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Joel C. Marrs, PharmD, FCCP, FASHP, FNLA, BCPS (AQ Cardiology), BCACP, CLS

  • Associate Professor, University of Colorado Skaggs School of Pharmacy and Pharmaceutical Sciences, Aurora, Colorado

http://www.ucdenver.edu/academics/colleges/pharmacy/Departments/ClinicalPharmacy/DOCPFaculty/H-P/Pages/MarrsJoelCPharmD.aspx

Glucose tolerance and the effect ofballoon angioplasty onhypertension inatherosclerotic renalmortality erectile dysfunction treatment vancouver order vimax with a mastercard, including a substudy of tolbutamide treatment erectile dysfunction supplements best order for vimax. Secondary hypertension: Sleep medical therapy for hypertensive patients with atherosclerotic renal artery Apnea erectile dysfunction caused by herpes order vimax 30caps otc. Daily usage and efficiency of remote home plasma metanephrinescomparedwith the combination of 24-hour urinary monitoring in hypertensive patients over a one-year period impotence yohimbe buy generic vimax 30caps on line. Evolving concepts in the pathophysiology erectile dysfunction causes prescription drugs proven vimax 30 caps, diagnosis and prevalence of hypertension: a systematic review impotence of organic origin icd 9 vimax 30 caps low price. Thegenetic treated hypertensive patients screened from clinical practice: results of basis of pheochromocytoma. A prospective study of the prevalence of primary aldosteronism in 1125 hypertensive patients. High incidence of primary aldosteronism in 199 patients referred with hypertension. Predictive value of preoperative tests in discriminating bilateral adrenal hyperplasia from an aldosterone-producing adrenal adenoma. Novel therapies blocking the renin-angiotensinaldosterone system in the management of hypertension and related disorders. Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study. Atkinson College of Medicine, Departments of Pathology and Pediatrics, the University of Florida, Gainesville, Florida 32610-0275 Correspondence: atkinson@ufi. This information is presented to the reader as a series of seminal historical discoveries that, when advanced through research, transformed our understanding of the roles for the immune system, genes, and environment in the formation of this disease. In addition, where longitudinal investigations of these three facets occurred, their roles within the development of type 1 diabetes, from birth to symptomatic onset and beyond, are discussed, including their most controversial elements. The disease is most tors contribute to this knowledge void, one beoften diagnosed in children and adolescents, using a failure in understanding the percentage of ually presenting with a classic trio of symptoms T1D cases that are errantly misclassified as type. Attempts pects for this disease remain either unclear or to distinguish T1D cases from those with T2D subject to significant debate within the medical have also resulted in a proposed new disease research community. Atkinson, and Peter Arvan Additional Perspectives on Type 1 Diabetes available at To be clear, geneity, or diagnosis, would include, but not be such confusion over disease classification in setlimited to , the growing problem of obesity tings of diabetes is not new because many terms (both childhood and adult) and health care pro. These exwe now refer to as T1D; each term eventually amples of infiuential changes likely refiect a sebeing replaced, to a large extent, as improveries of additional variables. Here too, avariety of ciated with immune-related genetic susceptibly, epidemiological notions. Yet,notallT1Dpatientspossessthese charat least on their surface, firm in their proposiacteristics; leading some to the proposed classition, whereas other concepts are less sure. Beyond this, although many autocific pathogenesis remains unclear (Imagawa immune disorders disproportionately affect et al. Interestingly, despite the proposal women,T1Dappearstoaffectmalesandfemales for adopting this new set of definitions for equally; but controversy does exist whether a 2 Cite this article as Cold Spring Harb Perspect Med 2012;2:a007641 Downloaded from perspectivesinmedicine. To lence rates for T1D are exceptionally interesting begin, for years, data regarding the incidence because they vary quite dramatically, with more and prevalence for T1D were far more predomthan a 350-fold variation in incidence among inant from studies performed in Europe rather reporting countries (Vandewalle et al. Although clear exceptions to tion (in the latter instance) was largely depenthis rule exist, it does remain noteworthy that dent on extrapolation of data obtained from a the incidence of T1D is positively related to dissmall and limited number of somewhat localtance north of the equator. Rates of more than T1D or T2D), to understand the infiuence of 20 cases per 100,000 per year are observed in race/ethnicity on the disease, and to address Sweden, Norway, Portugal, Great Britain, Canhow T1D and T2D differ in this U. This boring Cuba has an incidence of less than three notion finds