beneficial mutations can cause a species to evolve into forms that better survive their environment, a process called adaptation. new species are formed through the process of speciation, a process often caused by geographical separations that allow different populations to genetically diverge. the application of genetic principles to the study of population biology and evolution is referred to as the modern synthesis. as sequences diverge and change during the process of evolution, these differences between sequences can be used as a molecular clock to calculate the evolutionary distance between them. genetic comparisons are generally considered the most accurate method of characterizing the relatedness between species, an improvement over the sometimes deceptive comparison of phenotypic characteristics. the evolutionary distances between species can be combined to form evolutionary trees - these trees represent the common descent and divergence of species over time, although they cannot represent the transfer of genetic material between unrelated species ( known as horizontal gene transfer and most common in bacteria ). research and technologyedit model organisms and geneticsedit although geneticists originally studied inheritance in a wide range of organisms, researchers began to specialize in studying the genetics of a particular subset of organisms. the fact that significant research already existed for a given organism would encourage new researchers to choose it for further study, and so eventually a few model organisms became the basis for most genetics research. common research topics in model organism genetics include the study of gene regulation and the involvement of genes in development and cancer. organisms were chosen, in part, for convenience — short generation times and easy genetic manipulation made some organisms popular genetics research tools. widely used model organisms include the gut bacterium escherichia coli, the plant arabidopsis thaliana, baker ' s yeast ( saccharomyces cerevisiae ), the nematode caenorhabditis elegans, the common fruit fly ( drosophila melanogaster ), and the common house mouse ( mus musculus ). medical genetics researchedit medical genetics seeks to understand how genetic variation relates to human health and disease. when searching for an unknown gene that may be involved in a disease, researchers commonly use genetic linkage and genetic pedigree charts to find the location on the genome associated with the disease. at the population level, researchers take advantage of mendelian randomization to look for locations in the genome that are associated with diseases, a technique especially useful for multigenic traits not clearly defined by a single gene. once a candidate gene is found, further research is often done on the same gene ( called an ortholo


look for locations in the genome that are associated with diseases, a technique especially useful for multigenic traits not clearly defined by a single gene. once a candidate gene is found, further research is often done on the same gene ( called an orthologous gene ) in model organisms. in addition to studying genetic diseases, the increased availability of genotyping techniques has led to the field of pharmacogenetics — studying how genotype can affect drug responses. although it is not an inherited disease, cancer is also considered a genetic disease. the process of cancer development in the body is a combination of events. mutations occasionally occur within cells in the body as they divide. while these mutations will not be inherited by any offspring, they can affect the behavior of cells, sometimes causing them to grow and divide more frequently. there are biological mechanisms that attempt to stop this process ; signals are given to inappropriately dividing cells that should trigger cell death, but sometimes additional mutations occur that cause cells to ignore these messages. an internal process of natural selection occurs within the body and eventually mutations accumulate within cells to promote their own growth, creating a cancerous tumor that grows and invades various tissues of the body. dna can be manipulated in the laboratory. restriction enzymes are a commonly used enzyme that cuts dna at specific sequences, producing predictable fragments of dna. the use of ligation enzymes allows these fragments to be reconnected, and by ligating fragments of dna together from different sources, researchers can create recombinant dna. often associated with genetically modified organisms, recombinant dna is commonly used in the context of plasmids - short circular dna fragments with a few genes on them. by inserting plasmids into bacteria and growing those bacteria on plates of agar ( to isolate clones of bacteria cells ), researchers can clonally amplify the inserted fragment of dna ( a process known as molecular cloning ). ( cloning can also refer to the creation of clonal organisms, through various techniques. ) dna can also be amplified using a procedure called the polymerase chain reaction ( pcr ). by using specific short sequences of dna, pcr can isolate and exponentially amplify a targeted region of dna. because it can amplify from extremely small amounts of dna, pcr is also often used to detect the presence of specific dna sequences. dna sequencing and genomicsedit one of the most fundamental technologies developed to study genetics, dna sequencing allows researchers to determine the sequence of nucleotide


small amounts of dna, pcr is also often used to detect the presence of specific dna sequences. dna sequencing and genomicsedit one of the most fundamental technologies developed to study genetics, dna sequencing allows researchers to determine the sequence of nucleotides in dna fragments. developed in 1977 by frederick sanger and coworkers, chain - termination sequencing is now routinely used to sequence dna fragments. with this technology, researchers have been able to study the molecular sequences associated with many human diseases. as sequencing has become less expensive and with the aid of computational tools, researchers have sequenced the genomes of many organisms by stitching together the sequences of many different fragments ( a process called genome assembly ). these technologies were used to sequence the human genome, leading to the completion of the human genome project in 2003. new high - throughput sequencing technologies are dramatically lowering the cost of dna sequencing, with many researchers hoping to bring the cost of resequencing a human genome down to a thousand dollars. the large amount of sequences available has created the field of genomics, research that uses computational tools to search for and analyze patterns in the full genomes of organisms. genomics can also be considered a subfield of bioinformatics, which uses computational approaches to analyze large sets of biological data. - animal breeding - animal mate selection - animal strain differences - assortive mating - behavioural genetics - blood groups - family resemblance - genetic counselling - population genetics - genetic disorders - genetic engineering - human accelerated regions - hybrids ( biology ) - instinctive behaviour - reproductive technology - selective breeding - sexual reproduction - species differences - translocation ( chromosomes ) - ↑ genetikos, henry george liddell, robert scott, " a greek - english lexicon ", at perseus - ↑ genesis, henry george liddell, robert scott, " a greek - english lexicon ", at perseus - ↑ online etymology dictionary - ↑ griffiths et al. ( 2000 ), chapter 1 ( genetics and the organism ) : introduction - ↑ hartl d, jones e ( 2005 ) - ↑ weiling f ( 1991 ). historical study : johann gregor mendel 1822 – 1884. american journal of medical genetics 40 ( 1 ) : 1 – 25 ; discussion 26. - ↑ lamarck, j - b ( 2008 ). in encyclopædia britannica. retrieved from encyclopædia britannica online on 2008 - 03 - 16. - ↑ peter j. bowler, the mendelian revolution


, j - b ( 2008 ). in encyclopædia britannica. retrieved from encyclopædia britannica online on 2008 - 03 - 16. - ↑ peter j. bowler, the mendelian revolution : the emergency of hereditarian concepts in modern science and society ( baltimore : johns hopkins university press, 1989 ) : chapters 2 & 3. - ↑ 9. 0 9. 1 mendel, gj ( 1866 ). versuche uber pflanzen - hybriden. verhandlungen des naturforschenden vereins brunn 4 : 3 – 47. ( in english in 1901, j. r. hortic. soc. 26 : 1 – 32 ) english translation available online - ↑ genetics, n., oxford english dictionary, 3rd ed. - ↑ bateson w. letter from william bateson to alan sedgwick in 1905. the john innes centre. url accessed on 2008 - 03 - 15.. note that the letter was to an adam sedgwick, a zoologist at trinity college, cambridge, not " alan ", and not to be confused with the renown british geologist, adam sedgwick, who lived some time earlier. - ↑ genetic, adj., oxford english dictionary, 3rd ed. - ↑ bateson, w ( 1907 ). " the progress of genetic research ". wilks, w ( editor ) report of the third 1906 international conference on genetics : hybridization ( the cross - breeding of genera or species ), the cross - breeding of varieties, and general plant breeding, london : royal horticultural society. - initially titled the " international conference on hybridisation and plant breeding ", wilks changed the title for publication as a result of bateson ' s speech. - ↑ moore ja ( 1983 ). thomas hunt morgan — the geneticist. american zoologist 23 ( 4 ) : 855 – 865. - ↑ sturtevant ah ( 1913 ). the linear arrangement of six sex - linked factors in drosophila, as shown by their mode of association. journal of experimental biology 14 : 43 – 59. pdf from electronic scholarly publishing - ↑ avery ot, macleod cm, and mccarty m ( 1944 ). studies on the chemical nature of the substance inducing transformation of pneumococcal types : induction of transformation by a desoxyribonucleic acid fraction isolated from pneumococcus type iii. journal of experimental


1944 ). studies on the chemical nature of the substance inducing transformation of pneumococcal types : induction of transformation by a desoxyribonucleic acid fraction isolated from pneumococcus type iii. journal of experimental medicine 79 ( 1 ) : 137 – 158. 35th anniversary reprint available - ↑ hershey ad, chase m ( 1952 ). independent functions of viral protein and nucleic acid in growth of bacteriophage. the journal of general physiology 36 : 39 – 56. - ↑ judson, horace ( 1979 ). the eighth day of creation : makers of the revolution in biology, 51 – 169, cold spring harbor laboratory press. - ↑ watson jd, crick fhc ( 1953 ). molecular structure of nucleic acids : a structure for deoxyribose nucleic acid. nature 171 ( 4356 ) : 737 – 738. - ↑ watson jd, crick fhc ( 1953 ). genetical implications of the structure of deoxyribonucleic acid. nature 171 ( 4361 ) : 964 – 967. - ↑ sanger f, nicklen s, and coulson ar ( 1977 ). dna sequencing with chain - terminating inhibitors. nature 74 ( 12 ) : 5463 – 5467. - ↑ saiki rk, scharf s, faloona f, mullis kb, horn gt, erlich ha, arnheim n ( 1985 ). enzymatic amplification of β - globin genomic sequences and restriction site analysis for diagnosis of sickle cell anemia. science 230 ( 4732 ) : 1350 – 1354. - ↑ 23. 0 23. 1 human genome project information. human genome project. url accessed on 2008 - 03 - 15. - ↑ griffiths et al. ( 2000 ), chapter 2 ( patterns of inheritance ) : introduction - ↑ griffiths et al. ( 2000 ), chapter 2 ( patterns of inheritance ) : mendel ' s experiments - ↑ 26. 0 26. 1 26. 2 griffiths et al. ( 2000 ), chapter 3 ( chromosomal basis of heredity ) : mendelian genetics in eukaryotic life cycles - ↑ griffiths et al. ( 2000 ), chapter 4 ( gene interaction ) : interactions between the alleles of one gene - ↑ richard w. cheney. genetic notation. url accessed on 2008 - 03 - 18. - ↑ griffiths et al. ( 2000 ), chapter 2


