ] [ 22 ] [ 23 ] [ 24 ] The AP Stylebook , Chicago Manual of Style , and the Modern Language Association (MLA) have styled it similarly. [ 9 ] [ 25 ] [ 26 ] [ 27 ] Several observers have noted the importance of proper stylization, despite the seeming ridiculousness of worrying over such matters "at a time like this" (during the early days of the pandemic), recalling the confusion and prejudice which resulted from unclear or inconsistent naming as was the case with AIDS (which was called GRID /HTLV-III/LAV at various times) and non-A, non-B Hepatitis . They have also pointed out that future researchers will benefit from consistency when reviewing past data and research. [ 28 ] [ 29 ]
However, stylization as "Covid-19" has become common as well. Numerous news sources including The New York Times , CNN , Politico , The Wall Street Journal , NBCNews have presented the term with a capital C but all other letters as lower case. [ 30 ] As a result, use of "Covid-19" has become commonplace and even the accepted standard in some cases. [ 31 ] Use of "Covid-19" in news sources from the United Kingdom like The Guardian has also been the norm since most British newspapers only capitalize an entire acronym if the acronym is typically spelled out like " B-B-C " or " N-H-S " while acronyms which are pronounced as words, like " Nasa " or " Unicef " have their first letter capitalized and all subsequent letters lowercase. [ 28 ] [ 26 ]
While COVID-19 refers to the disease and SARS-CoV-2 refers to the virus which causes it, referring to the "COVID-19 virus" has been accepted. [ 9 ] [ 25 ] [ 29 ] Reference to SARS-CoV-2 as "the coronavirus" has become somewhat accepted despite such use implying that there is only one coronavirus species. Similarly, use of "COVID" for the disease (if first rendered as COVID-19) has been tolerated. Use of "the Coronavirus" to refer to the COVID-19 pandemic which began in December 2019 has also been accepted. Although such use does not specify the year or which coronavirus-related disease is being referred to, given its all-encompassing impact at the time, such references have been deemed justifiable. [ 26 ] [ 9 ] [ 25 ] [ 22 ] [ 31 ] Use of "the" when referring to the disease, virus, or 2019 pandemic has been quite varied with some requiring use of "the" while others have not. The Oxford English Dictionary noted that "the" is typically not used when referring to the disease, COVID-19, but is not uncommon when referring to the virus. [ 22 ] [ 10 ]
Reference to the virus and/or the disease as "corona", "the corona", and "the rona" has also arisen in various parts of the world. [ 10 ]
Numerous mutations and variants of SARS-CoV-2 have acquired colloquial vis-à-vis scientific labels for ease of pronunciation and usage, both in the lab and to some extent in mass media . The nomenclature draws from the corpus of mythology (both Greek and Scandinavian) and astronomy. [ 32 ]
Public messaging has been a concern given that these elements of popular reportage can be at variance with the Greek alphabet nomenclature established by the WHO ; [ 33 ] other schemes have been proposed. [ 34 ]
Arcturus ( XBB.1.16 ) was named on social media after the star; [ 35 ] Kraken ( XBB.1.5 ), Cerberus ( BQ.1.1 ), Typhon ( BQ.1 ), and Gryphon ( XBB ) were coined by evolutionary biologist T. Ryan Gregory (from his own personal nomenclature of mythical creatures); [ 36 ] whereas Pelican, Quail, and Mockingbird (variants of 20I/501Y.V1 ), have not gained wider usage. [ 37 ] The BA.2.86 variant was named 'pirola' ( sic ) by a group of scientists on social media in late 2023, and was brought to public attention by an August edition of the Wall Street Journal. [ 38 ] (Inasmuch as the World Health Organization has suggested using astronomy for its plethora of names, the Twitter user @JPWeiland suggested the obscure Jovian asteroid 1082 Pirola "for its uniqueness" and the possibility of shifting the nomenclature to Pi or Rho if needed.) [ 39 ] Two KP.2 variants which rose to prominence in the U.S. in late May 2024 are commonly known by the acronym FLiRT , the responsible mechanisms being a phenylalanine (F) to leucine (L) mutation and an arginine (R) to threonine (T) mutation in the virus's spike protein. [ 40 ]
Nicknames have also arisen for mutations such as Nelly (N501Y), Doug (and Douglas) (D614G), and even Eeek (E484K), initially meant as convenient labels in University of Bern lab discourse. [ 37 ]
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The CPK-MB test (creatine phosphokinase-MB), also known as CK-MB test , is a cardiac marker [ 3 ] used to assist diagnoses of an acute myocardial infarction , myocardial ischemia , or myocarditis . It measures the blood level of CK-MB (creatine kinase myocardial band), the bound combination of two variants (isoenzymes CKM and CKB ) of the enzyme phosphocreatine kinase . [ citation needed ]
In some locations, the test has been superseded by the troponin test . However, recently, there have been improvements to the test that involve measuring the ratio of the CK-MB1 and CK-MB2 isoforms. [ 4 ]
The newer test detects different isoforms of the B subunit specific to the myocardium whereas the older test detected the presence of cardiac-related isoenzyme dimers. [ citation needed ]
Many cases of CK-MB levels exceeding the blood level of total CK have been reported, especially in newborns with cardiac malformations, especially ventricular septal defects. This reversal of ratios is in favor of pulmonary emboli or vasculitis. An autoimmune reaction creating a complex molecule of CK and IgG should be taken into consideration. [ 5 ]
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CSF/serum albumin ratio is a test performed to compare the levels of albumin in the cerebrospinal fluid and the serum .
It is useful as a measure of the integrity of the blood–brain barrier . [ 1 ] [ 2 ] [ 3 ]
This medical diagnostic article is a stub . You can help Wikipedia by expanding it .
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The CSF/serum glucose ratio , also known as CSF/blood glucose ratio , is a measurement used to compare CSF glucose and blood sugar .
Because many bacteria metabolize glucose, and because the blood–brain barrier minimizes transversal, the ratio can be useful in determining whether there is a bacterial infection in the CSF.
The normal ratio is 0.6. [ 1 ]
It is used to distinguish between bacterial and viral meningitis, as it is often lowered in bacterial meningitis and normal in viral meningitis. [ 2 ]
This medical diagnostic article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/CSF/serum_glucose_ratio
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CVN45502 is a selective hypocretin (orexin) receptor 1 antagonist. It significantly reduces food intake and body weight in a mouse model of obesity. [ 1 ] Although HCRTR1 variants are significantly correlated with body weight in humans, it is not known if the drug has psychiatric side effects or could be combined with GLP-1 agonists . [ 2 ]
This medical article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/CVN45502
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CXL 1020 is an experimental drug that is being investigated as a treatment for acute decompensated heart failure . CXL 1020 functions as a nitroxyl donor; nitroxyl is the reduced, protonated version of nitric oxide . [ 1 ] Nitroxyl is capable of enhancing left ventricular contractility without increasing heart rate by modifying normal Ca 2+ cycling through the sarcoplasmic reticulum [ 2 ] as well as increasing the sensitivity of cardiac myofilaments to Ca 2+ . [ 3 ]
Patients with acute decompensated heart failure have diminished left ventricular systolic and/or diastolic functioning. [ 4 ] Impaired ventricular function can be a consequence of decreased sarcoplasmic reticulum Ca 2+ cycling and a corresponding decline in cardiomyocyte contraction. [ 2 ] Reduced ventricular functioning limits the ability of the ventricles to fill with blood and pump blood to the rest of the body.
There are two mechanisms through which CXL 1020 is able to enhance the movement of Ca 2+ in and out of the sarcoplasmic reticulum. Sarcoplasmic reticulum CaATPase (SERCA) is an energy-dependent ion pump found the sarcoplasmic reticulum of cardiac myocytes that is responsible for transporting Ca 2+ within the cytosol back in to the lumen of the sarcoplasmic reticulum. [ 2 ] The nitroxyl group that is donated by CXL 1020 initiates glutathiolation of SERCA at the cysteine 674 site, which in turn activates ATP-dependent Ca2+ transport. [ 5 ] Therefore, stimulation of SERCA leads to accelerated uptake of Ca 2+ from the cytosol of the cardiac myocyte.
Secondly, the nitroxyl group from CXL 1020 interacts with ryanodine receptors (RyR), specifically RyR2 , which is the predominant form found in cardiac tissue. [ 6 ] Ryanodine receptors are located within the membrane of the sarcoplasmic reticulum and function to release Ca 2+ required for myofilament activation (Guyton, 2006). Nitroxyl interacts with RyR2 to increase the probability of Ryanodine receptor opening, thereby enhancing Ca 2+ release from the sarcoplasmic reticulum. It is thought that nitroxyl modifies RyR2 function through its interaction with thiol groups present in the receptor, although the exact mechanism is unknown. [ 6 ]
Nitroxyl has also been shown to increase the sensitivity to cardiac myocytes to Ca 2+ , which in turn enhances the force of contraction. Its hypothesized that nitroxyl interacts with thiol groups present in myofilament proteins to increase the maximal Ca 2+ activated force of the myofilament, although the exact effect of nitroxyl on the myofilament is unknown. [ 3 ]
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In neuroscience , classical cable theory uses mathematical models to calculate the electric current (and accompanying voltage ) along passive [ a ] neurites , particularly the dendrites that receive synaptic inputs at different sites and times. Estimates are made by modeling dendrites and axons as cylinders composed of segments with capacitances c m {\displaystyle c_{m}} and resistances r m {\displaystyle r_{m}} combined in parallel (see Fig. 1). The capacitance of a neuronal fiber comes about because electrostatic forces are acting through the very thin lipid bilayer (see Figure 2). The resistance in series along the fiber r l {\displaystyle r_{l}} is due to the axoplasm 's significant resistance to movement of electric charge .
Cable theory in computational neuroscience has roots leading back to the 1850s, when Professor William Thomson (later known as Lord Kelvin) began developing mathematical models of signal decay in submarine (underwater) telegraphic cables. The models resembled the partial differential equations used by Fourier to describe heat conduction in a wire.
The 1870s saw the first attempts by Hermann to model neuronal electrotonic potentials also by focusing on analogies with heat conduction. However, it was Hoorweg who first discovered the analogies with Kelvin's undersea cables in 1898 and then Hermann and Cremer who independently developed the cable theory for neuronal fibers in the early 20th century. Further mathematical theories of nerve fiber conduction based on cable theory were developed by Cole and Hodgkin (1920s–1930s), Offner et al. (1940), and Rushton (1951).
Experimental evidence for the importance of cable theory in modelling the behavior of axons began surfacing in the 1930s from work done by Cole, Curtis, Hodgkin, Sir Bernard Katz , Rushton, Tasaki and others. Two key papers from this era are those of Davis and Lorente de Nó (1947) and Hodgkin and Rushton (1946).
The 1950s saw improvements in techniques for measuring the electric activity of individual neurons . Thus cable theory became important for analyzing data collected from intracellular microelectrode recordings and for analyzing the electrical properties of neuronal dendrites . Scientists like Coombs, Eccles , Fatt, Frank, Fuortes and others now relied heavily on cable theory to obtain functional insights of neurons and for guiding them in the design of new experiments.
Later, cable theory with its mathematical derivatives allowed ever more sophisticated neuron models to be explored by workers such as Jack, Rall , Redman, Rinzel, Idan Segev, Tuckwell, Bell, and Iannella. More recently, cable theory has been applied to model electrical activity in bundled neurons in the white matter of the brain. [ 1 ]
Note, various conventions of r m exist.
Here r m and c m , as introduced above, are measured per membrane-length unit (per meter (m)). Thus r m is measured in ohm ·meters (Ω·m) and c m in farads per meter (F/m). This is in contrast to R m (in Ω·m 2 ) and C m (in F/m 2 ), which represent the specific resistance and capacitance respectively of one unit area of membrane (in m 2 ). Thus, if the radius, a , of the axon is known, [ b ] then its circumference is 2 πa , and its r m , and its c m values can be calculated as:
These relationships make sense intuitively, because the greater the circumference of the axon, the greater the area for charge to escape through its membrane, and therefore the lower the membrane resistance (dividing R m by 2 πa ); and the more membrane available to store charge (multiplying C m by 2 πa ).
The specific electrical resistance , ρ l , of the axoplasm allows one to calculate the longitudinal intracellular resistance per unit length, r l , (in Ω·m −1 ) by the equation:
The greater the cross sectional area of the axon, πa 2 , the greater the number of paths for the charge to flow through its axoplasm, and the lower the axoplasmic resistance.
Several important avenues of extending classical cable theory have recently seen the introduction of endogenous structures in order to analyze the effects of protein polarization within dendrites and different synaptic input distributions over the dendritic surface of a neuron.
To better understand how the cable equation is derived, first consider an idealized neuron with a perfectly sealed membrane ( r m =∞) with no loss of current to the outside, and no capacitance ( c m = 0). A current injected into the fiber [ c ] at position x = 0 would move along the inside of the fiber unchanged. Moving away from the point of injection and by using Ohm's law ( V = IR ) we can calculate the voltage change as:
where the negative is because current flows down the potential gradient.
Letting Δ x go towards zero and having infinitely small increments of x , one can write ( 4 ) as:
or
Bringing r m back into the picture is like making holes in a garden hose. The more holes, the faster the water will escape from the hose, and the less water will travel all the way from the beginning of the hose to the end. Similarly, in an axon, some of the current traveling longitudinally through the axoplasm will escape through the membrane.
If i m is the current escaping through the membrane per length unit, m, then the total current escaping along y units must be y·i m . Thus, the change of current in the axoplasm, Δ i l , at distance, Δ x , from position x =0 can be written as:
or, using continuous, infinitesimally small increments:
i m {\displaystyle i_{m}} can be expressed with yet another formula, by including the capacitance. The capacitance will cause a flow of charge (a current) towards the membrane on the side of the cytoplasm. This current is usually referred to as displacement current (here denoted i c {\displaystyle i_{c}} .) The flow will only take place as long as the membrane's storage capacity has not been reached. i c {\displaystyle i_{c}} can then be expressed as:
where c m {\displaystyle c_{m}} is the membrane's capacitance and ∂ V / ∂ t {\displaystyle {\partial V}/{\partial t}} is the change in voltage over time.
The current that passes the membrane ( i r {\displaystyle i_{r}} ) can be expressed as:
and because i m = i r + i c {\displaystyle i_{m}=i_{r}+i_{c}} the following equation for i m {\displaystyle i_{m}} can be derived if no additional current is added from an electrode:
where ∂ i l / ∂ x {\displaystyle {\partial i_{l}}/{\partial x}} represents the change per unit length of the longitudinal current.
Combining equations ( 6 ) and ( 11 ) gives a first version of a cable equation:
which is a second-order partial differential equation (PDE).
By a simple rearrangement of equation ( 12 ) (see later) it is possible to make two important terms appear, namely the length constant (sometimes referred to as the space constant) denoted λ {\displaystyle \lambda } and the time constant denoted τ {\displaystyle \tau } . The following sections focus on these terms.
The length constant, λ {\displaystyle \lambda } (lambda), is a parameter that indicates how far a stationary current will influence the voltage along the cable. The larger the value of λ {\displaystyle \lambda } , the farther the charge will flow. The length constant can be expressed as:
The larger the membrane resistance, r m , the greater the value of λ {\displaystyle \lambda } , and the more current will remain inside the axoplasm to travel longitudinally through the axon. The higher the axoplasmic resistance, r l {\displaystyle r_{l}} , the smaller the value of λ {\displaystyle \lambda } , the harder it will be for current to travel through the axoplasm, and the shorter the current will be able to travel.
It is possible to solve equation ( 12 ) and arrive at the following equation (which is valid in steady-state conditions, i.e. when time approaches infinity):
Where V 0 {\displaystyle V_{0}} is the depolarization at x = 0 {\displaystyle x=0} (point of current injection), e is the exponential constant (approximate value 2.71828) and V x {\displaystyle V_{x}} is the voltage at a given distance x from x =0. When x = λ {\displaystyle x=\lambda } then
and
which means that when we measure V {\displaystyle V} at distance λ {\displaystyle \lambda } from x = 0 {\displaystyle x=0} we get
Thus V λ {\displaystyle V_{\lambda }} is always 36.8 percent of V 0 {\displaystyle V_{0}} .
Neuroscientists are often interested in knowing how fast the membrane potential, V m {\displaystyle V_{m}} , of an axon changes in response to changes in the current injected into the axoplasm. The time constant, τ {\displaystyle \tau } , is an index that provides information about that value. τ {\displaystyle \tau } can be calculated as:
The larger the membrane capacitance, c m {\displaystyle c_{m}} , the more current it takes to charge and discharge a patch of membrane and the longer this process will take. The larger the membrane resistance r m {\displaystyle r_{m}} , the harder it is for a current to induce a change in membrane potential. So the higher the τ {\displaystyle \tau } the slower the nerve impulse can travel. That means, membrane potential (voltage across the membrane) lags more behind current injections. Response times vary from 1–2 milliseconds in neurons that are processing information that needs high temporal precision to 100 milliseconds or longer. A typical response time is around 20 milliseconds.
If one multiplies equation ( 12 ) by r m {\displaystyle r_{m}} on both sides of the equal sign we get:
and recognize λ 2 = r m / r l {\displaystyle \lambda ^{2}={r_{m}}/{r_{l}}} on the left side and τ = c m r m {\displaystyle \tau =c_{m}r_{m}} on the right side. The cable equation can now be written in its perhaps best known form:
This is a 1D heat equation or diffusion equation for which many solution methods, such as Green's functions and Fourier methods, have been developed.
It is also a special degenerate case of the Telegrapher's equation , where the inductance L {\displaystyle L} vanishes and the signal propagation speed 1 / L C {\displaystyle 1/{\sqrt {LC}}} is infinite.
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The caduceus is the traditional symbol of Hermes and features two snakes winding around an often winged staff. Ancient sources associate Hermes with a variety of attributes, including wisdom, trade, deception, thievery, eloquence, negotiation, and alchemy . [ 1 ] [ 2 ] Nevertheless it is often used as a symbol of medicine, especially in the United States.
The modern use of the caduceus as a symbol of medicine became established in the United States in the late 19th and early 20th century as a result of well-documented mistakes and misunderstandings of symbology and classical culture. [ 3 ] [ 4 ] [ 5 ] [ 6 ] [ 7 ] [ 8 ] Critics of this practice say that the correct symbol for medicine is the Rod of Asclepius , which has only one snake and no wings. [ 7 ]
Before the ancient Romans and Greeks (about 2612 BCE ), older representations from Syria and India of sticks and animals looking like serpents or worms are interpreted by some as a direct representation of traditional treatment of dracunculiasis , the Guinea worm disease. [ 9 ]
While there is ample historical evidence of the use of the Caduceus, or Herald's Staff, to represent Hermes or Mercury (and by extension commerce and negotiation), early evidence of any symbolic association between the Caduceus and medicine or medical practice is scarce and ambiguous. It is likely linked to the alchemical "universal solvent", Azoth , the symbol of which was the caduceus.
