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hip fractures a practical guide to management

hip fractures a practical guide to management

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hip fractures a practical guide to managementThe current custom error settings for this application prevent the details of the application error from being viewed remotely (for security reasons). It could, however, be viewed by browsers running on the local server machine. Pedigrees review Biology is brought to you with support from the Amgen Foundation Biology is brought to you with support from the Our mission is to provide a free, world-class education to anyone, anywhere. Khan Academy is a 501(c)(3) nonprofit organization. Donate or volunteer today. The current custom error settings for this application prevent the details of the application error from being viewed remotely (for security reasons). It could, however, be viewed by browsers running on the local server machine. PhD, in Molecular Pathology (Second Edition), 2018 Other Considerations for Pedigree Construction and Interpretation Pedigree construction requires equal amounts of skill, science, and art. Those obtaining the pedigree must have a strong base of medical genetic knowledge, so as to know the important questions to ask and construct the pedigree correctly. In addition, careful attention must be paid to establishing trust, navigating social relationships, communicating effectively, and educating, all while ensuring the individual supplying the information is not being overwhelmed by the exercise. Family histories are deeply personal, and the psychosocial impact of the required informational gathering can be significant. Further, inaccurate information can result in misinterpretation and, ultimately, misdiagnosis. Whenever possible, reported diagnoses must be confirmed with medical records. The effort this requires should not be minimized, as privacy and confidentiality must be upheld for all family members throughout the process. Clinical molecular genetics seeks to identify genetic variation and to determine whether or not the observed genetic variation has a phenotypic effect.http://erimti.com/userfiles/ford-1710-tractor-parts-manual.xml

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Certainly, the latter cannot be accomplished without astute and thorough clinical evaluation and family history. Even an apparently negative family history is an important one that can guide test selection and result interpretation. In addition, the impact of pedigree analysis on genomic research is formidable. As a result of detailed pedigree assessment, numerous genes have been discovered, genotype:phenotype correlations elucidated, natural history knowledge obtained, and certainly inheritance patterns revealed. View chapter Purchase book Read full chapter URL: Apportionment of Autosomal Diversity with Subcontinental Markers Tony N. Frudakis, in Molecular Photofitting, 2008 EURO 1.0 PEDIGREES AS AN AID TO INTERPRETING RESULTS Pedigrees are useful for understanding the strengths and limitations of the European test, and instructive on how best to interpret results. One pedigree for the EURO 1.0 test is shown in Table 7-15. Table 7-15. Sample EURO 1.0 percentages for a real pedigree. NOR MED MIDEA SA Mother 44 26 30 0 Father 74 18 8 0 Child 1 70 15 15 0 Child 2 58 19 23 0 In the pedigree shown in Table 7-15, none of the four individuals characterized their ethnicity as Middle Eastern. It is clear that there is significant MED and MIDEA ancestry in the children, which we could conclude from the relatively high levels observed, but looking at the results in the entire pedigree it appears that although the MED ancestry in the children was contributed by both parents, the MIDEA ancestry came mainly from the mother. Both mother and father here are real people who described their heritage as continental European, but the MIDEA and SA result may provide a basis for a new genealogical line of investigation, one that is focused in time farther back than most genealogists consider with geopolitical records and surnames. This is true particularly for the mother’s side of the family tree (i.e., from where might this substantial and unexpected MIDEA ancestry have come?).http://globewheelers.com/userfiles/ford-1710-parts-manual-online.xml This pedigree was obtained from a real family. Typing actual family members may be difficult and time consuming (mainly, in collecting the samples), so it is much easier to simulate pedigrees. We have simulated over 120 pedigrees, and obtained satisfying results for all but two of them; a sampling of these pedigrees is shown in Table 7-16. Table 7-16. EURO 1.0 percentages for simulated pedigrees. The pedigree shown in Figure 4-20 (real people, not simulated) is the most discordant pedigree we