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As we know from earlier sessions generic 50 mg asendin with amex, this condition leads to heart disease cheap 50mg asendin mastercard, heart attack order asendin 50 mg fast delivery, and stroke asendin 50 mg mastercard. To prevent atherosclerosis from developing, children and teens should Not use tobacco. Health Resources for Parents Talking Points Some parents may not have their children tested for diabetes and high cholesterol because they think they cant afford a doctors visit. But, Medicaid is available in every state to provide heath and dental services for children under age 19 with low family incomes. When they call the free and confdential hotline, they will be connected directly to someone from their state who will help them apply. Depending on the state, they can do the application through the mail, over the phone, or even online. Talking Points There is increasing evidence that the build-up of plaque in the arteries of children and teenagers is linked to high cholesterol levels. Because there are no outward signs of this build-up, most people wont be aware of it until they have a heart attack or stroke as adults. The best way to avoid heart disease later in life is stop it before it begins in children. By eating healthy foods, not smoking, being physically active and keeping a healthy body weight, children and teenagers can delay or prevent heart disease later in life. Write the adult cholesterol numbers on a fipchart so they can see how close normal cholesterol levels are for children, teens, and adults. Blood Pressure Talking Points Childrens blood pressure should be measured starting at age three during a visit to the doctor, a school nurse, or a local clinic. Blood pressure should be measured with a child-sized blood pressure cuff, not an adult-sized cuff. If a childs numbers are higher than normal, the doctor will prescribe some type of treatment, starting with lifestyle changes, such as healthy eating and increased physical activity. Talking Points Increasing body weight, larger waistlines, and eating excess sodium in foods are related to higher blood pressure in children ages 8-17. If a child has high blood pressure, his or her blood cholesterol levels and blood sugar levels should be checked. Diabetes Talking Points Type 2 diabetes was once rare in children, but now its becoming more common. Type 2 diabetes in children can go undiagnosed (not found) for a long time because children may have no signs or only mild signs. Children and teens diagnosed with type 2 diabetes generally are between 10 and 19 years old, are overweight, and have family members who have type 2 diabetes. If a child has family members with type 2 diabetes and is overweight, the doctor should have him or her tested for diabetes. Most often, type 2 diabetes in children is a lifestyle diseasethe result of too much high-calorie junk food and too many sugary drinks, not being physically active, and being overweight. Talking Points If children have diabetes, it is important that they eat the right foods, check their blood glucose regularly, and take all diabetes medicines as prescribed by their doctor. Family support is very important because diabetes is stressful for both children and their families. Parents should be alert for signs of depression or eating problems in their child. In most cases, it can be prevented or delayed by a familys commitment to healthy eating and physical activity. Do parents know that lifestyle changes help kids with pre-diabetes or Type 2 diabetes? Its important that children know that diabetes can be controlled, and its important that they know that it must be controlled. It helps students with diabetes, their health care team, school staff, and parents work together to provide the best diabetes management in schools. At Risk for Overweight Talking Points Did you know that Childhood obesity rates remain high. Overall, obesity among our nations young people aged 2 to 19 years remains at about 17 percent. When you are taking in more energy, or calories, than you are burning the result is weight gain. Compared with children who have a normal weight, children who are overweight or obese are much more likely to have high blood pressure, high blood cholesterol, and diabetes as young adults. Same as adults, they are at greater risk for heart disease, heat attack, and stroke. Parents should ask their childrens doctor what a healthy weight range is for their child. Talking Points A healthy lifestyle, including healthy eating and physical activity, can lower the risk of becoming overweight and developing related risks and diseases. Remember, overweight children have a hard time because they may not be able to keep up with other children when physically active. One way to help families and communities live healthier lives is to promote healthy lifestyles at home, school, and in the community. Also, parents can take their children less often to fast-food places and can choose healthier foods and smaller amounts of food and drink if they do go. Parents can limit value or monster meals, which may contain more food than the family needs. Encourage parents to say: no to fried foods, desserts, chips and other salty snacks, and soft drinks. Children who often eat in restaurants, including fast-food restaurants, are more likely to become overweight and to have risk factors for heart disease and diabetes. Healthy Eating Talking Points When community health workers work in clinics, visit clients at home, or see them at other places in the community, they often see or work with entire families. If you see children who are overweight, very inactive, or eating unhealthy foods and drinking sugary drinks, take action by asking questions about the childrens eating habits and physical activity levels. Let the families know about places where their children can safely play actively and how the whole family can eat better. These are good questions to ask parents about their childrens eating habits Tell me what your child usually eats. Many of the unhealthy habits that lead to heart disease are habits we formed as children, especially the food choices we made. If parents make good food choices and stay physically active, their children are more likely to do the same. Parents should give their children water or low-fat and fat-free milk, and 100 percent fruit juice (in small amounts) to drink instead of soft drinks. But children aged 2 years and older should not drink whole milk because of the high amount of fat it contains. Low-fat (1%) milk and fat-free milk have all the nutrients of whole milk without the fat. Today in the United States, children arent eating the foods that will help them stay healthy and be free of heart disease as adults. Parents should replace high-fat snacks and sugary desserts with healthier choices such as fruits and vegetables.