The Guildhall Museum in London holds a 3rd-century oculist 's seal with Caduceus symbols both top and bottom. The seal was apparently used to mark preparations of eye medicine. [ 10 ] It is believed likely that rather than being evidence of a medical association per se , this is rather an allusion to the words of the Greek poet Homer who described the Caduceus as "possessing the ability to charm the eyes of men", which relates to the business of an oculist. [ 10 ]
Walter Friedlander proposed that early association of the Caduceus with medicine might have derived from the association of Hermes Trismegistus ("Thrice-Great Hermes") with early chemistry and medicine as aspects of alchemy as an esoteric practice. [ 3 ] He notes that "there are very definite connections between medicine and (Hermes)- Thoth , who later became known as Hermes Trismegistus. [ 11 ] [...] although these various factors may link Hermes/Mercury, along with his Caduceus, with alchemical medicine, they may just as well link all the other non-medical aspects of alchemy with Hermes/Mercury and the Caduceus". [ 12 ]
Despite a long tradition of interpretatio graeca (the tendency of the ancient Greeks to identify foreign deities with their own gods), determination of the equivalence of deities is a complex matter. The role of Hermes in the afterlife was limited to guiding souls of the deceased, whereas the powerful Egyptian god Thoth was truly lord of the underworld and master of death. Together with Osiris , he presided over the panel of forty-two divine judges that assessed the souls of the deceased for reward or punishment in the afterlife. [ 13 ] Thoth was at times depicted with two staves encircled by one cobra each, which might well have influenced the iconography of Hermes' caduceus. However, in ancient Egypt the snake staff represented the attribute of a powerful sorcerer, not a merchant or messenger. Compared to Hermes, Thoth was associated much more with magic and with potent actions preserving balance in the divine world, [ 14 ] than with the unpredictable whims of a trickster deity.
Depictions similar to the caduceus also occurred in bronze age Mesopotamia as devotional emblems for various major or minor deities , or as snakes embodying the deity itself. Ancient examples of attributes similar to the caduceus, or to aspects of Hermes' portfolio of divine roles, include the Sumerian messenger and snake god Nirah , the occasional depictions of the major goddess Innana holding a scepter with two winding snakes (which lacked the wings of a caduceus), and the benevolent Egyptian goddess Wadjet who was often depicted as a winged cobra.
If the caduceus was inspired by and adapted from an amalgam of serpent depictions in other cultures, probably with changes in explanatory myths and divine prerogatives, then Greek mythology might well have created an exaggerated impression that the origins of the caduceus were entirely separate from those of the rod of asclepius. From the perspectives of ethnography and literary history, their cultural and iconographic origins were probably deeply entwined as part of the complex and artistically fluid history of snakes as deities or as divine symbols for healing, magic and protective rituals. [ 15 ] [ better source needed ]
The Caduceus became a symbol of alchemy and pharmacy in medieval Europe. Its first appearance as a medical symbol can be traced back to 1st−4th century CE in oculists ' stamps that were found mostly in Celtic areas, such as Gaul , Germany and Britain, which had an engraving of the name of the physician, the name of the special medicine or medical formula and the disease for which the medicine was to be used. [ 16 ]
Medieval alchemy used the Caduceus to represent preparations containing quicksilver , later known as mercury. Quicksilver (named mercurius philosophorum ) was believed to be the basis of all substances and this element has been represented by the caduceus for many centuries. [ 17 ]
Based on the medieval European use of the caduceus to signify pharmacy, Bavarian printer Erhard Ratdolt used the caduceus in his medical manuscripts from 1486 CE. Others followed (not uncontroversially, see section Modern times below). Sir William Butts , physician to Henry VIII , was the first physician to adopt it as his emblem. [ 18 ] The rod of Asclepius , since the 5th century CE, resurfaced in 1544 CE. A publication of the medical writings of Avicenna , a Persian physician, had it at the frontispiece . [ citation needed ]
Beginning with the 16th century there is limited evidence of the use of the caduceus in what is arguably a medical context. However, this evidence is also ambiguous. In some cases it is clear that the caduceus symbolized wisdom, without any specific medical connotations. [ 3 ]
The caduceus appears in a general medical context in the printer's device used by the Swiss medical printer Johann Frobenius (1460–1527), who depicted the staff entwined with serpents and surmounted by a dove, with a biblical epigraph in Greek, "Be ye therefore wise as serpents and harmless as doves" (Matthew 10:16, here in the KJV translation), [ 5 ] in keeping with the connotations of the caduceus as a symbol of messengers and publishers based on the association of Hermes or Mercury with eloquence and negotiation. Friedlander observed that Frobenius could hardly be considered a medical printer, as had previously been asserted, noting that in a review of 257 of the works bearing this printer's device only one was related to medicine. Similar use of the caduceus in printers' marks continues to the present day, with companies including F. A. Davis Company still using the symbol as an element of their insignia.
There are a few other examples of use in this period. It may have been used as a symbol by Sir William Butts, physician to Henry VIII. [ 5 ] Similarly, physician John Caius , founder of Caius College, Cambridge , and at the time President of the Royal College of Physicians , during official visits to his eponymous college, had carried before him a silver caduceus on a cushion, and later presented this artefact to the college, where it remains in the college's possession. [ 19 ] This use was adduced by the medical historian (and primary apologist for the use of the caduceus in a medical context) Fielding Garrison to support his argument that the caduceus was used as a symbol of medicine as far back as the 16th century. However, as Walter Friedlander noted, "what Caius used was a non-specific herald's wand, rather than the caduceus of Hermes." In support of this assertion he quotes Caius's own words on why he chose a herald's wand as a symbol, making it clear that he chose it as a symbol of prudence. [ 3 ] This same passage was also earlier referenced by Engle in refuting Garrison's claim. Engle and Friedlander are not the only ones to have noted that the use of the Caduceus by Caius had nothing to do with supposed medical symbolism; as indicated in a publication produced by the Royal College of Physicians itself: "[...] by introducing the caduceus into the ceremony of the College of Physicians, Caius unintentionally added to the confusion between the two emblems for later times, when few people understand the visual signs with which he was so familiar." [ 20 ]
In support of the idea that the caduceus had a long-standing association with medicine, Garrison also mentioned the fact that the English medical printer Churchill used the symbol as a printer's device, beginning some time around 1844. Friedlander has examined this subject in detail, and shows that Churchill was well aware that the rod of Asclepius was the accepted symbol of medicine. He is, it seems, inclined to think that the adoption of the caduceus in this context probably had something to do with the relation between publishing and the role of Mercury as a messenger and scribe. He notes, however
That John Churchill adopted the caduceus as his printer's device independent of any idea that it symbolized medicine does not mean that, once having adopted it, it did not play some role in the caduceus coming to be accepted as a symbol of medicine, at least in the United States. During the remaining part of the nineteenth century several United States publishers appear to have copied or modified Churchill's caduceus and placed this mark on their medical books. Other contemporary British publishers did not use a caduceus and the caduceus had never been as widely connected to medicine in Great Britain or in Europe as it has been in the United States.
In any case, in Great Britain, as late as 1854, the distinction between the rod of Asclepius and the caduceus as symbols of two very different professions was apparently still quite clear. In his article On Tradesmen's Signs of London A.H. Burkitt notes that among the very old symbols still used in London at that time, which were based on associations between pagan gods and professions, "we find Mercury, or his caduceus , appropriate in trade, as indicating expedition. Esculapius , his Serpent and staff , or his cock , for professors of the healing art". [ 21 ]
Widespread confusion regarding the supposed medical significance apparently arose as a result of events in the United States that occurred in the second half of the 19th century. [ 7 ] As pointed out by Garrison, the caduceus had appeared on the chevrons of Army hospital stewards as early as 1856 [ 22 ] (William K. Emerson indicates the insignia was adopted earlier, in 1851). It has been asserted that this was a result of ignorance or misinterpretation regarding the pre-existing designation of the rod of Asclepius by the Surgeon General of the United States for this purpose. [ 10 ] Hospital stewards were not physicians; they played a supporting role preparing drugs for surgeons, supervising nurses and cooks, maintaining accounting and medical records, and in emergencies sometimes performed minor surgery or provided prescriptions. [ 23 ]
Later, in 1871, the Surgeon General designated the caduceus as the seal of the Marine Hospital Service (destined to become the U.S. Public Health Service in 1912). Gershen states that the change was for aesthetic reasons, [ 24 ] whereas Friedlander states the caduceus was adopted by the Marine Hospital Service "because of its relationship with merchant seamen and the maritime industry". [ 3 ]
The caduceus was formally adopted by the Medical Department of the United States Army in 1902 and was added to the uniforms of Army medical officers. According to Friedlander, this was brought about by one Captain Frederick P. Reynolds, although Bernice Engle states "the use of the caduceus in our army I believe to be due chiefly to the late Colonel Hoff, who has emphasized the suitability of the caduceus as an emblem of neutrality. [ 5 ] Reynolds had the idea rejected several times by the Surgeon General , but persuaded the new incumbent — Brig. Gen. William H. Forwood — to adopt it. This resulted in considerable controversy.
The Army and Navy Register of 28 June 1902 discusses the argument, which reflects the fact that a number of medical officers were unhappy with the choice. The article editor claims that the symbol was not chosen for its medical connotations and proposes the following symbolic interpretation: "the rod represents power, the serpents stand for wisdom and the two wings imply diligence and activity, qualities which are undoubtedly possessed by our Medical officers." [ 25 ] The editor also points out that the majority of Medical Corps personnel are not even doctors. According to this line of reasoning, the caduceus was never intended to be a symbol of medicine. The inconsistency was noticed several years later by the librarian to the Surgeon General , but for reasons which are not entirely clear, the symbol was not changed. [ 7 ]
Considerable light is shed on this confusion by an anonymous letter republished by Emerson, a historian of United States Army insignia and uniforms. He indicates that the April 1924 issue of The Military Surgeon printed a review of an earlier article that appeared in the Presse Médicale in which the author stated "There is nothing in history to justify the use of the caduceus as the emblem of the physician [...] it is most unfortunate that the 'confusion' exists." In an anonymous rebuttal contained in a letter to the editor published three months later in The Military Surgeon it was claimed that the late Col. John R. van Hoff was a member of the board that selected the emblem ("if he was not the one who was chiefly instrumental in its adoption"). In the letter to the editor reproduced by Emerson, the anonymous author claims
Hoff was far too scholarly and intelligent a man to commit the blunder of 'confusing' the caduceus with the serpent staff of Aesculapius. The sign of Mercury was deliberately adopted, as I have heard him state, because it was the emblem of the merchant and hence the emblem of the noncombatant. In junctures when it was necessary for a vessel to proclaim its nature, it was customary for a merchant vessel to indicate its noncombatant status by flying a flag which bore the emblem of Mercury, the God of the Merchant. The caduceus, in our use of it, is not distinctively the emblem of the physician, but the emblem of the whole Medical Department. The enlisted men of the medical department outnumber the physicians of that department. Besides the ambulance wagons, many vehicles are employed in field service in war which are not distinctively medical, but which are used for medical purposes. Both the enlisted men and the vehicles of the department (not to mention many other objects), should bear some sign of neutralization for protection. It seemed to Colonel Hoff and to the board that the Geneva cross, which in addition to its use as an emblem of neutrality is also the emblem of the Swiss Republic, there might well be substituted an emblem which is not the emblem of a foreign country, and the caduceus was selected, as the emblem which for many ages has served to indicate the noncombatant.
According to this view the caduceus was not intended to be a medical symbol (and, though explained differently, this reflects the view advanced by the editor commenting in The Army and Navy Register of 28 June 1902 discussed above). Nevertheless, after World War I the caduceus was employed as an emblem by both the Army Medical Department and the Navy Hospital Corps . [ citation needed ] Even the American Medical Association used the symbol for a time, but in 1912, after considerable discussion, the caduceus was abandoned by the AMA and the rod of Asclepius was adopted instead. [ 5 ]
The Army Medical Department (AMEDD) has included the Rod of Asclepius in its regimental coat of arms since its foundation in 1863. (Although now part of the AMEDD, the Army Medical Corps retains the caduceus for its own plaque and insignia.) The medical insignia of U.S. Air Force uses the rod of Asclepius.
Despite widespread acceptance of the caduceus as a medical symbol in the United States , it has been said that the rod of Asclepius has "the more ancient and authentic claim to be the emblem of medicine". [ 26 ] Most attempts to defend the caduceus's use in a medical context date from the last quarter of the 19th century through the first quarter of the 20th, and have been characterized as "based on flimsy and pseudo-historical research". [ 10 ]
In a survey of 242 logos used by organizations related to health or medicine, Friedlander found that professional associations were more likely to display the rod of Asclepius (62%), while organizations with a commercial focus were more likely to use the caduceus (76%). Hospitals were an exception (37% used a staff of Asclepius whereas 63% used a caduceus). Friedlander felt it likely that this might reflect the fact that "professional medical organizations have more often sought a real understanding of the meaning of the two symbols whereas commercial organizations have been less interested in the historical basis of their logo or insignia and more concerned with how well a certain symbol will be recognized by the iconographically unsophisticated audience they are trying to attract to their wares." [ 3 ]
The use of the caduceus in a medical context has long been frowned upon by many professionals, academics and others who are familiar with the historical significance of both symbols. This has occasioned impassioned remarks by those frustrated with the continuing confusion.
It is hard to trust a profession that cannot even get its symbols straight. Most physicians in the United States think that the symbol of their profession is something called the caduceus. But this is actually not true. [...] Historians have discovered that someone in the U.S. Army Medical Corps mistook the caduceus for the Aesculapion and introduced the Medical Corps' symbol at the beginning of the twentieth century. Soon thereafter, everyone in the United States was emulating the mistake.
It has been said that the caduceus is particularly inappropriate for use as a medical symbol due to its long associations with the Greek god Hermes , who was patron of commerce and traders as well as thieves, liars, and gamblers. [ 28 ]
As god of the high-road and the market-place Hermes was perhaps above all else the patron of commerce and the fat purse: as a corollary, he was the special protector of the traveling salesman. As spokesman for the gods, he not only brought peace on earth (occasionally even the peace of death), but his silver-tongued eloquence could always make the worse appear the better cause. From this latter point of view, would not his symbol be suitable for certain Congressmen, all medical quacks, book agents and purveyors of vacuum cleaners, rather than for the straight-thinking, straight-speaking therapeutist? As conductor of the dead to their subterranean abode, his emblem would seem more appropriate on a hearse than on a physician's car.
On the other hand, it has also been remarked – not without considerable irony – that commercial aims in medicine, especially in the United States of America, make the caduceus an appropriate symbol , at least for some physicians.
Well, so much for the caduceus. Somebody obviously got the wrong symbol for modern medicine–or did they? The caduceus seems to be an appropriate symbol for modern commercial medicine. Of particular relevance are the functions of escorting souls of the dead, wisdom, fertility, commerce, luck, eloquence, cheating and thieving. These have become symbolic of how medicine evolved in the late Twentieth Century.
Others are unapologetic about the association of medicine with commerce, recognizing the importance of "advertising essential for competitive marketing", and suggesting that it is up to individual physicians to choose between the two symbols, based on their own views about what associations are appropriate. [ 30 ] The AMA has used the Rod of Asclepius for over a century, [ 31 ] and its current logo since 2005. [ 32 ]
In North America, there are calls to clarify the symbol and to move to a uniform use of the rod of Asclepius. For example, the director of communications of the Minnesota Medical Association is quoted as saying, "If it's got wings on it, it's not really the symbol of medicine; some may find it hard to believe, but it's true. It's something like using the logo for the National Rifle Association when referring to the Audubon Society ". [ 33 ]
However, Andrew Weil , a proponent of alternative medicine , has suggested that the caduceus is appropriate as a medical symbol "because it embodies an esoteric truth that must be grasped to gain practical control over the shifting forces that determine health and illness." [ 34 ]
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A calcimimetic is a pharmaceutical drug that mimics the action of calcium on tissues, by allosteric activation of the calcium-sensing receptor that is expressed in various human organ tissues. Calcimimetics are used to treat secondary hyperparathyroidism (SHPT). [ 1 ] [ 2 ]
In the treatment of SHPT patients on dialysis calcimimetics does not appear to affect the risk of early death. [ 3 ] It does decrease the need for a parathyroidectomy but caused more issues with low blood calcium levels and vomiting . [ 3 ]
Cinacalcet was the first calcimimetic to be approved. Cinacalcet mimics calcium at the parathyroid hormone receptor . This binding will increase the sensitivity of calcium-sensing receptors (CaSR) on the parathyroid gland. As a result of the receptor "thinking" there is sufficient calcium, parathyroid hormone (PTH) secretion will be reduced. Lower calcium levels will be seen as well.
On August 25, 2015 Amgen Inc. announced that it had submitted a new drug application with the United States Food and Drug Administration for a new calcimimetic, etelcalcetide (formerly velcalcetide), for the treatment of SHPT in chronic kidney disease (CKD) patients on hemodialysis. Etelcalcetide is administered intravenously thrice weekly at the end of each dialysis session. Etelcalcetide binds to the CaSR on the parathyroid gland, which results in receptor activation and ultimately reduction in PTH.
Calcimimetics can be used concomitantly with vitamin D therapy.
Calcimimetic use can have side effects . Common side effects include: nausea and vomiting , hypocalcemia , and adynamic bone disease if intact parathyroid hormone (iPTH) levels drop below 100pg/mL.
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Calcinosis is the formation of calcium deposits in any soft tissue . [ 1 ] It is a rare condition that has many different causes. These range from infection and injury to systemic diseases like kidney failure .
The most common type of calcinosis is dystrophic calcification . This type of calcification can occur as a response to any soft tissue damage, including that involved in implantation of medical devices.
Metastatic calcification involves a systemic calcium excess imbalance, which can be caused by hypercalcemia , kidney failure , milk-alkali syndrome , lack or excess of other minerals, or other causes.
The cause of the rare condition of tumoral calcinosis is not entirely understood. It is generally characterized by large, globular calcifications near joints.
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NM_001033954 NM_007587 NM_001289444 NM_001305616
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Calcitonin is a 32 amino acid peptide hormone secreted by parafollicular cells (also known as C cells) of the thyroid (or endostyle ) in humans and other chordates [ 5 ] in the ultimopharyngeal body . [ 6 ] It acts to reduce blood calcium (Ca 2+ ), opposing the effects of parathyroid hormone (PTH). [ 7 ]
Its importance in humans has not been as well established as its importance in other animals, as its function is usually not significant in the regulation of normal calcium homeostasis . [ 8 ] It belongs to the calcitonin-like protein family .
