Nelson Jen An Chao, MD

• Professor of Medicine
• Donald D. and Elizabeth G. Cooke Cancer Distinguished Research Professor
• Professor in Immunology
• Research Professor of Global Health
• Professor in Pathology
• Member of the Duke Cancer Institute
• Chief, Division of Cell Therapy in the Department of Medicine
• Affiliate of the Regeneration Next Initiative

https://medicine.duke.edu/faculty/nelson-jen-chao-md

With a better understanding of the pathogenesis of diabetes asthmatic bronchitis 14 trusted 5mg singulair, it is now recognized that genetic or acquired factors that affect the pancreatic -cell structure and function as well as associated mechanisms such as amylin deposition and mitochondrial damage may give rise to a broad range of clinical manifestations with considerable overlap between type 1 and type 2 phenotypes asthma or out of shape cheap singulair 10mg on line. This will help to guide the treatment of these patients who often present at a young and have a long duration of diabetes ahead of them asthma 1st aid singulair 10 mg line, this makes them eopecially at risk for the long-term chronic complications of diabetes asthma treatment children generic singulair 10mg amex. Mutations in the hepatocyte nuclear factor-1alpha gene in Caucasian families originally classified as having Type I diabetes definition of asthma uk buy discount singulair 4mg line. Type 2 diabetes: evidence for linkage on chromosome 20 in 716 Finnish affected sib pairs asthma symptoms after eating singulair 10mg on line. Common variants of hepatocyte nuclear factor 1 are associated with type 2 diabetes in a Chinese population asthma related bronchitis purchase 4 mg singulair free shipping. Molecular mechanisms and clinical pathophysiology of maturity onset diabetes of the young asthma treatment doctor order 10mg singulair with mastercard. A rapid screening method for hepatocyte nuclear factor 1 alpha frameshift mutations; prevalence in maturity-onset diabetes of the young and late-onset non-insulin dependent diabetes. Genetic and clinical characteristics of maturity-onset diabetes of the young in Chinese patients. The ethnic distribution of antibodies to glutamic acid decarboxylase: presence and levels in insulin-dependent diabetes mellitus in Europoid and Asian subjects. A comparison of the epidemiology of youth-onset insulin-dependent diabetes mellitus between Japan and the United States (Allegheny County, Pennsylvania). Epidemiology of diabetes mellitus in children in Hong Kong: the Hong Kong childhood diabetes register. Islet autoimmunity status in Asians with young-onset diabetes (12­40 years): association with clinical characteristics, beta cell function and cardio-metabolic risk factors. Familial early onset type 2 diabetes in Chinese: the more significant roles of obesity and genetics than autoimmunity. The burden of mortality attributable to diabetes: realistic estimates for the year 2000. Metabolic and immunologic features of Chinese patients with atypical diabetes mellitus. Young Chinese adults with new onset of diabetic ketoacidosis: clinical course, autoimmune status and progression of pancreatic beta cell function. Genetic variants of hepatocyte nuclear factor-1beta in Chinese young-onset diabetic patients with nephropathy. Pancreatic islet cell toxicity of amylin associated with type-2 diabetes mellitus. Prevalence and clinicopathological characteristics of islet amyloid in Chinese patients with type 2 diabetes. Islet amyloid: a complication of islet dysfunction or an aetiological factor in Type 2 diabetes? Islet amyloid, increased A-cells, reduced B-cells and exocrine fibrosis: quantitative changes in the pancreas in type 2 diabetes. S20G mutant amylin exhibits increased in vitro amyloidogenicity and increased intracellular cytotoxicity compared to wild-type amylin. Amylin gene promoter mutations predispose to Type 2 diabetes in New Zealand Maori. The islet amyloid polypeptide (amylin) gene S20G mutation in Chinese subjects: evidence for associations with type 2 diabetes and cholesterol levels. Association studies of variants in the genes involved in pancreatic beta-cell function in type 2 diabetes in Japanese subjects. Etiological investigation of diabetes in young adults presenting with apparent type 2 diabetes. Latent autoimmune diabetes in adults: definition, prevalence, beta-cell function, and treatment. Differing frequency of autoantibodies to glutamic acid decarboxylase among Koreans, Thais, and Australians with diabetes mellitus. Clinical review: Type 1 diabetes and latent autoimmune diabetes in adults ­ one end of the rainbow. Insulin intervention to preserve beta cells in slowly progressive insulin-dependent (type 1) diabetes mellitus. Fulminant type 1 diabetes in Korea: high prevalence among patients with adult-onset type 1 diabetes. Exocrine pancreatic function (serum immunoreactive trypsin, fecal chymotrypsin, and pancreatic isoamylase) in Indian diabetics. Selective beta-cell loss and alpha-cell expansion in patients with type 2 diabetes mellitus in Korea. Polymorphic variations in the neurogenic differentiation-1, neurogenin-3, and hepatocyte nuclear