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For example, you may not be able to reasonably expect oneon-one education courses to create large-scale community change if the reach is limited. Make sure that your theory is not only clear and makes sense on paper, but that it is based on good underlying evidence about what increases screening rates and how people really change. Evidence can be based on previous work experience, literature and research, and professional opinions from colleagues and national organizations. Between the "if" and the "then," there should be solid evidence or some well-established connection supporting the idea that your initiative will work. For example, if your program plans to distribute pamphlets that encourage people to speak with health care providers about screening, there should be research that supports what you expect to happen. You should know if the message you are sending will resonate with that particular group, if the pamphlets will motivate participants to get screened, and if there are potential barriers to following through with your message. Many well-intentioned programs are not successful because the underlying research did not align with what the program expected to happen. Even if a program is incredibly effective, it is not likely that any single program will lead to community-level changes in screening rates, to say nothing of reducing colon cancer mortality. It would not be advisable for most programs to focus on community-level cancer incidence or screening rates as their evaluation focus. Instead, it is usually more appropriate to measure some of the more immediate program impacts. Example 2 Program theory for the Metropolitan Colon Cancer Collaborative: Staff distribute brochures and educational materials at community events. Example 3 Program theory for the Wellness Clinic: Clinic staff provide one-on-one education sessions. African American community members learn about the importance of screening and available community resources related to colorectal cancer screening. Wellness clinic patients gain knowledge and awareness of colorectal cancer screening options. African American community members talk to their families, friends, and health care providers about getting screened. Administrative tasks, such as training staff or doing paperwork, typically are not included in a program theory. These activities, while a necessary part of running a program, are usually not the important services that produce change in participants. Focus on the main services you provide ­ the ones you most count on to promote positive results. Simply put, a logic model is a picture of your theory ­ a drawing that shows how one thing leads to the next. A logic model uses short phrases to represent what is explained in the program theory. Most often, a logic model is presented in the form of a flow chart with multiple columns. The following components are usually included in a logic model: Inputs ­ any resources or materials used by the program to provide its activities. Outcomes are what you expect to change as a result of the participant receiving services. Outputs can tell you how much of a service was provided, but not whether the activity had the desired impact. For instance, it may be impressive to say that you distributed 10,000 brochures last year. One frequent approach is to illustrate the following three levels of outcomes, but there may be more or less. The first level of outcomes describes the short-term outcomes, or results of the program activities. Short-term outcomes typically refer to changes in knowledge or awareness, as these types of changes typically precede changes in behavior or practice. The next level describes intermediate outcomes, which usually refer to behavioral changes that follow knowledge and awareness changes. These outcomes usually refer to more global changes, such as a community-wide drop in colorectal cancer mortality.

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The factors that promote the progression of atherosclerosis and the development of complications typically induce plaque rupture and blood coagulation. A number of different bacterial and viral antigens have been identified in plaque. Another effect of smoking is vasoconstriction, which increases the risk of heart attack and stroke in arteries already narrowed by atherosclerosis. C-reactive protein, an acute-phase protein secreted during the inflammatory response, is associated with increased heart disease risk (see Chapter 22). Disorders characterized by abnormal levels of blood lipids are called hyperlipidemias or dyslipidemias. Oxidation may result from free-radical generation by macrophages and endothelial cells or various enzyme reactions. This lipoprotein profile, which is especially prevalent in individuals with metabolic syndrome and type 2 diabetes, is associated with an approximately threefold increased risk of coronary heart disease. Although pharmacological doses of a form of niacin may lower lipoprotein(a) levels, the benefit of treating lipoprotein(a) is not yet clear. Aging becomes a significant risk factor for men aged 45 or older and for women aged 55 or older. Plaque is caused by factors that damage the artery wall and promote blood coagulation. Although atherosclerosis can advance enough to fully block an artery, most heart attacks occur with less than 50 percent blockage. In angina pectoris and heart attacks, the pain or discomfort usually occurs in the chest region and may be perceived as a feeling of heaviness, pressure, or squeezing. In angina pectoris, the symptoms are often triggered by exertion, persist for several minutes, and subside with rest. In a heart attack, the pain may be severe, last longer, and occur without exertion. For some people, dietary and lifestyle changes may be the only treatment needed for managing cholesterol levels. Note