have observed yet, and it provides an opportunity to discuss how EURO 1.0 results should and should not be interpreted. In particular, it illustrates why it is better to draw conclusions about a sample’s or individual’s anthropological heritage from results of small pedigrees, even if incomplete (such as a child and a mother), rather than individual people (such as in this case, only the mother). In most forensics situations, this is not possible, but nonetheless this concept deserves some attention here because it illustrates how test error can manifest itself. A mother, father, and two children (STR paternity test positive) are shown in Table 7-17. None of the people had conducted an amateur genealogical study, but as with most people the two parents had a good idea of their predominant European ancestry. Via self-reporting, most (not necessarily all) of the mother’s recent ancestors three generations ago were known to have been English and German, and the father reported himself as a little over half Greek (exact percentage unknown). Table 7-17. Sample EURO 1.0 percentages for a real pedigree.https://formations.fondationmironroyer.com/en/node/14910 NOR MED MIDEA SA Mother 50 10 15 25 Father 55 40 5 0 Child 1 66 0 34 0 Child 2 35 45 0 20 The father’s results were more or less consistent with his expectations (particularly considering that most Greeks, Turks, and Italians show less MED ancestry, a measure of anthropological identity, than they expect from blood, which is derived from geopolitical, sociocultural, and very recent geographical identity). We have discussed the difference between anthropological and geopolitical ancestry as just discussed and in earlier chapters. As expected from self-reported ancestry of “a little more than half Greek,” the father shows relatively high MED ancestry with EURO 1.0 compared to the mother, who reported no Mediterranean or Southeastern European ancestry. Not expected from self-reporting in geopolitical terms, however, was the 15 MIDDEA and 25 SA ancestry for the mother. With an error caused by continuous allele frequencies of seven percentage points, it seems unlikely that this result is due to statistical error, and from this result we have good evidence for non-NOR, non-MED ancestry within the mother’s family tree—perhaps extending back a few hundred to a few thousand years ago. Looking at the children, the evidence is stronger. Child 1 is an example of an individual who obtained results that are somewhat discordant from those of his parents; we would have expected him to have scored somewhere between 5 and 15 MIDDEA, and 0 and 24 SA, but instead he scored 34 MIDDEA and 0 SA. Some of the discrepancy is likely due to the random nature of chromosome inheritance (genetic assortment) but some is undoubtedly due to test error. Child 2 showed less NOR and MIDDEA and more MED than expected, probably for the same reasons. Why is it that this pedigree so discordant. Recall that the average results are accurate to within 6 to 7 for any individual, meaning some people will exhibit 0 error, some 10 error, and a few 15 to 20 due to continuous allele frequencies. Say the mother has a 15 error in an opposite direction from one of her offspring—her 15 MIDDEA is really 30 and her son’s 34 is really 19. With the father at 5, the expected results for the son are 5 to 30 and the true value of 19 now make sense. Of over 126 pedigrees studied, it is unusual for a single child to show such divergence from expectations much less two in the same pedigree like this, our most discordant pedigree, but even in this case we can extract useful information. When we look at the results in the context of the pedigree, it is clear that the mother’s non-NOR and non-MED EURO 1.0 results are confirmed in her children (just not in the exact percentages we would expect, given the error associated with the test). The MIDDEA and SA ancestry observed in the children appears clearly to have come from the mother rather than the father. So, concluding that there is significant non-NOR and non- MED ancestry in this pedigree contributed from the mother’s ancestors is relatively safe. Note that concluding such from just one of the children, or even from the mother, is less secure. It is in confirming the result and its inheritance in the pedigree as a whole that we obtain the confidence to hypothesize that the mother’s and father’s anthropological heritage are different. Given our confidence from the pedigree, we can now ask from where might this MIDEA and SA ancestry have come. For example, perhaps some of her ancestors were Roma gypsy, or perhaps some were Bedouin Arabs who settled in Europe within the past 1,000 years. It so happens that the mother in this case felt such non-NOR, non-MED ancestry likely came from her mother rather than her father, since much more is known about the latter individual’s ancestors, but she could never know enough about either of them to know this for certain. For this reason, to form the most sound hypotheses of anthropological heritage, it is always better to test multiple individuals of a pedigree if possible. View chapter Purchase book Read full chapter URL: Osteogenesis Imperfecta David W. Rowe, Jay R. Shapiro, in Metabolic Bone Disease and Clinically Related Disorders (Third Edition), 1998 F Heritable Osteoporosis Pedigrees demonstrating familial transmission or clustering of osteopenia have been identified. 