factor1alpha genes contribute to glucose intolerance in a South Indian population. Impaired -cell function can be detected in genetically predisposed individuals. Responses to ingestion of mixed meals and to non-glucose stimuli are reduced with a decrease in maximal secretory capacity. Other histologic changes include a 30­50% decrease in islet mass and an alteration in the relative proportion of the islet cell population. Approximately 10% of patients have a late-onset form of autoimmune diabetes which may represent a hybrid of type 1 and type 2 diabetes Textbook of Diabetes, 4th edition. For many years it was controversial whether impaired -cell function or tissue insulin resistance was the underlying pathogenetic element. Until recently, it was generally thought that insulin resistance preceded -cell dysfunction and was the primary genetic factor, while -cell dysfunction was a late phenomenon brought about by exhaustion after years of compensatory hypersecretion [4­6]. During the past several years, however, the accumulation of evidence from sophisticated studies examining -cell function and tissue insulin sensitivity, both cross-sectionally and longitudinally, have swung the pendulum over to the concept that impaired -cell function is the primary underlying, probably genetic, defect [2,7­9]. The idea that insulin resistance could be the primary defect can be traced back to the classic studies of Himsworth & Kerr [10] more than 60 years ago, in which it was demonstrated that lean patients with early-onset diabetes were sensitive to exogenous injection of insulin, whereas obese patients with late-onset diabetes were resistant. The problem with interpretation of the results of these studies is that they failed to take the following into consideration: · Importance of the dynamics of insulin secretion. Plasma insulin (U/mL) 75 60 45 30 Increment at 30 min 15 0 80 Plasma glucose (mmol/L) 10 15 120 160 200 240 280 320 2-h plasma glucose (mg/dL) 360 2-h value 5 Figure 10. Moreover, restoration of early insulin responses either by insulin or an insulin secretogogue reduces late hyperinsulinemia [18,19]. Appropriateness of the plasma insulin level for the prevailing glucose level the major factor acutely regulating insulin is the plasma glucose concentration. As glucose is the predominant stimulus for insulin secretion, the prevailing plasma glucose concentration must be taken into consideration in judging whether the plasma insulin concentration is appropriate. For example, the plasma insulin level in an individual with diabetes whose plasma glucose concentration is 180 mg/dL (10 mmol/L) may be twice as great as that of an individual without diabetes with a plasma glucose concentration of 90 mg/dL (5 mmol/L), but is clearly inappropriate because the non-diabetic individual would have a plasma insulin level four times as great at the same hyperglycemia [20]. This reduction in early insulin response has been shown to diminish suppression of endogenous glucose production after glucose ingestion [16]; the resultant hyperglycemia provides a greater stimulus to the -cell, explaining the late (2 hour) hyperinsulinemia. The latter had often been erroneously interpreted to be the result of insulin resistance [4­6]. This adaptation, first demonstrated in the case of obesity in 1974, results in an increase in the -cell sensitivity to glucose [23]. The hyperbolic relationship between -cell function and tissue insulin sensitivity, first demonstrated by Bergman et al. In genetically predisposed individuals with normal glucose tolerance, impaired -cell function is demonstratable even when no insulin resistance is apparent [27­29]. During stage 2, decreases in insulin sensitivity emerge usually as a result of unhealthy lifestyles (environmental), and these, at least initially, are compensated for by an increase in -cell secretion so that glucose tolerance remains normal. During stage 3, -cell function deteriorates further to the point that when challenged, as during a glucose tolerance test or a standardized meal, postprandial glucose tolerance becomes abnormal. At this point, -cell function is clearly abnormal but sufficient to maintain normal fasting plasma glucose concentrations. In stage 4, there is further deterioration in -cell function noted at least in part from glucose toxicity as a result of postprandial hyperglycemia. Fasting plasma glucose concentrations increase in this stage because of an increase in basal endogenous glucose production. Finally, in stage 5, as a result of further deterioration 162 Abnormalities of Insulin Secretion and -Cell Defects Chapter 10 in -cell function, both fasting and postprandial glucose levels reach levels diagnostic of diabetes. Insulin sensitivity does not decrease per se with aging and decreases in insulin sensitivity when observed are most likely related to other factors such as changes in body composition and physical fitness. The conversion process requires the sequential action of three peptidase enzymes (prohormone convertases 2 and 3, and carboxypeptidase H) and produces four proinsulin conversion intermediates (32,33-split, 