that these are guidelines only and should not override the judgment of an attending physician. Obtain a complete lipoprotein profile from blood samples taken after a 9- to 12-hour fast. Currently, the saturated fat intake in the United States averages about 11 percent of total kcalories consumed. Choosing lean meats or fish, using fat-free or low-fat milk products, and avoiding certain types of bakery products are usually more effective ways of reducing saturated fat. Chapter 5 and Highlight 5 provide additional information about food selections that are low in saturated fat. This effect may be offset somewhat by limiting added sugars and including fiber-rich foods; ideally, the diet should include generous amounts of whole grains, legumes, fruits, and vegetables. Diets high in carbohydrate-especially those high in added sugars-can raise blood triglyceride levels in some people. Fibric acids (include gemfibrozil, clofibrate): Affect the production of proteins that help regulate lipoprotein synthesis and breakdown. In general, elevated triglyceride levels (150 mg/dL) are treated with weight management and moderate physical activity. Identify metabolic syndrome on the basis of the presence of three or more of the following risk determinants: · Abdominal obesity (waist measurement of more than 40 inches in men or more than 35 inches in women). Major drugs used for cholesterol lowering include: · Statins (include lovastatin, pravastatin): Reduce cholesterol synthesis in the liver. Bile acid sequestrants (include cholestyramine, colestipol): Bind bile acids in the small intestine, reducing reabsorption. If there is no improvement, elevated blood pressure and dyslipidemias should be actively treated. Maintaining a fat intake that is 25 to 35 percent of total kcalories may help with this goal.


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During that time, I would take at least one weekend summer camping trip every year to the park. During those trips, I would search for salamanders at night inside the park, since the Appalachian Mountains have some of the highest salamander diversity and abundance anywhere in the world. The Shenandoah salamander is one of the most challenging species to observe because it is nocturnal, lives only in the highest mountain areas of the park, and unlike with other salamanders, visitors are not permitted to flip over logs or rocks to look for it because it is an endangered species. I have seen one Shenandoah salamander, in 2015, but would like to observe them again, and hopefully take photographs of them. I will likely return to Shenandoah National Park in the summer of 2021 assuming it is safe to travel. The Shenandoah salamander is only found in very restricted habitats at the top of the highest mountains in Shenandoah National Park and is threatened by both acid rain and climate change. Furthermore, because salamanders feed preferentially during rainy and foggy weather, they are susceptible to impacts from acid deposition on their skin. The Shenandoah salamander already is restricted to the highest parts of Shenandoah National Park. Much like the birds in Hawaii discussed above, the salamander is already at the top of the mountain and cannot escape any higher to avoid the heat as temperatures continue to increase with climate change. I am disheartened that these threats will continue to harm the salamander, making it harder for me to observe them again in the future. I derive significant recreational and aesthetic benefits from seeing and photographing rare species in the wild. Any federal agency action - including the decreasing of vehicle emission standards - that harms these species or the habitat areas on which they rely also harms my interest and enjoyment in viewing the affected species. I have personal knowledge of the following facts and, if called as a witness, I would testify competently to them. As to those matters that reflect an opinion, they reflect my personal opinion and judgment on the matter. I became a member of Environment America because the health of our planet is in decline and we need to do something about it. There is power in numbers, and individual citizens can have more of an impact if they join together in a group. I have a respiratory condition called chronic allergic asthmatic bronchitis, which is affected by both pollens in the air and also air quality. Previously, I was diagnosed with acute asthmatic bronchitis because it only affected me during the spring. On September 6, 2019, I was diagnosed with chronic allergic asthmatic bronchitis because the condition now affects me all year long. My primary care physician has told me that my condition is caused by allergies and air pollution. My condition requires the daily use of a medically-prescribed inhaler to stop the chronic bronchospasms and cough. The increasing air pollution in what used to be an area with rather clean air has definitely impacted my quality of life. My blood pressure is affected because my condition causes my lungs to take in less oxygen so my circulatory system has to work harder. I also enjoy gardening but I am unable to garden as much as I would like to because of the increased severity of my condition. The smoke negatively affects my condition and makes it more difficult for me to breath. Both the smoke and ash act as bronchial and pulmonary irritants, which cause inflammation in the bronchial tubes making breathing difficult. Also, there were several days last year when ash was falling from the sky, and our air quality was deemed poor. Outdoor events were cancelled or camp was delayed, and people, especially those with respiratory conditions, were advised to stay indoors. I personally expect to purchase a car in the time-frame covered by the 2021 through 2026 model years. My current vehicle has over 140,000 miles on it and will need to be replaced during that period.