Historically calcitonin has also been called thyrocalcitonin. [ 9 ]
Calcitonin is formed by the proteolytic cleavage of a larger prepropeptide , which is the product of the CALC1 gene ( CALCA ). It is functionally an antagonist with PTH and Vitamin D3. The CALC1 gene belongs to a superfamily of related protein hormone precursors including islet amyloid precursor protein , calcitonin gene-related peptide , and the precursor of adrenomedullin .
Secretion of calcitonin is stimulated by:
The hormone participates in calcium (Ca 2+ ) metabolism. In many ways, calcitonin counteracts parathyroid hormone (PTH) and vitamin D .
More specifically, calcitonin lowers blood Ca 2+ levels in two ways:
High concentrations of calcitonin may be able to increase urinary excretion of calcium and phosphate via the renal tubules. [ 15 ] leading to marked hypocalcemia . However, this is a minor effect with no physiological significance in humans. It is also a short-lived effect because the kidneys become resistant to calcitonin, as demonstrated by the kidney's unaffected excretion of calcium in patients with thyroid tumors that secrete excessive calcitonin. [ 16 ]
In its skeleton-preserving actions, calcitonin protects against calcium loss from the skeleton during periods of calcium mobilization, such as pregnancy and, especially, lactation . The protective mechanisms include the direct inhibition of bone resorption and the indirect effect through the inhibition of the release of prolactin from the pituitary gland. The reason provided is that prolactin induces the release of PTH related peptide which enhances bone resorption, but is still under investigation. [ 17 ] [ 18 ] [ 19 ]
Other effects are in preventing postprandial hypercalcemia resulting from absorption of Ca 2+ . Also, calcitonin inhibits food intake in rats and monkeys, and may have CNS action involving the regulation of feeding and appetite.
Calcitonin lowers blood calcium and phosphorus mainly through its inhibition of osteoclasts. Osteoblasts do not have calcitonin receptors and are therefore not directly affected by calcitonin levels. However, since bone resorption and bone formation are coupled processes, eventually calcitonin's inhibition of osteoclastic activity leads to increased osteoblastic activity (as an indirect effect). [ 16 ]
The calcitonin receptor is a G protein-coupled receptor localized to osteoclasts [ 20 ] as well kidney and brain cells. It is coupled to a G s α subunit , thus stimulating cAMP production by adenylate cyclase in target cells. It may also affect the ovaries in women and the testes in men. [ citation needed ]
Calcitonin was first purified in 1962 by Douglas Harold Copp and B. Cheney at the University of British Columbia , Canada. [ 21 ] It was initially thought to be secreted by the parathyroid gland but was shown by Iain Macintyre and his team at the Royal Postgraduate Medical School, London, to be secreted by parafollicular cells of the thyroid gland . [ 22 ] Dr. Copp named the discovered hormone calcitonin because of its role in 'maintaining normal calcium tone'. [ 21 ]
Calcitonin assay is used in identifying patients with nodular thyroid diseases . It is helpful in making an early diagnosis of medullary carcinoma of thyroid. A malignancy of the parafollicular cells, i.e. medullary thyroid cancer (MTC), typically produces an elevated serum calcitonin level. Prognosis of MTC depends on early detection and treatment.
Calcitonin also has significantly impacted molecular biology , as the gene encoding calcitonin was the first gene discovered in mammalian cells to be alternatively spliced , now known to be a ubiquitous mechanism in eukaryotes . [ 23 ] [ 24 ]
Calcitonin has clinically been used for metabolic bone disorders for more than 50 years. [ 25 ] Salmon calcitonin is used for the treatment of:
It has been investigated as a possible non-operative treatment for spinal stenosis . [ 31 ]
The following information is from the UK Electronic Medicines Compendium [ 32 ]
Salmon calcitonin is rapidly absorbed and eliminated. Peak plasma concentrations are attained within the first hour of administration.
Animal studies have shown that calcitonin is primarily metabolised via proteolysis in the kidney following parenteral administration. The metabolites lack the specific biological activity of calcitonin. Bioavailability following subcutaneous and intramuscular injection in humans is high and similar for the two routes of administration (71% and 66%, respectively).
Calcitonin has short absorption and elimination half-lives of 10–15 minutes and 50–80 minutes, respectively. Salmon calcitonin is primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. Therefore, the metabolic clearance is much lower in patients with end-stage kidney failure than in healthy subjects. However, the clinical relevance of this finding is not known. Plasma protein binding is 30% to 40%.
There is a relationship between the subcutaneous dose of calcitonin and peak plasma concentrations. Following parenteral administration of 100 IU calcitonin, peak plasma concentration lies between about 200 and 400 pg/ml. Higher blood levels may be associated with increased incidence of nausea, vomiting, and secretory diarrhea.
Conventional long-term toxicity, reproduction, mutagenicity , and carcinogenicity studies have been performed in laboratory animals. Salmon calcitonin is devoid of embryotoxic, teratogenic, and mutagenic potential.
An increased incidence of pituitary adenomas has been reported in rats given synthetic salmon calcitonin for 1 year. This is considered a species-specific effect and of no clinical relevance. [ 33 ] Salmon calcitonin does not cross the placental barrier.
In lactating animals given calcitonin, suppression of milk production has been observed. Calcitonin is secreted into the milk.
Calcitonin was extracted from the ultimobranchial glands (thyroid-like glands) of fish, particularly salmon. Salmon calcitonin resembles human calcitonin, but is more active. At present, it is produced either by recombinant DNA technology or by chemical peptide synthesis . The pharmacological properties of the synthetic and recombinant peptides have been demonstrated to be qualitatively and quantitatively equivalent. [ 32 ]
Calcitonin can be used therapeutically for the treatment of hypercalcemia or osteoporosis . [ 34 ] In a recent clinical study, subcutaneous injections of calcitonin have reduced the incidence of fractures and reduced the decrease in bone mass in women with type 2 diabetes complicated with osteoporosis. [ 35 ]
Subcutaneous injections of calcitonin in patients with mania resulted in significant decreases in irritability, euphoria and hyperactivity and hence calcitonin holds promise for treating bipolar disorder . [ 36 ] However no further work on this potential application of calcitonin has been reported.
It may be used diagnostically as a tumor marker for medullary thyroid cancer , in which high calcitonin levels may be present and elevated levels after surgery may indicate recurrence. It may even be used on biopsy samples from suspicious lesions (e.g., lymph nodes that are swollen ) to establish whether they are metastases of the original cancer.
Cutoffs for calcitonin to distinguish cases with medullary thyroid cancer have been suggested to be as follows, with a higher value increasing the suspicion of medullary thyroid cancer: [ 37 ]
When over 3 years of age, adult cutoffs may be used
A Cochrane systematic review assessed the diagnostic accuracy of basal and stimulated calcitonin for Medullary Thyroid cancer. [ 38 ] Although both basal and combined basal and stimulated calcitonin testing presented high accuracy ( sensitivity : between 82% and 100%; specificity : between 97.2% and 100%), these results had a high risk of bias due to design flaws of included studies. [ 38 ] Overall, the value of routine testing of calcitonin for diagnosis and prognosis of Medullary Thyroid Cancer remains uncertain and questionable. [ 38 ]
Increased levels of calcitonin have also been reported for various other conditions. They include: C-cell hyperplasia , nonthyroidal oat cell carcinoma, nonthyroidal carcinoma and other nonthyroidal malignancies, acute kidney injury and chronic kidney failure , hypercalcemia , hypergastrinemia , and other gastrointestinal disorders, and pulmonary disease . [ 39 ]
Calcitonin is a polypeptide hormone of 32 amino acids, with a molecular weight of 3454.93 daltons. Its structure comprises a single alpha helix. [ 40 ] Alternative splicing of the gene coding for calcitonin produces a distantly related peptide of 37 amino acids, called calcitonin gene-related peptide (CGRP), beta type. [ 41 ]
The following are the amino acid sequences of salmon and human calcitonin: [ citation needed ] [ 42 ]
Cys-Ser-Asn-Leu-Ser-Thr-Cys-Val-Leu-Gly-Lys-Leu-Ser-Gln-Glu-Leu-His-Lys-Leu-Gln-Thr-Tyr-Pro-Arg-Thr-Asn-Thr-Gly-Ser-Gly-Thr-Pro
Cys-Gly-Asn-Leu-Ser-Thr-Cys-Met-Leu-Gly-Thr-Tyr-Thr-Gln-Asp-Phe-Asn-Lys-Phe-His-Thr-Phe-Pro-Gln-Thr-Ala-Ile-Gly-Val-Gly-Ala-Pro
Compared to salmon calcitonin, human calcitonin differs at 16 residues.
In addition to the injectable and nasal spray dosage forms of the salmon calcitonin, noninvasive oral formulations of the peptide are currently under clinical development. The short-half-life of this peptide in serum triggered several attempts to enhance plasma concentrations. The peptide is complexed with a macromolecule that acts as an absorption enhancer through the transcellular pathway and, additionally, protects the peptide from the harsh pH and enzymatic conditions of the GI tract. This complexation is weak, noncovalent and reversible and the drug remains chemically unmodified. After passage through the intestine, the delivery agent dissociates from the peptide. One of the extensively studied oral formulations is the disodium salts of 5-CNAC oral calcitonin. This novel oral platform in a number of clinical trials at different phases has demonstrated promising enhanced pharmacokinetic profile, high bioavailability, well-established safety and comparable efficacy to that of nasal calcitonin especially for treatment of postmenopausal bone loss. [ 25 ]
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A calculus ( pl. : calculi ), often called a stone , is a concretion of material, usually mineral salts, that forms in an organ or duct of the body. Formation of calculi is known as lithiasis ( / ˌ l ɪ ˈ θ aɪ ə s ɪ s / ). Stones can cause a number of medical conditions.
Some common principles (below) apply to stones at any location, but for specifics see the particular stone type in question.
Calculi are not to be confused with gastroliths , which are ingested rather than grown endogenously .
Calculi are usually asymptomatic, and large calculi may have required many years to grow to their large size.
In kidney stones , calcium oxalate is the most common mineral type (see nephrolithiasis ). Uric acid is the second most common mineral type, but an in vitro study showed uric acid stones and crystals can promote the formation of calcium oxalate stones. [ 1 ]
Stones can cause disease by several mechanisms: [ citation needed ]
A number of important medical conditions are caused by stones: [ citation needed ]
Diagnostic workup varies by the stone type, but in general: [ citation needed ]
Modification of predisposing factors can sometimes slow or reverse stone formation. Treatment varies by stone type, but, in general: [ citation needed ]
The earliest operation for curing stones is given in the Sushruta Samhita (6th century BCE ). [ 2 ] The operation involved exposure and going up through the floor of the bladder. [ 2 ]
The care of this disease was forbidden to the physicians that had taken the Hippocratic Oath [ citation needed ] because:
The word comes from Latin calculus "small stone", from calx " limestone , lime ", [ 3 ] probably related to Greek χάλιξ chalix "small stone, pebble, rubble", [ 4 ] which many trace to a Proto-Indo-European language root for "split, break up". [ 5 ] Calculus was a term used for various kinds of stones. In the 18th century it came to be used for accidental or incidental mineral buildups in human and animal bodies, like kidney stones and minerals on teeth. [ 5 ]
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The Calgary–Cambridge model ( Calgary-Cambridge guide ) is a method for structuring medical interviews . It focuses on giving a clear structure of initiating a session, gathering information, physical examination , explaining results and planning, and closing a session. It is popular in medical education in many countries.
The Calgary–Cambridge model involves:
This is designed to give a clear structure to the interview, and to help to build the relationship between the clinician and the patient. [ 1 ] The importance of nonverbal communication is noted. [ 1 ]
The model is based on 71 skills and techniques that improve patient interviews. [ 2 ] These include maintaining eye contact , active listening (not interrupting , giving verbal cues), summarizing information frequently, asking about patient ideas and beliefs, and showing empathy . [ 2 ]
The Calgary–Cambridge model was developed based on evidence from interviews of patients, and what made them successful. [ 3 ] It is generally focussed on the patient and their experience . [ 4 ] The guide of skills and techniques is generally seen as comprehensive. [ 5 ]
The Calgary–Cambridge model has been criticized for creating a separation between the process of interviewing a patient and the information gained. [ 1 ] The 71 skills are very difficult to incorporate simultaneously, making it more difficult to learn for clinicians than other techniques. [ 5 ]
The Calgary–Cambridge model is named after Calgary , Canada , and Cambridge , United Kingdom where the three authors worked. [ 6 ] It is popular in medical education in many countries. [ 1 ] [ 7 ] It has also been adapted for veterinarians . [ 8 ] Other models, such as the Global Consultation Rating Scale, have been based on the Calgary–Cambridge model. [ 9 ]
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Call–Exner bodies , giving a follicle-like appearance, are small eosinophilic fluid-filled punched out spaces between granulosa cells . [ 1 ] The granulosa cells are usually arranged haphazardly around the space.
They are pathognomonic for granulosa cell tumors .
Histologically, these tumors consists of monotonous islands of granulosa cells with "coffee-bean" nuclei. That same nuclear groove appearance noted in Brenner tumour , an epithelial-stromal ovarian tumor distinguishable by nests of transitional epithelial cells (urothelial) with longitudinal nuclear grooves (coffee bean nuclei) in abundant fibrous stroma. [ 2 ] [ 3 ]
They are composed of membrane-packaged secretion of granulosa cells and have relations to the formation of liquor folliculi which are seen among closely arranged granulosa cells.
They are named for Emma Louise Call (1847–1937), an American physician, and Sigmund Exner (1846–1926), an Austrian physiologist. [ 4 ] [ 5 ]
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Calomel is a mercury chloride mineral with formula Hg 2 Cl 2 (see mercury(I) chloride ). It was used as a medicine from the 16th to early 20th century, despite frequently causing mercury poisoning in patients. [ 5 ]
The name derives from Greek kalos (beautiful) and melas (black) because it turns black on reaction with ammonia . This was known to alchemists . [ 3 ]
Calomel occurs as a secondary mineral which forms as an alteration product in mercury deposits. It occurs with native mercury , amalgam , cinnabar , mercurian tetrahedrite , eglestonite , terlinguaite , montroydite , kleinite , moschelite , kadyrelite , kuzminite , chursinite , kelyanite , calcite , limonite and various clay minerals . [ 2 ]
The type locality is Moschellandsburg , Alsenz-Obermoschel , Rhineland-Palatinate , Germany . [ 3 ]
The substance later known as calomel was first documented in ancient Persia by medical historian Rhazes in year 850. Only a few of the compounds he mentioned could be positively identified as calomel, as not every alchemist disclosed what compounds they used in their drugs. [ 6 ] Calomel first entered Western medical literature in 1608, when Oswald Croll wrote about its preparation in his Tyroncium Chemicum . It was not called calomel until 1655, when the name was created by Théodore de Mayerne , [ 7 ] who had published its preparation and formula in “Pharmacopoeia Londinensis" in 1618. [ 6 ]
By the 19th century, calomel was viewed as a panacea , or miracle drug, and was used against almost every disease, including syphilis , bronchitis , cholera , ingrown toenails , teething , gout , tuberculosis , influenza , and cancer . During the 18th and early 19th centuries pharmacists used it sparingly; but by the late 1840s, it was being prescribed in heroic doses [ 8 ] —due in part to the research of Benjamin Rush , who coined the term "heroic dose" to mean about 20 grains (1.3 g) taken four times daily. [ 9 ] This stance was supported by Samuel Cartwright , who believed that large doses were "gentlest" on the body. [ 10 ] As calomel rose in popularity, more research was done into how it worked.
J. Annesley was one of the first to write about the differing effects of calomel when taken in small or large doses. [ 10 ] Through experimentation on dogs, Annesley concluded that calomel acted more like a laxative on the whole body rather than acting specifically on the vascular system or liver as previous physicians believed. [ 10 ] In 1853, Samuel Jackson described the harmful effects of calomel on children in his publication for Transactions of Physicians of Philadelphia. [ 8 ] He noted that calomel had harmful effects causing gangrene on the skin, loss of teeth, and deterioration of the gums. [ 8 ] On May 4, 1863, William A. Hammond , the United States' surgeon-general, stated that calomel would no longer be used in the army as it was being abused by soldiers and physicians alike. [ 8 ] This caused much debate in the medical field, and eventually led to his removal as surgeon-general. [ 11 ] Calomel continued to be used well into the 1890s and even into the early 20th century. [ 8 ] Eventually calomel’s popularity began to wane as more research was done, and scientists discovered that the mercury in the compound was poisoning patients.
Calomel was the main of the three components of the pill number 9 of the British army during the First World War. [ 12 ]
Calomel is used as the interface between metallic mercury and a chloride solution in a saturated calomel electrode , which is used in electrochemistry to measure pH and electrical potentials in solutions. In most electrochemical measurements, it is necessary to keep one of the electrodes in an electrochemical cell at a constant potential. This so-called reference electrode allows control of the potential of a working electrode. [ 13 ]
Calomel is a powder that is white when pure, and it has been used as a pigment in painting in 17th century South Americas art and in European medieval manuscripts. [ 14 ] When it is exposed to light or contains impurities it takes on a darker tint. [ 7 ] Calomel is made up of mercury and chlorine with the chemical formula Hg 2 Cl 2 . Depending on how calomel was administered, it affected the body in different ways. Taken orally, calomel damaged mainly the lining of the gastrointestinal tract. Mercury salts (such as calomel) are insoluble in water and therefore do not absorb well through the wall of the small intestine. Some of the calomel in the digestive system will likely be oxidized into a form of mercury that can be absorbed through the intestine, but most of it will not. [ 15 ] Oral calomel was actually the safest form of the drug to take, especially in low doses. Most of the calomel ingested will be excreted through urine and stool. [ 15 ]
Powdered forms of calomel were much more toxic, as their vapors damaged the brain. Once inhaled, the calomel enters the bloodstream and the mercury binds with the amino acids methionine, cysteine, homocysteine and taurine. [ 15 ] This is because of the sulfur group these amino acids contain, which mercury has a high affinity for. It is able to pass through the blood brain barrier and builds up in the brain. Mercury also has the ability to pass through the placenta , causing damage to unborn babies if a pregnant mother is taking calomel. [ 15 ]
Calomel was manufactured in two ways - sublimation and precipitation . When calomel first started being manufactured it was done through sublimation. Calomel made through sublimation tends to be a very fine white powder. [ 7 ] There was some controversy over the sublimation of calomel. Many argued that the more times calomel was sublimed, the purer it got. Opponents believed that the repeated sublimation made calomel lose some of its therapeutic ability. [ 6 ] In 1788 chemist Carl Wilhelm Scheele came up with the mechanism to make precipitated calomel. This became rapidly popular in the pharmaceutical industry because it was both a cheaper and safer form of production. [ 6 ] Precipitation also tended to form very pure calomel salts. [ 7 ]
Calomel was a popular medicine used during the Victorian period , and was widely used as a treatment for a variety of ailments during the American Civil War . The medication was available in two forms, blue pills and blue masses . [ 11 ] The blue pill was an oral form of calomel containing mercury that was often mixed with a sweet substance, like licorice or sugar in order to be taken by mouth. The blue mass was a solid form of calomel in which a piece could be pinched off and administered by any one of several possible routes ( e.g. orally, skin absorption, vapor inhalation) by a physician or other medical provider. Neither form of the medication came with a standardization of dosing. There was no way of knowing how much mercurous chloride each dose contained. [ 11 ]
Calomel was marketed as a purgative agent to relieve congestion and constipation; however, physicians at the time had no idea what the medication's mechanism of action was. They learned how calomel worked through trial and error. It was observed that small doses of calomel acted as a stimulant , often leading to bowel movements, while larger doses caused sedation . [ 8 ] During the 19th century, calomel was used to treat numerous illnesses and diseases like mumps, typhoid fever, and others—especially those that impact the gastrointestinal tract, such as constipation, dysentery, and vomiting. [ 9 ] As mercury softened the gums, calomel was the principal constituent of teething powders until the mid-twentieth century. [ 16 ] Babies given calomel for teething often suffered from acrodynia . [ 17 ]
It became popular in the late 18th century to give calomel in extremely high doses, as Benjamin Rush normalized the heroic dose. This caused many patients to experience many painful and sometimes life-threatening side effects.