support with at least two studies, cases per 100,000 per year. The mechanisms one in Europe, the other in the United States underlying these variances are unknown but, (Gillespie et al. For examnetic, autoantibody, and metabolic markers of ple, Sweden and Norway have reported a 3. Indeed, in the midannual increase in T1D rates, whereas Finland 1980s, a now oft-cited model was developed has observed a 2. This model for the and to be clear, like examples exist across the natural history of T1D suggests that genetically globe. These increases have largely been assusceptible individuals with a fixed number cribed to some unknown change in environof b cells are exposed to a putative environmenmental constituents because notions of genetic tal trigger, which induces b-cell autoimmunity. That said, pable of destroying b cells, resulting in a proafter yearsofreportssuggestingincreases,atleast gressive and predicable loss in insulin secretory one country, Sweden, has recently and quite unfunction. If 90% of the b cells have been destroyed, and confirmed in other populations, this would be there is a marked gap between the onset of aucause for optimism because current incidence toimmunity and the onset of diabetes. However, recently, some aspects of the equally across all age groups; that is, the most classical model have been modified to update profound elevations in incidence rates have knowledge gains (Fig. For been observed in the youngest individuals example, there are data to suggest that pancre(i. The modern model expands and updates the traditional model by inclusion of information gained through an improved understanding of the roles for genetics, immunology, and environment in the natural history of T1D. In short, despite being strongly cell loss in the pre-diabetic period has also reinfiuenced by genetic factors, T1D does not fit cently been subject to considerable debate, with any simple pattern of inheritance and is considsome proposing that the disorder may see its eredacomplex,multifactorialdisease(seeNoble symptomatic onset only following a period of and Erlich 2012). Indeed, continued identification of genes 1 in 20 risk of developing T1D, whereas the controlling disease susceptibility, improved ungeneral population of the United States have a derstanding of autoimmunity/mechanisms unone in 300 risk (Redondo et al. All of this said, a strange curiosity Cite this article as Cold Spring Harb Perspect Med 2012;2:a007641 5 Downloaded from perspectivesinmedicine. Atkinson A Islet antibody 1 Islet antibody 2 Islet antibody 3 Hyperglycemia Honeymoon phase Time B Effector T cells Regulatory T cells Time C Time Figure 2. An increase in the numbers of autoreactive effector T cells is controlled by an increase in the number of regulatory T cells. However, over time, a gradual disequilibrium of the cyclical behavior could occur, leading to the number of autoreactive effector T cells surpassing the number of regulatory T cells, which would no longer be capable of containing autoreactive effector T-cell responses and thereby lead to a decline in pancreatic islet function. This figure indirectly depicts the biological trends of the development of T1D, which may be attributed to the cyclical nature of the immunological events that lead to the attackor protection of b cells. Sucha phenomenon is usually the result of feedback-loop mechanisms, which, in the case of T1D, could be due to misdirected effector T cells that are not easily controlled by regulatory T cells. The infiammatory process of the pancreatic islets themselves may enhance b-cell proliferation and antigenic presentation, ultimately leading to the generation of more effector and regulatory T cells. In addition, as b-cell mass declines, the pressure on each b-cell to produce insulin increases, which may be sufficient to alter the recognition of b cells by the immune system and to alter their ability to regenerate and increase insulin production. The y-axis indicates the best estimate of the odds ratio for risk alleles at each of the indicated loci on the basis of currently published data. On the x-axis are indicated possible candidate genes within genomic regions in which convincing associations with T1D have been reported. On the basis of the known functions of these candidate genes, the corresponding bars in the graph depicting odds ratios have been color-coded to suggest possible roles of these loci in susceptibility to T1D. Atkinson T1D) has been mapped to a variable number of to the insulin-producing b cells (Atkinson et al. Disease association sponsible forinducingthe autoimmunity inT1D studies in case-control and family cohorts have also have yet to be elucidated (La Torre 2010). Other specific genes finding some damage,theever-elusivelocalviralinfection,dedegree of support for their infiuence on T1D fects in peripheral tolerance. Perhaps most interestbasic role for the cellular immune response, long ing,however,andaspointedoutbyothers (ConthoughtkeytothepathogenesisofT1D,hasbeen cannon et al. Given that nearly all studies performed man T1D are tied