65,66-split, des-31,32-split, and des-64,65-split proinsulins) before ultimately yielding insulin and C peptide (see Figure 6. Normally, a small amount of intact proinsulin and its conversion intermediates, mostly the des-31,32-split proinsulin, are released into the circulation along with insulin and C peptide. They are estimated to constitute 10­20 % of total immunoreactive insulin measured in the circulation during the basal state [39,40]. The events that lead to release of insulin from -cells are complex (see Chapter 6). In response to an acute square wave of hyperglycemia such as that used in hyperglycemic clamp experiments in humans or in studies of perfused rat pancreas, insulin release is biphasic (Figure 10. It is characterized by an acute increase in insulin release lasting approximately 10 minutes, termed first-phase release, followed by a slowly increasing second phase of insulin release that is more sustained and typically persists as long as glucose is elevated. The first-phase release has been related to insulin-secretory granules located close to the -cell plasma membrane (immediate releasable pool). The insulin secretion pattern throughout the day is more complicated than that seen during acute square wave of hyperglycemia in hyperglycemic clamp experiments. In vivo insulin secretion was found to be pulsatile, undergoing short (rapid) and long (ultradian) oscillations. The basis for these is still poorly understood, but there is evidence that the integrity of these responses is necessary for maintenance of normal glucose homeostasis [41]. These high frequency bursts occur every 5­15 minutes and account for the majority of insulin secreted in humans [42­44]. By contrast, inhibition of insulin 163 Part 3 Pathogenesis of Diabetes 2000 1000 pulses are less amplified after meals and less likely to follow plasma glucose oscillations [42,59]. The increased ratio is noted in the basal and stimulated insulin secretion states and indicates less successful proinsulin to insulin conversion within -cell secretory granules [39,40,60]. These include reduced first and second-phase responses to intravenous glucose (Figure 10. These rapid oscillations are superimposed on slower and larger ultradian oscillations (Figure 10. The ultradian oscillations are present during basal conditions and have clear amplification after meals. Such genes may affect -cell apoptosis, regeneration, glucose sensing, glucose metabolism, ion channels, energy transduction, microtubules/microfilaments and other islet proteins necessary for the synthesis, packaging, movement and release of secretory granules [72,73]. A second involves the gene encoding calpain-10, a cysteine protease that modulates insulin release as well as insulin effects on muscle and adipose tissue [75]. Commonly found abnormalities include absent first-phase and diminished second-phase release in response to hyperglycemia in hyperglycemic clamp experiments [53­55]. The ultradian 164 Abnormalities of Insulin Secretion and -Cell Defects Chapter 10 Normal 600 Pancreatic insulin secretion (pmol/mL) 500 400 300 200 100 0 0600 600 Pancreatic insulin secretion (pmol/mL) 500 400 300 200 100 0 0600 Pancreatic insulin secretion (pmol/mL) 900 800 700 600 500 400 300 200 100 0 0600 1000 Pancreatic insulin secretion (pmol/mL) 900 800 700 600 500 400 300 200 100 0600 1200 1200 Obese 1200 1800 2400 Clock time 0600 1800 2400 Clock time 0600 Figure 10. It was proposed that malnutrition in utero and during the first few months of life may damage -cell development; it is also possible that nutritional deficiency at this stage may program the -cell so as to limit its subsequent ability to adapt to overnutrition. The latter possibility is supported by the fact that the strongest link was Glucotoxicity There is abundant evidence that both prolonged [86] and acute hyperglycemia [87] can adversely affect -cell function. The mechanisms by which hyperglycemia exerts its adverse effects on -cells are complex and multifactorial. Evidence suggests that fatty acids inhibit glucose stimulated insulin secretion, impair insulin gene expression and, more importantly, promote -cell apoptosis [92]. It is not clear whether the defective incretin effect is merely a manifestation of a generalized reduction in -cell function as is the reduced insulin response to arginine [56,57,121,125]. Most obese individuals, however, compensate for their insulin resistance with an appropriate increase in insulin release and do not develop diabetes. Inadequate stimulation by incretins Incretins are hormones released by the gut in response to food ingestion, which augment insulin release in what is known as the incretin effect. In addition to promoting the biosynthesis and secretion of insulin [112], they increase -cell replication and inhibit its apoptosis in vitro and were found, in rodent model, to increase -cell mass [113­116]. These oligomers form and act inside the -cell, possibly causing endoplasmic reticulum stress-induced apoptosis [132,133]. In addition to increased systemic cytokines, these abnormalities involve acute-phase proteins and mediators associated with