Calomel, in high doses, led to mercury poisoning , which had the potential to cause permanent deformities and even death. Some patients experienced gangrene of the mouth generated by the mercury in the medicine, which caused the tissue on the cheeks and gums inside the mouth to break down and die. Some patients would lose teeth, while others were left with facial deformities. [ 11 ]
High doses of calomel would often lead to extreme cramping, vomiting, and bloody diarrhea; however, at the time, this was taken as a sign that the calomel was working to purge the system and rid the disease. [ 9 ] Calomel was often administered as a treatment for dysentery ; the effects of calomel would often worsen the severe diarrhea associated with dysentery and acted as a catalyst in speeding up the effects of dehydration. [ 11 ]
One victim was Alvin Smith , the eldest brother of Joseph Smith , founder of the Church of Jesus Christ of Latter-day Saints . [ 18 ] Alvin was suffering from a " bilious colic " better known as abdominal pain.
It was also used by Charles Darwin to treat his mysterious chronic gastrointestinal illness, which has recently been attributed to Crohn's disease . [ 19 ]
By the mid-19th century, some physicians had begun to question the usefulness of calomel. In 1863, the Surgeon General of the U.S. Army forbade calomel from inclusion in army medical supplies, a decision that angered many practicing doctors. The use of calomel gradually died out over the course of the late 19th and early 20th centuries, although its use persisted longer in the American South and American West . [ 9 ]
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Calyculins are natural products originally isolated from the marine sponge Discodermia calyx . [ 2 ] Calyculins have proven to be strong serine/threonine protein phosphatase inhibitors and based on this property, calyculins might be potential tumor-promoting agents.
A laboratory synthesis of calyculin A has been reported. [ 3 ]
Calyculin A is biosynthesized as a pyrophosphate containing phosphocalyculin A protoxins by a hybrid PKS-NRPS pathway within the sponge bacterial symbiont, " Candidatus Entotheonella" sp. [ 4 ]
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Camel urine is a liquid by-product of metabolism in a camel 's anatomy . Urine from camels has been used in medicine for centuries, being a part of ancient Bedouin , ayurvedic and Islamic Prophetic medicine . According to the World Health Organization , the use of camel urine as a medicine lacks scientific evidence . [ 1 ] After the spread of MERS-CoV infections, the WHO urged people to refrain from drinking "raw camel milk or camel urine or eating meat that has not been properly cooked".
Camel urine comes out as a thick syrup. [ 2 ] [ 3 ] [ 4 ] [ 5 ]
The kidneys and intestines of a camel are very efficient at reabsorbing water. Camels' kidneys have a 1:4 cortex to medulla ratio . [ 6 ] Thus, the medullary part of a camel's kidney occupies twice as much area as a cow's kidney. Secondly, renal corpuscles have a smaller diameter, which reduces surface area for filtration. These two major anatomical characteristics enable camels to conserve water and limit the volume of urine in extreme desert conditions. [ 7 ]
Each kidney of an Arabian camel has a capacity of around 0.86 litres and can produce urine with high chloride concentrations. Like the horse , the dromedary has no gall bladder , an organ that requires water to function. [ 8 ] Consequently, bile flows constantly. [ 9 ] Most food is digested and absorbed into the bloodstream from the small intestine. Any remaining liquids and roughage move into the large intestine.
In the Caraka-Samhita, camel urine is mentioned as being slightly bitter. It recommends it as a remedy for hiccups , cough, and hemorrhoids . [ 10 ] However, in the Yogacandrika, camel urine is referred to as having a remedial effect on various abdominal ailments. Furthermore, camel urine is prescribed for alleviating inflammation or =
edema, as per the Kāśyapa Samhitā. [ 11 ]
A hadith in Book 4 ( Ablution ) of al-Bukhari's collection narrated by Anas ibn Malik was used to promote the consumption of Arabian camel urine as a medicine. [ 12 ] [ 13 ] The climate of Medina did not suit some people, so Muhammad ordered them to follow his shepherd and drink his camel's milk and urine (as a medicine). So they followed the shepherd and drank the camel's milk and urine till their bodies became healthy. Then they killed the shepherd and drove away the camels. When the news reached Muhammad, he sent some people in their pursuit. When they were brought, he cut their hands and feet and their eyes were branded with heated pieces of iron. [ 14 ] [ 15 ] [ 16 ] The authentic hadith [ 17 ] also states "Some people of ‘Ukl or ‘Uraina tribe came to Medina and its climate did not suit them ... So the Prophet ordered them to go to the herd of Milch camels and to drink their milk and urine (as a medicine). ... So they went as directed and after they became healthy". [ 14 ] Bukhari also narrated, an otherwise identical version of this Hadith, without the mention of " urine ". [ 18 ] The event has also been recorded in Sahih Muslim , History of the Prophets and Kings and Kitāb aṭ-ṭabaqāt al-kabīr . [ 19 ] [ 20 ] [ 21 ]
Indian Islamic scholar Mohammad Najeeb Qasmi notes various theories proposed by Hanafi and Shaafi’e scholars for a canonical understanding of the implications. This book refers to topical application of milch camel urine as the actual word of the saying has the word Azmadu which means to apply a layer of something. [ 22 ] However, Bachtiar Nasir , an Islamic scholar, advocated for and defended the consumption of camel urine, claiming the mixture of camel urine and milk has medicinal benefits. [ 23 ]
In Middle Eastern societies, camel urine is consumed as medicine, but some see its use as najis [ 24 ] — ritually unclean according to Islam Law. [ 25 ] However, in the Arabian Peninsula , bottled camel urine is still sold and consumed as prophetic medicine. [ 26 ] [ 27 ]
Avicenna in The Canon of Medicine noted that a mixture of camel milk and urine can be beneficial for some diseases such as dropsy and jaundice . [ 28 ]
In Yemen , camel urine is consumed and used for treating ailments, though it has been widely denounced. [ 15 ] Some salons are said to use it as a treatment for hair loss . [ 15 ] The camel urine from a virgin camel is priced at twenty dollars per liter, with herders saying that it has curative powers. It is traditionally mixed with milk. [ 15 ]
Certain preclinical studies have claimed that camel urine possesses various therapeutic advantages, including antimicrobial, anti-inflammatory, anticancer properties, and potential cardiovascular benefits. For example, in 2012, a study conducted at the Department of Molecular Oncology of King Faisal Specialist Hospital and Research Center , and published in the Journal of Ethnopharmacology , found that camel urine contains anti-cancerous agents that are cytotoxic against various, but not all, human cancer cell lines in vitro . [ 29 ]
A study published on the World Health Organization 's Eastern Mediterranean Health Journal found that camel urine showed no clinical benefits in cancer patients, with two of the participants developing brucellosis . [ 1 ] Given the lack of scientific evidence supporting the use of camel urine as a traditional medicine, it is advisable to discontinue its promotion. [ 1 ]
In 2017, a joint study by King Faisal University and the University of Hong Kong found that experimental infections of dromedaries with MERS-CoV did not show any evidence of virus in the urine. Therefore, the camel urine is an unlikely source of virus transmission to humans. [ 30 ] [ 31 ]
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Cameron Health was a medical device developer based in San Clemente, California , US. Cameron Health had its European office, Cameron Health BV, in Arnhem , The Netherlands . The privately held company's focus was on a new generation of minimally invasive implantable cardioverter-defibrillator (ICD) which they called a Subcutaneous Implantable Defibrillator (S-ICD). Cameron Health's approach avoided implanting transvenous leads into the heart , which had been the usual procedure for cardiac devices. Instead, the Cameron ICD was entirely implanted outside the thoracic wall.
In June 2012, Boston Scientific acquired Cameron Health for a total sum of $1.3 Billion, paid out incrementally as various revenue milestones were achieved. [ 1 ] As of February 2016 [update] , Boston Scientific still markets the S-ICD system. [ 2 ]
Every ICD is designed to detect heart rhythms consistent with a catastrophic failure of the body's natural regulation of the heartbeat, which, untreated, could result in death. When an ICD detects a serious arrhythmia , it issues an electrical impulse to the heart muscle, of a magnitude sufficient to cause the heart to revert to a normal rhythm. ICDs with transvenous leads administer this shock to the interior of the heart muscle; the Cameron Health device generated a more powerful shock which can be effective from outside the heart. In the view of Cameron Health, transvenous leads into the heart needlessly complicated the process of implanting a device, and raised other issues and risks which their less invasive approach avoids. [ 3 ]
The Cameron Health subcutaneous ICD sat outside the ribcage and has no connection to the interior of the heart. The surgical procedure for implantation was minimally invasive as opposed to the traditional procedure of threading leads into the subclavian venous system, through the superior vena cava and into one or more endocardial areas of the heart, a procedure often requiring a cardiologist with specialized training in electrophysiology . [ 4 ] In addition to the risks inherent in cardiac surgery, the leads have themselves proved to be a weakness in some ICD designs. [ 5 ] According to one estimate, patients with ICDs have a 20 percent chance of lead failure within 10 years, and replacing the leads carries a risk of death of between two and five percent. [ 6 ] Some device manufacturers have had to replace defective leads which exposed implanted individuals to unnecessary shocks or other malfunctions, in some cases possibly resulting in fatalities. [ 7 ] [ 8 ]
The Cameron Health S-ICD had the disadvantage of being somewhat bulkier than existing ICDs. [ 6 ] Also, this kind of ICD did not include a pacemaker, which narrowed the range of patients for whom it would be appropriate; it was estimated that a majority of patients receiving combination pacemaker/ICD implants would qualify for a pure ICD. These patients tended to have genetic or other conditions predisposing them to sudden cardiac death due to a failure of the heart of maintain a normal rhythm. [ 9 ]
A trial involving 53 patients, who were temporarily implanted with S-ICDs, was reported in 2005 at the European Society of Cardiology Congress. [ 10 ] A second series of 55 trial patients was conducted in 2008 and 2009 in 10 centers in Europe and New Zealand . Of the 55 patients, 53 had two instances of fibrillation and in 52 these were successfully converted. These findings were reported to European Union authorities in 2009, and resulted in approval for marketing the device. A study of 300 patients is in progress for US approvals. [ 6 ] [ 11 ] Small nonrandomized early-phase studies primarily intended to show the feasibility of an entirely subcutaneous ICD were updated, combined and published in May 2010. In this report, the system successfully and consistently detected and converted episodes of ventricular fibrillation that were induced during electrophysiological testing. In the European trial of 55 patients, after 46 patient-years of follow-up, 54 of 55 patients were alive, and the single death was due to renal failure. In this trial the system successfully detected and treated 12 episodes (100%)of spontaneous, sustained ventricular tachyarrhythmia in three patients, prior to the onset of syncope, and with no adverse events. One of the three patients was successfully treated for seven successive episodes of ventricular tachycardia , a condition known as a "VT storm".
Boston Scientific acquired an exclusive option to purchase Cameron Health in 2004, and made an undisclosed equity investment in the company at that time. [ 12 ] In 2008, several additional investors organized by the investment company Piper Jaffray [ 13 ] and including PTV Healthcare Capital, Delphi Ventures, Sorrento Ventures, Three Arch Partners and Versant Ventures provided just over $50 million to finance the continuing operation of the company. [ 14 ]
In June 2012, Boston Scientific officially acquired Cameron Health for a total sum of $1.3 Billion, paid out incrementally as various revenue milestones were achieved. [ 1 ]
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The Cameron Prize for Therapeutics of the University of Edinburgh is awarded by the College of Medicine and Veterinary Medicine to a person who has made any highly important and valuable addition to practical therapeutics [ a ] in the previous five years. The prize, which may be awarded biennially, was founded in 1878 by Andrew Robertson Cameron of Richmond, New South Wales, with a sum of £2,000. The University's senatus academicus may require the prizewinner to deliver one or more lectures or to publish an account on the addition made to practical therapeutics. [ 2 ] A list of recipients of the prize dates back to 1879.
Rockefeller Institute for Medical Research
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Camptocormia , also known as bent spine syndrome (BSS), is a symptom of a multitude of diseases that is most commonly seen in the elderly. It is identified by an abnormal thoracolumbar spinal flexion, which is a forward bending of the lower joints of the spine, occurring in a standing position. In order to be classified as BSS, the anterior flexion (the lower back bending) must be of 45 degrees anteriorly. This classification differentiates it from a similar syndrome known as kyphosis . [ 2 ] Although camptocormia is a symptom of many diseases, there are two common origins: neurological and muscular. Camptocormia is treated by alleviating the underlying condition causing it through therapeutic measures or lifestyle changes.
Camptocormia comes from two Greek words, meaning "to bend" (κάμπτω, kamptō ) and "trunk" (κόρμος, kormos ), and was coined by Alexandre-Achille Souques and B. Rosanoff-Saloff. [ 3 ] These two men also created the definition of the disease that is widely accepted today. [ 2 ]
When the disorder was first clinically studied around the time of First World War , it was believed to be a psychogenic conversion disorder that resulted from the severe trauma of war. Souques and others treated patients with psychological therapy and early versions of electrotherapy . Samuel A. Sandler used a similar approach to treat soldiers during the Second World War . [ 2 ] The view of BSS as a conversion disorder led to a lack of awareness about the conditions and few diagnoses by physicians.
As time progressed and advances were made in knowledge of neuroscience and physiology, biological mechanisms behind the irregular bending were identified. The current medically preferred term for the condition is bent spine syndrome , because of the psychological origin associated with camptocormia . [ 2 ]
BSS is not limited to the elderly but has an average age of onset of 66 years [ 2 ] and is more common amongst men.
The primary symptom of camptocormia is abnormal forward bending of the torso . This bending becomes worse while walking but does not appear when the affected individual is lying down in a horizontal position. This alleviation of the condition indicates that it is a manifestation of another disease or ailment and is not due to a spine that is actually bent. [ 2 ] This is somewhat ironic, since the medically accepted name for the condition is bent spine syndrome.
In an affected individual, the abnormal bending consists of an anterior flexion greater than 45 degrees. [ 4 ] Because of this bending and the physical limitations caused by the conditions associated with the disease, it is usually impossible for an affected person to achieve a fully erect position. In addition, patients with camptocormia often experience low back pain as a result of the condition. BSS often appears in individuals with Parkinson's disease , muscular dystrophies , endocrine disorders , inflammatory conditions ( myositis ), or mitochondrial myopathies . [ 1 ] As previously mentioned, the disease is more common in older individuals.
When initially identified, camptocormia was classified as a psychogenic disease. Although the condition is sometimes a psychogenic manifestation, camptocormia typically originates from either muscular or neurological diseases. However, due to the wide variety of pathologies resulting in camptocormia, there is no singular cause that is most influential for the condition.
Myopathic origin BSS can be secondary to various muscular disorders or occur as a primary idiopathy . [ 2 ] These etiologies are termed secondary and primary BSS respectively. Idiopathic primary BSS is a late-onset myopathy with progressive muscular weakness that is detected on the spinal extensor muscles in elderly patients and is more predominant in females. [ 2 ] The pathogenesis of primary BSS is typically related to fibrosis and fatty infiltration of muscular tissues and to mitochondrial changes due to the aging process. [ 2 ] Specifically, weakening occurs in the paravertebral muscles of patients. These paravertebral muscles have a great influence over the walking stance and gait of a patient, so fatty infiltration and degradation of these muscle lead to the characteristics that easily define BSS, such as the anterior flexion of the back combined with an ability to keep upright with any kind of support (e.g., holding onto a table). [ 4 ]
Secondary BSS can have a multitude of causes, making it hard to pinpoint to a specific muscular disorder. Some examples of diseases that have secondary BSS as a symptom are myopathies caused by muscular dystrophies , neuromuscular disorders , and inflammatory muscle diseases ; metabolic or endocrine disorders; and mitochondrial myopathies. [ 2 ]
A multitude of neurological disorders cause BSS, including motor neuron disease , CNS disorders, and early amyotrophic lateral sclerosis . [ 2 ] Usually, the bent spine is caused by dysfunctioning extensor spinal muscles with a neurological cause.
Neurological origin BSS may also result from damage to the basal ganglia nuclei that are a part of the cerebral cortex , which play a major role in bodily positioning. Damage to this part of the brain can inhibit proper flexion and extension in the muscles necessary for maintaining an upright position. Additionally, the neurotransmitter dopamine plays a key role in the operation of basal ganglia . An abnormally low dopamine concentration, such as that associated with Parkinson's disease , causes dysfunction in the basal ganglia and the associated muscle groups, leading to BSS. [ 2 ] Studies have estimated the prevalence of BSS in people affected by Parkinson's to be between 3% and 18%. [ 1 ]
Several gene mutations have been identified in patients with camptocormia. These include the RYR1 gene in axial myopathy, the DMPK gene in myotonic dystrophy, and genes related to dysferlinopathy and Parkinson's disease. These genes could serve as targets for gene therapy to treat the condition in the years to come. [ 5 ]
In order to qualify a patient's condition as BSS, the bending angle must be greater than 45 degrees. While the presence of the condition is very easy to note, the cause of the condition is much more difficult to discern. Conditions not considered to be BSS include vertebral fractures, previously existing conditions, and ankylosing spondylitis . Lower-back CT scans and MRIs can typically be used to visualize the cause of the disease. [ 5 ] Further identification of the cause can be done by histochemical or cellular analysis of muscle biopsy.