2000 ), chapter 4 ( gene interaction ) : interactions between the alleles of one gene - ↑ richard w. cheney. genetic notation. url accessed on 2008 - 03 - 18. - ↑ griffiths et al. ( 2000 ), chapter 2 ( patterns of inheritance ) : human genetics - ↑ griffiths et al. ( 2000 ), chapter 4 ( gene interaction ) : gene interaction and modified dihybrid ratios - ↑ mayeux r ( 2005 ). mapping the new frontier : complex genetic disorders. the journal of clinical investigation 115 ( 6 ) : 1404 – 1407. - ↑ griffiths et al. ( 2000 ), chapter 25 ( quantitative genetics ) : quantifying heritability - ↑ luke a, guo x, adeyemo aa, wilks r, forrester t, lowe w jr, comuzzie ag, martin lj, zhu x, rotimi cn, cooper rs ( 2001 ). heritability of obesity - related traits among nigerians, jamaicans and us black people. int j obes relat metab disord 25 ( 7 ) : 1034 – 1041. abstract from ncbi - ↑ pearson h ( 2006 ). genetics : what is a gene?. nature 441 ( 7092 ) : 398 – 401. - ↑ prescott, l ( 1993 ). microbiology, wm. c. brown publishers. - ↑ griffiths et al. ( 2000 ), chapter 8 ( the structure and replication of dna ) : mechanism of dna replication - ↑ gregory sg et al. ( 2006 ). the dna sequence and biological annotation of human chromosome 1. nature 441 : 315 – 321. free full text available - ↑ alberts et al. ( 2002 ), ii. 4. dna and chromosomes : chromosomal dna and its packaging in the chromatin fiber - ↑ griffiths et al. ( 2000 ), chapter 2 ( patterns of inheritance ) : sex chromosomes and sex - linked inheritance - ↑ griffiths et al. ( 2000 ), chapter 7 ( gene transfer in bacteria and their viruses ) : bacterial conjugation - ↑ griffiths et al. ( 2000 ), chapter 7 ( gene transfer in bacteria and their viruses ) : bacterial transformation - ↑ griffiths et al. ( 2000 ), chapter 5 ( basic eukaryotic chromosome mapping ) : nature of crossing - over - ↑ griffiths et al. ( 2000 ), chapter 5 ( basic eukaryotic chromosome mapping ) : linkage maps - ↑ berg jm, tymoczko j


basic eukaryotic chromosome mapping ) : nature of crossing - over - ↑ griffiths et al. ( 2000 ), chapter 5 ( basic eukaryotic chromosome mapping ) : linkage maps - ↑ berg jm, tymoczko jl, stryer l, clarke nd ( 2002 ). biochemistry, 5th edition, new york : w. h. freeman and company. i. 5. dna, rna, and the flow of genetic information : amino acids are encoded by groups of three bases starting from a fixed point - ↑ crick, f ( 1970 ) : central dogma of molecular biology ( pdf ). nature 227, 561 – 563. pmid 4913914 - ↑ alberts et al. ( 2002 ), i. 3. proteins : the shape and structure of proteins - ↑ alberts et al. ( 2002 ), i. 3. proteins : protein function - ↑ how does sickle cell cause disease?. brigham and women ' s hospital : information center for sickle cell and thalassemic disorders. url accessed on 2007 - 07 - 23. - ↑ imes dl, geary la, grahn ra, lyons la ( 2006 ). albinism in the domestic cat ( felis catus ) is associated with a tyrosinase ( tyr ) mutation. animal genetics 37 ( 2 ) : 175. - ↑ medlineplus : phenylketonuria. nih : national library of medicine. url accessed on 2008 - 03 - 15. - ↑ brivanlou ah, darnell je jr ( 2002 ). signal transduction and the control of gene expression. science 295 ( 5556 ) : 813 – 818. - ↑ alberts et al. ( 2002 ), ii. 3. control of gene expression – the tryptophan repressor is a simple switch that turns genes on and off in bacteria - ↑ jaenisch r, bird a. epigenetic regulation of gene expression : how the genome integrates intrinsic and environmental signals. nature genetics 33 ( 3s ) : 245 – 254. - ↑ chandler vl ( 2007 ). paramutation : from maize to mice. cell 128 : 641 – 645. - ↑ griffiths et al. ( 2000 ), chapter 16 ( mechanisms of gene mutation ) : spontaneous mutations - ↑ kunkel ta ( 2004 ). dna replication fidelity. journal of biological chemistry 279 ( 17 ) : 16895 – 16898. - ↑


↑ griffiths et al. ( 2000 ), chapter 16 ( mechanisms of gene mutation ) : spontaneous mutations - ↑ kunkel ta ( 2004 ). dna replication fidelity. journal of biological chemistry 279 ( 17 ) : 16895 – 16898. - ↑ griffiths et al. ( 2000 ), chapter 16 ( mechanisms of gene mutation ) : induced mutations - ↑ griffiths et al. ( 2000 ), chapter 17 ( chromosome mutation i : changes in chromosome structure ) : introduction - ↑ sawyer sa, parsch j, zhang z, hartl dl ( 2007 ). prevalence of positive selection among nearly neutral amino acid replacements in drosophila. proc. natl. acad. sci. u. s. a. 104 ( 16 ) : 6504 – 10. - ↑ griffiths et al. ( 2000 ), chapter 24 ( population genetics ) : variation and its modulation - ↑ griffiths et al. ( 2000 ), chapter 24 ( population genetics ) : selection - ↑ griffiths et al. ( 2000 ), chapter 24 ( population genetics ) : random events - ↑ darwin, charles ( 1859 ). on the origin of species, 1st, 1, john murray.. related earlier ideas were acknowledged in darwin, charles ( 1861 ). on the origin of species, 3rd, xiii, john murray. - ↑ gavrilets s ( 2003 ). perspective : models of speciation : what have we learned in 40 years?. evolution 57 ( 10 ) : 2197 – 2215. - ↑ wolf yi, rogozin ib, grishin nv, koonin ev ( 2002 ). genome trees and the tree of life. trends genet. 18 ( 9 ) : 472 – 479. - ↑ the use of model organisms in instruction. university of wisconsin : wisconsin outreach research modules. url accessed on 2008 - 03 - 15. - ↑ ncbi : genes and disease. nih : national center for biotechnology information. url accessed on 2008 - 03 - 15. - ↑ davey smith, g, ebrahim, s ( 2003 ). ‘ mendelian randomization ’ : can genetic epidemiology contribute to understanding environmental determinants of disease?. international journal of epidemiology 32 : 1 – 22. - ↑ pharmacogenetics fact sheet. nih : national institute of general medical sciences. url accessed on 2008 - 03 - 15. - ↑ strachan t, read ap ( 1999 ). human molecular genetics 2, second edition, john wiley


##acogenetics fact sheet. nih : national institute of general medical sciences. url accessed on 2008 - 03 - 15. - ↑ strachan t, read ap ( 1999 ). human molecular genetics 2, second edition, john wiley & sons inc.. chapter 18 : cancer genetics - ↑ lodish et al. ( 2000 ), chapter 7 : 7. 1. dna cloning with plasmid vectors - ↑ lodish et al. ( 2000 ), chapter 7 : 7. 7. polymerase chain reaction : an alternative to cloning - ↑ brown ta ( 2002 ). genomes 2, 2nd edition. section 2, chapter 6 : 6. 1. the methodology for dna sequencing - ↑ brown ( 2002 ), section 2, chapter 6 : 6. 2. assembly of a contiguous dna sequence - ↑ service rf ( 2006 ). the race for the $ 1000 genome. science 311 ( 5767 ) : 1544 – 1546. - alberts b, johnson a, lewis j, raff m, roberts k, and walter p ( 2002 ). molecular biology of the cell, 4th edition. - griffiths ajf, miller jh, suzuki dt, lewontin rc, and gelbart wm ( 2000 ). an introduction to genetic analysis, new york : w. h. freeman and company. - hartl d, jones e ( 2005 ). genetics : analysis of genes and genomes, 6th edition, jones & bartlett. - lodish h, berk a, zipursky ls, matsudaira p, baltimore d, and darnell j ( 2000 ). molecular cell biology, 4th edition. | this page uses creative commons licensed content from wikipedia ( view authors ). |


individual differences | methods | statistics | clinical | educational | industrial | professional items | world psychology | fetal alcohol spectrum disorders ( fasd ) describes a continuum of permanent birth defects caused by maternal consumption of alcohol during pregnancy, which includes, but is not limited to fetal alcohol syndrome ( fas ). over time, as it became apparent through research and clinical experience that a range of effects ( including physical, behavioral, and cognitive ) could arise from prenatal alcohol exposure, the term fetal alcohol spectrum disorders, or fasd, was developed to include fetal alcohol syndrome ( fas ) as well as other conditions resulting from prenatal alcohol exposure. there are a number of other subtypes with evolving nomenclature and definitions based on partial expressions of fas, including partial fetal alcohol syndrome ( pfas ), alcohol - related neurodevelopmental disorder ( arnd ), alcohol - related birth defects ( arbd ), and fetal alcohol effect ( fae ). the term fetal alcohol spectrum disorders is not in itself a clinical diagnosis but describes the full range of disabilities that may result from prenatal alcohol exposure. currently, fetal alcohol syndrome ( fas ) is the only expression of prenatal alcohol exposure that is defined by the international statistical classification of diseases and related health problems and assigned icd - 9 and icd - 10 diagnoses. since the original syndrome of fetal alcohol syndrome ( fas ) was reported in 1973, four fasd diagnostic systems that diagnose fas and other fasd conditions have been developed in north america : - the institute of medicine ' s guidelines for fas, the first system to standardize diagnoses of individuals with prenatal alcohol exposure, - the university of washington ' s " the 4 - digit diagnostic code, " which ranks the four key features of fasd on a likert scale of one to four and yields 256 descriptive codes that can be categorized into 22 distinct clinical categories, ranging from fas to no findings, - the centers for disease control ' s " fetal alcohol syndrome : guidelines for referral and diagnosis, " which established general consensus on the diagnosis fas in the u. s. but deferred addressing other fasd conditions, and - canadian guidelines for fasd diagnoses, which established criteria for diagnosing fasd in canada and harmonized most differences between the iom and university of washington ' s systems. each diagnostic system requires that a complete fasd evaluation include assessment of the four key features of fasd, described below. a positive