endothelial cell activation [145]. Most of these changes are small and their contribution to -cell failure is unclear. Other histologic changes include a decreased islet mass, an alteration in the relative proportion of the islet cell population (see below), and variable degrees of fibrosis of islets and endocrine tissue [131,149­151]. These deposits are localized in the pancreas and are not part of a systemic amyloidosis disorder. It is still not clear what triggers this process and whether this simply reflects islet cell deterioration and destruction. Similar deposits, nevertheless, can be found in a minority of people without diabetes, especially with aging [131]. The decline in -cell mass is caused by a decrease in the number of cells rather than the volume of individual cells. A several-fold increase in -cell apoptosis without an adequate compensatory increase in replication or neogenesis rate is responsible for the reduction in cell numbers Figure 10. Insulin-containing -cells (labeled brown with immunoperoxidase) are clustered towards the periphery of the islet and are very reduced in number. In a patient with type 2 diabetes, amyloid (Am) fibrils closely surround the -cells (B) and deeply invaginate the distorted cell membrane. The genetic basis of type 2 diabetes mellitus: impaired insulin secretion versus impaired insulin sensitivity. Insulin resistance and non-insulin-dependent diabetes mellitus: cellular and molecular mechanisms. The importance of -cell failure in the development and progression of type 2 diabetes. Noninsulin-dependent diabetes mellitus: a genetically programmed failure of the beta cell to compensate for insulin resistance. Impaired glucose tolerance as a disorder of insulin action: longitudinal and cross-sectional studies in Pima Indians. Insulin response to glycemic stimulus: relation of delayed initial release to carbohydrate intolerance in mild diabetes. Role of reduced suppression of glucose production and diminished early insulin release in impaired glucose tolerance. Loss of early phase of insulin release in humans impairs glucose tolerance and blunts thermic effect of glucose. Effect of loss of first-phase insulin secretion on hepatic glucose production and tissue glucose disposal in humans. Importance of early insulin secretion: comparison of nateglinide and glyburide in previously diet-treated patients with type 2 diabetes. Use of the oral glucose tolerance test to assess -Cell and glucagon changes the -cell mass is either unchanged or slightly increased [131,151]; this would result in a relative increase in -cells because -cell mass decreases. This has been correlated with reduced -cell function and could therefore be a secondary phenomenon involving glucose toxicity, lipotoxicity and resistance to insulin. Although this exacerbates the consequences of impaired insulin release on hepatic glucose production [16], it is likely to be a secondary phenomenon, because it is readily correctable by physiologic insulin replacement [161]. Studies have reported -cell mass to be either increased [162] or with no significant change [151,152]. Current evidence favors the concept that the predominant genetic impact involves impaired insulin secretion whereas additional acquired elements, and thus potentially preventable factors, also adversely affect -cell function and tissue responses to insulin. Much of the research focus in recent years is directed toward understanding the molecular and genetic basis of the disease. Being a polygenic disorder, multiple different polymorphisms that diminish -cell function are likely to be identified. New therapies that preserve -cell function and eventually reverse the defects may be developed in the future. Gender, autoantibodies, and obesity in newly diagnosed diabetic patients aged 40­75 years. Physiologic evaluation of factors controlling glucose tolerance in man: measurement of insulin sensitivity and B-cell glucose sensitivity from the response to intravenous glucose. Pancreatic B-cell defects in gestational diabetes: implications for the pathogenesis and prevention of type 2 diabetes. The natural history of insulin-dependent diabetes mellitus in Denmark: long term survival with and without diabetic complications. Insulin secretion, insulin action, and hepatic glucose production in identical twins discordant for non-insulin-dependent diabetes mellitus. Beta-cell function in subjects spanning the range from normal glucose tolerance to overt diabetes: a new analysis. Effect of aging on glucose homeostasis: accelerated deterioration of beta-cell function in individuals with impaired glucose tolerance. Relationships among age, proinsulin conversion, and betacell function in nondiabetic humans. Impact of intra-abdominal fat and age on insulin sensitivity and beta-cell function. Disproportionate elevation of immunoreactive proinsulin in type 2 (non-insulin-dependent) diabetes mellitus and in experimental insulin resistance. In humans at least 75% of insulin secretion arises from punctuated insulin secretory bursts. Pulsatile insulin secretion accounts for 70% of total insulin secretion during fasting.