Camptocormia is becoming progressively found in patients with Parkinson's disease . [ 4 ] The diagnosis of Parkinson's-associated camptocormia includes the use of imaging of the brain and the spinal cord, along with electromyography or muscle biopsies.
Muscle biopsies are also a useful tool to diagnose camptocormia. Muscle biopsies found to have variable muscle fiber sizes and even endomysial fibrosis may be markers of bent spine syndrome. In addition, disorganized internal architecture and little necrosis or regeneration is a marker of camptocormia.
Patients with camptocormia present with reduced strength and stooped posture when standing due to weakened paraspinous muscles (muscles parallel to the spine). Clinically, limb muscles show fatigue with repetitive movements. [ 5 ] Paraspinous muscles undergo fat infiltration. Electromyography may be used as well in diagnosis. On average, the paraspinous muscles of affected individuals were found to be 75% myopathic, while limb muscles were 50% percent myopathic. [ 5 ] Creatine kinase activity levels in skeletal muscle are a diagnostic indicator that can be identifiable through blood tests.
Due to the wide range of causes of camptocormia, there is no one treatment that suits all patients. In addition, there is no specific pharmacological treatment for primary BSS. The use of analgesic drugs depends entirely on the intensity of the back pain. Muscular-origin BSS can be alleviated by positive lifestyle changes, including physical activity, walking with a cane, a nutritious diet, and weight loss. Worsening of symptoms is possible but rare in occurrence. [ 2 ]
Treatment of the underlying cause of the disease can alleviate the condition in some individuals with secondary BSS. Other treatment options include drugs, injections of botulinum toxin , electroconvulsive therapy , deep brain stimulation , and surgical correction. [ 6 ] Unfortunately, many of the elderly individuals affected by the BSS are not treated surgically due to age-related physical ailments and the long postoperative recovery period. [ 4 ]
This condition can lead to excess pressure on the spine, causing pain and discomfort. [ 5 ] If the spine is bent too far, a patient may have difficulties breathing because of the pressure of the spine pressed against the lungs. Camptocormia may also lead to muscle weakness in the upper back and to arthritis and other bone-degeneration diseases. [ 5 ] Because of loss of bone strength, injury to the spine and slipped discs become increasingly significant. Camptocormia can lead to infection, tumors, and diseases of the endocrine system and connective tissues. The success of the treatment method is largely dependent on the patient, but response to therapeutic methods is generally low.
Clinical studies have revealed that camptocormia may be hereditary; however, the inheritance mechanism remains unclear. [ 2 ] Current areas of research include molecular and genetic studies aimed at elucidating a possible inheritance model along with molecular pathological mechanisms and proteins responsible for BSS. This research will help will facilitate improvement in the classification, diagnosis, and treatment of the condition. In addition, new technologies and animal models of postural abnormalities are being developed to understand camptocormia and design more effective treatment methods. [ 5 ]
One treatment methodology that is very promising for the treatment of camptocormia is deep brain stimulation . Previously, deep brain stimulation and bilateral stimulation of the subthalamic nucleus and/or globus pallidus internus have been used to treat patients with Parkinson's disease. [ 6 ] Studies have shown that similar treatments could be used on patients with severe camptocormia. By using the Burke-Fahn-Marsden Dystonia Rating Scale before and after treatment, it was found that patients experienced significant functional improvement in the ability to walk. [ 6 ]
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The Canada Gairdner Wightman Award is annually awarded by the Gairdner Foundation to a Canadian who has demonstrated outstanding leadership in the field of medicine and medical science.
Source: Gairdner- Past Recipients
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https://en.wikipedia.org/wiki/Canada_Gairdner_Wightman_Award
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The Canada Ukraine Surgical Aid Program or CUSAP is a mission of Canadian doctors led by Oleh Antonyshyn, a Canadian plastic surgeon of Ukrainian descent. [ 1 ] Initiated by the Canada-Ukraine Foundation in 2014 following the Revolution of Dignity , CUSAP's volunteer doctors provide free treatment to patients, while the Canada-Ukraine Foundation covers operating costs. [ 2 ] [ 3 ] [ 4 ]
From 2014 to 2022, the mission was based in Kyiv. In 2022, with the beginning of the Russian full-scale invasion, the surgical assistance program was relocated to the hospital in Czeładz , Poland. [ 5 ] [ 6 ] [ 7 ]
In April 2014, after the shootings on the Maidan, a Ukrainian-American physician, activist, and philanthropist Ulana Suprun , who served as Director of Humanitarian Initiatives for the Ukrainian World Congress, appealed to the Canada-Ukraine Foundation for medical assistance to Ukrainians wounded during the Revolution of Dignity. [ 2 ] [ 8 ] [ 9 ] [ 10 ]
In March 2014, to assess the state of affairs and the possibilities of medical assistance, the Canada-Ukraine Foundation organized a trip of several representatives of the organization who had medical specialization, including Antonyshyn, [ 10 ] a plastic surgeon at Toronto's Sunnybrook Health Sciences Centre, professor in the Department of Plastic, Reconstructive, and Aesthetic Surgery at the University of Toronto, and a member of the Canadian Ukrainian diaspora. [ 2 ] [ 11 ]
The delegation visited several hospitals in Kyiv where Ukrainians with severe injuries were treated and also visited hospitals in Donetsk . [ 9 ] After visiting at least 20 hospitals all over Ukraine, Oleh Antonyshyn and the leadership of the Canada-Ukraine Foundation established the Canada Ukraine Medical missions. After eight years, it was renamed to the Canada Ukraine Surgical Aid Program (CUSAP). [ 2 ] [ 9 ]
In November of the same year, at the invitation of Antonyshyn, 25 volunteer surgeons, anesthesiologists, and nurses arrived in Ukraine from Canada to carry out a mission to treat patients who were injured during the Revolution of Dignity and those who were wounded in Eastern Ukraine . [ 12 ] [ 13 ] The medical team was assembled across Canada, including Victoria , Vancouver , Edmonton , Winnipeg and Toronto . More than 60 patients from Ukraine with complex post-traumatic conditions and distortions were consulted. A total of 37 reconstructive surgeries were performed on 30 patients. [ 2 ] [ 14 ] [ 15 ]
Between 2014 and 2020, Antonyshyn and the surgical aid team conducted five missions. During each mission, they treated about 40 patients, and by the fifth mission, the medical team was regularly consulting 100 patients. [ 10 ] [ 16 ] [ 17 ]
From 2014 to 2020, the Canadian Mission of Plastic Surgeons was based in Kyiv, and Canadian doctors also performed on-site surgeries in Lviv and Odesa . Over the years of the mission's work in Ukraine, the Canada-Ukraine Foundation has contributed almost 2 million Canadian dollars to Ukrainian hospitals. [ 18 ] [ 19 ]
In 2016, Antonyshyn was awarded the State Award "For Merit" of the III Degree by Presidential Decree. [ 20 ]
In 2017, Antonyshyn received the M. Ochrymovych Humanitarian Award, also known as the Helping Hands Humanitarian Award, from the Ukrainian Canadian Social Services Toronto (UCSST) organization. [ 21 ] [ 22 ] [ 23 ]
With the outbreak of Russia's full-scale war against Ukraine, the Canada Ukraine Surgical Aid Program relocated to Poland. [ 1 ] Operating rooms were set aside in the hospital in Czeładź, [ 24 ] where volunteer doctors from Canada provide orthopedic and plastic surgery to seriously wounded military and civilians, [ 25 ] [ 4 ] who have suffered mine-blast injuries. [ 26 ] [ 27 ] Ukrainian surgeons are also involved in the postoperative care and recovery of the victims. [ 1 ] [ 28 ] [ 29 ] [ 3 ]
In 2022, Polish Prime Minister Mateusz Morawiecki visited the hospital in Czeładź to thank Canadian doctors who operate on seriously wounded war veterans and civilian Ukrainians. [ 30 ] [ 31 ] [ 32 ]
At the beginning of the large-scale invasion, the CUSAP team received more than 120 applications from doctors of various specialties from across North America who wanted to treat Ukrainian patients on a volunteer basis. [ 9 ] One of the mission participants is Steve McCabe, who, together with his team, was the first in the world to perform an arm transplant. The doctor has been participating in CUSAP missions since 2014. [ 33 ] [ 34 ] [ 35 ] [ 36 ]
For some facial reconstructions, plastic surgeons use patients' bones from other parts of the body, or artificial implants printed on a 3D printer. [ 1 ] [ 4 ] [ 16 ]
Operations are performed with the participation of medical specialists from various fields, including maxillofacial surgeons and neurosurgeons, which has a multidisciplinary approach to treatment. [ 2 ] [ 37 ] [ 9 ]
According to Polish law, foreign doctors are prohibited from treating patients in the country without first confirming their qualifications. The Polish government and the Polish Ministry of Health simplified this procedure for CUSAP doctors and issued a 3-week authorization for Canadian doctors to treat patients. [ 38 ] [ 24 ]
On September 11, 2014, the Ukrainian Canadian community in Toronto hosted a charity event, "Unite for Ukraine", to raise funds for the first mission of plastic surgeons to Ukraine. The event was sponsored by Canadian businessman Eugene Melnyk , the Canadian entrepreneur and proprietor of the NHL's Ottawa Senators . The gathering included the attendance of then Prime Minister Stephen Harper , renowned hockey figure Wayne Gretzky , and other notable attendees. [ 15 ] The evening raised over 200,000 Canadian dollars. Other donors included representatives of the Canada-Ukraine Foundation, Canadian corporations, and other institutions, which allocated CAD 500,000 for the second and third missions. [ 39 ] [ 40 ]
CUSAP's last four missions were funded by donor support raised via the Ukraine Humanitarian Appeal, established in 2022 as a joint initiative of the Ukrainian Canadian Congress (UCC) and the Canada-Ukraine Foundation (CUF). [ 41 ] [ 38 ]
The Canada Ukraine Surgical Aid Program is also supported by the Ministry of Health of Ukraine, the Ministry of Defense of Ukraine, and the Ministry of Health of Poland. [ 37 ] [ 18 ] [ 38 ] Also, in 2023, Sunnybrook Health Sciences Centre , in collaboration with the Canada-Ukraine Foundation, launched an educational initiative for Ukrainian surgeons. This program aims to improve patient care in Ukraine through joint training and exchange of experience. During each mission, 15-20 Ukrainian doctors are trained in craniofacial surgery. [ 42 ] [ 43 ] [ 44 ] [ 45 ]
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The Canadian Cardiovascular Society ( CCS ) is the national voice for cardiovascular physicians and scientists in Canada. The CCS is a membership organization that represents more than 1,800 professionals in the cardiovascular field. Its mission is to promote cardiovascular health and care through knowledge translation, professional development and leadership in health policy. [ 1 ]
The official journal of the Canadian Cardiovascular Society is the Canadian Journal of Cardiology (editor-in-chief – Stanley Nattel).
On April 2, 2014, the society released a list of "Five Things Physicians and Patients Should Question" as part of the Choosing Wisely Canada campaign. [ 2 ] CCS recommendations include:
1. Don’t perform stress cardiac imaging or advanced non-invasive imaging when initially evaluating patients when there are no cardiac symptoms present unless the patient has high-risk markers. [ 3 ] [ 4 ]
2. Don’t perform annual stress cardiac imaging or advanced non-invasive imaging in asymptomatic patients in a routine follow-up. [ 5 ]
3. Don’t perform stress cardiac imaging or advanced non-invasive imaging in pre-operative assessment for patients who are scheduled to undergo low-risk non-cardiac surgery. [ 3 ]
4. Don’t perform echocardiography in routine follow-up for adult patients who have mild, asymptomatic native valve disease with no change in signs or symptoms. [ 3 ]
5. Don’t order annual electrocardiograms (ECGs) in patients who are low-risk and do not have any symptoms. [ 6 ]
The Canadian Cardiovascular Society Angina Grading Scale is commonly used for the classification of severity of angina : [ 7 ]
It is similar to the New York Heart Association Functional Classification of heart failure .
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The Canadian Headache Society ( CHS ) is an organization of health care professionals in Canada devoted to headache care, research and education. CHS makes recommendations for the diagnostic criteria [ 1 ] as well as guidelines for the nonpharmacologic and pharmacological management of migraine headache in clinical practice. [ 2 ] [ 3 ] Headache Network Canada – a Canadian registered charity – and CHS maintain an educational website in joint partnership on the subject of headache disorders; both for the general public and health care professionals.
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The Canadian Journal of Surgery is a bimonthly peer-reviewed open access medical journal covering surgery . It was established in 1957 and is published by the Canadian Medical Association . The current editors-in-chief are Edward J. Harvey and Chad Ball. The journal is sponsored by the Canadian Association of General Surgeons , Canadian Society for Vascular Surgery , Canadian Association of Thoracic Surgeons , and Canadian Society of Surgical Oncology .
The journal was established as a result of a collaboration between Canadian departments of surgery , the Royal College of Physicians and Surgeons of Canada , and the Canadian Medical Association . In 1957, leading surgical groups asked the Canadian Medical Association to undertake the publishing of the journal. The founding editorial board consisted of the chairs of surgery at the 12 medical schools in Canada at the time. The president of the Royal College of Physicians and Surgeons of Canada chaired the board. [ 1 ] The first issue was published on 1 October 1957. The Royal College of Physicians and Surgeons of Canada subsidized the journal until 1991 when it withdrew in favor of its own journal, Annals of the Royal College of Physicians and Surgeons of Canada . [ 2 ] Jean Couture then arranged for the Canadian Association of General Surgeons to become the major sponsor of the journal. [ 2 ] Currently the Canadian Journal of Surgery, at 60 years of continuous publication, is the longest surviving journal of record of surgery in 300 years of organised surgery in Canada . [ 3 ]
Journal Citation Reports shows that as of the end of 2016, the Canadian Journal of Surgery had published 5917 citable articles. The average citation per article was 6.9 so that its Impact Factor increased yearly from 0.5 in 2006 to 2.544 in 2017. The journal's h-index is 55 with a normalized Eigenfactor score of 0.42. [ 4 ]
The following persons are or have been editor-in-chief of the journal: [ 5 ]
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The Canary Foundation is a non-profit organization dedicated to discovering highly sensitive and specific biomarkers of early stage cancer and building tests for these markers. [ 1 ] The research goal is to be able to identify cancer through a simple blood test , soon after its development, so that treatment has a higher chance of success.
It was founded in 2004 by former Cisco Systems executive vice president Don Listwin . [ 1 ] As of 2006 [update] , the Science Team included the Nobel Laureate Lee Hartwell , and had partnerships with multiple cancer research centers, including the Fred Hutchinson Cancer Research Center , Stanford University Medical Center , BC Cancer Agency , and University of California, San Francisco Helen Diller Family Comprehensive Cancer Center.
In June 2009, the Canary Foundation, together with Stanford University , committed $20 million to the creation of a research center dedicated to improving cancer early detection. [ 2 ]
This article about a medical , pharmaceutical or biotechnological corporation or company is a stub . You can help Wikipedia by expanding it .
This oncology article is a stub . You can help Wikipedia by expanding it .
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A cancer-associated fibroblast ( CAF ) (also known as tumour-associated fibroblast ; carcinogenic-associated fibroblast; activated fibroblast) is a cell type within the tumor microenvironment that promotes tumorigenic features by initiating the remodelling of the extracellular matrix or by secreting cytokines. CAFs are a complex and abundant cell type within the tumour microenvironment; [ 1 ] the number cannot decrease, as they are unable to undergo apoptosis . [ 2 ]
CAFs have been found to be abundant in a tumour stroma. [ 3 ] [ 4 ] Myofibroblasts and fibroblasts make up CAFs. [ 5 ]
The functions of these CAFs have been known to stimulate angiogenesis , supporting the formation of tumours and thus proliferation of cancer cell and metastasis . [ 6 ] [ 7 ] Cancer cells are usually also drug resistant, which is contributed by CAFs. [ 4 ] As such, this interaction is being studied for potential anti-cancer therapy. [ 8 ]
Normal fibroblasts aid in the production of components of the extracellular matrix such as collagens , fibres, glycosaminoglycans and glycoproteins and are therefore vital in tissue repair in wound healing. [ 9 ]
CAFs however, are derived from either normal fibroblasts, pericytes , smooth muscle cells, fibrocytes or mesenchymal stem cells [ 10 ] These CAFs then go on to support tumour growth by secreting growth factors such as Vascular Endothelial Growth Factor ( VEGF ), Platelet Derived Growth Factor ( PDGF ) and Fibroblast Growth Factor ( FGF ) and other chemokines to stimulate angiogenesis and thus the growth of a tumour. [ 11 ]
CAFs produce a number of proteins that are specific to the origin of the cells. [ 12 ] However, as there are no specific protein to CAFs, a combination of these proteins are then used as markers to identify CAFs [ 4 ] High levels of the marker would mean a low prognosis due to the stage of cancer.
Markers for CAFs are notably similar to those of surrounding tumour-associated cells but at the same time, display massive heterogeneity of behaviour, appearance and genotype. [ 19 ]
In 2017 Swedish researchers tried to classify molecularly distinct fibroblasts into groups depending on their differential expression of markers. They found overlapping expression patterns which supported the idea that there are transitional states and even identified pluripotency in some patients’ activated fibroblasts (suggesting progenitor cells).
Pleotropic functions (e.g. tumour-promoting and tumour-inhibiting) require cell plasticity. [ 20 ]
While there are positive markers for CAFs, there are also negative markers namely; cytokeratin and CD3, as CAFS do not have epithelial and endothelial characteristics. [ 21 ]
The origins of CAF differ depending on the tumour histotype and where the tumour originated in the first place but can be broadly separated into 4 categories. The origin of each type of CAF has a role in determining the function of that specific cell. [ 1 ] [ 23 ]
These CAFs arise from fibroblasts within the vicinity of the tumour that have been recruited by cancer derived growth factor. This process is similar to active inflammation with the main difference between these two processes being that, in cancer, the fibroblasts can't be deactivated which has led to tumours being referred to as “wounds that do not heal.” [ 24 ] It is believed that most CAFs arise from differentiated resident fibroblast cells. [ 25 ]
The normal fibroblast cells receive a hormone signal from nearby cancer cells, indicating that it must become activated, and is thus classed as a CAF. [ 2 ] It is unclear why normal fibroblasts transition into CAFs but it has been found that by adding transforming growth factor-β to fibroblasts in culture they start to display features of CAFs. [ 26 ] TGF-β is known to control the activation of fibroblasts in inflammation.