455 Subjects with this phenotype also display scoliosis and mild joint laxity. From the experience gained studying the milder forms of OI, there is reason to believe that abnormalities of type I collagen (or other matrix components) may be present in certain of these families. 456 A number of determined attempts to discern such patients from unselected osteoporotic patients 52 or pedigrees with familial osteoporosis have been unrewarding. 53 Nevertheless, it can be expected that variable degrees of osteopenia, reflecting the underlying defect of collagen or other matrix protein, do account for the transition in phenotype between type I OI and heritable osteoporosis. The problem is how to distinguish this potential subgroup clinically from other forms of osteoporosis. View chapter Purchase book Read full chapter URL: Managing Pedigree and Genotype Data Stephen P. Bryant, in Guide to Human Genome Computing (Second Edition), 1998 2.1 Pedigrees The pedigree ( Figure 3.1 ) is the unit of information in a linkage analysis. The observations on a pedigree have a special kind of interdependency, determined by the mechanism of genetic inheritance. Human pedigrees or genealogies can be classified into several kinds on the basis of the distribution of affecteds (i.e. individuals expressing a particular trait) ( Table 3.1 ). Figure 3.1. An example pedigree, shown in conventional graphical form. Each square or circle represents a person. Squares represent males and circles females. The unique identifier for each person is given below each symbol. A diagonal line through the symbol means that the person is known to be dead. A vertical line is used to connect parents with offspring. A horizontal line is used to join sibships and also to join parents. A trait T is segregating in the family, inherited as an autosomal dominant, fully penetrant trait with two phenotypes: (1) affected (shown as a black-filled symbol), and (2) unaffected (shown as a white-filled symbol). People with unknown T phenotype contain an interrogation mark (?). Codominant marker loci A, B, C, D and E (from top of diagram to bottom) are also shown. Genotypes are given as pairs of alleles A i A j, B i B j, C i C j, D i D j or E i E j Unknown genotypes are scored as 00. Paternal alleles are shown on the left of each genotype pair, maternal on the right. Alleles unambiguously inherited from the same grandparent are shown boxed, as black (grandpaternal) and white (grandmaternal). Crossovers are shown as a change of phase from grandpaternal to grandmaternal, or vice versa. Table 3.1. Classification of family types, by distribution of affecteds Family type Description Simplex Single affected offspring, with parental information Sib-pairs Pairs of affected siblings, with or without parental information Sib-sets As above, with more than two offspring Relative pairs Pairs of relatives in relationships other than sibs, with or without information from other family members Extended General case, multiplex families in arbitrary degrees of relationship For simple family types such as sib-pairs or nuclear three-generational families, there typically exist a large number of identical family structures. For more complicated family types ( Figure 3.1 ), there is typically only one family of a given structure and distribution of affecteds in any one study. These differences influence how the information from different families can be combined, but do not impact on how the data are stored or managed. View chapter Purchase book Read full chapter URL: Fundamentals of heredity Judy S. Crabtree PhD, in Clinical Precision Medicine, 2020 Pedigrees A pedigree is a graphical representation of a family tree that uses symbols to represent different individuals and assists with the recognition of genetic patterns. At the most fundamental level, pedigree symbols include a square for males, a circle for females, diamonds for individuals of unknown gender, and lines to indicate relationships. Affected individuals are indicated by filled symbols, carriers have a dot within the symbol, and a diagonal line through the symbol indicates the individual is deceased. Single horizontal lines indicate a mating pair, and double horizontal lines indicate consanguineous mating. View