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Pedigree Analysis hair loss help dutasteride 0.5mg line, Applications hair loss kidney failure dutasteride 0.5mg visa, and Genetic Testing 145 any discordance among monozygotic twins is usually due to environmental factors hair loss with lupus buy 0.5 mg dutasteride with amex, because monozygotic twins are genetically identical gene therapy hair loss cure generic 0.5 mg dutasteride with amex. The use of twins in genetic research rests on the important assumption that, when concordance for monozygotic twins is greater than that for dizygotic twins, it is because monozygotic twins are more similar in their genes and not because they have experienced a more similar environment. The degree of environmental similarity between monozygotic twins and dizygotic twins is assumed to be the same. Because they look alike, identical twins may be treated more similarly by parents, teachers, and peers than are nonidentical twins. Evidence of this similar treatment is seen in the past tendency of parents to dress identical twins alike. In spite of this potential complication, twin studies have played a pivotal role in the study of human genetics. Asthma is characterized by constriction of the airways and the secretion of mucus into the air passages, causing coughing, labored breathing, and wheezing (Figure 6. Asthma is a major health problem in industrialized countries and appears to be on the rise. The incidence of childhood asthma varies widely; the highest rates (from 17% to 30%) are in the United Kingdom, Australia, and New Zealand. A number of environmental stimuli are known to precipitate asthma attacks, including dust, pollen, air pollu- tion, respiratory infections, exercise, cold air, and emotional stress. Allergies frequently accompany asthma, suggesting that asthma is a disorder of the immune system, but the precise relation between immune function and asthma is poorly understood. A genetic study of childhood asthma was conducted as a part of the Twins Early Development Study in England, an ongoing research project that studies more than 15,000 twins born in the United Kingdom between 1994 and 1996. These twins have been assessed for language, cognitive development, behavioral problems, and academic achievement at ages 7 and 9, and the genetic and environmental contributions to a number of their traits were examined. Parents of the twins were asked whether either of their twins had been prescribed medication to control asthma; those children receiving asthma medication were considered to have asthma. Concordances of the monozygotic and dizygotic twins for asthma are shown in Table 6. The concordance value for the monozygotic twins (65%) was significantly higher than that for the dizygotic twins (37%), and the researchers concluded that, among the 4-year-olds included in the study, asthma was strongly influenced by genetic factors. The fact that even monozygotic twins were discordant 35% of the time indicates that environmental factors also play a role in asthma. Low concordance for monozygotic twins indicates that environmental factors play a significant role. What conclusion can you draw about the role of genetic factors in determining differences in the trait Methods Compare the body-mass index of adopted children with those of their adoptive and biological parents. Mother Thin Obese Adoptee weight class ies were instrumental in showing that schizophrenia has a genetic basis. Adoption studies have also shown that obesity, as measured by body-mass index, is at least partly influenced by genetics (Figure 6. Adoption studies assume that the environments of biological and adoptive families are independent. This assumption may not always be correct, because adoption agencies carefully choose adoptive parents and may select a family that resembles the biological family. Thus, some of the similarity between adopted persons and their biological parents may be due to these similar environments and not due to common genetic factors. In addition, offspring and the biological mother share the same environment during prenatal development. This approach is one of the most powerful for distinguishing the effects of genes and environment on characteristics. For a variety of reasons, many children each year are separated from their biological parents soon after birth and adopted by adults with whom they have no genetic relationship. These adopted persons have no more genes in common with their adoptive parents than do two randomly chosen persons; however, they do share an environment with their adoptive parents. In contrast, the adopted persons have 50% of their genes in common with each of their biological parents but do not share the same environment with them.