CAFs can also be recruited from a remote source, such as the bone marrow. For example, fibroblasts recruited from the bone marrow were found in breast cancer. [ 27 ]
CAFs can also be derived from differentiation of other cell types such as mesenchymal stem cells, which was proved in murine models with cancers such as glioma, breast, pancreatic and gastric cancers. [ 27 ] Another suggested origin is differentiation of endothelial or epithelial cells via trans-differentiation or epithelial to mesenchymal transition, respectively. [ 28 ] [ 29 ]
Less common origin of CAFs is by differentiation of other tumor adjacent cells such as epithelial or endothelial cells, adipocytes, pericytes and smooth muscle cells. [ 27 ] Adipocytes, especially white adipocytes transdifferentiate into CAFs upon activation with TGF-β1. Through TGF-β1 can be transformed also peritoneal mesothelial cells. [ 30 ]
It has been suggested that CAFs are better conceptualised as a “cell state” [ 8 ] Research has found that CAF trans-differentiation can be caused by epigenetic factors. [ 31 ]
In general, the presence and density of cancer associated fibroblasts (CAF) point towards a bad prognosis for the patient, and so, are pro-tumour. These could however be used as markers for diagnosis and therapies, thus diagnosing at an earlier stage.
The presence of podoplanin in CAFs has been found to play a fundamental role in worsening the prognosis of patients with lung adenocarcinoma; this could however be helpful as a marker to diagnose at an early stage. [ 32 ]
In oesophageal adenocarcinomas, CAFs release the ECM (Extracellular Matrix) protein periostin and promote tumour cell growth through paracrine signalling. However, blocking specific integrin receptors and pathways can ceases the invasion of tumor cells. [ 33 ] The greater the density of CAFs found in oral cancer, the poorer the prognosis, as this significantly decreases the 5 year survival rate. Being female in this study also proved to be a bigger risk factor, with men being protected more against the effects. [ 34 ]
Cancer-associated fibroblasts negatively influence the outcome of oncological diseases. These cells create a stromal niche for cancer cells and especially cancer stem cells, where they employ both paracrine and direct cell-contact to maintain stemness in cancer stem cells. In turn, this enables these cancer stem cells to escape chemotherapy and radiotherapy, while the cancer-associated fibroblasts also create an environment that allows cancer cells to escape the action anti-tumour immunity. [ 35 ] In turn, this promotes the cancer process through tumour growth and also fosters angiogenesis, metastasis and immune evasion. CAF express various cytokines and factors, which activate and contribute to pathways favouring tumorigenesis. [ 36 ] They may disrupt normal cell functions, such as cell cycle regulation and cell death, or signal to specific types of cells to mobilize and activate their pro-tumour actions. [ 37 ] Furthermore, it has been found that the effect of CAF on neoplastic cells is unique to the type of tumour cells.
Cytokine release from CAFs have been linked to breast carcinomas through the metabolism and production of androgen synthesis enzymes. [ 38 ] Furthermore, on the topic of the progression of breast cancer, CAFs induces the release growth factors such as FGF and HGF which in turn induces the hyperproliferation of epithelial cells of the breast. EMT [ clarification needed ] and ECM reorganisation are further mechanisms by which the CAFs induce cancer. [ 39 ] FSP1, which is secreted by CAFs, promotes tumours through another method - by altering the tumour microenvironment (TME). [ 40 ] Some CAFs also recycle the by-products of anaerobic metabolism by resorting to other metabolic pathways to sustain the growth of cancer cells. [ 41 ] [ 42 ]
CAFs can produce cytokine TGF-β which has inhibitory effect on T cells, macrophages and neutrophils thus they are not able to promote immune response against the tumor. [ 17 ]
Immune system is greatly affected by CAFs. CAFs promote the recruitment of monocytes and induce their differentiation into pro-tumorigenic macrophage subset M2. In breast cancer secretion of monocyte chemotactic protein-1 , stromal-derived factor 1 and chitinase 3-like 1 is a signal for monocyte migration and differentiation into M2 subset. Similar effect was observed in prostate carcinoma. [ 30 ] In pancreatic cancer, other cytokines have central role in monocyte differentiation into M2 subset such as M-CSF1, IL-6 and CCL2 . Other cytokines such as IL-8 , IL-10 , TGF-β also participate. [ 30 ] Such M2 macrophages then further activate progression of CAFs. [ 43 ]
CAFs have inhibitory effects on NK cells by releasing prostaglandin E2 (PGE2). In hepatocellular carcinoma besides PGE2, indoleamine 2,3-dioxygenase (IDO) is suppressing NK cells. [ 30 ]
In the restriction of anti-tumor immunity are crucial regulatory T cells (Treg; Foxp3+). CAFs stimulate migration, induction and maintenance of Treg cells which depends on the chemokines CCL5 and CXCL12. [ 30 ]
Critical for anti-tumor immunity are cytotoxic CD8+ T cells. [ 30 ] CAFs decrease their infiltration into tumor by releasing chemokine CXCL12 and cytokines IL-6 and TGF-β. However, for T cell movement restriction in tumors is also responsible hypoxia, which leads to decrease of expression of adhesion molecules on endothelial cells. [ 30 ] Other mechanism how T cells are suppressed by CAFs is high expression of checkpoint molecules such as PD-L1, PD-L2, B7-H3/H4, galactins and the enzyme IDO. [ 30 ] CAFs in pancreatic cancer upregulate PD-1, CTLA-4 or TIM-3 on both CD4+ and CD8+ T cell surfaces. [ 30 ]
Angiogenesis is an essential aspect of tumour development. In order for a tumour to grow and significantly increase in size, it must have a sufficient blood supply. If the tumour is unable to develop the blood supply it requires, cells within the tumour will begin to die and further growth will be halted. Angiogenic factors such as vascular endothelial growth factor (VEGF), stromal cell-derived factor 1 (SDF-1), fibroblast growth factor (FGF) and platelet-derived growth factor (PDGF) are expressed by CAF to encourage the growth of new blood vessels. [ 4 ] Some of these factors may also recruit cells that are vital to the angiogenic process, for instance SDF-1 attracts bone-marrow derived endothelial cells. [ 44 ]
CAF have been found to promote tumour metastasis in numerous ways. Firstly, they may alter gene expression and have been found to upregulate specific genes involved in pro-tumorigenic pathways including heat shock factor 1 (HSF1). [ 44 ] They can also interfere with the function of tumour suppressor genes, such as Tumour protein p53, leading to higher rates of cell proliferation due to the loss of control of the cell cycle. [ 44 ] Additionally, CAF have the ability to break down proteins in the extracellular matrix and basement membranes leading to disruption to the normal structure allowing cells to move away from their primary region. The group of proteins known as the matrix metalloproteinases are key to this process. [ 4 ] CAF also direct the movement of neoplastic cells by using the Rho-dependent signaling pathway to create tracks for these cells in the matrix. [ 37 ]
In some cases, the characteristics of CAF provide therapeutic resistance. Soluble factor resistance occurs when CAF either directly secrete signals (cytokines or growth factors) or influence the cells around them to give off similar signals, which reduce the efficacy of therapeutic drugs. For instance, this can either be done by an increased secretion of antiapoptotic factors or by altering the cell environment (e.g. pH) to counteract the actions of the drug. [ 4 ] Another form is cell adhesion- mediated drug resistance. [ 37 ] This involves the tight attachment of neoplastic cells to the extracellular matrix or stromal cells. For example, secretion of TGF-beta allows cancerous cells to bind more successfully to the extracellular matrix thus evading the action of some cancer drugs.
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Cancer-related fatigue is a symptom of fatigue that is experienced by nearly all cancer patients. [ 1 ]
Among patients receiving cancer treatment other than surgery, it is essentially universal. Fatigue is a normal and expected side effect of most forms of chemotherapy , radiation therapy , and biotherapy . [ 2 ] On average, cancer-related fatigue is "more severe, more distressing, and less likely to be relieved by rest" than fatigue experienced by healthy people. [ 2 ] It can range from mild to severe, and may be either temporary or a long-term effect.
Fatigue may be a symptom of the cancer, or it may be the result of treatments for the cancer.
The pathophysiology of cancer-related fatigue is poorly understood. It may be caused by the cancer or the effects it has on the body, by the body's response to the cancer, or by the cancer treatments .
Fatigue is a common symptom of cancer. [ 3 ] One meta-analysis estimated that around 43% of individuals with cancer report experiencing fatigue. [ 4 ] The study also highlighted that fatigue levels can differ depending on factors like the type of cancer, the stage of treatment, and gender. Notably, women were found to experience more severe fatigue than men. [ 4 ]
Some fatigue is caused by cancer treatments. This may show a characteristic pattern. For example, people on many chemotherapy regimens often feel more fatigue in the week after treatments, and less fatigue as they recover from that round of medications. People receiving radiation therapy , by contrast, often find their fatigue steadily increases until the end of treatment. [ 3 ]
A systematic review and meta-analysis found that approximately 42% of working cancer survivors report experiencing cancer-related fatigue. [ 5 ] The analysis also identified emotional distress as a possible contributing factor to ongoing fatigue symptoms. These findings suggest that both physical and psychological factors may influence fatigue in working survivors, indicating the potential value of supportive workplace strategies [ 5 ]
Proposed mechanisms by which cancer can cause fatigue include an increase in pro-inflammatory cytokines , dysregulation of the hypothalamic-pituitary-adrenal axis , disruption of circadian rhythms , muscle loss and cancer wasting , and genetic problems. [ 2 ] Additionally, some forms of cancer may cause fatigue through more direct mechanisms, such as a leukemia that causes anemia by preventing the bone marrow from producing blood cells efficiently. A relationship between Interleukin 6 and fatigue has been observed in studies, albeit inconsistently. Increased markers of sympathetic nervous system activity are also associated with cancer related fatigue. [ 6 ]
The National Comprehensive Cancer Network recommends that every cancer patient be systematically screened for fatigue at the first visit with an oncologist , throughout treatment, and afterwards. [ 2 ] Screening typically involves a simple question, like "On a scale of one to ten, how tired have you felt during the last week?"
More detailed information may be collected in a symptom journal .
Some causes of cancer-related fatigue are treatable, and evaluation is directed towards identifying these treatable causes. Treatable causes of cancer-related fatigue include: anemia , pain , emotional distress , sleep disturbances , nutritional disturbances, decreased physical fitness and activity, side effects from medications (e.g., sedatives ), abuse of alcohol or other substances. [ 2 ] Additionally, other medical conditions , such as infections , heart disease , or endocrine dysfunction (e.g., hot flashes ), can cause fatigue, and may also need treatment.
The National Comprehensive Cancer Network defines cancer-related fatigue as "a distressing persistent, subjective sense of physical, emotional and/or cognitive tiredness or exhaustion related to cancer or cancer treatment that is not proportional to recent activity and interferes with usual functioning". [ 2 ]
Cancer-related fatigue is a chronic fatigue (persistent fatigue not relieved by rest), but it is not related to chronic fatigue syndrome . [ 3 ] Cancer-related fatigue occurs in a significant proportion of cancer survivors, both during and after cancer treatment. [ 7 ] A review of current evidence indicates that exercise is the most effective way of ameliorating cancer-related fatigue. [ 7 ]
Cancer related fatigue is common in patients undergoing treatment for prostate cancer . [ 8 ] A systematic review of the prevalence of cancer-related fatigue in men with prostate cancer was performed. [ 9 ] The analysis indicated that fatigue is a common symptom, occurring in about 40% of men with prostate cancer especially among those using hormone therapy. [ 9 ]
Cancer-related fatigue is a prevalent and significant symptom among breast cancer patients, often lasting for years after treatment. [ 10 ] An empirical study regarding cancer-related fatigue in breast cancer patients identified different groups of patients based on their fatigue levels, with nearly half (47.5%) falling into an "exhausted" group, characterized by high fatigue severity and interference in daily activities, along with elevated stress, anxiety, depression, and sleep disturbance, significantly impacting quality of life. [ 10 ]
Treatment depends on the patient's overall situation. A patient who is in active treatment may have different priorities than a person who has completed treatment, or who is at the end of life.
Some management strategies may help all patients and could be supported by the work of an Occupational Therapist . These include scheduling high-priority tasks during the patient's best time of day, using labor-saving devices, delegating tasks to caregivers, and avoiding unimportant activities, so that the patient will have more energy available for other activities. [ 11 ]
Patients who are not at the end of life may benefit from physical exercise or physical therapy . [ 12 ] Engaging in physical activity may reduce fatigue. [ 2 ] [ 13 ] [ 14 ] [ 15 ] Forms of exercise that have been proven to be most effective are more aerobic exercise such as walking, running, cycling, and swimming. [ 16 ] These forms of activity can be done at various levels of intensity and have been proven as an effective way of improving quality of life for cancer patients. [ 17 ] A network meta-analysis evaluated the effectiveness of various exercise modalities in alleviating CRF among breast cancer patients. The findings indicated that yoga was the most effective, followed by combined aerobic and resistance exercises. [ 18 ] In addition to general exercise and yoga, other mind-body practices such as Qigong have demonstrated potential benefits in managing CRF.
With its focus on the integration of inner awareness, breathing, and body, yoga differs from general aerobic exercise. [ 19 ] Hatha yoga , a commonly practiced and accessible form of yoga, integrates physical postures ( asanas ) and breathwork ( pranayama ) and was featured in several interventions evaluated for their effectiveness in reducing cancer-related fatigue. Mixed types of yoga—those combining physical postures, breathing control, and mindfulness—were associated with increased patient adherence and improved fatigue outcomes. [ 19 ] Physical postures, often involving gentle stretching and movement, contributed to improved physical function, especially when paired with breathwork or meditative elements. [ 19 ] Breathing techniques alone, such as pranayama-based interventions, also demonstrated positive effects on fatigue management by potentially modulating stress and supporting emotional well-being. These interventions were most effective when delivered as part of a strategy that included both supervised group sessions and ongoing self-practice. As a low-intensity form of exercise, yoga practice of 150 minutes or greater per week is considered safe and effective for alleviating cancer-related fatigue. [ 19 ]
Qigong is a traditional Chinese practice that combines gentle movements, breathing exercises, and meditation to cultivate and maintain health and well-being. Research has consistently found that Qigong practice relieved cancer-related fatigue. [ 20 ] A systematic review and meta-analysis of randomized controlled trials found that Qigong practice is comparable to the effects of other intervention therapies for cancer-related fatigue, including Western exercise. [ 20 ] Mindful Exercises like Qigong may offer an alternative strategy for individuals who find it difficult to adhere to or adapt to medium or high-intensity aerobic exercise. Larger reductions in fatigue were observed among patients with higher baseline fatigue scores following Qigong intervention. [ 20 ] Different styles of Qigong, such as Taiichi Qigong, Badu Anjin Qigong, and Guolin Qigong, have been used in studies examining their effects on cancer-related fatigue.
In addition to yoga and Qigong, other mindfulness-based interventions (MBIs) have been studied for their potential in managing cancer-related fatigue. These interventions typically aim to help individuals become more aware of present-moment experiences, including physical sensations and thought processes, while adopting a nonjudgmental and accepting attitude. [ 21 ]
One of the most frequently studied MBIs is Mindfulness-Based Stress Reduction (MBSR), a structured program that uses practices such as body scanning, mindful breathing, and gentle movement to help individuals recognize and accept discomfort without judgment or avoidance. MBSR has been shown in multiple studies to reduce symptoms of fatigue and emotional distress in oncology populations. [ 21 ]
Mindfulness-Based Cognitive Therapy (MBCT) builds upon the MBSR model by incorporating elements of cognitive therapy , particularly techniques aimed at helping individuals identify and disengage from repetitive or negative thought patterns. MBCT interventions have been used to support patients in reducing cognitive reactivity, which may contribute to the emotional and psychological aspects of fatigue. [ 21 ]
Mindfulness-Based Cancer Recovery (MBCR) is an adaptation of MBSR specifically tailored for individuals with cancer. It focuses on addressing the unique psychological and physical challenges faced by cancer patients through mindfulness training. While fewer studies have evaluated MBCR compared to MBSR or MBCT, preliminary evidence suggests potential benefits in improving fatigue-related outcomes. [ 21 ]
Recent research has explored several complementary approaches for managing cancer-related fatigue (CRF), including microbiome -based therapies, nurse-led interventions, and melatonin supplementation. A systematic review examining the use of probiotics and synbiotics found preliminary evidence suggesting they may help reduce CRF symptoms, though the authors emphasized the need for more extensive clinical trials to confirm their effectiveness. [ 22 ] Another systematic review focusing on nurse-led interventions showed that multidisciplinary strategies—particularly those involving physical activity and psychological support—can be beneficial in easing fatigue among cancer patients. [ 23 ] Additionally, a meta-analysis on melatonin supplementation reported that taking melatonin, especially for periods of 13 weeks or longer, may lead to noticeable improvements in fatigue severity. [ 24 ]
While antidepressants are ineffective at reducing fatigue in non-depressed cancer patients, psychostimulants such as methylphenidate and amphetamines may reduce fatigue in some patients. [ 2 ] [ 25 ] [ 26 ] [ 27 ] [ 28 ] Methylphenidate may be effective in the management of cancer-related fatigue. If methylphenidate were to be used in patients with CRF, it would be prudent to restrict its use to patients with advanced disease or for short-term use in patients on active treatment. The clear advantage of methylphenidate in cancer is its rapid onset of action within 24–48 hours, and so the drug can be discontinued if ineffective. [ 29 ]
At the end of life, fatigue is usually associated with other symptoms, especially anemia, side effects from many medications and previous treatments, and poor nutritional status. [ 2 ] Pain, difficulty breathing , and fatigue form a common symptom cluster. Fatigue often increases as patients with advanced cancer approach death. As a result, people who are dying often sleep much more than a healthy person. [ 30 ] [ 31 ]
If the fatigue is caused or exacerbated by a specific medical condition, such as anemia, then treatment of that medical condition should reduce the fatigue.
Fatigue caused by the cancer or its treatment often resolves if treatment is successful. However, some patients experience long-term or chronic fatigue. When strict definitions are used, about 20% of long-term, disease-free cancer survivors report fatigue. [ 2 ] Under looser definitions, up to half of cancer survivors report fatigue. [ 2 ] However, these studies are largely limited to patients with breast cancer , or peripheral stem cell transplant or bone marrow transplant patients, and the incidence may be different for survivors of other cancers.