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The duration and intensity of the exercise dictate the type and amount of fuel that is needed, which needs to be balanced against our ability to supply that fuel. High temperatures can increase the rate of fluid loss or the accumulation of body heat, and even change the rate at which carbohydrate fuel is burned. Finally, our preparation-how well we are able to fuel and hydrate before an event or during events-must be considered. But sometimes poor recovery is our own doing-for example, if we dehydrate and restrict food intake in the lead-up to an event to meet a weigh-in target. You may be able to recall times when you have had symptoms such as headaches, heavy legs, light-headedness, confusion, or stomach problems. These symptoms may give clues to what is preventing your body from performing at its best. In simplistic terms, in explosive efforts such as jumps and lifts, most of the fuel is supplied not by burning fat or carbohydrate fuel but anaerobically (without oxygen), via high-energy phosphate compounds within the muscle cell. Repeated short bursts tax the regeneration of creatine phosphate, though creatine supplementation can counter this. But more likely, it will be the build-up of acidity (the hydrogen ions accompanying the production of lactate) and other by-products of this fuel use that cause the burning sensation and fatigue. Aside from ensuring that you have adequate glycogen stores, you can limit these effects by finding ways to increase muscle and blood buffering of the hydrogen ions. As the exercise goes on for longer-and necessarily at a lower intensity-aerobic metabolism becomes more important. For this, your muscles burn a fuel mixture of fat (relatively unlimited supply in the body) and carbohydrate (limited supply), with the proportions depending on factors like: · · · · the intensity of exercise (the carbohydrate contribution is greater at a higher workload) the duration of exercise (carbohydrate contribution typically declines over the duration of the event) your pre-event diet (consuming carbohydrate in the hours before exercise increases the carbohydrate contribution to fuel) your level of training (training allows you to exercise at the same absolute workload with a higher fat; lower carbohydrate mix) Team sports usually involve a mixture of (anaerobic) high-intensity bursts, interspersed with (aerobic) recovery periods. Meanwhile, athletes in steady-state events, such as running or cycling, gravitate to a predominantly aerobic workload just below the threshold at which blood lactate starts accumulating. Of course, steady-state is a relative term, since even the longest races will involve periods of higher-intensity work as athletes stage breakaways, surge up hills or sprint to the finish. The likely cause is the exhaustion of muscle glycogen, which forces the muscle to turn to fat and blood glucose for energy. This often happens in conjunction with muscle glycogen depletion, but in some sensitive individuals it may occur as an independent event. The smart athlete will try to avoid both of these consequences of carbohydrate depletion. Some athletes may start an event with a fluid deficit-from deliberate dehydration to make a weight category or from failure to rehydrate in hot weather or after previous exercise. A deficit can also arise during exercise as athletes fail to replace the fluid lost in sweat when their bodies try to cool themselves. Just like a car, you produce heat as a by-product of work, and this must be dissipated to keep your body at its preferred temperature. The harder you work and the heavier you are, the more sweat will be produced to cool you down. Athletes who have heavy sweat loss, low fluid intake or both are at risk of incurring a fluid mismatch that will affect their performance and perhaps health. A body-fluid deficit has creeping physiological effects-increasing body temperature, increasing heart rate, and increasing the perceived effort involved in exercise. There is still a lot of discussion about the true effect of dehydration on exercise performance. The following summarises current thinking: · In laboratory studies, the effect of dehydration on prolonged exercise is related to the size of the fluid deficit. It may thus be more detrimental to an athlete in an unpredictable, skill-based activity like a team game than to a runner who just needs to keep putting one foot in front of another! The effects of dehydration build continuously, so the point at which it becomes a disadvantage is determined by our ability to detect a difference. In lab-based studies, we can detect an impairment of endurance and the performance of prolonged aerobic or intermittent exercise with a fluid deficit of as little as 2 per cent of body weight. In real-life sport, the differences between winning and losing can be far smaller than our ability to detect differences in performance in the lab. So it is possible that on-field performance impairments result from smaller levels of dehydration, or have greater effects on competition outcomes, than is seen in our current studies. On the other hand, laboratory studies cannot mimic some of the things in real-life sport that might reduce the effects of dehydration on performance-ranging from the motivation of competition to the effect of wind and air flow out in the open. So we may be overestimating the effects of dehydration based on the results of our laboratory studies.