chapter Purchase book Read full chapter URL: Towards Automatic Risk Analysis for Hereditary Non-Polyposis Colorectal Cancer Based on Pedigree Data Munevver Kokuer. Elements of the feature vector are binary variables except for two ratios which are continuous. Since our data set (i.e. number of pedigrees) is small, we cannot afford to use an independent test set for assessing the performance of the systems developed. To overcome this difficulty, we employed the leave-one-out method. This training-testing leave-one-out procedure is repeated for each pedigree in the database. View chapter Purchase book Read full chapter URL: Hereditary Hearing Impairment Rena Ellen Falk, Arti Pandya, in Emery and Rimoin's Principles and Practice of Medical Genetics, 2013 142.6.6 Mitochondrial Pedigrees with nonsyndromic sensorineural deafness and a maternal inheritance pattern are well known, though the proportion of mitochondrial HL among all nonsyndromic hearing impairment is not clear. While most cases manifest nonsyndromic HL, maternal inheritance of HL in association with diabetes, skin manifestations, neuromuscular symptoms, retinitis pigmentosa and other ocular findings has been reported as well. The most common mitochondrial gene defect leading to nonsyndromic HL is the homoplasmic A1555G mutation in the mitochondrial small ribosomal RNA gene ( 177 ). This mutation alone is not sufficient to cause the deafness phenotype, and additional nuclear modifier genes are thought to be necessary for phenotypic expression. Several of these modifier genes have been identified and appear to involve mitochondrial RNA processing ( 178, 179 ). Importantly, the A1555G mitochondrial mutation also predisposes to aminoglycoside ototoxicity. Hence, review of the pedigree and genetic testing can prevent exposure to aminoglycosides in at-risk maternally related family members of such patients. Four additional mutations in the same small ribosomal RNA gene have also been shown to predispose to aminoglycoside ototoxicity, but occur less commonly than the A15555G substitution ( 180 ). Three additional mitochondrial mutations in and around the tRNAser (UCN) gene, which lead to nonsyndromic HL, have been identified in pedigrees from all over the world (reviewed by Fischel-Ghodsian ( 181 ) ). These mutations appear to be nearly homoplasmic in the majority of cases, and the exact pathophysiological relationship between the mitochondrial mutations and HL remains unclear. Of note, a recent study ( 182 ) suggested that concomitant use of salicylates, chosen for their antioxidant effect, decreased the risk of aminoglycoside ototoxicity, though it did not address the question of genetic susceptibility in the study cohort. As noted above, some mitochondrial mutations have been implicated in the occurrence of auditory neuropathy. View chapter Purchase book Read full chapter URL: Genetics of Melatonin W. Schloot,. N. Birau, in Melatonin: Current Status and Perspectives, 1981 Psoriasis vulgaris. Pedigrees do not fit a simple mode of inheritance. In some cases autosomal dominant inheritance has been described. The genetic mechanism determining psoriasis is very obscure. There may be a predisposition to react to various metabolic and toxic stimuli. Most cases seem to be sporadic. The risk of recurrence for a patient's child is 20 if one parent is affected. Besides the hypothesis of an autosomal dominant trait with modifying genes or incomplete penetrance and varying expressivity there is a hypothesis of polygenic trait (the expression is controlled by many genes). Metabolic abnormalities have been described by Hammarstrom and coworkers (1975). They found an increased concentration of nonesterified arachidonic acid and other compounds of prostraglandin metabolism in the epidermis of psoriasis. The disorder of arachidonic acid is very profound. Patients with psoriasis have a severe disorder of melatonin secretion (Birau and Schloot, 1979). Day-time levels are extremely low and the normal nocturnal rise does not occur. Family studies are in progress. Treatment with psoralen (8-methoxy-psoralen) rises serum melatonin concentration and may be an effective tool in curing psoriasis (Birau, 1980). The suggested antimitotic effect of melatonin presumedly is of importance for the regulation of increased epidermal mitotic rate and decreased cell turnover time. View chapter Purchase book Read full chapter URL: Recommended publications Info icon Mitochondrion Journal The American Journal of Human Genetics Journal Molecular Genetics and Metabolism Journal Browse books and journals About ScienceDirect Remote access Shopping cart Advertise Contact and support Terms and conditions Privacy policy We use cookies to help provide and enhance our service and tailor content and ads. By continuing you agree to the use of cookies. Mendel's