diagnosing fasd in canada and harmonized most differences between the iom and university of washington ' s systems. each diagnostic system requires that a complete fasd evaluation include assessment of the four key features of fasd, described below. a positive finding on all four features is required for a diagnosis of fas, the first diagnosable condition of fasd that was discovered. however, prenatal alcohol exposure and central nervous system damage are the critical elements of the spectrum of fasd, and a positive finding in these two features is sufficient for an fasd diagnosis that is not " full - blown fas. " diagnoses are described in a following section. key features of fasdedit each of the key features of fasd can vary widely within one individual exposed to prenatal alcohol. while consensus exists for the definition and diagnosis of fas across diagnostic systems, minor variations among the systems lead to differences in definitions and diagnostic cut - off criteria for other disgnoses across the fasd continuum. ( the central nervous system ( cns ) damage criteria particularly lack clear consensus. ) a working knowledge of the key features is helpful in understanding fasd diagnoses and conditions, and each are reviewed with attention to similarities and differences across the four diagnostic systems. in terms of fasd, growth deficiency is defined as significantly below average height, weight or both due to prenatal alcohol exposure, and can be assessed at any point in the lifespan. growth measurements must be adjusted for parental height, gestational age ( for a premature infant ), and other postnatal insults ( e. g., poor nutrition ), although birth height and weight are the preferred measurements. deficiencies are documented when height or weight falls at or below the 10th percentile of standardized growth charts appropriate to the patient ' s population. criteria for fasd are least specific in the iom diagnostic system ( " low birth weight..., decelerating weight not due to nutrition..., [ or ] disproportional low weight to height " p. 4 of executive summary ), while the cdc and canadian guidelines use the 10th percentile as a cut - off to determine growth deficiency. the " 4 - digit diagnostic code " allows for mid - range gradations in growth deficiency ( between the 3rd and 10th percentiles ) and severe growth deficiency at or below the 3rd percentile. growth deficiency ( at severe, moderate, or mild levels ) contributes to diagnoses of fas and pfas


( pfl ) is measured in millimeters with either calipers or a clear ruler and then compared to a pfl growth chart, also developed by the university of washington. all four diagnostic systems have agreed upon this method for determining fas facial feature severity rankings. ranking fas facial features is complicated because the three separate facial features can be affected independently by prenatal alcohol. central nervous system damage edit central nervous system ( cns ) damage is the primary key feature of any fasd diagnosis. prenatal alcohol exposure, a teratogen, can damage the brain across a continuum of gross to subtle impairments, depending on the amount, timing, and frequency of the exposure as well as genetic predispositions of the fetus and mother. while functional abnormalities are the behavioral and cognitive expressions of the fasd disability, cns damage can be assessed in three areas : structural, neurological, and functional impairments. all four diagnostic systems allow for assessment of cns damage in these areas, but criteria vary. the iom system requires structural or neurological impairment for a diagnosis of fas, but also allows a " complex pattern " of functional anomalies for diagnosing pfas and arnd. the " 4 - digit diagnostic code " and cdc guidelines allow for a positive cns finding in any of the three areas for any fasd diagnosis, but functional anomalies must measure at two standard deviations or worse in three or more functional domains for a diagnoses of fas, pfas, and arnd. the " 4 - digit diagnostic code " also allows for an fasd diagnosis when only two functional domains are measured at two standard deviations or worse. the " 4 - digit diagnostic code " further elaborates the degree of cns damage according to four ranks : - definite - structural impairments or neurological impairments for fas or static encephalopathy. - probable - significant dysfunction of two standard deviations or worse in three or more functional domains. - possible - mild to moderate dysfunction of two standard deviations or worse in one or two functional domains or by judgment of the clinical evaluation team that cns damage cannot be dismissed. - unlikely - no evidence of cns damage. structural abnormalities of the brain are observable, physical damage to the brain or brain structures caused by prenatal alcohol exposure. structural impairments may include microcephaly ( small head size ) of two or more standard deviations below the average, or other abnormalities in brain structure ( e. g


damage to the brain or brain structures caused by prenatal alcohol exposure. structural impairments may include microcephaly ( small head size ) of two or more standard deviations below the average, or other abnormalities in brain structure ( e. g., agenesis of the corpus callosum, cerebellar hypoplasia ). microcephaly is determined by comparing head circumference ( often called occipitofrontal circumference, or ofc ) to appropriate ofc growth charts. other structural impairments must be observed through medical imaging techniques by a trained physician. because imaging procedures are expensive and relatively inaccessible to most patients, diagnosis of fasd is not frequently made via structural impairments except for microcephaly. when structural impairments are not observable or do not exist, neurological impairments are assessed. in the context of fasd, neurological impairments are caused by prenatal alcohol exposure which causes general neurological damage to the central nervous system ( cns ), the peripheral nervous system, or the autonomic nervous system. a determination of a neurological problem must be made by a trained physician, and must not be due to a postnatal insult, such as a high fever, concussion, traumatic brain injury, etc. all four diagnostic systems show virtual agreement on their criteria for cns damage at the neurological level, and evidence of a cns neurological impairment due to prenatal alcohol exposure will result in a diagnosis of fas or pfas, and functional impairments are highly likely. neurological problems are expressed as either hard signs, or diagnosable disorders, such as epilepsy or other seizure disorders, or soft signs. soft signs are broader, nonspecific neurological impairments, or symptoms, such as impaired fine motor skills, neurosensory hearing loss, poor gait, clumsiness, poor eye - hand coordination, or sensory integration dysfunction. many soft signs have norm - referenced criteria, while others are determined through clinical judgment. when structural or neurological impairments are not observed, all four diagnostic systems allow cns damage due to prenatal alcohol exposure to be assessed in terms of functional impairments. functional impairments are deficits, problems, delays, or abnormalities due to prenatal alcohol exposure ( rather than hereditary causes or postnatal insults ) in observable and measurable domains related to daily functioning, often referred to as developmental disabilities. there is no consensus on a specific pattern of functional impairment


abnormalities due to prenatal alcohol exposure ( rather than hereditary causes or postnatal insults ) in observable and measurable domains related to daily functioning, often referred to as developmental disabilities. there is no consensus on a specific pattern of functional impairments due to prenatal alcohol exposure and only cdc guidelines label developmental delays as such, so criteria ( and fasd diagnoses ) vary somewhat across diagnostic systems. the four diagnostic systems list various cns domains that can qualify for functional impairment that can determine an fasd diagnosis : - evidence of a complex pattern of behavior or cognitive abnormalities inconsistent with developmental level in the following cns domains - sufficient for a pfas or arnd diagnosis using iom guidelines - performance at two or more standard deviations on standardized testing in three or more of the following cns domains - sufficient for an fas, pfas or static encephalopathy diagnosis using 4 - digit diagnostic code - general cognitive deficits ( e. g., iq ) at or below the 3rd percentile on standardized testing - sufficient for an fas diagnosis using cdc guidelines - performance at or below the 16th percentile on standardized testing in three or more of the following cns domains - sufficient for an fas diagnosis using cdc guidelines - performance at two or more standard deviations on standardized testing in three or more of the following cns domains - sufficient for an fas diagnosis using canadian guidelines ten brain domainsedit a recent effort to standardize assessment of functional cns damage has been suggested by an experienced fasd diagnostic team in minnesota. the proposed framework attempts to harmonize iom, 4 - digit diagnostic code, cdc, and canadian guidelines for measuring cns damage viz - a - viz fasd evaluations and diagnosis. the standardized approach is referred to as the ten brain domains and encompasses aspects of all four diagnostic systems ' recommendations for assessing cns damage due to prenatal alcohol exposure. the framework provides clear definitions of brain dysfunction, specifies empirical data needed for accurate diagnosis, and defines intervention considerations that address the complex nature of fasd with the intention to avoid common secondary disabilities. the proposed ten brain domains include : - achievement, adaptive behavior, attention, cognition, executive functioning, language, memory, motor skills, sensory integration or soft neurological problems, social communication the fetal alcohol diagnostic program ( fadp ) uses unpublished minnesota state criteria of performance at 1. 5 or more standard deviations on standardized testing in three or more of the ten brain domains to determine cns damage. however, the ten brain domains are


the fetal alcohol diagnostic program ( fadp ) uses unpublished minnesota state criteria of performance at 1. 5 or more standard deviations on standardized testing in three or more of the ten brain domains to determine cns damage. however, the ten brain domains are easily incorporated into any of the four diagnostic systems ' cns damage criteria, as the framework only proposes the domains, rather than the cut - off criteria for fasd. prenatal alcohol exposureedit prenatal alcohol exposure is determined by interview of the biological mother or other family members knowledgeable of the mother ' s alcohol use during the pregnancy ( if available ), prenatal health records ( if available ), and review of available birth records, court records ( if applicable ), chemical dependency treatment records ( if applicable ), or other reliable sources. exposure level is assessed as confirmed exposure, unknown exposure, and confirmed absence of exposure by the iom, cdc and canadian diagnostic systems. the " 4 - digit diagnostic code " further distinguishes confirmed exposure as high risk and some risk : - high risk - confirmed use of alcohol during pregnancy known to be at high blood alcohol levels ( 100mg / dl or greater ) delivered at least weekly in early pregnancy. - some risk - confirmed use of alcohol during pregnancy with use less than high risk or unknown usage patterns. - unknown risk - unknown use of alcohol during pregnancy. - no risk - confirmed absence of prenatal alcohol exposure. amount, frequency, and timing of prenatal alcohol use can dramatically impact the other three key features of fasd. while consensus exists that alcohol is a teratogen, there is no clear consensus as to what level of exposure is toxic. the cdc guidelines are silent on these elements diagnostically. the iom and canadian guidelines explore this further, acknowledging the importance of significant alcohol exposure from regular or heavy episodic alcohol consumption in determining, but offer no standard for diagnosis. canadian guidelines discuss this lack of clarity and parenthetically point out that " heavy alcohol use " is defined by the national institute on alcohol abuse and alcoholism as five or more drinks per episode on five or more days during a 30 day period. " the 4 - digit diagnostic code " ranking system distinguishes between levels of prenatal alcohol exposure as high risk and some risk. it operationalizes high risk exposure as a blood alcohol concentration ( bac ) greater than 100mg / dl delivered at least weekly in early pregnancy. this bac level is typically reached by a 55kg female drinking six to eight beers in one sitting. for many adopted