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It is recognised that weight gain, overweight and obesity are associated with increased occurrence, morbidity and mortality in several cancer sites. Current estimates suggest that significant proportions of these cancers can be reduced through decreases in excess body fat. In addition to overall body size, adult weight gain (since age 18 years and since menopause) is thought to be a risk factor for the development of postmenopausal breast [10] and possibly colon [11] cancer. Current evidence has prompted researchers to question whether obesity management might be an opportunity for cancer prevention [13]. Metabolic syndrome may also increase cancer risk, suggesting that the metabolic disturbances associated with this disorder promote genetic instability. Raised oestrogens these are likely to contribute to the greater risk of breast and endometrial cancers in obese patients. Exposure to increased oestrogen levels (especially in postmenopausal women), whether from endoge nous production or exogenous when taken as hor mone replacement therapy, is a wellestablished risk factor for breast and uterus cancers [16]. In addition, cancersitespecific mechanisms have been postulated in relation to tissue damage caused by obesity. For example, increasing gall stones has been implicated as a factor in gallbladder cancer, and increased gastrooesophageal reflux in patients with abdominal obesity has been implicated in the development of oesophageal cancer [17]. The relationship between colorectal cancer and obesity is thought to be related primarily to the effect of obesity in increased inflammation that might account for why the disease risk is reduced with antiinflammatory agents such as aspirin [18]. After 8 years, there was a 9% difference between intervention and control groups in breast cancer incidence. Body weight was not an intervention target; however, after 5 years followup, those who received the dietary intervention weighed a statisti cally significant 2. Modest weight loss is associated with cancer risk reduction (which would be considered highly desir able if a drug was being tested), and there appears to be a dose­response relationship, with higher weight loss associated with greater risk reduction. In women, mortality from all cancers was again reduced, but only in those who had obe sityrelated illnesses: by 37% if they lost 0. Bariatric surgery studies of weight loss and cancer risk A number of studies have now reported reduced can cer incidence following bariatric surgery. Similar findings were reported in the Utah Obesity Study, where total cancer incidence was 27% lower after gastric bypass in women, with little impact on men [28]. A Canadian cohort study reported a reduction of 78% cancer risk over 5year followup, with a notable 83% reduction for breast cancer [29]. Where positive effects have been reported, these suggest that significant weight loss can reduce cancer risk within a relatively short time period, with marked differences by gender. It is important within such studies to focus on weight loss (shown to be effective) rather than diet or physical activity alone. Both components are likely to have significant effects on cancer risk, but the combined effect is greater. Fundamental to the design of weight loss trials (and prior to the investment in expensive, long term followup trials) is the development and feasi bility testing of robust and acceptable interventions that can demonstrate weight reduction in people at risk of developing cancer. Subjects were recruited from a breast cancer family history clinic and from the general population. Oestradiol is consid ered a causal mediator for postmenopausal breast and endometrial cancers, and the authors conclude that even modest weight loss could have substantial and fairly immediate effects on risk. They suggest that a 10% weight loss is associated with a reduction of free oestradiol levels by about onethird. All participants were advised to maintain their current activity levels throughout the trial and did not receive specific advice on physical activity. The impact of this magnitude of weight loss is unclear, given the scarcity of evidence, but observational studies of weight loss suggest sig nificant cancer risk reduction [21]. Longterm tri als of weight loss interventions and cancer outcomes may not be feasible, given the numbers required and the length of followup. However, weight loss trials in patients with cancer (notably breast cancer) are underway [33]. Quality of life, measured using a patientgenerated index questionnaire [35], also improved in 14 of the 17 patients (82%). Participants reported adher ence related to tailored advice, personalised feed back and family support.