Experiencing fatigue before treatment, being depressed or anxious, getting too little exercise, and having other medical conditions are all associated with higher levels of fatigue in post-treatment cancer survivors. [ 2 ] Receiving multiple types of treatments, such as chemotherapy and radiation, is associated with more fatigue. [ 3 ] Older adults have a higher risk of long-term fatigue. [ 3 ]
Cancer-related fatigue has consistently been found to be one of the most prevalent and distressing symptoms in childhood cancer survivors. [ 35 ] The International Late Effects of Childhood Cancer Guidelines Harmonization Group (IGHG) has published recommendations regarding the surveillance of fatigue in survivors of childhood cancer. [ 36 ] These recommendations include regular screenings of fatigue in survivors of childhood cancer. Survivors of pediatric brain tumors report more fatigue after end of treatment than survivors of acute lymphoblastic leukemia, but both groups experience more fatigue than healthy children and adolescents. [ 37 ] While considered a long-term effect of the treatment, children and adolescents experience fatigue already during the treatment for acute lymphoblastic leukemia and this side-effect of treatment remains in some patients after the treatment has ended. [ 38 ] Fatigue after treatment for pediatric brain tumors does not automatically resolve itself, but requires surveillance and interventions. [ 39 ]
Cancer-related fatigue in older adults is the most distressing symptom of cancer, as described by those still undergoing treatment and survivors alike. This is especially distressing for older adults, as 60% of cancer diagnoses are in people 65 and up. [ 40 ] An issue with identifying the cause of cancer-related fatigue is the potential of comorbidities . Beyond cancer and treatment related fatigue, older adults may suffer from frailty syndrome or various age-related issues. Moreover, there is a rise in fatigue reported in older adults when compared to studies of the past. [ 41 ] Some existing methods of treating fatigue in older adults include exercise, education, and prescribing antidepressants. [ 42 ] Depression is especially prevalent in older adults with cancer. The existence of depressive symptoms in an already at risk group further exacerbates the decreased quality of life in this group. Due to the other comorbidities existing in this group, depression is often overlooked, which contributes to why older adults with cancer are one of the most at-risk groups for committing suicide. [ 43 ] Fatigue in older adults with cancer is a long lasting and dangerous symptom that requires surveillance and informed aid.
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Cancer symptoms are changes in the body caused by the presence of cancer. They are usually caused by the effect of a cancer on the part of the body where it is growing, although the disease can cause more general symptoms such as weight loss or tiredness. There are more than 100 different types of cancer with a wide range of signs and symptoms which can manifest in different ways. [ 2 ]
Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. [ 3 ] [ 4 ] Cancer can be difficult to diagnose because its signs and symptoms are often nonspecific, meaning they may be general phenomena that do not point directly to a specific disease process. [ 5 ]
In medicine, a sign is an objective piece of data that can be measured or observed, as in a high body temperature (fever), a rash, or a bruise. [ 6 ] A symptom, by contrast, is the subjective experience that may signify a disease, illness or injury, such as pain, dizziness, or fatigue. [ 7 ] Signs and symptoms are not mutually exclusive, for example a subjective feeling of fever can be noted as sign by using a thermometer that registers a high reading. [ 7 ]
Because many symptoms of cancer are gradual in onset and general in nature, cancer screening (also called cancer surveillance) is a key public health priority. This may include laboratory work, physical examinations, tissue samples, or diagnostic imaging tests that a community of experts recommends be conducted at set intervals for particular populations. Screenings can identify cancers before symptoms develop, or early in the disease course. [ 8 ] Certain cancers can be prevented with vaccines against the viruses that cause them (e.g., HPV vaccines as prevention against cervical cancer). [ 9 ]
Additionally, patient education about worrisome symptoms that require further evaluation is paramount to reduce morbidity and mortality from cancer. Symptoms that cause excess worry, symptoms that persist or are unexplained, and/or the appearance of several symptoms together particularly warrant evaluation by a health professional. [ citation needed ]
Cancer may produce symptoms in one or more of the following ways: [ citation needed ]
Symptoms of cancer may be nonspecific changes to the individual's sense of physical well-being (constitutional symptoms), or may localize to a particular organ system or anatomic region. [ citation needed ]
The following symptoms may be manifestations of an underlying cancer. [ 12 ] [ 13 ] [ 14 ] Alternatively, they may point to non-cancerous disease processes, benign tumors, or even be within the physiological range of normal. They may appear at the primary site of cancer or be symptoms of cancer metastasis, or spread. Further workup by a trained healthcare professional is required to diagnose cancer. [ 13 ]
Blood in sputum (hemoptysis)
Shortness of breath (dyspnea)
Unusual diarrhea or constipation
Continuing indigestion or heartburn
Abdominal pain, bloating, or nausea
Blood in the stool
Enlarged liver
Any abnormal bleeding , including menstrual irregularities*, bleeding from the vagina
blood in urine
Uterine, ovarian or vaginal cancer
Unexplained rash
Unusual lump
Changes in a mole *
Oral cancers, or other cancers of the tissues where they develop
**These are often evaluated with the ABCD mnemonic for changes in
Changes in skin texture, e.g. dimpling
Inversion of nipples
Unusual or bloody discharge
Fractures, esp. spinal
Swollen lymph node or unusual lump
Lymphomas
New-onset seizures
Vertigo
When patients present with "suspicious symptoms", healthcare providers follow specific guidelines or diagnostic pathways to evaluate for potential cancer. Healthcare professionals face challenges of distinguishing potentially serious symptoms as opposed to common benign conditions. Recent research in the UK has shown that some cancer types often require multiple consultations before confirmed diagnosis. Understanding these diagnostic challenges is crucial for both the healthcare providers and patients in navigating the cancer diagnostic process effectively and ethically. [ 15 ]
A healthcare professional may pursue a formal diagnostic workup to evaluate symptoms of cancer. The tests ordered will depend upon the type of cancer suspected. These may include the following: [ 16 ]
Modern approaches to cancer detection have evolved beyond traditional symptom recognition because of new technologies that can potentially identify cancers at earlier, more treatable stages.
Cancer biomarkers provide crucial information about the different states of cells when transitioning from healthy to malignant cancer conditions. Recent research has shown proof of extensive biomarker technologies that show potential for early cancer detection, primarily focusing on minimally invasive approaches. These minimaly invasive approaches are being developed to complement traditional screening methods. Essentially, these modern technologies and how they can detect cancer at earlier stages rather than traditional symptom recognition, could overall potentially improve survival rates. [ 17 ]
Liquid biopsies allow for minimally invasive molecular characterizations of cancers through the detection of circulating different cells and their DNA. This technology offers guidance on how these approaches could be beneficial for detection of early cancer symptoms before they actually develop, potentially leading to earlier intervention and improved outcomes. [ 18 ]
Artificial intelligence (AI) applications in cancer diagnosis across clinical practices, while also keeping in mind the potential challenges, could be a beneficial impact for cancer screening and diagnostic processes. AI algorithms can analyze medical images, detect patterns in biomarker data, and help identify patients who are high-risk and may benefit from more extensive screening and applications like ai. These technologies could aim to assist healthcare professionals in screening asymptomatic patients, investigating symptomatic patients, and diagnosing cancer more effectively than just traditional methods alone. [ 19 ]
Cancers treatments may include surgery , chemotherapy , radiation therapy , hormonal therapy , targeted therapy (including immunotherapy such as monoclonal antibody therapy ) and synthetic lethality , most commonly as a series of separate treatments (e.g. chemotherapy before surgery). Some of these cancer therapies may produce treatment-related, or secondary, symptoms, including:
Symptoms that require immediate treatment include:
Cancer-related symptom burden refers to the cumulative impact of physical, psychological, and emotional symptoms —such as pain , fatigue , nausea , and emotional distress (e.g., anxiety, depression)—experienced by individuals with cancer due to the disease and its treatment. This burden encompasses both the severity of these symptoms and the patient's perception of their impact on daily life and overall well-being. [ 22 ]
In 2013, the Eastern Cooperative Oncology Group (ECOG), informed by recommendations from an expert panel from the Center for Medical Technology Policy and comprehensive systematic reviews, established core symptoms that represent commonly reported cancer-related (including treatment-related) symptoms for the purposes of clinical research and assessment of quality of care. [ 23 ] [ 24 ] [ 25 ] [ 26 ] Individuals with breast, prostate, colorectal, and lung cancers—of all disease stages and phases of care—were represented in their large multi-center study. These symptoms include, but are not limited to:
Other patient-reported outcomes such health-related quality of life (HRQoL) , a broader construct which subjectively assesses life as a whole, may be confused with cancer-related symptom burden. Both constructs are considered when effectively defining endpoints in cancer clinical trials that share a common goal of symptom reduction. [ 22 ] Contrary to HRQoL, cancer-related symptom burden focuses more on the impact of nonspecific, often co-occurring symptoms, and symptom clustering which are not are not monitored as closely as other toxicities within clinical settings, to ultimately inform symptom management. [ 22 ]
Measures that assess for cancer-related symptom burden recognize that patients can experience multiple symptoms as a result of disease and/or treatment. Collectively, they can be thought of as an indicators of symptom severity and the perception of the extent to which these symptoms affect daily functioning. [ 22 ]
A variety of PROs are utilized to assess symptom burden among cancer patients participating in cancer clinical research. Common measures recommended due to their psychometric properties and utility in cancer clinical research include:
Many of these measures also have adapted versions according to specific cancer and/or illness type. [ 24 ] In addition to clinical trials, many PROs are increasingly being collected within ambulatory care settings to inform symptom management and intervention as well as through electronic methods such as electronic patient-reported outcomes .
There is no formal diagnosis for cancer-related symptom burden as it is conceptualized as a constellation of concerns commonly reported by individuals with cancer, any of which, may be endorsed at any time before, during, or after treatment and throughout the cancer control continuum . [ 27 ]
Accurate assessment of cancer-related symptom burden requires repeatedly measuring the types, severity, and effects symptoms that patients experience throughout their cancer journey. Scientific review studies have advocated for standardization among PROs to capture this information in a consistent manner. [ 28 ] [ 29 ] [ 23 ] [ 24 ] Existing measures allow clinicians to measure the severity of symptoms and follow their progression over time to ensure timely interventions can be made to minimize any negative patient impacts.
Further, scientific reviews have identified common clusters of symptoms in cancer patients such as fatigue, pain, and depression. Identification of such clusters is important since they can contribute to increased symptom burden and negatively impact quality of life. [ 30 ] Holistic diagnostic methods that recognize the interactions between several symptoms are important to appropriately diagnosing and treating these symptoms. [ 30 ] Standardized PROs along with identification of common symptom clusters can help provide clinicians with the necessary information to manage symptom burden in a timely manner, thereby improving patient care and outcomes. [ 30 ]
Recent research on ePROs have provided general support for the implementation of ePRO-based interventions to improve symptom burden, quality of life, and survival among individuals with cancer. [ 31 ] Additionally, among patients receiving specific treatments, these interventions were found to be effective in reducing symptom burden and promoting better quality of life. [ 31 ]
A scientific review also highlighted potential non-pharmacological interventions for individuals with cancer experiencing pain concerns and facing social disparities such as identifying as an ethnic minority, having low income, and vulnerable women. [ 32 ] This study revealed a high risk of bias across studies evaluating education, coaching, and online support group interventions and underscored the need to further investigate supportive care interventions that are responsive to the needs of individuals facial social disparities. [ 32 ]
Another review of randomized controlled trials evaluating nursing interventions aimed at reducing symptom burden in adult cancer patients highlighted some clinically meaningful reductions in symptom burden but cautioned against making any definitive conclusions and potential generalizations regarding key components, circumstances, and target population of the interventions and called for further research. [ 33 ]
There is also some support for the potential utility of mindfulness based interventions (MBIs) in reducing symptom burden among individuals with cancer. [ 34 ]
Comprehensive review studies demonstrate that symptom burden can often persist beyond completion of primary treatment. A meta-analysis that included breast, gynecological, prostate, and colorectal cancer survivors showed that fatigue, pain, and psychological distress persisted well beyond treatment completion, ultimately impacting quality of life negatively. [ 35 ] This in turn, highlights the need for continued symptom monitoring, management, and supportive care that is responsive to the long-term needs of cancer survivors. [ 35 ]
Additionally, studies suggest that cancer patients with advanced disease often have several different co-occurring symptoms, which translates into a high overall burden. One scientific review revealed that pain, fatigue, and depression symptoms overlapped in a way that negatively impacted daily functioning and quality of life in these patients. [ 30 ] Understanding and treating these symptom clusters from a holistic palliative care perspective is critical to patients' outcomes and quality of life. [ 30 ]
The general increase observed in both symptom burden and HRQoL in late stage vs. early stage disease across 10 cancer types studied in a recent scientific review, also underscores the need for earlier detection and intervention to promote survival as well as minimize the adverse effects on symptom burden and HRQoL. [ 36 ]
These findings underscore the need for comprehensive, ongoing symptom assessment and treatment across the cancer control continuum [ 27 ] to improve cancer patient outcomes and reduce symptom burden.
Recent research has revealed that cancer-related symptom burden varies widely by race and ethnicity. For example, a retrospective analysis of symptom burden by race and ethnicity in a large cohort of cancer patients revealed that racial and ethnic minority patients experienced greater symptom burden than non-Hispanic White patients. [ 37 ]
Additionally, studies on social determinants of health and symptom burden in cancer treatment suggest that marginalized cancer survivors might experience significantly greater symptom burden including higher frequency and severity, and higher levels of depression and anxiety. [ 38 ] Supporting this notion, findings from a review that examined quality of life among U.S. Latino cancer survivors revealed that compared to other racial/ethnic communities, Hispanic/Latinos reported higher symptom burden across several HRQoL domains. [ 39 ] Further, there is some evidence to suggest a disparity in the reporting of symptom burden within routine cancer care among individuals who identify as Black. [ 37 ]
Overall research on potential symptom burden disparities among individuals with cancer from historically-marginalized populations is currently limited. Another recent review that examined cognitive impairment among Black, Hispanic, and Asian breast cancer survivors from the U.S. revealed that Black and Hispanic patients were more likely to report cognitive impairment concerns relative to White patients, pre and post chemotherapy. [ 40 ] Additionally, Black cancer survivors reported greater cognitive concerns when compared to their White counterparts. [ 40 ]
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Cancer/testis (CT) antigens are a group of proteins united by their importance in development and in cancer immunotherapy . In general, expression of these proteins is restricted to male germ cells in the adult animal. However, in cancer these developmental antigens are often re-expressed and can serve as a locus of immune activation. Thus, they are often classified as tumor antigens . The expression of CT antigens in various malignancies is heterogeneous and often correlates with tumor progression. [ 1 ] CT antigens have been described in melanoma , liver cancer , lung cancer , bladder cancer , and pediatric tumors such as neuroblastoma . Gametogenesis offers an important role for many of these antigens in the differentiation, migration, and cell division of primordial germ cells, spermatogonia spermatocytes and spermatids . [ 2 ] Because of their tumor-restricted expression and strong in vivo immunogenicity, CT antigens are identified as ideal targets for tumor specific immunotherapeutic approaches and prompted the development of several clinical trials of CT antigens-based vaccine therapy. CT antigens have been found to have at least 70 families so far, including about 140 members, most of which are expressed during spermatogenesis. Their expression are mainly regulated by epigenetic events, specifically, DNA methylation. [ 3 ]
The Ludwig Institute for Cancer Research (LICR) maintains the "CTDatabase." [ 4 ] This database is an authoritative list of known CT antigens. It also serves as a repository into which new candidates can be entered.
Important CT antigens in cancer therapy include MAGE-A1 , MAGE-A3 , MAGE-A4, NY-ESO-1 , PRAME , CT83 and SSX2 .
With the development of tumor-associated antigens (TAA), the first clone of a human tumor antigen, melanoma antigen-1 (MAGE-1) was reported in 1990s, which elicited an autologous cytotoxic T-lymphocyte (CTL) response in a melanoma patient. [ 5 ] Further studies found that MAGE-1 (renamed MAGE-A1 later) was expressed in various cancers of different histological origin but not in normal tissues excluding testis and placenta . Later on, using T-cell epitope cloning technology, other tumor antigens with same properties were identified, including MAGE-A2, MAGE-A3, BAGE and GAGE-1. With the new approach, serological analysis of cDNA expression libraries (SEREX), several novel similar antigens were discovered, including SSX-2, NY-ESO-1, etc. Beyond these immunological methods, some gene expression techniques, including mRNA pools comparison, differential display, cDNA oligonucleotide array analysis and bioinformatic analysis, identified a multitude of tumor genes with a cancer/testis restricted expression profile. As the growing of this family, this type of tumor antigens, the genes of which expressing limitedly in malignancies of various histotypes, but not in normal tissue except testis and placenta, was named cancer testis antigen (CT antigens) by Old (1997) and Chen (1998). [ 6 ] [ 7 ] So far, at least 70 families of CT antigens with over 140 members have been identified and listed in a database established by the Ludwing Institute for Cancer Research. [ 8 ]
CT antigens can be divided by whether they are encoded on the X chromosome (X-CT antigens genes) or not (non-X-CT antigens genes). It has been estimated that 10% of genes on the X chromosome belong to X-CT antigens families. The X-CT antigens genes represent more than half of all CT antigens and often constitute multigene families organized in well-defined clusters long the X chromosome, while the genes of non-X-CT antigens are distributed throughout the genome and are mostly single-copy genes.
In normal testis, X-CT antigens genes are expressed primarily on the spermatogonia that are proliferate germ cells, while non-X-CT antigens are expressed in later stages of germ-cell differentiation, such as on spermatocytes . In normal placenta, CT antigens genes are less common, and MAGE-A3, MAGE-8, MAGE-A10, XAGE-2 and XAGE-3 have been found there. The mRNA of CT antigens was also found in some somatic tissues such as pancreas , liver and spleen , but the level is normally less than 1% of that in testis.
The expression of CT antigens genes were measured mainly by RT-PCR in transcription level and by immunohistochemistry (IHC) analysis in protein level. In tumor tissues, CT antigens are distributed widely but heterogeneously, expressing largely in melanoma , bladder and non-small cell lung cancers, moderately in breast and prostate cancers, poorly in kidney and colon cancers and in hematologic malignancies . Some reports suggest that multiple CT antigens tend to be co-expressed in the same neoplastic lesion.
The expression of CT antigens genes are exclusively regulated by epigenetic events both in normal and cancer tissues, while DNA methylation and histone post-translational modification remain the most widely characterized epigenetic factors here. [ 9 ]
DNA methylation is commonly found to lead to silencing of gene expression with the covalent addition of a methyl group catalyzed by DNA methyltransferases (DNMTs). It is found so far that the non-expression in normal somatic tissues of CT antigens genes is caused by the methylation in their promoters and the different promoter methylation status is directly responsible for the highly heterogeneous intratumor expression of CT antigens in different cancers. This promoter methylation heterogeneity was found to be inherited by daughter cells.