work led him to the understanding that traits, such a plant height, are carried in DNA. DNA is found in all living cells. It Controls all functions inside the cell.Cancel anytime. Share this document Share or Embed Document Sharing Options Share on Facebook, opens a new window Share on Twitter, opens a new window Share on LinkedIn, opens a new window Share with Email, opens mail client Copy Text Related Interests Zygosity Dominance (Genetics) Allele Genetics Genotype Footer menu Back to top About About Scribd Press Our blog Join our team. Quick navigation Home Books Audiobooks Documents, active. Griffiths AJF, Gelbart WM, Miller JH, et al. Modern Genetic Analysis. New York: W. H. Freeman; 1999. By agreement with the publisher, this book is accessible by the search feature, but cannot be browsed. Modern Genetic Analysis. Show details Griffiths AJF, Gelbart WM, Miller JH, et al. New York: W. H. Freeman; 1999. Search term The investigator traces theThe geneticX-linked. The four categories are discussed in the following sections. Figure 4-17 Symbols used in human pedigree analysis.(After W. F. Bodmer and L. L. Cavalli-Sforza, Genetics, Evolution, and Man. Freeman and Company.) Autosomal Recessive Disorders The unusual phenotype of a recessive disorder is determined by homozygosity for a recessive allele, and the unaffected phenotype is determined by the corresponding dominant allele. In. Chapter 3 we saw that phenylketonuria (PKU) is aPKU is determined by an allele that we can call p, andTherefore, sufferers of this disease are ofWhen we know that both male and femaleThe following typical pedigree illustrates the key point thatFurthermore, we can deduceHence, the pedigree canIf the couple were to have, say, 20In the case of a rare recessive allele, in the population most of these alleles will be foundThe reason is a matter of probability: to conceive aThe formation of anInbreeding (mating between relatives) increases the chance that a mating will be between twoIndividuals III-5 and III-6 are first cousins and produce two children. You can see from the figure that an ancestor who is a heterozygote may produce many descendantsMatings between relatives thus run a higher risk of producingIt is for this reason thatGene symbols normally are not included in pedigree charts, but genotypes are inserted hereThe inheritance and molecular genetics of albinism are integratedThe phenotype is caused by homo-zygosity for a recessive allele,In the pedigree, parents heterozygous for. The three panels at the bottomAn example of a rare autosomalIn this case, people with normal stature are genotypicallyFigure 4-21 The human achondroplasia pheno-type, illustrated by a family of five sisters and twoMost members of theAgain, the representation of bothThe phenotype appearsThis is relatively rare, but must be kept in mind as a possibility.) A typical pedigree for aOnce again,As with recessiveHuntington’s disease is an example of an autosomal dominant disorder. The phenotype is one ofHowever, it is a late-onsetThis tragic pattern has led to a drive toLet’s look at aMost human populations are dimorphic for theThis makes it clear that the allele for ability to tasteNotice, however, that almost allSuch a pedigree thus differs from those of rare recessive disorders, forFigure 4-23 Pedigree for the ability to taste the chemical PTC. MESSAGE Phenotypes with X-linked recessive inheritance typically show theThis is because a femalePerhaps the best-known example is hemophilia, a malady in which a person’s blood fails toThe most common type ofAlexis, the son of the last czar of Russia, inherited the allele ultimately from Queen. Victoria, who was the grandmother of his mother Alexandra. Nowadays, hemophilia can beIt is interesting to note that inFor example, one exemption was for the sons of women whoseDuchenne muscular dystrophy is a fatal X-linked recessive disease. The phenotype is aGenerally the onset is before the age of 6, with confinementThe gene for Duchenne muscular dystrophy has now beenSuch insight holds out hope for aA rare X-linked recessive phenotype that is interesting from the point ofPeople afflicted. They have female external genitalia, a blindTestes may be present either in the labia or in the abdomen. AlthoughThe condition is notThe reason for the insensitivity is thatIn humans, femalenessFigure 4-24 Pedigree showing that X-linked recessive alleles expressed in males are then carriedNote that III-3 and III-4 cannot be distinguished phenotypically. Figure 4-25 The inheritance of the X-linked recessive condition hemophilia in the royal families of. Europe. A recessive allele causing hemophilia (failure of blood clotting) arose in theThere are few examples of X-linked dominant phenotypes in humans. One is hypophosphatemia, a. The mechanisms of X-linked dominance and recessiveness in humans