A high and positive correlation was observed between full length asthma symptoms checklist cheap singulair 5mg free shipping, muzzle length to tail asthma control test singulair 10 mg overnight delivery, thoracic diameter asthmatic bronchitis airways cheap 5 mg singulair with amex, tail length asthma 2014 movie soundtrack buy generic singulair 10 mg, head circumference and length (0 asthma night cough singulair 4mg free shipping,9 asthma nos definition cheap 4mg singulair fast delivery, P0 asthmatic bronchitis with acute exacerbation order 4mg singulair with mastercard,05) chronic asthmatic bronchitis icd 10 cheap singulair 4 mg without a prescription. The results obtained showed that the correlation between corporal and testicular biometrics and seminal characteristics could be predictive criteria for seminal quality of wild felids. In addition, testicle size showed an important correlation with sperm concentration and plasmatic membrane structural integrity. Therefore, the obtained results contribute to a better understanding of the wild male felids. Four days after hormone administration, ovaries were recovered, and all visible follicles with a 3­6 mm diameter were aspirated for the oocyte recovery using a 21 G needle attached to a 5. After, oocytes were denuded and assessed for the presence of first polar body using a stereomicroscope. Then, oocytes were stained with Hoechst 33342 (10 g/mL) for 15 min and visualized with a fluorescent microscope for identification of nuclear status in second metaphase. All data were expressed as mean ± standard error and analysed by the chi-square test (P < 0. A total of 172 follicles were aspirated after four sessions of ovarian stimulation. Several studies report the role of leptin in maintenance of normal reproductive function, regulating folliculogenesis, oogenesis and estrous cycle. The aim of this study was to investigate immunolocalization of leptin receptors (Ob-R) in the ovary of galea spixii. The sections were photomicrographed and color intensity of the reaction was measured. In order to quantify the intensity of the positive reactions of each ovary structure, three sections were selected for each structure and analyzed by three independent observers, following the criteria: absence (1), weak (2), moderate (3), strong (4) and very strong (5). Strong immunoreaction was observed in oocyte and theca cells, moderate in ovarian stromal cells and large luteal cells and weak stained in granulosa, endothelial, perivascular and small luteal cells. When compared to receptor expression along follicular development it was observed that the oocyte and the theca cells remained with expression at the same intensity. However, the granulosa cells showed strong stained in the preantral stages, whereas in the antral follicles it expressed low intensity. Thus, the presence of leptin receptor in the main structures of ovary suggest that this hormone acts fundamental role in the reproduction of this species. Morphological characterization of the female and male reproductive system of the ocelot (Leopardus pardalis): Preliminary data L. This specie is widely studied as to its conservation, but it lacks studies on its morphology. Thus, this study aimed to describe the morphology of male and female reproductive systems of ocelot in order to obtain more information, which may be useful for the reproductive management of this species. In the macroscopic description of the ocelot females, the findings showed that the ovaries are pairs and are located dorsally in the sub lumbar region and caudally to the kidneys. When longitudinally sectioned, we can observe the functional structures of the ovaries, composed of the medullary region, stromal rich in blood vessels and external parenchymal region, surrounded by tunica albuginea. The uterine tubes, which are also pairs, perform the communication between the ovaries and the uterus. The uterus is bicornuated, in which the uterine horns extend into the abdominal cavity reaching the ovary sac and being suspended by the suspending ligament of the uterus. The uterine body has small dimensions and is followed by the cervix, which is composed of a thick wall of smooth musculature. The uterine cervix performs the communication between the uterus and the vagina which is composed of circular thick muscle fibers that make up the longitudinal folds. In males, the scrotum is located in the perineal region as an extension of the abdominal epithelium, in the form of a membranous pouch divided by a median septum, which separates the two testicles that are rounded ovoid, with concave lateral border and another medial straight. Covered by a thin serous membrane and located at the middle edges of the testicles are the epididymis, extending from the cranial end to the caudal, formed by head, body and tail. The head of the epididymis, the most prominent portion of the structure, is located in the cranial portion of the gonad, firmly attached to the vaginal tunica. The prostate is composed of a large, irregularly shaped, compact mass located caudally to the urinary vesicle and cranially to the bulbourethral gland, which presents in two pairs with rounded conformation, located dorsolaterally to the pelvic urethra and caudally to the prostate. The foreskin is thick and covered by hairs, with its ventrally turned orifice, through which urine and semen are ejected. From a cross section can be observed their cavernous bodies that are surrounded by tunica albuginea, erectile tissue and deep artery. The microscopic findings of the organs composing the male and female reproductive systems of ocelot are being analyzed and will be presented later. Profile of the ejaculate of a Jaguarundi through the pharmacological ejaculation and urethral