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The Endangered Species Act lists factors that are used to help determine candidates to add to the Endangered Species list. It is necessary to identify which species are imperiled (and why) before effective measures can be put into place for species recovery. In addition, readily available sources-such as your natural history museum, library and newspaper website/archive- offer additional material on the status of local species. The website for the Fish and Wildlife Service Endangered Species Program is. Be sure you are able to navigate through these sites prior to showing them to the class. Show students where they can find out more information about endangered species that are specific to their state and/or county. Explain to students that each of them will investigate an animal and a plant species that are currently endangered within their state/county. Students should then choose one of their identified species and develop a poster board presentation. What is the difference between it and the endangered species they have already studied, in terms of population, habitat, and other factors? What organizations/agencies in your county/region might have an impact on how species are classified? National organizations such as the National Audubon Society and the Sierra Club have local chapters that can be called upon to speak about locally endangered species and conservation efforts. Find a guest speaker to invite to the class to talk about local endangered species. Have students prepare three open-ended questions that they could possibly ask the guest speaker. Inform the students that the questions should not be personal in nature and should result in an open ended response. Instruct students about appropriate behavior and respect when presented with a guest speaker. Inform students of any assignments they will need to complete (essay, quiz, report, etc. Remind speaker of the amount of time he/she have to speak, leaving enough time for class questions. Spend the beginning of the next class period discussing the experience and the information learned with the students. Assign different groups of students to a) make arrangements with the speaker, b) prepare for the speakers needs, c) introduce the speaker and encourage questions, d) follow up with a thank you letter. What are the most critical conservation-related issues facing local plant/animal species? Handout: Guest Speaker Worksheet Local Expert/Guest Speaker Worksheet: Name: Date: Name of Speaker: Title: 32 Organization or Agency: What is the role of this organization or agency in conservation of endangered species? The questions should not be closed ended questions (those that result in yes/no responses. These resources provide a wealth of information about geology, zoology, marine science, entomology, paleontology, and mineralogy and often life and earth science specimens. In addition, they often have extensive educational programs for both teachers and students. Explain to the students that during their tour of the location, they are to identify and characterize 6-8 local species to generate their own guided tour onto poster board. Students should take notes about the exhibits ­ species, habitat, interesting facts, etc. Students should summarize their information as if they were giving a guided tour of each exhibit. The summaries and images should be displayed into a creative fashion onto poster board. Alternatively: If a field trip cannot be scheduled, students may be able to take a virtual tour of a museum, zoo, botanic gardens or other facility on their website. Does your local museum do an adequate job expressing the issues associated with endangered species? Homework Exploring Your State Wildlife Action Plan Congress asked every state and territory to develop a wildlife action plan to examine the health of wildlife and prescribe actions to conserve wildlife and habitats before they become rarer and more difficult to protect. Summarize the total number of species found in your state, the number of species in need of conservation in your state, and the number of species listed as threatened/endangered in your state.

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Patients with hepatic encephalopathy should avoid excessive protein consumption, and their protein intake should be spread throughout the day so that they consume only modest amounts at each meal. Protein restriction is not helpful, however, because inadequate protein can worsen malnutrition and wasting. In an attempt to normalize altered amino acid ratios in brain tissue and improve mental status, some health care providers may prescribe enteral formulas with reduced aromatic amino acids and added branched-chain amino acids. Clinical studies testing the use of these formulas have yielded mixed results, however, and their routine use is not currently recommended. Many patients with cirrhosis are insulin resistant and require medications or insulin to manage their hyperglycemia. These individuals should follow the dietary guidelines for diabetes: consume mostly complex carbohydrates, and consume them at regular intervals throughout the day. In patients with fat malabsorption, fat intake may be restricted to less than 30 percent of total kcalories or as necessary to control steatorrhea. Severe steatorrhea warrants supplementation of the fat-soluble vitamins, calcium, magnesium, and zinc (see Chapter 24). Therefore, the treatment usually includes both a moderate sodium restriction (to no more than 2000 milligrams of sodium per day) and diuretic therapy to promote fluid loss. Potassium intake should be monitored if a potassium-wasting diuretic (such as furosemide) is used. Many patients find low-sodium diets unpalatable, so some health practitioners may allow a more liberal sodium intake and depend on diuretics to mobilize excess fluids. If patients do not respond to sodium restriction and diuretic therapy, fluid may be removed from the abdomen by surgical puncture (paracentesis) or may be diverted to the bloodstream using a catheter (peritoneovenous shunt). Fluid restriction may be necessary when ascites is accompanied by a low concentration of serum sodium. If the sodium level falls below 128 milliequivalents per liter, the fluid intake should be limited to 1200 to 1500 milliliters daily; with a sodium level below 125 milliequivalents per liter, fluids should be restricted to 1000 to 1200 milliliters per day. If steatorrhea is present, fat-soluble nutrients can be provided in a water-soluble form. Patients with esophageal varices may find it easier to ingest supplements in liquid form. Enteral and Parenteral Nutrition Support In patients who are unable to consume enough food, tube feedings may be infused overnight as a supplement to oral intakes or may replace oral feedings entirely. Although standard formulas are often appropriate, an energy-dense, moderate-protein, low-electrolyte formula may be necessary for patients with ascites or fluid restrictions. In patients with esophageal varices, the feeding tube should be as narrow and flexible as possible to prevent rupture and bleeding. Parenteral nutrition support should be considered for patients who are unable to tolerate enteral feedings due to intestinal obstruction, gastrointestinal bleeding, or uncontrollable vomiting. To avoid excessive fluid delivery, patients with ascites typically require concentrated parenteral solutions, which are infused into central veins. Although he recognizes that he has an alcohol problem and recently entered an alcohol rehabilitation program, he is still drinking. According to family members, he is showing signs of mental deterioration, such as forgetfulness and an inability to concentrate. Compare the results of his laboratory tests with the values shown in Table 25-3 (p. Describe the development of that type of problem in liver disease, and explain how the diet is usually adjusted for such a patient. Describe each of the following complications of liver disease: portal hypertension, jaundice, and gastroesophageal varices. The primary causes of cirrhosis in the United States are hepatitis C infection and alcohol abuse. Symptoms of cirrhosis include fatigue, gastrointestinal disturbances, anorexia, and weight loss.