risk exposure as a blood alcohol concentration ( bac ) greater than 100mg / dl delivered at least weekly in early pregnancy. this bac level is typically reached by a 55kg female drinking six to eight beers in one sitting. for many adopted or adult patients and children in foster care, records or other reliable sources may not be available for review. reporting alcohol use during pregnancy can also be stigmatizing to birth mothers, especially if alcohol use is ongoing. in these cases, all diagnostic systems use an unknown prenatal alcohol exposure designation. a diagnosis of fas is still possible with an unknown exposure level if other key features of fasd are present at clinical levels. confirmed absence of exposureedit confirmed absence of exposure would apply to planned pregnancies in which no alcohol was used or pregnancies of women who do not use alcohol or report no use during the pregnancy. this designation is relatively rare, as most patients presenting for an fasd evaluation are at least suspected to have had a prenatal alcohol exposure due to presence of other key features of fasd. while the four diagnostic systems essentially agree on criteria for fetal alcohol syndrome ( fas ), there are still differences when full criteria for fas are not met. this has resulted in differing and evolving nomenclature for other conditions across the spectrum of fasd, which may account for such a wide variety of terminology. most individuals with deficits resulting from prenatal alcohol exposure do not express all features of fas and fall into other fasd conditions. the canadian guidelines recommend the assessment and descriptive approach of the " 4 - digit diagnostic code " for each key feature of fasd and the terminology of the iom in diagnostic categories, excepting arbd. fetal alcohol syndrome or fas is the only expression of fasd that has garnered consensus among experts to become an official icd - 9 and icd - 10 diagnosis. to make this diagnosis or determine any fasd condition, a multi - disciplinary evaluation is necessary to assess each of the four key features for assessment. generally, a trained physician will determine growth deficiency and fas facial features. while a qualified physician may also assess central nervous system structural abnormalities and / or neurological problems, usually central nervous system damage is determined through psychological, speech - language, and occupational therapy assessments to ascertain clinically significant impairments in three or more of the ten brain domains. prenatal alcohol exposure risk may be assessed by a qualified physician, psychologist, social worker, or chemical health counselor. these professionals work together as a team


to ascertain clinically significant impairments in three or more of the ten brain domains. prenatal alcohol exposure risk may be assessed by a qualified physician, psychologist, social worker, or chemical health counselor. these professionals work together as a team to assess and interpret data of each key feature for assessment and develop an integrative, multi - disciplinary report to diagnose fas ( or other fasd conditions ) in an individual. other fasd diagnosesedit other fasd conditions are partial expressions of fas, and here the terminology shows less consensus across diagnostic systems, which has led to some confusion for clinicians and patients. a key point to remember is that other fasd conditions may create disabilities similar to fas if the key area of central nervous system damage shows clinical deficits in two or more of the ten brain domains. essentially, growth deficiency and / or fas facial features may be mild or nonexistent in other fasd conditions, but clinically significant brain damage of the central nervous system is present. in these other fasd conditions, an individual may be at greater risk for adverse outcomes because brain damage is present without associated visual cues of poor growth or the " fas face " that might ordinarily trigger an fasd evaluation. such individuals may be misdiagnosed with primary mental health disorders such as adhd or oppositional defiance disorder without appreciation that brain damage is the underlying cause of these disorders, which requires a different treatment paradigm than typical mental health disorders. while other fasd conditions may not yet be included as an icd or dsm - iv - tr diagnosis, they nonetheless pose significant impairment in functional behavior because of underlying brain damage. partial fas ( pfas ) edit previously known as atypical fas in the 1997 edition of the " 4 - digit diagnostic code, " patients with partial fetal alcohol syndrome have a confirmed history of prenatal alcohol exposure, but may lack growth deficiency or the complete facial stigmata. central nervous system damage is present at the same level as fas. these individuals have the same functional disabilities but " look " less like fas. - growth deficiency - growth or height may range from normal to deficient - fas facial features - two or three fas facial features present - central nervous system damage - clinically significant structural, neurological, or functional impairment in three or more of the ten brain domains - prenatal alcohol exposure - confirmed prenatal alcohol exposure alcohol - related neurodevelopmental disorder ( arnd )


nervous system damage - clinically significant structural, neurological, or functional impairment in three or more of the ten brain domains - prenatal alcohol exposure - confirmed prenatal alcohol exposure alcohol - related neurodevelopmental disorder ( arnd ) edit alcohol - related neurodevelopmental disorder ( arnd ) was initially suggested by the institute of medicine to replace the term fae and focus on central nervous system damage, rather than growth deficiency or fas facial features. the canadian guidelines also use this diagnosis and the same criteria. while the " 4 - digit diagnostic code " includes these criteria for three of its diagnostic categories, it refers to this condition as static encephalopathy. the behavioral effects of arnd are not necessarily unique to alcohol however, so use of the term must be within the context of confirmed prenatal alcohol exposure. arnd may be gaining acceptance over the terms fae and arbd to describe fasd conditions with central nervous system abnormalities or behavioral or cognitive abnormalities or both due to prenatal alcohol exposure without regard to growth deficiency or fas facial features. - growth deficiency - growth or height may range from normal to minimally deficient - fas facial features - minimal or no fas facial features present - central nervous system damage - clinically significant structural, neurological, or functional impairment in three or more of the ten brain domains - prenatal alcohol exposure - confirmed prenatal alcohol exposure fetal alcohol effects ( fae ) edit this term was initially used in research studies to describe humans and animals in whom teratogenic effects were seen after confirmed prenatal alcohol exposure ( or unknown exposure for humans ), but without obvious physical anomalies. smith ( 1981 ) described fae as an " extremely important concept " to highlight the debilitating effects of brain damage, regardless of the growth or facial features. this term has fallen out of favor with clinicians because it was often regarded by the public as a less severe disability than fas, when in fact its effects can be just as detrimental. alcohol - related birth defects ( arbd ) edit formerly known as possible fetal alcohol effect ( pfae ), alcohol - related birth defects ( arbd ) was a term proposed as an alternative to fae and pfae the iom presents arbd as a list of congenital anomalies that are linked to maternal alcohol use but have no key features of fasd. pfae and arbd have fallen out of favor because these anomalies are not necessarily specific to maternal alcohol


. 13 6. 14 6. 15 institute of medicine ( iom ), stratton, k. r., howe, c. j., & battaglia, f. c. ( 1996 ). fetal alcohol syndrome : diagnosis, epidemiology, prevention, and treatment. washington, dc : national academy press. isbn 0309052920 - ↑ 7. 0 7. 1 7. 2 7. 3 7. 4 7. 5 7. 6 7. 7 7. 8 7. 9 fetal alcohol syndrome : guidelines for referral and diagnosis ( pdf ). cdc ( july 2004 ). retrieved on 2007 - 04 - 11 - ↑ 8. 0 8. 1 8. 2 8. 3 8. 4 8. 5 8. 6 8. 7 chudley a, conry j, cook j, et al ( 2005 ). fetal alcohol spectrum disorder : canadian guidelines for diagnosis. cmaj 172 ( 5 suppl ) : s1 – s21. - ↑ 9. 0 9. 1 9. 2 9. 3 clinical growth charts. national center for growth statistics. retrieved on 2007 - 04 - 10 - ↑ jones, k. l., & smith d. w. ( 1975 ). the fetal alcohol syndrome. teratology, 12 ( 1 ), 1 - 10. - ↑ astley, s. j., & clarren, s. k. ( 1996 ). a case definition and photographic screening tool for the facial phenotype of fetal alcohol syndrome. journal of pediatrics, 129 ( 1 ), 33 - 41. - ↑ astley, s. j., stachowiak, j., clarren, s. k., & clausen, c. ( 2002 ). application of the fetal alcohol syndrome facial photographic screening tool in a foster care population. journal of pediatrics, 141 ( 5 ), 712 - 717. - ↑ lip - philtrum guides. fas diagnostic and prevention network, university of washington. retrieved on 2007 - 04 - 10 - ↑ 14. 0 14. 1 14. 2 fas facial features. fas diagnostic and prevention network, university of washington. retrieved on 2007 - 04 - 10 - ↑ astley, susan. backside of lip - philtrum guides ( 2004 ) ( pdf ). university of washington, fetal alcohol syndrome diagnostic and prevention network. retrieved on [ [ 2007 - 04 - 11 ] - ↑ west, j. r. ( ed. )


susan. backside of lip - philtrum guides ( 2004 ) ( pdf ). university of washington, fetal alcohol syndrome diagnostic and prevention network. retrieved on [ [ 2007 - 04 - 11 ] - ↑ west, j. r. ( ed. ) ( 1986 ). alcohol and brain development. new york : oxford university press. - ↑ 17. 0 17. 1 fadp - fetal alcohol diagnostic program - ↑ 18. 0 18. 1 18. 2 18. 3 18. 4 18. 5 lang, j. ( 2006 ). ten brain domains : a proposal for functional central nervous system parameters for fetal alcohol spectrum disorder diagnosis and follow - up. journal of the fas institute, 4, 1 - 11. can be downloaded at http : / / www. motherisk. org / jfas _ documents / jfas _ 5012 _ final _ e12 _ 6. 28. 6. pdf - ↑ u. s. department of health and human services. ( 2000 ). national institute on alcohol abuse and alcoholism. tenth special report to the u. s > congress on alcohol and health : highlights frfom current research. washington, dc : the institute. - ↑ 20. 0 20. 1 20. 2 streissguth, a. ( 1997 ). fetal alcohol syndrome : a guide for families and communities. baltimore : brookes publishing. isbn 1 - 55766 - 283 - 5. - ↑ malbin, d. ( 2002 ). fetal alcohol spectrum disorders : trying differently rather than harder. portland, or : fascets, inc. isbn 0 - 9729532 - 0 - 5. - ↑ smith, d. w. ( 1981 ). fetal alcohol syndrome and fetal alcohol effects. neurobehavioral toxicology and teratology, 3, 127. - ↑ aase, j. m., jones, k. l., & clarren, s. k. ( 1995 ). do we need the term fae? pediatrics, 95 ( 3 ), 428 - 430. - ↑ sokol, r. j., & clarren, s. k. ( 1989 ). guidelines for use of terminology describing the impact of prenatal alcohol on the offspring. alcoholism : clinical and experimental research, 13 ( 4 ), 597 - 598. - samhsa fetal alcohol spectrum disorders center of excellence - u. s. congressional caucus on fetal alcohol spectrum disorders - nofas - uk | this page