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Both hu- mans and transgenic mice recognized the same immunodominant epi- topeswheninjected with viruses (Engelhard et al purchase 50 mg asendin with amex. This was shown in a study of human infection by Epstein-Barr virus (Burrows et al purchase asendin 50mg fast delivery. Interference occurs even when the antagonist occurs in relatively low concentration and is presented on dierent cells from the partner epitope order asendin 50 mg line. Mutual interference suggests that hosts jointly infected with cp26 and cp29 will be less eective in clearing parasites than singly infected hosts or hosts with other combinations of strains order asendin 50mg fast delivery. In the case of Plasmodium falciparum,itappears that variant peptides interfere with immunity suciently to inuence the distribution of antigenic variation in the parasite population. Often the host has several B and T cell specici- ties that match the various antigens of a parasite, but the host amplies only a subset of matching specicities. I discussed in earlier sections various factors that inuence immunodominancethe particular subset of antigens that stimulate an immune reaction from among the broader set of antigens that could potentially stimulate a response. The sequence in which the host encounters antigenic variants inu- ences the specicity of the immune response. The rst observations of sequential eects were made on inuenza infections (Francis 1953; Fazekas de St. These authors called sequential eects original antigenic sin because the rst antigenic expo- sure inuenced response to later antigens. Ifthehost encounters A rst, then secondary in- fection with A stimulates a secondary immune response, a,withrel- atively higher specicity for A and weaker specicity for A (original order). If the host encounters A rst, then secondary infection with A stimulates a secondary response, a,withhigher specicity for A and weaker specicity for A (reversed order). This case is similar to the rst, in which se- quential stimulation by A and then A causes a cross-reactive response a against secondary challenge by A (original order). Thus, ini- tial priming of cross-reactive memory cells by rst exposure to A is re- quired to generate a response to secondary challenge by A. The third pattern of sequential eects occurs when parasite challenge raises a specic immune response against several epitopes (g. Thus, a strong response against a constant epitope represses the response against the changed epitope. It is not known how memory B or T cells reduce stimulation of naive clones during a secondary challenge. The rapid response from memory cells may keep parasite density below the threshold required to stim- ulate naive B or T cells. This would be a form of indirect repression mediated by the population dynamics of the parasite and the specic immune cells. Alternatively, the memory cells may exert a more direct form of re- pression (Janeway et al. Binding kinetics determine winners and losers in the competition between B cell lineages with dierent antibody specici- ties (Rao 1999). Equilibrium anity dominates early in the competition, whereas on-rates dominate later during anity maturation. How can one study the biochemical andstructuralattributesthatde- termine the binding kinetics of antibodies and epitopes? With regard to equilibrium anity, one can compare structurally the dierent anti- bodies from the naive repertoire in relation to their success in binding aparticularepitope and stimulating its B cell lineage. With regard to the shaping of on-rates, the hypermutation and selection during an- ity maturation produce a lineal sequence of substitutions that enhances on-rates and perhaps also increases o-rates. This is a superb opportunity to relate structure to function via the kinetic