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In four species the shift was significant and in two species the shift was approximately a month earlier (Forister and Shapiro 2003, p. As summarized by Parmesan (2006), climate variables explained 85 percent of the variation in flight date, with warmer, drier winters driving early flight. While none of the species in the study were in the genus Euphydrys, seven of the species were in the Nymphalidae family. The date of first flight was also observed to have increased in 26 out of 35 butterfly species in the United Kingdom (Roy and Sparks 2000 as cited in Parmesan 2006, p. Since prediapause larval Bay checkerspot butterflies are small and do not travel far, this would likely result in increased larval mortality. A second concern with climate change is amount and frequency of rain events, drought, and heat waves. Increased frequency and duration of drought would likely result in higher larval mortality. Summary of Factor E: the threats from climate change and wildfire are significant threats especially in conjunction with the current narrow distribution and small population size of the subspecies. Climate change and wildfire in conjunction with other impairment of habitat due to invasive and non-native vegetation, nitrogen deposition, and fragmentation and loss of habitat resulting from development, represent major threats to the Bay checkerspot butterfly. The Service has no information regarding the impact of pesticides on the Bay checkerspot butterfly beyond a general understanding that pesticides are harmful to a variety of species, including lepidopterans, and that pesticides are being applied in areas adjacent to extant occurrences of Bay checkerspot butterflies and may be applied within areas currently occupied by the butterfly. There are many paths to accomplishing the recovery of a species and recovery may be achieved without fully meeting all recovery plan criteria. For example, one or more criteria may have been exceeded while other criteria may not have been accomplished. In that instance, we may determine that, over all, the threats have been minimized sufficiently, and the species is robust enough to downlist, or delist the species. In other cases, new recovery approaches and/or opportunities unknown at the time the recovery plan was finalized may be more appropriate ways to achieve recovery. Likewise, new information may change the extent that criteria need to be met for recognizing recovery of the species. We focus our evaluation of species status in this 5-year review on progress that has been made toward recovery since the species was listed (or since the most recent 5-year review) by eliminating or reducing the threats discussed in the five-factor analysis. In that context, progress towards fulfilling recovery criteria serves to indicate the extent to which threat factors have been reduced or eliminated. Core population ­ Adult populations of at least 8,000 butterflies, or populations of at least 20,000 postdiapause larvae, in 12 of 15 consecutive years, at each of the following areas: Kirby, Metcalf, San Felipe, Silver Creek Hills, Santa Teresa Hills, and Edgewood Park. Total population across all core areas should be at least 100,000 adults or 300,000 post-diapause larvae in each of the 12 years, with no recent severe decline. Has criterion been met: Criterion 1 has not been met; in fact, populations have continued to decline since listing. For specific information regarding size of populations in core areas, see the Abundance section above. Satellite populations ­ Adult populations of at least 1,000 butterflies, or populations of at least 3,000 postdiapause larvae, in 10 of 15 consecutive years, at each of at least nine distinct areas: three in San Mateo County, five in Santa Clara County, and one in Contra Costa County. Adult populations of at least 300 butterflies, or populations of at least 1,000 postdiapause larvae, in 8 of 15 consecutive years, at each of at least 18 additional distinct areas: 5 in San Mateo County, 10 in Santa Clara County, 1 in Alameda County, and 2 in Contra Costa County. To be "distinct," populations should be separated by at least 1 kilometer (3,000 feet) of unsuitable, unrestorable habitat. Satellite populations in Alameda and Contra Costa Counties are unlikely to be established naturally due to the distance between them and extant populations being several times greater than the known dispersal capabilities of the butterfly. Even if all recently occupied core and secondary habitats in San Mateo and Santa Clara Counties were occupied, the likelihood of recolonization and persistence in sites at distances greater than 5 miles from occupied core areas would be low (Harrison et al. One peer reviewer on the proposed revised Critical Habitat designation for the Bay checkerspot butterfly commented that San Bruno Mountain was not within easy dispersal distance for the Bay checkerspot butterfly (Launer, in litt. A second peer reviewer stated that dispersal between San Bruno Mountain and Pulgas Ridge (approximately 10 miles south) is unlikely and should not be counted on as part of the metapopulation dynamics for the butterfly (Weiss, in litt.