are somewhat complicated byThis topic will be covered in. Chapter 16. Calculating Risks in Pedigree Analysis When a disease allele is known to be present in a family, knowledge of simple gene For example, a married couple finds out that each had an uncle with. Tay-Sachs disease (a severe autosomal recessive disease). The pedigree is as follows: The probability of their having a child with Tay-Sachs can be calculated in the followingTherefore, they effectively constituted aThus if the father isHence the probability of the man’s being aCompany. Bookshelf ID: NBK21257 Modern Genetic Analysis. New York: W. H. Freeman; 1999. Human Pedigree Analysis. Disable Glossary Links In this Page Autosomal Recessive Disorders Autosomal Dominant Disorders X-Linked Recessive Disorders X-Linked Dominant Disorders Calculating Risks in Pedigree Analysis Recent Activity Clear Turn Off Turn On Human Pedigree Analysis - Modern Genetic Analysis Human Pedigree Analysis - Modern Genetic Analysis Your browsing activity is empty. Activity recording is turned off. Turn recording back on See more. The current custom error settings for this application prevent the details of the application error from being viewed remotely (for security reasons). It could, however, be viewed by browsers running on the local server machine. Big Idea Pedigrees are not just for dogs. Lesson Author Mariana Garcia Serrato San Jose, CA Grade Level Seventh grade Subjects Science Heredity Genetics Standards MS-LS1-5 Construct a scientific explanation based on evidence for how environmental and genetic factors influence the growth of organisms. MS-LS3-1 Develop and use a model to describe why structural changes to genes (mutations) located on chromosomes may affect proteins and may result in harmful, beneficial, or neutral effects to the structure and function of the organism. MS-LS3-2 Develop and use a model to describe why asexual reproduction results in offspring with identical genetic information and sexual reproduction results in offspring with genetic variation. SP4 Analyzing and interpreting data SP7 Engaging in argument from evidence XC-SSM-MS-3 Models are limited in that they only represent certain aspects of the system under study. Hook 5 minutes I start this lesson by asking the students if they have ever heard the word pedigree, and ask what that word means to them. I show the first two slides of the Pedigree presentation (which includes a Star Wars and a Harry Potter family tree), and ask what they think the different lines depicted mean. This allows the students to collaborate with each other searching for the best explanation ( SP7 ), and analyze pedigree charts ( SP4 ). Through the work and conversation, the students are engaging in using the pedigree charts (models) to understand and predict behaviors of biological systems ( CCC Systems and System Models Models are limited in that they only represent certain aspects of the system under study ). Read my reflection on Practice Towards Mastery to see how I find resources when this happens. Pedigrees Charts Student Work Pedigree charts Closure 5 minutes To close this lesson, I have the students use write a post-it note on my reflective chart. This chart is posted at the front of the room, and gives me a quick reference into student thinking and attitudes in the classroom. All Rights Reserved. Privacy Policy Legal. Which of the following describes the probability of hemophilia in the offspring of a man who does not have hemophilia and a woman whose father is a hemophiliac? The condition where no antigens are present on the blood cells (type O blood) is a recessive trait. Which set of parents can most likely produce a child with type O blood? The other parent does not have the PKU alleles. What is the chance that the couple will have a child with phenylketonuria? A woman who does not have hitchhiker's thumb marries a man who is heterozygous for hitchhiker's thumb. What is the probable genotypic ratio of their children? What percent of offspring are expected to have an orange phenotype if the parent plants are orange (RR') and yellow (R'R')? This hypothesis is supported by which observation? In which circumstance would he most likely show the trait coded for by the recessive allele. Please try one of the quick links below or go back to the previous page. Go Back Het kan zijn dat de pagina niet meer bestaat of is verhuisd. Misschien kunnen we u verder helpen met de onderstaande links. If you answer incorrectly, it will explain the right answer. Then drag letters in to fill the squares for the potential children’s alleles. This will check if you are correct. Sex linked Traits (Bio Project) If you wish not to see this then stop the video after 1:57 fast forward and restart at 2:45. This video continues talking about the really BIG cows, and how we have bred for them.