with functions related to imto date have involved immunological charactermune responsiveness. One important reason relates to the limited number of cases that have been available Autoimmunity, Autoantibodies, for study. Of and Cellular Immunity these, few have been studied in depth, and most As previously indicated, T1D is an autoimmune lack the techniques of modern technologies. Curiously, it remains uncells are absent, leaving a situation of so-called clear why the autoimmunity in T1D is specific pseudo-atrophic islets devoid of b cells. However, those with T1D is typically characterized by a recent studies in animal models of T1D purdecrease (or absence) of insulin-producing bporting a crucial role for B-lymphocytes in discells along with a pancreatic islet cell infiltrate ease development have opened the door for a composed of T-lymphocytes, B-lymphocytes, previously unappreciated role for autoantibodmacrophages, and lesser numbers of other cells ies in the presentation of self-antigens to the representing the immune response (for review, cytotoxic T cells responsible for b-cell destrucsee Foulis 2008). This concept has alsofi have not, in most settings, been considered ethdrawn support in human T1D studies in which ically feasible (for safety reasons) and autopsy therapeutic benefits were seen, over the short tissuefromsubjectsrecentlydiagnosedwithT1D term, in recent-onset T1D patients treated is rare, major programs have recently been eswith the B-lymphocyte-depleting agent antitablished to obtain these tissues for research. With time, it is anticipatimmune linage in disease pathogenesis (Clynes ed that tissues obtained from these programs 2010). Specifically, when presantibody/autoantigen combinations remains ent at higher titers, at a younger age, or with the (Taplin 2008; Zhang et al. Atkinson nearly all do so) use the so-called biochemical autoantibody in those with the aforementioned autoantibodies. In combination ated autoantibodies a relatively easy biomarker with a growing understanding of genetic susfor studies of the disease, the reality for such a ceptibility, autoantibodies allow for us to accunotion in everyday practice has often proved rately predict which patients will develop T1D, otherwise. Indeed, based on studies of large popof the start of exogenous insulin therapy, beulations (both general population and families) cause insulin antibodies. Briefiy, studmost important of the T1D-associated autoanies of cellular immunity in T1D have been limtibodies, at least in terms of predictive value. Characteristics of the initial antibody response cited as evidence for this activity (Gale 2008). Although ple, persons with autoimmunity may also be 12 Cite this article as Cold Spring Harb Perspect Med 2012;2:a007641 Downloaded from perspectivesinmedicine. Beyond this, questions regarding marked replication in the research community the specificity of these antibodies used to detect (Atkinson et al. This virus in pancreatic sections, for patients with said, very recently, cross-reactivity between the T1D, have come under increased scrutiny b-cell-specific protein (insulin) and bovine a(Richardson et al. As a result, much casein has been noted and holds interesting pomore effort will be required to link this virus tential for molecular mimicry (Adler et al. To this end, data exist suggesting that been subject to multiple reports touting their newly diagnosed T1D subjects had lower serum implication for T1D development (Borchconcentrations of this metabolite than healthy Johnsen et al. In addition, polymorphisms with time, these associations have either not in the vitamin D metabolism gene have recently been subject to replication by others or firm been implicated with this disorder (Bailey et al. Atkinson exposure (a factor infiuencing the synthesis of velop in the presence of environmental factors vitamin D) could modulate this metabolite, one eliciting strong Th2-like immunity. Toxic them) truly associated with the development doses of nitrosamine compounds can also cause of the disease be identified. In addition, the diabetes through the generation of free radicals, complexity of these efforts must go beyond but the effect of dietary nitrate, nitrite, or nitrothe simplicity of previous efforts and delve samine exposure on human T1D risk remains into areas not subject to much in the way of unclear (Kostraba et al. In the end, it will be important to deterinteracts with genetic factors, affording either mine whether these factors ultimately contribsusceptibility or resistance to the disease (Fig. In support of this, there has been a parallel rise in the rates of asthma and Much has been learned in the last 40 years reallergy to that in T1D. The aforementioned hygarding the pathogenesis and natural history of giene hypothesis proposes that early exposure to T1D. That said, a major motivation driving reinfective agents in early childhood is necessary search efforts in these areas was a belief that such for maturation of the neonatal immune regains would result in a means to prevent as well sponse.