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At first, the number of cells in the embryo doubles approximately every 24 hours; later the rate slows, and only one doubling occurs during the final 10 weeks of pregnancy. At 8 weeks, the 11/4-inch embryo has a complete central nervous system, a beating heart, a digestive system, well-defined fingers and toes, and the beginnings of facial features. Each organ grows to maturity according to its own schedule, with greater intensity at some times than at others. Most successful pregnancies last 38 to 42 weeks and produce a healthy infant weighing between 61/2 and 9 pounds. An adverse influence felt late temporarily impairs development, but a full recovery is possible. Critical Periods Times of intense development and rapid cell division are called critical periods- critical in the sense that those cellular activities can occur only at those times. If cell division and number are limited during a critical period, full recovery is not possible (see Figure 14-3). The development of each organ and tissue is most vulnerable to adverse influences (such as nutrient deficiencies or toxins) during its own critical period (see Figure 14-4). The critical period for neural tube development, for example, is from 17 to 30 days gestation. Consequently, neural tube development is most vulnerable to nutrient deficiencies, nutrient excesses, or toxins during this critical time- when most women do not even realize that they are pregnant. Any abnormal development of the neural tube or its failure to close completely can cause a major defect in the central nervous system. Figure 14-5 shows photos of neural tube development in the early weeks of gestation. Normal development An adverse influence felt early permanently impairs development, and a full recovery never occurs. In the later stages of development (green area of the bars), the tissues continue to grow and change, but the events are less critical in that they are relatively minor or reversible. Key: Critical development Continued development Central nervous system Heart Ears Reminder: the neural tube is the structure that eventually becomes the brain and spinal cord. Any failure of the neural tube to close or to develop normally results in central nervous system disorders such as spina bifida and anencephaly. Successful development of the neural tube depends, in part, on the vitamin folate. At 6 weeks, the neural tube (outlined by the delicate red vertebral arteries) has successfully closed. Neural Tube Defects In the United States, approximately 30 of every 100,000 newborns are born with a neural tube defect; some 1000 or so infants are affected each year. The two most common types of neural tube defects are anencephaly and spina bifida. Pregnancies affected by anencephaly often end in miscarriage; infants born with anencephaly die shortly after birth. Spina bifida is characterized by incomplete closure of the spinal cord and its bony encasement (see Figure 14-6 on p. The meninges membranes covering the spinal cord often protrude as a sac, which may rupture and lead to meningitis, a life-threatening infection. Spina bifida is accompanied by varying degrees of paralysis, depending on the extent of the spinal cord damage. Common problems include clubfoot, dislocated hip, kidney disorders, curvature of the spine, muscle weakness, mental handicaps, and motor and sensory losses. The cause of neural tube defects is unknown, but researchers are examining several gene-gene, gene-nutrient, and gene-environment interactions. Reminder: A neural tube defect is a malformation of the brain, spinal cord, or both during embryonic development. The two main types of neural tube defects are spina bifida (literally, "split spine") and anencephaly ("no brain"). A woman who has previously had an infant with a neural tube defect may be advised by her physician to take folate supplements in doses ten times larger-4 milligrams daily. Because high doses of folate can mask the symptoms of the pernicious anemia of a vitamin B12 deficiency, quantities of 1 milligram or more require a prescription. Most over-the-counter multivitamin supplements contain 400 micrograms of folate; prenatal supplements usually contain at least 800 micrograms.