asa - interpret carriage - control characters asa [ file... ] the asa utility will write its input files to standard output, mapping carriage - control characters from the text files to line - printer control sequences in an implementation - dependent manner. the first character of every line will be removed from the input, and the following actions will be performed : if the character removed is : - the rest of the line will be output without change. - a newline character will be output, then the rest of the input line. - one or more implementation - dependent characters that causes an advance to the next page will be output, followed by the rest of the input line. - the newline character of the previous line will be replaced with one or more implementation - dependent characters that causes printing to return to column position 1, followed by the rest of the input line. if the " + " is the first character in the input, it will have the same effect as the space character. the action of the asa utility is unspecified upon encountering any character other than those listed above as the first character in a line. - a pathname of a text file used for input. if no file operands are specified, the standard input will be used. the standard input will be used only if no file operands are specified. see the input files section. the input files must be text files. the following environment variables affect the execution of asa : - provide a default value for the internationalisation variables that are unset or null. if lang is unset or null, the corresponding value from the implementation - dependent default locale will be used. if any of the internationalisation variables contains an invalid setting, the utility will behave as if none of the variables had been defined. - if set to a non - empty string value, override the values of all the other internationalisation variables. - determine the locale for the interpretation of sequences of bytes of text data as characters ( for example, single - as opposed to multi - byte characters in arguments and input files ). - determine the locale that should be used to affect the format and contents of diagnostic messages written to standard error. - determine the location of message catalogues for the processing of lc _ messages. the standard output will be the text from the input file modified as described in the description section. the following exit values are returned : - all input files were output successfully. - an error occurred. the following command : permits the viewing of file ( created by a program using fortran - style carriage


the cpsc and the fda came together yesterday to issue a warning to parents and caregivers to stop using infant sleep positioners immediately as two recent deaths underscore concerns about suffocation. you may remember the recent recall of the nap nanny. well, now the cpsc is issuing a general warning with regard to sleep positioners after reviewing reports of 12 known infant deaths associated with the products which have occurred over the past 13 years. most of the infants suffocated after rolling from a side to a stomach position. in addition to the 12 reported deaths, the cpsc has received dozens of reports of infants who were placed on their backs or sides in sleep positioners, only to be found later in potentially hazardous positions within or next to the sleep positioners. the most common types of sleep positioners are : - sleeping bolsters, usually a flat or inclined mat with round or triangular cushions on each side of a baby ( see figure 1 ) and - wedge - style positioners, which elevate a baby ’ s head higher than its body, sometimes by placing the infant in an attached, diaper - like sling ( see figure 2 ). with bolster - style positioners, if a baby is placed on its stomach or if a baby rolls from its side to its stomach, his or her mouth and nose can become pressed against a bolster or other parts of the device. even if placed on its back, a baby may move upward or downward in the positioner, entrapping its face against a bolster or becoming trapped between the positioner and the crib side or bassinet. a baby placed on a wedge - style positioner can scoot upward so that its head falls off and hangs over the high edge of the positioner, or the baby may scoot or roll down the wedge so that its mouth and nose are pressed into the positioner. the baby ’ s movement may also cause the positioner to flip on top of the baby, trapping the baby underneath the positioner or between the positioner and the side of the crib. many of these devices have been marketed with medical claims that they reduce the risk of sids by keeping a child on their back, help with food digestion and reflux ( gerd ), ease colic, and / or prevent flat head syndrome. however, the fda and the cpsc have stated that there is currently no scientific evidence supporting these claims and they believe that any benefit from using these devices is outweighed by the risk of


ease colic, and / or prevent flat head syndrome. however, the fda and the cpsc have stated that there is currently no scientific evidence supporting these claims and they believe that any benefit from using these devices is outweighed by the risk of suffocation. the fda, which has jurisdiction over products making medical claims, is now contacting all manufacturers of infant sleep positioners, including those it had previously cleared with medical claims, and requesting that they stop marketing them until they submit scientific data showing that the benefits of their products outweigh the risk of suffocation or other serious harm. the fda has also indicated it will be contacting retailers to ask them to stop selling the devices. the fda and cpsc warn parents, caregivers, and healthcare professionals to take this warning seriously and follow these recommendations : ( 1 ) stop using infant sleep positioners. using a device to hold an infant in a particular position is dangerous and unnecessary. ( 2 ) never put pillows, infant sleep positioners, comforters, or quilts under the baby or in the crib. ( 3 ) always place an infant to sleep on his / her back, and not their sides, at night and during nap time. fda pediatric expert susan cummins, m. d., m. p. h., says, “ the safest crib is a bare crib, ” and summarizes the above recommendations with the “ abcs of safe sleep — alone on the back in a bare crib. ” if you enjoy reading purebebe, please tell your friends and click on “ sign me up! ” under “ email subscription ” on the right rail of the screen. by subscribing to our emails, you are telling us that you dig our site and want to read more of our healthy baby news and topics! other recent recalls : similac baby formula recalled nap nanny® recall : what you should know cpsc vote to issue safety standards that will eliminate drop - side cribs massive crib recall announced : what you should know double check your children ’ s medicine to subscribe to recall announcements and product safety alerts from the cpsc, click here.


mexico - messico photo by eddie adams " anger is energy, it ’ s a force. if an act of injustice doesn ’ t provoke anger in me, it could be seen as indifference, passivity. it ’ s injustice that motivates us to do something, to take risks, knowing that if we don ’ t, things will remain the same. " one of the foremost human rights attorneys in mexico, digna ochoa was also a nun. as defense attorney at prodh ( centro de derechos humanos miguel agustin pro juarez, known as centro pro, or " the pro " ), ochoa took on some of mexico ’ s most politically charged cases, including the defense of alleged members of the zapatista insurgency in chiapas. she won acquittals in several highly publicized cases. in many cases, ochoa ’ s clients were subjected to torture and due process violations. ochoa herself was threatened with death, abducted, and subjected to extensive harassment. just a few weeks after she was interviewed for the book, speak truth to power, two men assaulted her in her own apartment. they blindfolded her, tied her up, interrogated her, threatened her, and pressured her to sign a statement. they cut her phone line, and opened a gas valve in a closed room. miraculously, she survived. her attackers left stolen files during an attack a few months earlier, while the next day prodh staff found their offices had been broken into and ransacked. nevertheless, ochoa went right back to work at the pro. in recent years human rights advocates, government investigators, and opposition leaders have been murdered in mexico. the inter - american court of human rights has required the mexican government to take steps to assure the safety of prodh staff in the wake of this pattern of persecution against the organization. on october 19, 2001, however, digna ochoa was found shot dead at her office in mexico city. her killers also left a death threat against other members of prodh. mexican special prosecutor margarita guerra, who led an inquiry into the violent death of internationally recognized advocate then stunned the human rights community in 2003 by disparaging the activist ’ s human rights work, discounting any motive for her to have been targeted for murder, and concluding that her death was probably a suicide. this troubling pronouncement further emphasized the deplorable state of the mexican justice system that ms. ochoa worked so tirelessly to reform. digna ochoa was killed because


and concluding that her death was probably a suicide. this troubling pronouncement further emphasized the deplorable state of the mexican justice system that ms. ochoa worked so tirelessly to reform. digna ochoa was killed because of her human rights work. she and other members of the prodh have worked on cases of torture and other serious human rights violations in which mexican officials have been implicated. as a result, these defenders of human rights have been the target of many threats and attacks digna ochoa was posthumously bestowed with the ludovic trarieux international human rights prize in 2003. centro de derechos humanos “ miguel agustin pro juarez ” i am a nun, who started life as a lawyer. i sought a religious community with a social commitment, and the protection of human rights is one of the things that my particular community focuses on. they have permitted me to work with an organization that fights for human rights, called centro pro, supporting me economically, morally, and spiritually. this has been a process of building a life project, from a social commitment to a spiritual one with a mystical aspect. my father was a union leader in veracruz, mexico. in the sugar factory where he worked, he was involved in the struggles for potable water, roads, and securing land certificates. i studied law because i was always hearing that my father and his friends needed more lawyers. and all the lawyers charged so much. my father was unjustly jailed for one year and fifteen days. he then disappeared and was tortured — the charges against him were fabricated. this led to my determination to do something for those suffering injustice, because i saw it in my father ' s flesh. when i first studied law, i intended to begin practicing in the attorney general ’ s office, then become a judge, then a magistrate. i thought someone from those positions could help people. after i got my degree, i became a prosecutor. i remember a very clear issue of injustice. my boss, who was responsible for all of the prosecutions within the attorney general ’ s office, wanted me to charge someone whom i knew to be innocent. there was no evidence, but my boss tried to make me prosecute him. i refused, and he prosecuted the case himself. up until that time, i was doing well. the job was considered a good one, because it was in a coffee - producing area and the people there had lots of money. but i realized that i was doing the same thing that everyone did, serving