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The first physical introduction should take no longer than one hour erectile dysfunction education purchase 30 caps vimax visa, prolonging this with each attempt erectile dysfunction drugs nz buy cheap vimax 30caps online. If the introduction is between one male and a coalition erectile dysfunction treatment manila generic vimax 30caps line, the new male is introduced to each coalition member separately impotence from vasectomy order vimax without prescription. Firstly erectile dysfunction doctors buffalo ny generic 30caps vimax overnight delivery, the two groups were placed in adjourning pens for a period of six months erectile dysfunction doctors in alexandria va buy discount vimax 30caps on-line. Aggressive behaviour was rarely observed, they more or less avoided each other until one of the males was relocated to another institution. Subsequently, the remaining sibling joined up with the other pair and formed a triadic coalition. This can last for a few weeks until the keepers are positive that the animals have accepted each other. Depending on the interactions between the animals, they are left together or separated and introduced again the next day. In general, an introduction follows a threestep approach: 1) Animals need to have visual and olfactory contact for a few weeks or months before physical access. Animals behaving extremely aggressive (as some mild aggression is expected) need to be separated. Animals accepting each other can be left together or separated and introduced daily for longer periods of time. Introduction of cheetah to new environment: Compared to other species, the cheetah adapts easily to a new situation, taking only a few days to acclimate to their new environment. In case the animal is transported to another institution this can take around 1 to 2 weeks. Before releasing a cheetah into its new enclosure, it is preferable to keep the animal in a smaller holding area for the animal to acclimate to its new environment and daily routine. When the animal recognizes the area as a secure place and feeding area, access to the entire exhibit can be offered. The diet for cheetahs, new to an institution, should be gradually converted from the originating zoo to the new (Kleinman, 1997). Well-planned and managed exhibits have the potential to supply the animals with environmental enrichment and the public with more interesting and educational enclosures. While planning, the following factors need to be assessed: 1) Risks for the animals, for example as a consequence of animals in heat. During this period animals change their behaviour and conflicts can arise between the species. Additionally, newborns may experience harassment by other species and fall prey to them. In order to avoid this, it is advised to choose species with different dietary requirements. Cheetahs have been successfully introduced with Black and White rhinoceros in the past. At Leipzig zoo, they currently house a cheetah female group together with a male and female Black rhino. Prior to the introduction of both species, each was placed alone in the enclosure for a few days. Except for some mild attacks from the rhinos towards the cheetahs, there are no major conflict or injuries perceived. At Boras Djurpark located in Sweden, cheetahs are kept together with White rhinos. Another example is the combination with pygmy hippo in Bangkok Safari World, but surely multiple other examples have not been listed yet. This chapter discloses several strategies to facilitate breeding and how to handle in case mating is succeeded. For instance, housing hoofstock or other natural prey species have shown to increase reproduction, whereas housing natural competing predators has decreased reproduction success. Zoos that house cheetahs in groupstructures similar to their wild counterparts have higher breeding success, institutions that want to breed cheetahs should try to achieve a similar constellation (Wielebnoswski, 2002; Chadwick, 2014). Furthermore, it is advised to separate males and females not only physically but also visually, as they can form a sibling bond making them less likely to breed (Ziegler-Meeks, 2009). Lastly, rotating the animals to new enclosures, the introduction of new animals to each other or any novel situation can stimulate breeding activity, therefore it is recommended to do so. Introductions between cheetahs of the opposite sex differ from an introduction with the same sex in duration and purpose. When introducing animals, with the purpose to breed, there is an internal motivation of the cheetahs, working in favour of the caretakers. Moreover, the timespan the animals need to be with each other can be as short as one hour, in order to be successful. Therefore, an introduction with the purpose of mating follows a different pathway. A crucial role for succesfull introductions is the experience of the staff in recognizing the behaviour of the animals (Bus, 2015). This is vital for preventing fights and injuries between two animals and form successful breeding pairs. Females have very subtle key behaviours during oestrus that indicate they are ready to mate. When zookeepers monitor positive behaviour of the animals it is time to physically introduce the aninals to each other, there still might be some aggression (as seen in the wild). Usually, copulation occurs Figure 11: Mating (Safari de Peaugres) 33 Contents within the first hour and lasts around 30-45 seconds (Figure 11). After copulation the male exhibits a flehmen response and hisses, whereas the female is seen rolling from side to side (Frank, 2005). There are different opinions and experiences concerning the mating of cheetahs in captivity. One issue is, whether or not a female should be introduced to a single male or a coalition. In the wild females are more likely to encounter a coalition, as they defend territories around female hotspots (Caro, 1993). However, it remains unclear if the female only mates with the dominant male or with several coalitionmembers (Gottelli, 2007). What has been proven is that females are promiscuous and have cubs with multiple paternities (Gottelli, 2007). Conceivable multiple singletons, several males of one coalition or they mate with