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There are marked differences in per capita -tocopherol supply among different countries ranging from approximately 8-10 mg/head/day. This variation can be ascribed mainly to the type and quantity of dietary oils used in different countries and the proportion of the different homologues in the oils (Table 25). For example, sunflower seed oil contains approximately 55 mg -tocopherol/100 g in contrast to soybean oil that contains only 8 mg/100 ml (34). Soybean, a rich source of the less biologically active form, is most commonly used in northern European countries whereas sunflower seed oils, which mainly contain the form, are generally used in southern Europe (30). Even for vitamin E with its important biologic antioxidant properties, there was no consistent evidence for protection against chronic disease from dietary supplements. There is very little clinical evidence of deficiency disease in humans except in certain inherited conditions where the metabolism of vitamin E is disturbed. Even biochemical evidence of poor vitamin E status in both adults and children is minimal. Meta-analysis of data collected within European countries indicates that optimum intakes may be implied when plasma concentrations of vitamin E exceed 25­30 µmol/L of lipid-standardized -tocopherol (35). However, this approach should be treated with caution, as plasma vitamin E concentrations do not necessarily reflect intakes or tissue reserves because only 1 percent of the body tocopherol may be in the blood (36) and the amount in the circulation is strongly influenced by circulating lipid (37). The erythrocytes of subjects with values below this concentration of vitamin E may show evidence of an increasing tendency to haemolyze when exposed to oxidizing agents and thus such values should be taken as an indication of biochemical deficiency (38). Furthermore, although the high intake of soybean oil with its high content of -tocopherol substitutes for the intake of -tocopherol in the British diet, a comparison of -tocopherol-cholesterol ratios found almost identical results in two groups of randomly selected, middle-aged adults in Belfast (Northern Ireland) and Toulouse (France), two countries with very different intakes of -tocopherol (34) and cardiovascular risk (31). As indicated above, however, plasma concentrations in France and Northern Ireland suggest that an increased amount of dietary vitamin E is not necessary to maintain satisfactory plasma concentrations (31). At present, data are not sufficient to formulate recommendations for vitamin E intake for different age groups except for infancy. There is some indication that new-born infants, particularly if born prematurely, are vulnerable to oxidative stress because of low body stores of vitamin E, impaired absorption, and reduced transport capacity resulting from low concentrations at birth of circulating low-density lipoproteins (49). However, term infants almost achieve adult plasma vitamin E concentrations in the first week (50) and although the concentration of vitamin E in early human milk can be variable, after 12 days it remains fairly constant at 0. No specific recommendations concerning the vitamin E requirements in pregnancy and lactation have been made by other advisory bodies (42, 43) mainly because there is no evidence of vitamin E requirements different from those of other adults and presumably also as the increased energy intake would compensate for the increased needs for infant growth and milk synthesis. Vitamin E appears to have very low toxicity, and amounts of 100­200 mg of the synthetic all-rac-tocopherol are consumed widely as supplements (28, 29). Evidence of prooxidant damage has been associated with the feeding of supplements but usually only at very high doses. Future research More investigation is required of the role of vitamin E in biologic processes which do not necessarily involve its antioxidant function. Similarly, more investigation is required of the growing evidence that inadequate vitamin E status may increase susceptibility to infection particularly by allowing the genomes of certain relatively benign viruses to convert to more virulent strains (52). Intervention trials with morbidity and mortality endpoints may take years to complete. Relative susceptibility of microsomes from lung, heart, liver, kidney, brain and testes to lipid peroxidation: correlation with vitamin E content. Purification and partial characterisation of an -tocopherol-binding protein from rabbit heart cytosol. Vitamin E requirements, transport, and metabolism: Role of -tocopherol-binding proteins. Kinetics of rat peripheral nerve, forebrain and cerebellum -tocopherol depletion: Comparison with different organs. Uptake, storage and excretion of chylomicra-bound 3H-alpha-tocopherol by the skin of the rat. Impaired ability of patients with familial isolated vitamin E deficiency to incorporate -tocopherol into lipoproteins secreted by the liver. Dietary vitamin E and the attenuation of early lesion development in modified Wattanabe rabbits. Effect of oral supplementation with D-tocopherol on the vitamin E content of Human low density lipoprotein and resistance to oxidation. Randomised trial of alpha-tocopherol and beta-carotene supplements on incidence of major coronary events in men with previous myocardial infarction.


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