catheterization K. Cunha3 1 Department of Animal Reproduction and Veterinary Obstetrics, School of Veterinay Medicine and Animal Science, Federal University of Bahia, Brazil; 2Zoo botanical Park Getulio Vargas, Salvador, Bahia, Brazil; 3Setor of diagnosis by image of the Veterinary Clinic of the Salvador University, Salvador, Bahia, Brazil. Electroejaculation is the most used method to obtain semen in felines but is a technique that requires special equipment and trained operator, besides stimulating the animal, requiring larger anesthetic doses. Pharmacological ejaculation with urethral catheterization is a safe alternative with no effect on sperm quality. This study evaluate the ejaculate profile of a Jaguarundi (Puma yagouaroundi) obtained through pharmacological ejaculation. The specimen was kept in captivity at the Zoo botanical Park Getulio Vargas (Salvador, Bahia), weighed 6,3 kg, was already in sexual maturity and received a diet based on beef and chicken, presenting no malnutrition or health problems. The animal was chemically restrained with a combination of 0,1mg/kg of medetomidine hydrochloride (1mg/ml Vetoquinol Orion Pharma, Group Orion, Italy. The prepuce and penis were washed with sterile saline solution and a sterile urethral tomcat catheter (13cm x 1mm, Provar Ltda, Sгo Paulo, Brazil) was introduced in the penile urethra until 7 cm, 20 after the pharmacological induction. Before the procedure, the prostate was digitally stimulated through the rectum and a 1 mL syringe was connected to the catheter and negative pressure was applied to increase suction. After the procedure, the anesthesia was reverted by administration of 0,25 mg/kg antipamezole (4,28 mg/ml, Vetoquinol Orion Pharma, Group Orion, Italy). To obtain the kinetics parameters, 5µL of diluted semen were evaluated under a microscope (100x magnification). The sperm concentration was accessed by counting the spermatozoa in a Neubauer chamber. The semen (5µL) was added in a 1:10 proportion solution of distilled deionized water and incubated at 37єC for 5 min. This solution was evaluated under a microscope and the reactive spermatozoa was calculated by counting the percentage of ones that whose flagella swelled and curled and diminishing by the percentage of the sperms that presented curled tails in the morphological test. The diluted semen was fixed in buffered saline formal and the stained smear was evaluated for its morphology under phase-contrast microscopy (1000x magnification). The urethral catheterization after medetomidine and ketamine administration is an efficient inducer of ejaculation in Jaguarundi; the sample obtained had no quality change and was not contamined with urine. Semen collection in a captive margay (Leopardus wiedii) by urethral catheterization after pharmacological induction R. Pharmacological induction for semen collection comes as an alternative to electroejaculation due to its simpler and effective protocol. This method does not require highly specialized equipment or trained operator and reduces the risk of urine contamination in comparison to the electroejaculation. Studies contemplating this method for the margay (Leopardus wiedii) were not found in the literature. The species exemplar was a male captive adult who was a sexual mature animal and showed no malnutrition or health issues signs. The animal was chemically restrained with a combination of 0,1mg/kg of medetomidine hydrochloride (1mg/ml Vetoquinol Orion Pharma, Group Orion, Italia. The prepuce and penis were washed with sterile saline solution and a sterile urethral tomcat catheter (13mm x 1mm, with front opening only, Provar Ltda, Sгo Paulo, Brazil) was introduced in the penile urethra until 7 cm. A 1 mL syringe was connected to the catheter and negative pressure was applied to increase suction. After the procedure, the anesthesia was reverted by administration of 0,25 mg/kg antipamezole (4,28 mg/ml, Vetoquinol Orion Pharma, Group Orion, Italia). To obtain the parameters of sample kinetics, 5µL of diluted semen were evaluated under a microscope (100x magnification). An aliquot of this solution was evaluated under a microscope and the reactive spermatozoa was calculated by counting the percentage of ones that whose flagella swelled and curled and diminishing by the percentage of the spermatozoa that presented curled tails in the morphological test. One hundred cells were counted and classified individually as normal, major defects or minor defects. The animal was successfully anesthetized and through this technique, it was possible to collect the sperm sample with adequate quality, therefore this methodology did not affect it. Therefore, the urethral catheterization post anesthesia induction with medetomidine and ketamine combined is a practical and effective protocol for sperm collection that can be used in a Leopardus wiedii as it has been used with others wild felines. Vaginal microbiota at the different phases of the estrus cycle in Dasyprocta prymnolopha Wagler, 1831 A. Menezes1,4 Post-graduation Program in Veterinary Medicine, Federal University of Campina Grande, Health Center and Rural Technology, Patos, Paraнba, Brazil; 2Academic Unit of Veterinary Medicine of the Federal University of Campina Grande, Health Center and Rural Technology, Patos, Paraнba, Brazil; 3Department of Veterinary Medicine, Federal Rural University of Pernambuco, Recife, Pernambuco, Brazil; 4Department of Morphology of the Federal University of Rio Grande do Norte, Natal, Rio Grande do Norte, Brazil. During the estrus cycle, several populations of microorganisms present enzymes that allow them to prepare for survival and multiplication in the vaginal environment. The increase in glycogen that occurs at some phases of the