multiple males from different coalitions. Introducing a male and female together can take place via different pathways: 1) Introducing the female to one male. Therefore the options that give the animals the opportunity to choose a particular (or more than one) individual may influence acceptance, and as a consequence thereof, reproductive success (Asa, 2011). During pregnancy, meals should be increased and fasting days terminated (Ziegler-Meeks, 2009). Small, whole carcasses should be fed in order for them to receive all necessarly nutrients. If the female lives in a group she should be separated as soon as pregnancy is suspected or confirmed (Fitch-Snyder, 1988). There are three alternatives to assess the pregnancy status of a cheetah: 1) Faecal progestin tests: this method can only be carried out after 70 days postbreeding. After that point, females having a false pregnancy start to lose weight, whereas pregnant females will continue to put on weight. At first by reducing their food intake 1 to 5 days prior to parturition and stop eating altogether 1 to 2 days before giving birth. Before parturition females may seem restless, they are observed pacing around the enclosure or entering and exiting the den regularly, also smelling and scraping the bedding. Getting closer to labor, females will stay in the maternity den, grooming and an increase of respiration can be seen. Parturition can range from 30 minutes to 14 hours and can arise at any time, day and night. Therefore, it is recommended to install a camera inside the maternity den, have a one-way glass or a small window on one of the walls in order to check on the animals without being seen or smelled (Ziegler-Meeks, 2009). Complications may occur and if that happens the veterinarian should be notified (Ziegler-Meeks, 2009). As soon as the females have given birth it is advised to restain access to the main outside enclosure. The average litter size is 3 to 4 cubs, but litter sizes may range from 1 to 8 cubs. The slide needs to be closed behind her, to reduce the chance of taking the cubs with her until they are old enough. During the night depending on the temperature and the female, she is either locked in the indoor enclosure or left to go in the indoor and the small outside enclosure. During the lactation period, cheetahs should not have any contact with other conspecifics and all forms of disturbance should be kept to an absolute minimum after birth (Fitch-Snyder, 1988). Extreme caution is required while handling first time mothers, as keepers have no prior experience on the behaviour reaction of the mother. If staffmembers enter the den, mothers may stop nursing properly, try to move the cubs to another place or even abandon them. Therefore, zookeepers should enter the den through a different opening while the female is separated and cannot enter the den. Keepers should not touch the cubs, however, if necessarly for chipping, sexing or veternairy reasons the cubs should be handled with gloves. Females will usually stay in the den during the first 72 hours after giving birth, excluding small periods of time where they eat, drink, defecate or urinate. After this period, the mother will start going out of the den for short amounts of time (Ziegler-Meeks, 2009). From this point unwards, the bedding will need to be checked daily in order to remove food or clean if the female has urinated inside, this should be done with prudence. During the first 48 hours it is not necessary to offer the female food, though different institutions offer food the same day or the day thereafter. In the event no deviation is perceived, favourite foods may be offered at 35 Contents different locations (Ziegler-Meeks, 2009). During lactation, provide whole carcasses to compensate the energetic demands during this period. Female siblings are allowed to stay with their brothers until their first oestrus before separating the siblings. Male siblings should remain together for life, even when transferred to other zoos (Caro, n. In places with warmer temperatures, some cheetahs have been observed to rear the cubs outside, without the protection of a den. Checking the health of mother and her cubs may be difficult or not possible at all. Furthermore, at 3 weeks old, the cubs will start to move with more freedom than in a den. The mother might try to continually pick them up in an effort to keep the cubs together, confiding the animals to a smaller space might be necessary (ZieglerMeeks, 2009). An alternative to hand rearing may be euthanasia, especially when behavioural problems are expected in the future. Another alternative to hand rearing may be to cross-foster cheetah cubs (Figure 12). Especially, when a singleton is born it is recommended to try and find another cheetah with a litter of similar age and size. Successful introductions have been witnessed when impregnating the new cub in the urine and faeces of the females litter (Ziegler-Meeks, 2009). The protocol contains information on maternal milk composition, the different milk formulas and the calculations to be made in order to decide the amount of formula to administer. Furthermore, it contains information about common digestive problems, weaning and housing. This behaviour may lead to the lack of specific stimulation needed for the development of species-specific behaviour, leading to social, maternal and sexual disruptions (Kleinman, 1997). As soon as possible the 36 Contents cubs should be weaned and placed in an enclosure where they can see their conspecifics. At Safaripark Beekse Bergen 2 singletons were reintroduced with their mothers after being weaned and the mothers accepted the cubs immediately. As cheetahs need to stay with their mother for at least 1fi (male cubs) to 2 years (female cubs), institutions should have the facilities to house the cubs for at least 2 years. The easiest solution to limit undesirable reproduction is holding female cheetahs separate from the males (common practice). Such methods include: sterilization, castration or implants with hormones for either females or males. Both populations are managed completely separate, as the Northern and Southern cheetah are 2 genetically distinct populations.

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