The third phenotypic ratio is not really a ratio: all the offspring have the same phenotype (uniform progeny) hair loss 8 yr old girl generic 0.5mg dutasteride free shipping. If we are interested in the ratios of genotypes instead of phenotypes hair loss in men experiencing 0.5 mg dutasteride with amex, there are only three outcomes to remember (Table 3 hair loss cure timeline buy 0.5mg dutasteride visa. These simple phenotypic and genotypic ratios and the parental genotypes that produce them provide the key to understanding crosses for a single locus and hair loss cure yet generic dutasteride 0.5mg overnight delivery, as you will see in the next section, for multiple loci. Understanding the nature of these crosses will require an additional principle, the principle of independent assortment. Dihybrid Crosses In addition to his work on monohybrid crosses, Mendel crossed varieties of peas that differed in two characteristics-a dihybrid cross. For example, he had one homozygous variety of pea with seeds that were round and yellow; Basic Principles of Heredity Experiment Question: Do alleles encoding different traits separate independently Relating the Principle of Independent Assortment to Meiosis An important qualification of the principle of independent assortment is that it applies to characters encoded by loci located on different chromosomes because, like the principle of segregation, it is based wholly on the behavior of chromosomes in meiosis. Each pair of homologous chromosomes separates independently of all other pairs in anaphase I of meiosis (see Figure 2. Genes that happen to be located on the same chromosome will travel together during anaphase I of meiosis and will arrive at the same destination-within the same gamete (unless crossing over takes place). Genes located on the same chromosome therefore do not assort independently (unless they are located sufficiently far apart that crossing over takes place every meiotic division, as will be discussed fully in Chapter 7). Genes located close together on the same chromosome do not, however, assort independently. If we consider only the shape of the seeds, the cross was Rr Rr, which yields a 3: 1 phenotypic ratio (3/4 round and 1 /4 wrinkled progeny, see Table 3. The cross was Yy Yy, which produces a 3: 1 phenotypic ratio (3/4 yellow and 1/4 green progeny). We can now combine these monohybrid ratios by using the multiplication rule to obtain the proportion of progeny with different combinations of seed shape and color. The proportion of progeny with round and yellow seeds is 3/4 3 (the probability of round) /4 (the probability of yel9 low) /16. Rr Yy (a) Expected proportions for first character (shape) Expected proportions for second character (color) Expected proportions for both characters Rr Rr Yy Yy Cross Rr Yy Rr Yy Cross 2. Now follow each branch of the diagram, multiplying the probabilities for each trait along that branch. Another branch leads from round to green, yielding round and green progeny, and so forth. We calculate the probability of progeny with a particular combination of traits by using the multiplication rule: the probability of round (3/4) and yellow (3/4) seeds is 3/4 3/4 9/16. The advantage of the branch diagram is that it helps keep track of all the potential combinations of traits that may appear in the progeny. It can be used to determine phenotypic or genotypic ratios for any number of characteristics. Using probability is much faster than using the Punnett square for crosses that include multiple loci. Genotypic and phenotypic ratios can be quickly worked out by combining, with the multiplication rule, the simple ratios in Tables 3. The probability method is particularly efficient if we need the probability of only a particular phenotype or genotype among the progeny of a cross. Suppose we needed to know the probability of obtaining the genotype Rr yy in the F2 of the dihybrid cross in Figure 3. The probability of obtaining the Rr genotype in a cross of Rr Rr is 1/2 and that of obtaining yy progeny in a cross of Yy Yy is 1/4 (see Table 3. Using the multiplication rule, we find the probability of Rr yy to be 1/2 1/4 1/8. To illustrate the advantage of the probability method, consider the cross Aa Bb cc Dd Ee Aa Bb Cc dd Ee. Suppose we wanted to know the probability of obtaining offspring with the genotype aa bb cc dd ee. If we used a Punnett square to determine this probability, we might be working on the solution for months. However, we can quickly figure the probability of obtaining this one genotype by breaking this cross into a series of single-locus crosses: Progeny cross Aa Aa Bb Bb cc Cc Dd dd Ee Ee Genotype aa bb cc dd ee Probability 1 /4 1 /4 1 /2 1 /2 1 /4 Wrinkled 14 / yy rr yy 14 / Green = 1 16 / Wrinkled, green 14 / 3.