processes that regulate the immune response. Quantitative models help to develop hypotheses that can be tested by experimental perturbation. For example, Rao (1999) suggested that competition for helper T cells determines the expansion of B cell lineages. He tested this idea by manipulating the pool of helper T cells, and found that reducing the helper T cell pool did lower stimulation to B cell lineages. Raos quantitative model could be expanded into a mathematical anal- ysis, with interactions between binding rates, pool sizes for dierent B and T cell lineages, and the rules of competition that determine which lineages succeed. Such a model presents clear hypotheses about the quantitative interactions that regulate immunity. Those hypotheses call attention to the sorts of experimental perturbations that should be in- formative. Their model focused on competition between immune cell lineages for stimulation by epitopes. Immune cells receive relatively stronger stimulation as their matching epitopes increase in numbers. The strongest immune- epitope match leads to the largest, immunodominant population of im- mune cells. That immunodominant lineage expands until its killing ef- fect reduces the parasite population within the host down to a point of balance. At that balance point, the parasite population stimulates division of the immunodominant population of immune cells just enough to match the tendency of the immune cell population to die o. In turn, the immu- nodominant immune cells reduce the parasites just enough to balance their births and deaths and hold the parasite population at a constant level. Other immune cell lineages receive weaker stimulation by the par- asites because of their weaker binding characteristics to epitopes. Those subdominant lineages decline because the dominant lineage pushes par- asite abundance down tothepoint where the weaker stimulation re- ceived by the subdominant lineages cannot overcome their tendency to decline. Can such idealized mathematical models capture the complex molec- ular and kinetic details of the immune response? On the one hand, immunodominance is shaped in part by competition between lineages of immune cells, and thus the population dynamics of competition contribute in some way to the pat- terns of immunodominance. The mathematical abstraction pays o as long as one understands the goal: to bring into sharp focus a hypothesis about how essential processes shape immunodominance. If one suspects that the distinction between equilibrium anity and kinetic on-rates matters in an essential way for immunodominance, then an extended mathematical model would pro- vide testable predictions about that aspect of the system. Iemphasizetheseissues here because the dynamics of immune cells andparasite populations within each infected host provide one of the few subjects that has been developed mathematically (Nowak and May 2000). The simple principles from those models do seem to be impor- tant, if only because the rules of population dynamics must play a key role in shaping how populations of immune cells and parasites interact. One can, of course, make more specic mathematical models to pre- dict the dynamics ofparticularparasites or the role of particular mo- lecular mechanisms. And that is exactly what we want: tests of clearly and logically formulated quantitative predictions. Helper T cells pro- vide an important stimulus in the development of an antibody response. Thus, an antigen must have two epitopes to stimulate a robust B cell response with anity maturation. Several factors likely aect the degree to which helper T cell epitopes modulate the immunodominance of B cellepitopes. In particular, ahelperTcellepitope near the hypervariable region of thehepatitis C virus envelope gene aids in generation of antibodies to the hypervariable region.