Histone are fundamentally componential proteins in chromosomes containing flexible N-terminal tails protruding from the nucleosomes , providing targets for different modifications. The N-terminal lysine residues are often acetylated histone acetyltransferases (HAT) adding acetyl groups, while histone deacetylases (HDAC) works oppositely. The inhibition of HDAC by specific inhibitors (HDACi) is found to associate with the CT antigens expression in human malignancies. In addition, histone methylation is also involved in the gene expression of CT antigens, with activation and repression.
Germ cells share some features with cancers. The motile and penetrating features and colonization of primitive germ cells resemble the migration of cancer cells from primary tumor to metastasis . Also, during spermatogenesis , germ cells exhibit characteristics similar to cancer cells. These phenomena led to the hypothesis that the activation of CT antigens in normal stomatic tissues related to tumorigenesis . Although the function of CT antigens is far from understanding, increasing studies have found more evidences for some of the properties of CT antigens in recent years.
MAGE-A1 might repression the expression of genes required for differentiation during the spermatogenesis and be involved in the inhibition of cellular differentiation in cancer cells, contributing to tumorigenesis. MAGE-A11 was found to be involved in the regulation of androgen-receptor function by modulating its internal domain interactions. More studies support that the expression of MAGE genes in cancer cells might contribute to the malignant phenotype and the resistance to chemotherapeutic drugs. Besides, GAGE-7 was reported to have antiapoptotic properties. Some SSX family members was found to induce altered gene expression patterns, resulting in the malignant phenotype in cancers.
Multiple CT antigens have been shown to promote cancer cell growth, like SSX2 in melanoma, and might also be functional in treatment responses to cytotoxic or growth inhibitory anti-cancer drugs.
CT antigens are frequently expressed in malignant tumors, especially in metastases, when compared with the rare expression in benign neoplastic lesions.
The activation of meiotic programs in cancer cells may contribute to the genome instability, and the meiosis -specific CT antigens might be involved in this process, such as SPO11, SCP1 and HORMAD1. Moreover, some CT antigens combined with other proteins have been shown to support productive mitosis in cancer cells. [ 10 ]
In normal tissues, CT antigens are exclusively expressed in testis, making it no access to the immune system. Besides, the existence of blood-testis barrier and the lack of human leukocyte antigen (HLA) class I expression on the surface of germ cells prevent the immune system interacting with CT antigens proteins and recognizing it as invading structures. Thus, CT antigens can be regarded as essentially tumor-specific targets when they are expressed in cancers.
Distinct CT antigens encode for different antigenic peptides presented to the immune system in association with various HLA class I or HLA class II allospecificities, eliciting both CTL and humoral immune responses.
The implication of CTA peptides as vaccinating agents relies on the characterization of immunogenic peptides from selected CTA and the identification of the respective HLA class I antigen restriction. To date, MAGE-A3-derived peptides have been used as vaccines in HLA-A1-positive patients with tumor expressing the respective antigen. MAGE-A peptides have also been used in vaccines consisting of peptide-loaded monocyte-derived dendritic cells (DC). Besides peptide vaccines, recombinant full-length MAGE-A3 and NY-ESO-1 proteins are currently being evaluated as anti-cancer vaccines in a series of clinical trials.
Given some drawbacks and limitation of the inter- and intratumoral heterogeneous expression of CT antigens from the CT antigens-based vaccination, the promoter methylation in regulating CT antigens expression can be combined into the therapy to therapeutically modulate CT antigens expression in neoplastic cells.
Infiltrating T cells therapy have been shown to apparently induce tumor regression with durable complete responses in melanoma. Expending from this approach to other types of cancers, the difficulties of obtaining tumor-infiltrating lymphocytes come out. In this case, the tumor-reactive T cells can be engineered to express recombinant or chimeric T-cell receptors against common tumor antigens where CT antigens could be a high priority target. Their frequent expression in many types of cancer makes CT antigen-directed T-cell therapy applicable to many types of cancer. [ 11 ]
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https://en.wikipedia.org/wiki/Cancer/testis_antigens
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Cancer is a biweekly peer-reviewed scientific journal covering oncology . The journal was established in 1948. It is an official journal of the American Cancer Society and is published by Wiley-Blackwell on behalf of the society. The first editor-in-chief was Fred W. Stewart , who held that position until 1961. The current editor-in-chief is Suresh S. Ramalingam, and the previous one was Fadlo R. Khuri . Cancer Cytopathology was published as a section from 1997 until 2008, when it was split into a separate journal. [ 1 ]
The journal is abstracted and indexed in:
According to the Journal Citation Reports , the journal has a 2015 impact factor of 5.649, ranking it 26th out of 211 journals in the category "Oncology". [ 12 ]
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https://en.wikipedia.org/wiki/Cancer_(journal)
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The Cancer Act 1939 ( 2 & 3 Geo. 6 . c. 13) is an Act of Parliament of the United Kingdom passed in 1939 to:
As of December 2014, the sole remaining provision is in respect of advertising to treat or cure cancer, all other provisions having been repealed or subsumed into other legislation. The Act does not apply in Northern Ireland.
The Act's most notable provision is a clause prohibiting taking any part in publication, except under specified conditions, of advertisements that "offer to treat any person for cancer, or to prescribe any remedy therefor, or to give any advice in connection with the treatment thereof". Prosecutions do take place, but are rare. [ 1 ]
The expression "advertisement" includes any notice, circular, label, wrapper or other document, and any announcement made orally or by any means of producing or transmitting sounds.
The Act provides for exceptions in making material available to registered medical and nursing personnel and pharmacists , and for material produced by hospitals and local authorities.
According to an answer given in the House of Commons on 12 June 2014 [ 2 ] [ 3 ] there were 21 convictions under the Act between 1984 and 2013, and from then until 12 June 2014 there have been another four.
Convictions that have been reported in the press include:
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https://en.wikipedia.org/wiki/Cancer_Act_1939
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Cancer Causes & Control is a peer-reviewed medical journal published by Springer Science+Business Media , covering research on the epidemiology , causes, and control of cancer . According to the Journal Citation Reports , the journal has a 2020 impact factor of 2.506. [ 1 ]
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Cancer Cell is a peer-reviewed scientific journal scientific journal that publishes articles that provide major advances in cancer research and oncology. The journal considers manuscripts that answer important questions relevant to naturally occurring cancers. Areas covered include basic cancer biology, therapeutic development, translational research, cancer model development, multi-omics and computational biology . Cancer Cell is also interested in publishing clinical investigations, in particular those that lead to establishing new paradigms in the treatment, diagnosis, or prevention of cancers; those that provide important insights into cancer biology beyond what has been revealed by preclinical studies; and those that are mechanism-based proof-of-principle clinical studies.
Cancer Cell is internationally regarded as one of the top cancer research and oncology journals. According to the Journal Citation Reports , the 2022 impact factor of the journal is 50.3. It is part of the Cell Press portfolio, which is owned by Elsevier . Issues are published monthly in print and online versions. All content becomes available for free one year after publication. In January 2021, Cancer Cell became a Transformative Journal as part of Elsevier's efforts to increase Open Access content. [ 1 ] [ 2 ]
Cancer Cell publishes Research, Review, and Perspective articles, in addition to opinion pieces such as Letters, Commentaries, Previews, Spotlight, and Voices. The journal often publishes a yearly special issue with a compilation of review articles around a common topic. In the Cancer Cell website, articles can be browsed by Issue, Collection, early online access ("Online Now"), or annual "Best of Cancer Cell ".
Cancer Cell was launched in 2002 with the publication of its inaugural issue on February 1, 2002. In an Editorial published in this first issue, Editor-in-Chief Mariana Resnicoff introduced Cancer Cell as "An exciting forum for cancer research". [ 3 ] Following in the footsteps of the Cell Press flagship journal Cell , the goal of Cancer Cell was to publish cutting-edge findings in cancer research and to provide great author service by having a team of dedicated scientific editors that hold the highest standards of excellence, editorial consistency, and author service. Li-Kuo Su became Editor-in-Chief in 2003 and is recognized for promoting the journal's growth and establishing it as one of the most reputable cancer research journals. He retired from his editorial activities in 2019. Steve Mao became Cancer Cell 's Editor-in-Chief in 2020 after serving as senior editor at Cell and Science .
In the April 2020 special issue of Cancer Cell , Steve Mao published the editorial "Changing for a Better Future" [ 4 ] delineating his views for the journal. This Editorial reiterated the journal's commitment to scientific excellence and introduced key changes. While Cancer Cell is traditionally considered a journal interested in strong mechanistic studies, the Editorial highlights its interest in translational and clinical studies, as well in discovery papers that scientifically sound and conceptually bold. In line with the Cell Press rebranding strategy launched in 2020, [ 5 ] Steve Mao vowed to continue publishing "Science that Inspires". The Editorial also states the editors' commitment to increase communication with its scientific community and authors, as well as to work with authors to improve the revision process of manuscripts under consideration.
In 2020, Cancer Cell made a number of changes to increase diversity and inclusion of underrepresented minorities in cancer research and oncology. In June 2020, the journal announced the new members of its advisory board (previously editorial board), which includes a higher representation of female scientists (>40%) and physicians (~50%) and higher geographical and ethnic diversity. [ 6 ] That same month, the Cell Editorial Team published the editorial "Science has a racism problem", [ 6 ] acknowledging the underrepresentation of Black scientists in STEM in the wake of the murders of George Floyd, Breonna Taylor, and Ahmaud Arbery. These events, in conjunction with the anti-immigration policies of the Trump administration in the U.S., led to a Summer of social reckoning in the scientific community. Cancer Cell joined the cancer research and oncology communities and their call for action and change by dedicating its September 2020 issue to the importance of diversity and immigration in cancer research in the U.S. and publishing a series of opinion pieces by scientists and clinicians that represent several minorities (immigrants, Black, Latinx, LGBTQ) and their allies. [ 7 ] [ 8 ] [ 9 ] The journal has also published several articles that address ethnic health disparities and aim to increase the representation of non-Caucasian populations in cancer research and oncology. [ 10 ] [ 11 ] [ 12 ] [ 13 ] [ 14 ]
As a part of Cell Press, Cancer Cell has supported Black in Cancer and the #BlackInCancerWeek campaign on Twitter. The journal also participated in the creation of the "Rising Black Scientists Award", a cash award granted to one undergraduate student and one graduate student or postdoctoral trainee "meant to break down barriers and create opportunities by providing funds to support professional development". [ 15 ]
In January 2021, Cell Press introduced the Inclusion and Diversity Statement, in which authors may choose to disclose information related to how they are increasing their effort to promote genetic diversity in their study subjects, participation of minorities, and balancing gender representation, to name a few. [ 16 ]
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https://en.wikipedia.org/wiki/Cancer_Cell_(journal)
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Cancer Cell International is a peer-reviewed scientific journal that publishes papers on various aspects of cancer cell . The journal was established in 2001 and is published by Springer Science+Business Media . [ 1 ]
Cancer Cell International is an open-access , online-only journal which publishes articles focused on cancer cell. [ 2 ]
Journal publishes also articles on cancer studies with the data from experiments. Publish research articles based on data in many fields, from cell proliferation to apoptosis , etc. [ 3 ]
As of 2022 editors-in-Chief are Domenico Coppola from Moffitt Cancer Center and Yasumasa Kato from Ohu University . [ 4 ]
The journal is abstracted and indexed for example in: [ 5 ]
According to the Journal Citation Reports , the journal has a 2021 impact factor of 6.436. [ 6 ]
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https://en.wikipedia.org/wiki/Cancer_Cell_International
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The Journal of the National Cancer Institute ( JNCI ) is a peer-reviewed medical journal covering research in oncology that was established in August 1940. It is published monthly by Oxford University Press and is edited by Patricia A. Ganz . It was merged with Cancer Treatment Reports in January 1988. JNCI used to be the official journal of the U.S. National Cancer Institute (NCI); however, in 1996, the NCI and JNCI agreed to grow apart. Over the next five years, JNCI became independent of the NCI.
A related publication is Journal of the National Cancer Institute Monographs ( JNCI Monographs ), established in 1959, which publishes manuscripts from cancer and cancer-related conferences, as well as groups of papers on specific subjects related to cancer. In January 1986, Cancer Treatment Symposia was merged with JNCI Monographs . Additionally, JNCI Cancer Spectrum ( JNCI CS ) is a fully open access journal, which was established in 2017. It is published bimonthly by Oxford University Press and is edited by Ronald Chen .
The history of JNCI is linked to that several other journals. A full history of JNCI and JNCI Monographs is presented below.
JNCI is indexed and abstracted in:
According to the Journal Citation Reports , the journal has a 2014 impact factor of 12.583, ranking it 8th out of 211 journals in the category "Oncology". [ 13 ]
JNCI Monographs is indexed and abstracted in
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https://en.wikipedia.org/wiki/Cancer_Chemotherapy_Reports
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Cancer Chemotherapy and Pharmacology is a peer-reviewed medical journal covering oncological pharmacotherapy . It was established in 1978 and is published by Springer Science+Business Media . The editors-in-chief are Jan Hendrik Beumer ( University of Pittsburgh School of Pharmacy ) and Étienne Chatelut (Institut Claudius-Regaud). According to the Journal Citation Reports , the journal has a 2020 impact factor of 3.333. [ 1 ]
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Cancer Cytopathology is a monthly peer-reviewed scientific journal which covers practice of cytopathology and its related oncology -based disciplines. It is one of three official journals of the American Cancer Society and is published by Wiley-Blackwell on behalf of the society. The current editor-in-chief is William C. Faquin. Cancer Cytopathology was published as a section of Cancer from 1997 until 2008 when it was split into a separate journal. [ 1 ]
The journal is abstracted and indexed in:
According to the Journal Citation Reports , the journal has a 2020 impact factor of 5.284, ranking it 16th out of 77 journals in the category "Pathology" and 83rd out of 242 journals in "Oncology". [ 11 ]
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Cancer Discovery is a monthly peer-reviewed medical journal published by the American Association for Cancer Research . It covers research and clinical trials related to the study of cancer . The editors-in-chief are Lewis C. Cantley and Luis A. Diaz . [ 1 ] The journal was established in 2011. [ 1 ]
The journal is abstracted and indexed in:
According to the Journal Citation Reports , the journal has a 2020 impact factor of 39.397. [ 6 ]
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https://en.wikipedia.org/wiki/Cancer_Discovery_(journal)
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Cancer Epidemiology, Biomarkers & Prevention is a peer-reviewed medical journal devoted to research in the field of cancer epidemiology . Topics include descriptive, analytical, biochemical, and molecular epidemiology , the use of biomarkers to study the neoplastic and preneoplastic processes in humans, chemoprevention and other types of prevention trials, and the role of behavioral factors in cancer etiology and prevention . It is published by the American Association for Cancer Research and co-sponsored by the American Society of Preventive Oncology .
Indexed by ISI Cancer Epidemiology, Biomarkers & Prevention collected an impact factor of 5.057 as reported in the 2018 Journal Citation Reports by Thomson Reuters, ranking it 48 out of 230 journals in the category Oncology [ 2 ] and ranking it 13 out of 186 journals in the category Public, environmental & occupational health . [ 3 ]
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https://en.wikipedia.org/wiki/Cancer_Epidemiology,_Biomarkers_&_Prevention
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Cancer Epidemiology (formerly known as Cancer Detection & Prevention ) is a peer reviewed journal devoted to epidemiological cancer research. According to the Journal Citation Reports , the journal has a 2020 impact factor of 2.984. [ 2 ]
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Cancer Immunology, Immunotherapy is a monthly peer-reviewed medical journal published by Springer Science+Business Media . According to the Journal Citation Reports , the journal has a 2020 impact factor of 6.968. [ 1 ] As of 2024, the impact factor is 4.8. [ 2 ]
Immunology includes the use of certain components of the immune system ( antibodies, cells & cytokines), etc. for the treatment of various cancers and autoimmune diseases and the manipulation of immune system through vaccines for the prevention and treatment of infectious and allergic diseases.
What Kind of cancer does immunotherapy treat?
Immunotherapy is a promising treatment option for advanced lung cancer, alone or in combination with conventional treatments like chemotherapy or surgery. Several FDA- approved immunotherapies offer treatment options to children and adults with Hodgkin and non-Hodgkin lymphoma.
Can you survive cancer with immunotherapy?
Immunotherapy has shown success in 15 different types of cancers including lung cancer, head and neck cancer, bladder cancer, kidney cancer, and Hodgkin lymphoma.
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Cancer Immunology Research is a monthly peer-reviewed medical journal published by the American Association for Cancer Research . It covers research and clinical trials related to the study of cancer immunology . The editors-in-chief are Robert D. Schreiber and Philip Greenberg . [ 1 ] The journal was established in 2013. [ 1 ]
The journal is abstracted and indexed in:
According to the Journal Citation Reports , the journal has a 2021 impact factor of 12.020. [ 6 ]
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https://en.wikipedia.org/wiki/Cancer_Immunology_Research
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Cancer Informatics is a peer-reviewed open access medical journal focusing on the application of computational biology to cancer research . It was established in 2005 and was originally published by Libertas Academica . SAGE Publications became the publisher in September 2016. [ 1 ] The editor in chief is J. T. Efird .
The journal is abstracted and indexed in:
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Cancer Investigation is a peer-reviewed medical journal in the field of basic and clinical oncology . [ 1 ] The editor in chief is Gary Herbert Lyman . [ 2 ] It is currently indexed for MEDLINE.
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Cancer Letters is a peer-reviewed medical journal established in 1975 that focuses on the rapid publication of original research on multidisciplinary aspects of cancer . The editor-in-chief is M. Schwab .
Cancer Letters is abstracted and indexed in BIOSIS , Chemical Abstracts , Current Contents /Life Sciences, EMBASE , MEDLINE , Oncology Information Service , PASCAL and FRANCIS , and Scopus .
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Cancer Management and Research is a peer-reviewed medical journal covering research on cancer . It is published by Dove Medical Press .
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Cancer Medicine is a monthly peer-reviewed open-access medical journal covering oncology . It was established in 2012 and is published by John Wiley & Sons . The editor-in-chief is Stephen Tait (Institute of Cancer Sciences, University of Glasgow ). According to the Journal Citation Reports , the journal has a 2020 impact factor of 4.452. [ 1 ]
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Cancer Prevention Research is a peer-reviewed medical journal that publishes original studies, reviews, and commentaries in the fields of cancer prevention and interception. It was launched in 2008 by its publisher, the American Association for Cancer Research . The journal's current editors-in-chief are Raymond N. DuBois and Michael N. Pollak, who were appointed in 2018.
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