Further myonecrosis during reperfusion occurs due to rapidinfluxofcalciumionsandgenerationoftoxicoxygenfreeradicals hair loss nutritional deficiency buy 0.5mg dutasteride with visa. Electron microscopic changes i) Disappearance of perinuclear glycogen granules within 5 minutes of ischaemia hair loss cure zone order dutasteride 0.5 mg with visa. Chemical and histochemical changes i) Glycogen depletion in myocardial fibres within 30 to 60 minutes of infarction hair loss quora safe dutasteride 0.5mg. Measurement of their levels in serum is helpful in making a diagnosis and plan management hair loss with chemo buy dutasteride 0.5mg overnight delivery. TherearetwotypesofcTn: d a) cardiac troponin T (cTnT); and b) cardiac troponin I (cTnI). Both troponin levels remain high for much longer duration; cTnI for 7-10 days and cTnT for 10-14 days. A small percentage of cases may result from other causes such as emboli, coronary arteritis and myocarditis. M/E Salient features are as under: i) Therearescatteredareasofdiffusemyocardialfibrosis,especiallyaround the small blood vessels in the interstitial tissue of the myocardium. The most important cause is coronary atherosclerosis; less commonly it may be due to coronary vasospasm and other non-ischaemic causes. The mechanism of sudden death by myocardial ischaemiaisalmostalwaysbyfatalarrhythmias,chieflyventricularasystole orfibrillation. G/A At autopsy, such cases reveal most commonly critical atherosclerotic coronary narrowing (more than 75% compromised lumen) in one or more of the three major coronary arterial trunks with superimposed thrombosis or plaque-haemorrhage. Even mild hypertension (blood pressure higher than 140/90 mmHg) of sufficient duration may induce hypertensive heart disease. The stress of pressure on the ventricular wall causes increased production of myofilaments, myofibrils, other cell organelles and nuclear enlargement. The thickness of the left ventricular wall increases from its normal 13 to 15 mm up to 20 mm or more. Initially, there is concentric hypertrophy of the left ventricle (without dilatation). But when decompensation and cardiac failure supervene, there is eccentric hypertrophy (with dilatation) with thinning of the ventricular wall and there may be dilatation and hypertrophy of right heart as well. M/E the changes include enlargement and degeneration of myocardial fibreswithfocalareasofmyocardialfibrosis. Thus, cor pulmonale is the right-sided counterpart of the hypertensive heart disease just described. Depending upon the rapidity of development, cor pulmonale may be acute or chronic: Acute cor pulmonale occurs following massive pulmonary embolism resulting in sudden dilatation of the pulmonary trunk, conus and right ventricle. Chronic cor pulmonale is more common and is often preceded by chronic pulmonary hypertension. Following chronic lung diseases can cause chronic pulmonary hypertension and subsequent cor pulmonale: i) Chronic emphysema ii) Chronic bronchitis iii) Pulmonary tuberculosis iv) Pneumoconiosis v) Cysticfibrosis vi) Hyperventilation in marked obesity (Pickwickian syndrome) vii) Multiple organised pulmonary emboli. The most common underlying mechanism causing increased pulmonary blood pressure (pulmonary hypertension) is by pulmonary vasoconstriction, activation of coagulation pathway and obliteration of pulmonary arterial vessels. Pulmonary hypertension causes pressure overload on the right ventricle and hence right ventricular enlargement. G/A In acute cor pulmonale, there is characteristic ovoid dilatation of the right ventricle, and sometimes of the right atrium. In chronic cor pulmonale, there is increase in thickness of the right ventricular wall from its normal 3 to 5 mm up to 10 mm or more. In spite of its name suggesting an acute arthritis migrating from joint to joint, it is the heart rather than the joints whichisfirstandmajororganaffected. The disease is seen more commonly in poor socioeconomic strata of the society living in damp and overcrowded places which promote interpersonal spread of the streptococcal infection. It is still common in the developing countries of the world, particularly prevalent in Indian subcontinent (India, Pakistan, Bangladesh, Nepal, Afghanistan), some Arab countries, subSaharan Africa and some South American countries. However, the mechanism of lesions in the heart, joints and other tissues is not by direct infection but by induction of hypersensitivity or autoimmunity in a susceptible host. Socioeconomic factors like poverty, poor nutrition, density of population, overcrowding in quarters for sleeping etc are associated with spread of infection. The geographic distribution of the disease, as already pointed out, shows higher frequency and severity of the disease in the developing countries of the world where the living conditions in underprivileged populationsaresubstandardandmedicalfacilitiesareinsufficient.