until that time, i was doing well. the job was considered a good one, because it was in a coffee - producing area and the people there had lots of money. but i realized that i was doing the same thing that everyone did, serving a system that i myself criticized and against which i had wanted to fight. i decided to quit and with several other lawyers opened an office. i had no litigation experience whatsoever. but i was energized by leaving the attorney general ’ s office and being on the other side, the side of the defense. the first case i worked on was against judicial police officers who had been involved in the illegal detention and torture of several peasants. we wanted to feel like lawyers, so we threw ourselves into it. our mistake was to take on the case without any institutional support. i had managed to obtain substantial evidence against the police, so they started to harass me incessantly, until i was detained. first, they sent telephone messages telling me to drop the case. then by mail came threats that if i didn ’ t drop it i would die, or members of my family would be killed. i kept working and we even publicly reported what was happening. the intimidation made me so angry that i was motivated to work even harder. i was frightened, too, but felt i couldn ’ t show it. i always had to appear — at least publicly — as if i was sure of myself, fearless. if i showed fear they would know how to dominate me. it was a defense mechanism. then, i was kidnapped and held incommunicado for eight days by the police. they wanted me to give them all the evidence against them. i had hidden the case file well, not in my office, not in my house, and not where the victims lived, because i was afraid that the police would steal it. now, i felt in the flesh what my father had felt, what other people had suffered. the police told me that they were holding members of my family, and named them. the worst was when they said they were holding my father. i knew what my father had suffered, and i didn ’ t want him to relive that. the strongest torture is psychological. though they also gave me electric shocks and put mineral water up my nose, nothing compared to the psychological torture. there was a month of torture. i managed to escape from where they were holding me. i hid for a month after that, unable to communicate with my family. it was a month


mineral water up my nose, nothing compared to the psychological torture. there was a month of torture. i managed to escape from where they were holding me. i hid for a month after that, unable to communicate with my family. it was a month of anguish and torture, of not knowing what to do. i was afraid of everything. i eventually got in touch with my family. students at the university, with whom i had always gotten along very well, had mobilized on my behalf. after i " appeared " with the help of my family and human rights groups in jalapa, veracruz, i was supported by lawyers, most of whom were women. the fact that i was in veracruz caused my family anguish. at first i wanted to stay, because i knew we could find the police who detained me. we filed a criminal complaint. we asked for the police registries. i could clearly identify some of the officers. but there was a lot of pressure about what i should do : continue or not with the case? my life was at risk, and so were the lives of members of my family. after a month of anguish, my family, principally my sisters, asked me to leave jalapa for a while. for me, but also for my parents. i came to mexico city. the idea was to take a three - month human rights course for which i had received a scholarship. i met someone at the human rights course who worked at centro pro, one of the human rights groups involved on my behalf. one day he said, " look, we ’ re just setting up the center and we need a lawyer. work with us. " i had never dreamed of living in mexico city, and i didn ’ t want to. but i accepted, because the conditions in jalapa were such that i couldn ’ t go back. two really good women lawyers in jalapa with a lot of organizational support took up the defense case i had been working on. this comforted me, because i knew the case would not be dropped — i had learned the importance of having organizational backup. so i started to work with centro pro in december 1988. since i began working with the organization, i ’ ve handled a lot of cases of people like my father and people like me. that generates anger, and that anger becomes the strength to try to do something about the problem. at work, even though i give the appearance of seriousness and resolve, i ’ m trembling inside. sometimes i want to cry, but i know that i


that generates anger, and that anger becomes the strength to try to do something about the problem. at work, even though i give the appearance of seriousness and resolve, i ’ m trembling inside. sometimes i want to cry, but i know that i can ’ t, because that makes me vulnerable, disarms me. at this time, because of what happened to me, i needed the help of a psychoanalyst, but i wasn ’ t ready to accept it. the director of centro pro prepared me to accept that support. he was a jesuit and psychologist. for six months, i didn ’ t know he was a therapist. when i found out, i asked him why he hadn ’ t told me. " you never asked, " he said. we became very close. he was my friend, my confessor, my boss, and my psychologist, too, although i also had my psychoanalyst. the idea of a confessor came slowly to me. in jalapa, i had been supported by some priests. when i first " appeared, " the first place i was taken was a church. i felt secure there, though as a kid, i had never had much to do with priests, besides attending church. to me they were people who accepted donations, delivered sacraments, and were power brokers. it made an impression on me to see priests committed to social organizations, supporting people. since i ’ ve been at centro pro, we ’ ve gone through some tough times, like the two years of threats we received beginning in 1995. once again it was me who was being threatened. my first reaction was to feel cold shivers. i went to the kitchen with a faxed copy of the threat and said to one of the sisters in the congregation, " luz, we ’ ve received a threat, and they ’ re directed at me, too. " and luz responded, " digna, this is not a death threat. this is a threat of resurrection. " that gave me great sustenance. later that day another of my lawyer colleagues, pilar, called me to ask what security measures i was taking. she was — rightfully — worried. i told her what luz had said and pilar responded, " digna, the difference is that you ’ re a religious person. " and i realized that being a person of faith and having a community, that having a base in faith, is a source of support that others don ’ t have. now, some people said to me that


that you ’ re a religious person. " and i realized that being a person of faith and having a community, that having a base in faith, is a source of support that others don ’ t have. now, some people said to me that my reaction was courageous. but i ’ ve always felt anger at the suffering of others. for me, anger is energy, it ’ s a force. you channel energy positively or negatively. being sensitive to situations of injustice and the necessity of confronting difficult situations like those we see every day, we have to get angry to provoke energy and react. if an act of injustice doesn ’ t provoke anger in me, it could be seen as indifference, passivity. it ’ s injustice that motivates us to do something, to take risks, knowing that if we don ’ t, things will remain the same. anger has made us confront police and soldiers. something that i discovered is that the police and soldiers are used to their superiors shouting at them, and they ’ re used to being mistreated. so when they run into a woman, otherwise insignificant to them, who demands things of them and shouts at them in an authoritarian way, they are paralyzed. and we get results. i consider myself an aggressive person, and it has been difficult for me to manage that within the context of my religious education. but it does disarm authorities. i normally dress this way, in a way that my friends call monklike. that ’ s fine. it keeps people off guard. i give a certain mild image, but then i can, more efficiently, demand things, shout. for example, one time there was a guy who disappeared for twenty days. we knew he was in the military hospital, and we filed habeas corpus petitions on his behalf. but the authorities simply denied having him in custody. one night we were informed that he was being held at a particular state hospital. we went the next day. they denied us access. i spent the whole morning studying the comings and goings at the hospital to see how i could get in. during a change in shifts, i slipped by the guards. when i got to the room where this person was, the nurse at the door told me i could not go in. " we are not even allowed in, " she said. i told her that i would take care of myself ; all i asked of her was that she take note of what i was going to do and that if they did something to me, she should call


are not even allowed in, " she said. i told her that i would take care of myself ; all i asked of her was that she take note of what i was going to do and that if they did something to me, she should call a certain number. i gave her my card. i took a deep breath, opened the door violently and yelled at the federal judicial police officers inside. i told them they had to leave, immediately, because i was the person ’ s lawyer and needed to speak with him. they didn ’ t know how to react, so they left. i had two minutes, but it was enough to explain who i was, that i had been in touch with his wife, and to get him to sign a paper proving he was in the hospital. he signed. by then the police came back, with the fierceness that usually characterizes their behavior. their first reaction was to try to grab me. they didn ’ t expect me to assume an attack position — the only karate position i know, from movies, i suppose. of course, i don ’ t really know karate, but they definitely thought i was going to attack. trembling inside, i said sternly that if they laid a hand on me they ’ d see what would happen. and they drew back, saying, " you ’ re threatening us. " and i replied, " take it any way you want. " after some discussion, i left, surrounded by fifteen police officers. meanwhile i had managed to record some interesting conversations. they referred to " the guy who was incommunicado, " a term that was very important. i took the tape out and hid the cassette where i could. the police called for hospital security to come, using the argument that it wasn ’ t permitted to have tape recorders inside the hospital. i handed over the recorder. then they let me go. i was afraid that they would kidnap me outside the hospital. i was alone. i took several taxis, getting out, changing, taking another, because i didn ’ t know if they were following me. when i arrived at centro pro, i could finally breathe. i could share all of my fear. if the police knew that i was terrified when they were surrounding me, they would have been able to do anything to me. sometimes, without planning and without being conscious of it, there is a kind of group therapy among the colleagues at centro pro. we show what we really feel, our fear. we cry. there ’ s a group


able to do anything to me. sometimes, without planning and without being conscious of it, there is a kind of group therapy among the colleagues at centro pro. we show what we really feel, our fear. we cry. there ’ s a group of us who have suffered physically. on the other hand, my religious community has helped me manage my fear. at times of great danger, group prayer and study of the bible and religious texts helps me. praying is very important. faith in god. that has been a great source of strength. and i ’ m not alone anymore. as a christian, as a religious person, i call myself a follower of christ who died on the cross for denouncing the injustices of his time. and if he had to suffer what he suffered, what then can we expect? for years after my father was tortured, i wanted revenge. then, when i was the torture victim, the truth is that the last thing i wanted was revenge, because i feared that it would be an unending revenge. i saw it as a chain. three years after coming to mexico city i remember that a person came to tell me that they had found two of the judicial police officers who tortured me. the person asked if i wanted him to get them and give them their due. at first, i did have a moment when i thought yes. but i thought about it and realized that i would simply be doing what they did. i would have no right to speak about them as i am talking about them now. i would have been one of them. i rarely share my own experience of torture. but i remember talking to a torture victim who was very, very angry, for whom the desire for revenge was becoming destructive. i shared my own experience, and that made an impression on him. but if we don ’ t forgive and get over the desire for revenge, we become one of them. you can ’ t forget torture, but you have to learn to assimilate it. to assimilate it you need to find forgiveness. it ’ s a long - term, difficult, and very necessary undertaking. if you don ’ t step up to those challenges, what are you doing? what meaning does your life have? it is survival. when i began to work, when i took that case in which they made me leave jalapa, i was committed to doing something against injustice. but there was something else that motivated me, and i have to recognize it, even though it causes me shame. what


work, when i took that case in which they made me leave jalapa, i was committed to doing something against injustice. but there was something else that motivated me, and i have to recognize it, even though it causes me shame. what motivated me as well as the commitment was the desire to win prestige as a lawyer. thanks to the very difficult situation that i lived through, i realized what was wrong. what a shame that i had to go through that in order to discover my real commitment, the meaning of my life, the reason i ’ m here. in this sense, i ’ ve found something positive in what was a very painful experience. if i hadn ’ t suffered, i wouldn ’ t have been able to discover injustice in such depth. maybe i wouldn ’ t be working in centro pro. maybe i wouldn ’ t have entered the congregation. maybe i wouldn ’ t have learned that the world is a lot bigger than the very small world that i had constructed. thanks to a very difficult, painful experience for me and my family and my friends, my horizons were broadened. sometimes i say to myself, " what a way for god to make you see things. " but sometimes without that we aren ’ t capable of seeing. speak truth to power ( umbrage, 2000 )


training to compete develop the engine the player - specializes the players in this stage are generally around 16 - 19 years old for boys and around 15 - 18 years old for girls players are more likely to have committed themselves to rugby as their chief sport. they are more willing to invest a significant amount of time and energy to become successful. they are driven and are fiercely competitive with a greater capacity for all game related competencies. players pay more attention to developing themselves as positional specialists in order to undertake their functional roles. players at this stage are capable of independent thinking and of taking greater responsibility while also contributing more toward problem solving. the coach - facilitates since players have the capacity for greater input, the role of the coach shifts towards facilitation. allowing opportunity for opinions and problem solving is critical if players are to develop confidence and relative autonomy. the coach will still need to employ teaching, challenging and guiding skills where appropriate. the emphasis should be on developing players ’ ability to navigate rather than replicate. the game - outcomes the game becomes fiercely competitive with positional specialists influencing games, mini units and units well are synchronized and team play concentrates on reducing errors and maximizing success. the focus is on achieving desired outcomes with respect to attacking and defensive goals ( team, unit, mini - unit ).