Estrogen is also a potent antioxidant and may reduce lipid peroxidation in the atherosclerotic arterial wall asendin 50 mg fast delivery. Animal studies demonstrated that estrogen buy asendin 50 mg on line, and estrogen and progesterone significantly alter atherosclerotic plaque formation in ovariectomized monkeys fed a high fat diet (30) discount 50 mg asendin with amex. Animal and human studies have also demonstrated that estrogen receptors exist on vascular smooth muscle cells and that estrogen can alter endothelial function by enhancing coronary artery dilation and coronary blood flow in normal and atherosclerotic coronary arteries (31) purchase asendin 50mg on-line. Estrogen has also been shown to have an effect on the balance between thrombosis and fibrinolysis (32). Concerns have been raised about the risk of estrogen replacement therapy with regard to the potential negative effects on lipids and coagulation, and the risk of certain cancers (33). In addition, the combined effects of long term estrogen and progesterone on the cardiovascular system are unknown. In addition, there was a higher rate of venous thromboembolic complications in women treated with hormones than in women given placebo. Further studies are needed to determine whether these results are applicable to all postmenopausal women with established coronary disease. Guide to risk reduction for women Raloxifene, a selective estrogen receptor modulator with estrogen-antagonistic effects in the breast and uterus, has been shown to alter serum lipids and coagulation factors favourably in postmenopausal women (36). Further trials are needed to determine whether these effects are associated with a reduction in cardiovascular events in postmenopausal women. Guidelines for preventive cardiology for women recently produced by a joint American Heart Association/American College of Cardiology medical/scientific consensus panel have been reviewed and supported in Canada (Table 1) (37). The scientific basis for recommendations and areas of potential future recommendations are presented below. The complex interaction among psychosocial, socioeconomic and health behaviours needs to be studied further, especially in women. Studies should be done to evaluate interactions between behavioural and socioeconomic factors in women. Patterns of coronary heart disease morbidity and mortality in the sexes: A 26-year follow-up of the Framingham population. Cardiovascular disease in women: A statement for healthcare professionals from the American Heart Association. Adherence to National Cholesterol Education Program Treatment goals in postmenopausal women with heart disease. Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. Medical Research Council trial of treatment of hypertension in older adults: principal results. Effect of antihypertensive drug treatment on cardiovascular outcomes in women and men: A meta-analysis of individual patient data from randomized, controlled trials. Acute myocardial infarction and combined oral contraceptives: results of an international multicentre case-control study. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Estrogen and progestin compared with simvastatin for hypercholesterolemia in postmenopausal women. A comparison of estrogen replacement, pravastatin, and combined treatment for the management of hypercholesterolemia in postmenopausal women. Postmenopausal estrogen use, cigarette smoking, and cardiovascular morbidity in women over 50. Effects of estrogen or estrogen/progestin regimens on heart disease risk factors in postmenopausal women. Inhibition of coronary artery atherosclerosis by 17-beta estradiol in ovariectomized monkeys. Relation of hormone-replacement therapy to measures of plasma fibrinolytic activity. The use of estrogens and progestins and the risk of breast cancer in postmenopausal women. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. Effects of raloxifene on serum lipids and coagulation factors in healthy postmenopausal women. Among these elderly Canadians, 37% of women and 24% of men had at least two of the following risk factors: smoking, obesity, elevated cholesterol and elevated blood pressure. Except for smoking, elderly women have a higher prevalence of risk factors than elderly men. However, if current trends continue, there will be more smokers among women than among men. Furthermore, among the elderly, 12% have diabetes, and 75% do not exercise regularly three or more times per week. However, the high density lipoprotein cholesterol level may be a better predictor. However, the absolute risk (calculated as the risk of individuals developing events during a defined period) is much higher in the elderly. In other words, after 65 years of age, the relative risk attenuates, but the event rate (absolute risk) is much higher than in those aged less than 65 years. Why should we assess and treat high risk elderly patients to increase their life expectancy by one or two years? The issue is not only a question of treatment to increase life expectancy by a couple of years but also of treatment to improve quality of life. Preventing a stroke or congestive heart failure has an impact on the quality of life of the patient and on health care cost. For some clinicians, the problem is related to the maximum age at which these persons should be actively treated. To solve this problem, clinicians should consider the prognostic impact of risk factors in the elderly as outlined above as well as the physiological age of the elderly. Although there are a few clinical trials involving the elderly with high blood pressure (11,12), there are no such large clinical trials in the elderly with dyslipidemia. These last interventions have been shown to significantly reduce the rate of recurrent stroke in elderly patients with symptomatic stenosis of 70% to 99%, as outlined in the chapter on stroke (Level I, Grade A). Atrial fibrillation is associated with 20% and 30% risk of stroke if the patient is aged 70 to 79 and more than 80 years of age, respectively. At least two out of three strokes can be prevented by anticoagulant therapy with warfarin administered to patients with atrial fibrillation. Lifestyle: Smoking is a preventable risk factor in the elderly (17); within three to five years of smoking cessation, the risk decreases to that of persons who have never smoked.

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