The ceramide is hair loss radiation cheap dutasteride 0.5 mg mastercard, in turn hair loss treatment youtube order dutasteride 0.5 mg on line, cleaved by ceramidase into sphingosine and a free fatty acid (Figure 17 hair loss 4 months after childbirth buy cheap dutasteride 0.5 mg online. In the severe infantile form (Type A hair loss vitamin deficiency buy 0.5 mg dutasteride fast delivery, which shows less than 1% of normal enzymic activity), the liver and spleen are the primary sites of lipid deposits and are, therefore, greatly enlarged. The lipid consists primarily of the sphingomyelin that cannot be degraded (Figure 17. A less severe variant (Type B, which shows 5% or more of normal activity) with a later age of onset and a longer survival time causes little to no damage to neural tissue, but lungs, spleen, liver, and bone marrow are affected, resulting in a chronic form of the disease. Although Niemann-Pick disease occurs in all ethnic groups, Type A occurs with greater frequency in the Ashkenazi Jewish population. Like the phospholipid sphingomyelin, glycolipids are derivatives of ceramides in which a long-chain fatty acid is attached to the amino alcohol sphingosine. They are located in the outer leaflet of the plasma membrane, where they interact with the extracellular environment. As such, they play a role in the regulation of cellular interactions (for example, adhesion and recognition), growth, and development. Glycosphingolipids are antigenic and are the source of blood group antigens, various embryonic antigens specific for particular stages of fetal development, and some tumor antigens. Genetic disorders associated with an inability to properly degrade the glycosphingolipids result in lysosomal accumulation of these compounds. The number and type of carbohydrate moieties present determine the type of glycosphingolipid. Neutral glycosphingolipids the simplest neutral (uncharged) glycosphingolipids are the cerebrosides. These are ceramide monosaccharides that contain either a molecule of galactose (forming ceramide-galactose or galactocerebroside, the most common cerebroside found in myelin, as shown in Figure 17. Ceramide oligosaccharides (or globosides) are produced by attaching additional monosaccharides to a glucocerebroside, for example, ceramideglucose-galactose (also known as lactosylceramide). The additional monosaccharides can include substituted sugars such as N-acetylgalactosamine. Acidic glycosphingolipids Acidic glycosphingolipids are negatively charged at physiologic pH. Additional numbers and letters in the subscript designate the monomeric sequence of the carbohydrate attached to the ceramide. Sulfatides: these sulfoglycosphingolipids are sulfated galactocerebrosides that are negatively charged at physiologic pH. Enzymes involved in synthesis the enzymes involved in the synthesis of glycosphingolipids are glycosyltransferases that are specific for the type and location of the glycosidic bond formed. Degradation of glycosphingolipids Glycosphingolipids are internalized by endocytosis as described for the glycosaminoglycans. All of the enzymes required for the degradative process are present in lysosomes, which fuse with the endocytotic vesicles. The lysosomal enzymes hydrolytically and irreversibly cleave specific bonds in the glycosphingolipid. Sphingolipidoses In a normal individual, synthesis and degradation of glycosphingolipids are balanced, so that the amount of these compounds present in membranes is constant. If a specific lysosomal acid hydrolase required for degradation is partially or totally missing, a sphingolipid accumulates. Lysosomal lipid storage diseases caused by these deficiencies are called sphingolipidoses. The result of a specific acid hydrolase deficiency may be seen dramatically in nerve tissue, where neurologic deterioration can lead to early death. Common properties: A specific lysosomal hydrolytic enzyme is deficient in the classic form of each disorder. Therefore, usually only a single sphingolipid (the substrate for the deficient enzyme) accumulates in the involved organs in each disease. Genetic variability is also seen because a given disorder can be caused by any one of a variety of mutations within a single gene. The sphingolipidoses are autosomal-recessive diseases, except for Fabry disease, which is X linked. The incidence of the sphingolipidoses is low in most populations, except for Gaucher and Tay-Sachs diseases, which, like Niemann-Pick disease, show a high frequency in the Ashkenazi Jewish population.