save the clean air act to fight global warming scientific consensus is clear : we must reduce the level of atmospheric carbon dioxide to 350 parts per million ( ppm ) or below to avoid global catastrophe. unfortunately, pending climate legislation isn ' t going to get us to 350 ppm - - but the clean air act could. to reach 350 ppm, carbon pollution from the united states and other developed countries must be reduced by 45 percent or more below 1990 levels by 2020. but the senate climate bill would reduce emissions by just 4 percent below those levels. ( the house bill sets even weaker targets. ) clearly, the road map to 350 ppm won ' t be found in pending legislation. rather, the path to achieving 350 ppm must utilize the clean air act, which provides indispensable tools for reducing pollution from smokestacks and other big polluters, and also requires the environmental protection agency to set a science - based national pollution limit for greenhouse gases. - under the act, the epa is required to set a limit on the amount of carbon pollution that different sources, such as coal - fired power plants, oil refineries, and cement factories, may emit. - the act requires each new or modified source of carbon pollution to show that the proposed facility will use the best available carbon control technology before it can be built. - finally, the act requires the epa to use the best available science and set a national limit - - such as 350 ppm - - on the total amount of carbon pollution that may exist in the ambient air. epa has not yet set that limit, and will be prevented from ever doing so if the current climate bill becomes law. the clean air act is a comprehensive system of pollution control with a proven track record of saving the public money and protecting our planet ' s health. it can work immediately to curb carbon pollution, either by itself or in conjunction with new climate legislation. now, more than ever, is the time to enforce the clean air act - - not to gut it. we need you to stand with us to save the clean air act today. - if you haven ' t yet written to your senators urging them to save the clean air act, click here to send them a message now. - please call your senators and urge them to save the clean air act - - the entire clean air act. personal calls from constituents make a big difference. call ( 202 ) 224 - 3121 and ask for your senators ' office, or visit https : / / salsa. democracyinaction.


emergency & security medications, attention deficit disorder, and hepatitis medication in school school personnel may assist a student to manage prescription and non - prescription medication only under the directions of a physician. prescription medication will be accepted only in the container properly labeled by the pharmacist. this label will serve as the physician ’ s written instructions. the parent must fill out medication consent forms, available in the front office. students may carry a 1 - day supply of non - prescription medication with them, as long as they also carry a note from the parent specifying the name of the medication and dose to be taken. all medication requested to be administered by school personnel must be checked in with school personnel and kept in a locked cupboard. the student may carry emergency medication / inhalers with parent and physician written instruction. school personnel will accept changes in medication dosages only with the new properly labeled pharmacy container reflecting the dosage and / or time changes. parents are responsible for transportation of medication to and from school. parents are responsible for refilling the school ’ s supply of medication and keeping track of that supply. parents are responsible for the preparation of all tablets ( e. g., halving tablets ). parents are responsible for picking up all unused medication at the end of the school year. adhd / add and medications an increasing number of students are being diagnosed as having an attention deficit disorder and are being placed on medication by their physicians. there is still much to learn about attention disorders, and controversy about the appropriateness of prescribing medication. our role as educators is to provide instruction, make reasonable accommodations, observe behavior and provide feedback to parents and physicians when asked. we have the responsibility of cooperating with a physician and parent when a child is placed on medication following the procedures outline in school board policy 5665, administering medication in school ( see appendix a ). we do not have the training or authority to prescribe medication. consult with district nurses, psychologists, or social workers if you have questions about adhd / add. due to the continuing high local incidence rate of hepatitis b, we will again follow the recommendations of the lane county health department in restricting the use of home prepared foods for use at school sponsored events. food prepared by the cafeteria staff, pre - packaged or “ store bought ” items, and food cleaned and cooked at school under staff supervision are acceptable to share at school. this restriction applies specifically to all school functions that include students, parents, or other members of the community. while the restrictions do not apply to events that


louis xv and science : the most beautiful instruments authors : engineer : claude - simeon passemant ( 1702 - 1769 ) ; clockmaker : louis dauthiau ( 1730 - 1809 ) ; sculptors and bronze artists : jean - jacques and philippe caffieri ( 1725 - 1772 ) date : presented to the royal academy of science on 23 august 1749, presented to the king in 1750. mechanism : 1749 ; bronze : 1753 characteristics / origins : gilt bronze, enamel, steel, copper and glass. versailles, musee national des chateaux de versailles et de trianon © chateau de versailles, christian milet the extraordinary astronomical clock was added to the clock cabinet in january 1754. engineer claude - simeon passemant designed the timepiece, clockmaker louis dauthiau crafted the mechanism and sculptors and bronze artists jacques and philippe ii caffieri made the case. it shows the date, real time, average time, phases of the moon and movements of the planets according to copernicus. a moving sphere crowns the exceptional rocaille work, which measures over two metres tall. a bronze globe features all the countries engraved with the main cities. it is amidst rocks and waterfalls serving as the universal horizon. the academy of science examined and approved the clock in august 1749 before the duc de chaulnes presented it to louis xv at choisy on 7 september 1750. the king acquired it that year. it was put in the clock cabinet, attesting to louis xv ' s interest in the mechanical arts and clocks ; the room actually got its name because of the large astronomical clock dials in the wainscoting showing the sunrises and moonrises every day. the king ' s scientific interests led him to amplify that daily experience by having the passemant clock installed in this room. video in french


for one aes is built for three key sizes 128, 192 or 256 bits. currently, brute - forcing 128 bits is not even close to feasible. hypothetically, if an aes key had 129 bits, it would take twice as long to brute - force a 129 bit key than a 128 bit key. this means larger keys of 192 bits and 256 bits would take much much much longer to attack. it would take so incredibly long to brute - force one of these keys that the sun would stop burning before the key was realized. that ' s a big freaking number. that ' s how many possibly keys there are. assuming the key is random, if you divide that by 2 then you have how many keys it will take on average to brute - force aes - 256 in a sense we do have the really big cipher keys you are talking of. the whole point of a symmetric key is to make it unfeasible to brute - force. in the future, if attacking a 256bit key becomes possible then keysizes will surely increase, but that is quite a ways down the road. the reason rsa keys are much larger than aes keys is because they are two completely different types of encryption. this means a person would not attack a rsa key the same as they would attack an aes key. attacking symmetric keys is easy. - start with a bitstring - decrypt ciphertext with that bitstring. - if you can read it, you succeeded. - if you cannot read it then increment the bitstring attacking an rsa key is different... because rsa encryption / decryption works with big semi - prime numbers... the process is mathy. with rsa, you don ' t have to try every possible bit string. you try far fewer than 2 ^ 2048 bitstrings... but it ' s still not possible to bruteforce. this is why rsa and aes keys differ in size. to sum up everything and answer your question in 1 sentence. we don ' t need ridiculously big symmetric keys because we already have ridiculously big symmetric keys. 256 bit encryption sounds wimpy compared to something like a 2048 bit rsa key, but the algorithms are different and can ' t really be compared ' bit to bit ' like that. in the future if there is a need to longer keys then there will be new algorithms developed to handle larger keys. and if we ever wanted to go bigger on current hardware,


unions have been fighting the 1 % vs 99 % fight for more than 100 years. now the rest of us are learning that this fight is also our fight. the story of organized labor has been a story of working people banding together to confront concentrated wealth and power. unions have been fighting to get decent wages, benefits, better working conditions, on - the - job safety and respect. now, as the reagan revolution comes home to roost, taking apart the middle class, the rest of us are learning that this is our fight, too. the story of america is a similar story to that of organized labor. the story of america is a story of we, the people banding together to fight the concentrated wealth and power of the british aristocracy. our declaration of independence laid it out : we were fighting for a government that derives its powers from the consent of us, the people governed, not government by a wealthy aristocracy telling us what to do and making us work for their profit instead of for the betterment of all of us. it was the 99 % vs the 1 % then, and it is the 99 % vs the 1 % now. we, the people democracy is when we, the people decide things together — collectively — for the common good of all of us. our country originated from the idea of we, the people banding together to watch out for and protect each other, so we can all rise together for the common good, or “ general welfare. ” collectively we make decisions, and the result of this collective action is decisions that work for all of us instead of just a few of us. this is the founding idea of our country. unions protect the interests of working people the same is true for unions. unions work to bring we - the - people democracy to the workplace. like the old story about how it is harder to break a bundle of sticks than the same sticks one stick at a time, unions are organizations of working people, banding together so their collective power can confront the power of concentrated wealth. by banding together in solidarity, working people are able to say, “ no, you can ’ t do that!, ” and bargain for a better life for all of us. organized labor sets the standard the benefits that unions win don ’ t just go to the union members, they become the standard. when labor won the fight for an 8 - hour day and 40 - hour workweek with overtime pay, that became the standard. when labor fought for minimum wages, that became the standard, when labor fought


the union members, they become the standard. when labor won the fight for an 8 - hour day and 40 - hour workweek with overtime pay, that became the standard. when labor fought for minimum wages, that became the standard, when labor fought for workplace safety, that became the standard. labor ’ s fight is a fight to set the standard for the rest of us. labor stands up to the 1 %, and uses their organized power ( bundle of sticks ) to win better pay, benefits and working conditions for the 99 %. “ although it is true that only about 20 percent of american workers are in unions, that 20 percent sets the standards across the board in salaries, benefits and working conditions. if you are making a decent salary in a non - union company, you owe that to the unions. one thing that corporations do not do is give out money out of the goodness of their hearts. ” – molly ivins. working people banding together to bargain with management — “ collective ” bargaining — is a fundamental right in the united states, but this right has eroded along with the rest of our democracy. for many years, the mechanisms of government that were supposed to enforce these rights were “ captured ” and instead were working against the rights of working people. bob borosage explains, in, the forgotten leading actor in the american dream story, globalization gave manufacturers a large club in negotiations — concessions or jobs get shipped abroad. and often the reality was concessions and jobs got shipped abroad. corporations perfected techniques, often against the law, to crush organizing drives, and stymie new contracts for the few that succeeded. the national labor relations board, stacked with corporate lobbyists under republican presidents, turned a blind eye to systematic violations of the law. so now union workers are down to about 7 percent of the private workforce. virtually the only growing unions are public employees — teachers, nurses, cops. not surprisingly, conservative republican governors, led by wisconsin ’ s scott walker and ohio ’ s john kasich, used the budget squeeze caused by the great recession to go after these unions, combining layoffs with efforts to eviscerate the right of public employees to organize and negotiate. the fight is on “ only a fool would try to deprive working men and working women of their right to join the union of their choice. ” – dwight d. eisenhower. dorian warren, at salon in america ’ s last hope : a strong labor movement, writes, the fate of the labor movement is the fate of american democracy. without


their right to join the union of their choice. ” – dwight d. eisenhower. dorian warren, at salon in america ’ s last hope : a strong labor movement, writes, the fate of the labor movement is the fate of american democracy. without a strong countervailing force like organized labor, corporations and wealthy elites advancing their own interests are able to exert undue influence over the political system, as we ’ ve seen in every major policy debate of recent years. yet the american labor movement is in crisis and is the weakest it ’ s been in 100 years. that truism has been a progressive mantra since the clinton administration. however, union density has continued to decline from roughly 16 percent in 1995 to 11. 8 percent of all workers and just 6. 9 percent of workers in the private sector. unionized workers in the public sector now make up the majority of the labor movement for the first time in history, which is precisely why — a la wisconsin and 14 other states — they have been targeted by the right for all out destruction. … contrary to the intent of the 1935 national labor relations act, which made it national policy to encourage and promote collective bargaining, the nlra now provides incentives for employers to break the law routinely and ignore any compulsion to negotiate collective agreements. when there is little outrage for the daily violations of workers ’ liberty ( employers fire workers illegally in 1 in 3 union campaigns for attempting to exercise freedom of association ), our democracy is in peril. restore the middle class unions brought us a middle class, and now that the power of organized labor has eroded we find ourselves in a fight to keep the middle class. borosage again, we emerged from world war ii with unions headed towards representing about 30 % of the workforce. fierce struggles with companies were needed to ensure that workers got a fair share of the rewards of their work. unions were strong enough that non - union employers had to compete for good workers by offering comparable wages. unions enforced the 40 - hour week, overtime pay, paid vacations, health care and pensions, and family wages. strong unions limited excesses in corporate boardrooms, a countervailing power beyond the letter of the contract. as profits and productivity rose, wages rose as well. when unions were weakened and reduced, all that changed. productivity and profits continued to rise, but wages did not. the ratio of ceo pay to the average worker pay went from 40 to 1 to more than 350 to 1. ceos were given multimillion - dollar pay incentives to cook


that changed. productivity and profits continued to rise, but wages did not. the ratio of ceo pay to the average worker pay went from 40 to 1 to more than 350 to 1. ceos were given multimillion - dollar pay incentives to cook their books and merge and purge their companies. unions were not strong enough to police the excess. america let multinationals define its trade and manufacturing strategy, hemorrhaging good jobs to mercantilist nations like china. the result was the wealthiest few captured literally all the rewards of growth. and 90 % of america struggled to stay afloat with stagnant wages, rising prices and growing debt. support bargaining rights for labor we all need to understand that labor ’ s fight is our fight. now that labor is under attack across the country, we need to understand that we are also under attack. as labor loses rights and power, all of our pay and benefits fall back. we need to support the rights of working people to organize into unions and bargain collectively, to fight our fight, the 99 % vs the 1 %. this battle right now is the whole ball game. “ to a right - winger, unions are awful. why do right - wingers hate unions? because collective bargaining is the power that a worker has against the corporation. right - wingers hate that. ” – janeane garofalo


winsor mccay, pioneering animator and comic strip artist, was a native of spring lake, michigan. spring lake is also where he began his career in art. his father, robert mccay, and mother janet ran a grocery store in the village. while it is probable that winsor was born in 1867 during a visit to his mother ’ s family in ontario, mccay stated that he was born september 26, 1871, in spring lake, michigan. he always considered spring lake his hometown. in 1880, the goodrich steamship alpena, en route from nearby grand haven to chicago, was wrecked in a terrible storm and sank to the bottom, carrying with it nearly one hundred passengers. at the age of thirteen, young winsor drew a picture of the wreck on the blackboard of union school, which he attended on exchange street. the illustration was photographed and copies were sold as postcards. a panel from the comic strip little nemo in slumberland ( 1905 - 1914 ) mccay ’ s comic strips included little nemo in slumberland and dream of the rarebit fiend. mccay created the very first animated cartoon in america with the release of little nemo in 1911 ( see video link below ). many in the animation world hail mccay today as the “ father of animation. ” as a tribute, the highest award that an animator can receive is an “ annie, ” which is the winsor mccay award for lifetime achievement in animation. when disneyland first opened in 1955, so the story goes, walt disney took robert mccay, son of spring lake native winsor mccay, on a guided tour. he stopped near the end and said, “ you know, this should really belong to your father. ”


the coral is at the mercy of natural circumstances like water quality and starfish population, but can be aided by human intervention. the first step to take will be decreasing population and co2 emissions. coral cover in the great barrier reef has dropped by more than half over the last 27 years, according to scientists, a result of increased storms, bleaching and predation by population explosions of a starfish which sucks away the coral ’ s nutrients. at present rates of decline, the coral cover will halve again within a decade, though scientists said the reef could recover if the crown - of - thorns starfish can be brought under control and, longer term, global carbon dioxide emissions are reduced. “ this latest study provides compelling evidence that the cumulative impacts of storms, crown - of - thorns starfish ( cots ) and two bleaching events have had a devastating effect on the reef over the last three decades, ” said john gunn, chief executive of the australian institute of marine science. coral reefs are an important part of the marine ecosystem as sources of food and as protection for young fish. they are under threat around the world from the effects of bleaching, due to rising ocean temperatures, and increasing acidification of the oceans, which reduces the corals ’ ability to build their calcium carbonate structures. the great barrier reef is the most iconic coral reef in the world, listed as a unesco world heritage site and the source of $ a5bn ( £3. 2bn ) a year to the australian economy through tourism. the observations of its decline are based on more than 2, 000 surveys of 214 reefs between 1985 and 2012. the results showed a decline in coral cover from 28 % to 13. 8 % – an average of 0. 53 % a year and a total loss of 50. 7 % over the 27 - year period. the study was published on monday in the proceedings of the national academy of sciences journal ( subscription ). two - thirds of the coral loss has occurred since 1998 and the rate of decline has increased in recent years, averaging around 1. 45 % a year since 2006. “ if the trend continued, coral cover could halve again by 2022, ” said peter doherty, a research fellow at the institute. tropical cyclones, predation by cots, and bleaching accounted for 48 %, 42 %, and 10 % of the respective estimated losses. in the past seven years the reef has been affected by six major cyclones. cyclone hamish, for example, ran along the reef, parallel to the


and bleaching accounted for 48 %, 42 %, and 10 % of the respective estimated losses. in the past seven years the reef has been affected by six major cyclones. cyclone hamish, for example, ran along the reef, parallel to the coast for almost 930 miles ( 1, 500km ), leaving a trail of destruction much greater than the average cyclone, which usually crosses the reef on a path perpendicular to the coast. the starfish problem was first recorded in 1962 at green island off cairns. “ when we say outbreaks, we mean explosions of cots populations to a level where the numbers are so large that they end up eating upwards of 90 % of a reef ’ s coral, ” gunn said. “ since 1962 there have been major outbreaks every 13 - 14 years. ” the evidence suggests that outbreaks of cots start two or three years after major floods in northern rivers. in september, scientists at the international union for conservation of nature announced that caribbean coral reefs are on the verge of collapse, with less than 10 % of the reef area showing live coral cover. the collapse was due to environmental issues, including over - exploitation, pollution and climate change. david curnick, marine and freshwater programme co - ordinator at the zoological society of london, said many of the most endangered coral species around the world were also under severe pressure from the aquarium trade. “ corals are notoriously hard to propagate in captivity and therefore the trade is still heavily dependent on harvesting from the wild. ”. ” he said the results of the great barrier reef survey were not surprising and the challenge for conservationists was to limit the localised threats to give reefs a chance to recover and develop resilience against the effects of climate change. “ this is challenging but entirely achievable and there are many community - led projects around the world demonstrating this. ” corals can recover if given the chance. but this is slow – in the absence of cyclones, cots and bleaching, the great barrier reef can regrow at a rate of 2. 85 % a year, the scientists wrote. removing the cots problem alone would allow coral cover to increase at 0. 89 % a year. reducing cots means improving water quality around the rivers at the northern end of the reef to reduce agricultural run - off – high levels of nutrients flowing off the land feed and allow high survival of cots larvae. another option is some form of biological control of populations – gunn said there were promising results from research on naturally