reproductive cycle favors the predominance of acidophil organisms among the heterogeneous group that forms the normal vaginal flora6. Knowledge of the diseases that affect the reproductive system of wild animals can contribute to control of reproductive disorders and help in the implementation of reproductive management programs, by selecting fertile animals for mating, gamete freeze drying and artificial insemination14. There is very little information on health management of the most frequent diseases, that can damage health in captivity8 therefore knowing the microbiological dynamic in healthy situations may help in the identification, treatment and control of such reproductive pathologies, potentializing the productivity of these captive animals. The objective of the present study was to identify and characterize the prevalence of bacteria existing in the vagina of agouti (Dasyprocta prymnolopha) in the different phases of the estrus cycle. Two complete estrus cycles were followed in a total of 12 healthy females of the species, where, by cytological collections with sterile swabs, samples were replicated in culture media and then the colonies were identified by carbohydrate battery. A high variety of colonies was obtained, with bacteria with considerable pathogenic potential among some bacteria common to various mammal species. Among the phases of the estrus cycle analyzed, only in the material collected in the metaestrus were was not verified absence of growth of bacteria colonies of the females analyzed. The Estrus and proestrus presented the highest percentage of absence of growth of bacteria colonies of the collections made. It was concluded that knowledge of the microbiota in the reproductive system of wild animals can favor early diagnosis of reproductive pathologies, potentializing all the productive and conservationist process of the species, as for example the agouti. Bowers regarding the efficacy and appropriateness of sex reassignment surgery as a medically necessary treatment for gender dysphoria (May 7, 2016) Appx1Appx47 Appx48Appx51 Appx52Appx55 Appx56Appx68 Appx69Appx70 Appx71Appx109 Appx110Appx115 Appx116Appx123 Appx124Appx128 Appx129Appx139 Pages 48 through 70, containing the regulation at issue, 38 C. Department of Veterans Affairs Letter from Members of Congress (June 22, 2016) Letter from Michael P. Department of Veterans Affairs (July 29, 2016) Letter from Members of Congress to Secretary Robert A. Increased understanding of both gender dysphoria and surgical techniques 1n this area has improved significantly and is now widely accepted as medically necessary treatment. Increased understanding of both gender dysphoria and surgical technfques in this area has improved significantly and is now widely accepted as medically necessary treatment. Increased understanding of both gender dysphoria and surgical techniques in this area has improved significantly and is now widely accepted as medically necessary treatment. Angela Prudhomme, Congressional Relations Officer, at (202) 461-6471 or by email at Angela. Effective: January 19, 2017 Currentness (a) Subject to paragraphs (b) and (c) of this section, the following hospital, outpatient, and extended care services constitute the "medical benefits package" (basic care and preventive care): (1) Basic care. Care referred to in the "medical benefits package" will be provided to individuals only if it is determined by appropriate healthcare professionals that the care is needed to promote, preserve, or restore the health of the individual and is in accord with generally accepted standards of medical practice. Care is deemed to promote health if the care will enhance the quality of life or daily functional level of the veteran, identify a predisposition for development of a condition or early onset of disease which can be partly or totally ameliorated by monitoring or early diagnosis and treatment, and prevent future disease. Care is deemed to preserve health if the care will maintain the current quality of life or daily functional level of the veteran, prevent the progression of disease, cure disease, or extend life span. Care is deemed to restore health if the care will restore the quality of life or daily functional level that has been lost due to illness or injury. This exclusion does not apply to veterans who are released from incarceration in a prison or jail into a temporary housing program (such as a community residential re-entry center or halfway house). Gender refers to the behavioral, cultural, or psychological traits that a society associates with male and female sex. Where there are questions or concerns related to room assignments, an ethics consultation may be requested. The Office of Patient Care Services (10P4) is responsible for the contents of this Directive. Questions related to medical care may be referred to Specialty Care Services (10P4E) at (202) 461-7120. Questions related to mental health care may be referred to the Office of Mental Health Services (10P4M) at (202) 461-7310. Intersex individuals may or may not have interest in changing gender or in acting in ways that are discordant with their assigned gender. Sex refers to the classification of individuals as female or male on the basis of their reproductive organs and functions. Transgender is a term used to describe people whose gender identity (sense of themselves as male or female) or gender expression differs from that usually associated with their sex assigned at birth. Male-to-female (MtF) transsexuals are a subset of transgender individuals who are male sex at birth but self-identify as female and often take steps to socially or medically transition to female, including feminizing hormone therapy, electrolysis, and surgeries. Female-to-male (FtM) transsexuals are a subset of transgender individuals who are female sex at birth but self-identify as male and often take steps to socially or medically transition to male, including masculinizing hormone therapy and surgeries. Sex reassignment surgery includes any of a variety of surgical procedures (including vaginoplasty and breast augmentation in MtF transsexuals and mastectomy and phalloplasty in FtM transsexuals) done simultaneously or sequentially with the explicit goal of transitioning from one sex to another. Intersex individuals are born with reproductive or sexual anatomy and/or chromosome pattern that do not seem to fit typical definitions of male or female. People with intersex conditions are often assigned male or female gender by others at birth. Medical Facility Director, Chief of Staff, and Associate Director for Patient Care Services or Nurse Executive. Appx57 Case: 17-1460 Document: 126 Page: 61 Filed: 01/03/2018 (a) Patients will be addressed and referred to based on their self-identified gender. Room assignments and access to any facilities for which gender is normally a consideration. For example, a MtF patient over the age of 50 may be offered breast cancer screening and may wish to discuss the benefits and harms of prostate cancer screening with her provider. A FtM transsexual patient may be offered screening for breast and cervical cancer. The prevalence of transgender individuals is not known in general or in the Veteran population. This agenda includes appropriate data gathering on sexual orientation and gender identity in public health research tools and electronic health records. Based on these data, the estimated prevalence of Male-to-Female (MtF) to Female-toMale (FtM) transsexual individuals is approximately 3:1 in the general population. This prevalence ratio is likely to be higher in the predominantly male Veteran population. It is important to note that FtM transsexual individuals are also part of the Veteran population. Intersex Veterans, that is, individuals who are born with reproductive or sexual anatomy and/or chromosome pattern that do not seem to fit typical definitions of male or female, may or may not identify as transgender. The term "transgender" refers to gender identity or the sense of oneself as male, female, or other. The terms "gay" (in the case of men) and "lesbian" (in the case of women) refer to sexual orientation. The sexual orientation of gay and lesbian persons is attraction to the same gender whereas heterosexual persons are attracted to the opposite gender. A transgender Veteran may identify as heterosexual ("straight"), gay, lesbian, bisexual. For example, an individual may be assigned the physical status of "female" at birth and identify as female throughout her lifetime, with or without knowledge of an intersex condition. Some intersex persons with male chromosomes who have been assigned female become gender dysphoric even without knowing that they were "reassigned" at, or near, birth. Knowing someone has an intersex condition gives you no information about their gender identity or sexual orientation. Sex reassignment surgery includes any of a variety of surgical procedures done simultaneously or sequentially with the explicit goal of transitioning from one gender to another. This term includes surgical revision of a previous sex reassignment surgery for cosmetic purposes. For all treatments and procedures, informed consent and shared decision-making needs to be the basis for individualized care that weighs the possible benefits and harms, with an emphasis on the lowest (safest) dose to achieve benefits. The goal of cross-sex hormone therapy in treatment of MtF transgender patients is to suppress testosterone levels and introduce estrogen to achieve a pre-menopausal female hormonal range. The effects are decreased facial and body hair, redistribution of fat, breast development and prostate and testicular atrophy. Risks include venous thromboembolism, liver dysfunction, hypertension, and cardiovascular disease. As with any medical therapy, benefits Appx62 Case: 17-1460 Document: 126 Page: 66 Filed: 01/03/2018 and harms of treatment need individualization using principles of shared decision-making, with an emphasis upon the lowest (safest) dose to achieve benefits. The effects are increased facial and body hair and muscle, acne, permanent deepening of the voice, cessation of menses, redistribution of fat mass, and clitoral enlargement. Risks include hypertension, erythrocytosis, liver dysfunction, lipid changes, weight gain, and sodium retention.

Nutrition education improves metabolic outcomes among older adults with diabetes mellitus: results from a randomized controlled trial asthma treatment canada purchase singulair 4 mg with mastercard. Sigal1 asthma symptoms green mucus purchase singulair 5 mg mastercard,2 asthma definition 1 generic singulair 10mg without prescription,3 1 2 Ottawa Hospital Research Institute asthmatic bronchitis pictures cheap singulair 5 mg with visa, University of Ottawa asthma definition que cheap singulair 4mg without a prescription, Ottawa asthma symptoms 4 days singulair 4mg online, Ontario asthma symptoms running singulair 10mg overnight delivery, Canada Faculty of Health Sciences asthma treatment in hospital singulair 5mg with amex, University of Ottawa, Ottawa, Ontario, Canada 3 Faculties of Medicine and Kinesiology, University of Calgary, Calgary, Alberta, Canada · Regular exercise increases insulin sensitivity in both individuals with and without diabetes. Glucose production and glucose disposal increase in parallel in order to maintain blood glucose homeostasis. To maximize the impact of lifestyle measures on glycemic control, combined aerobic and resistance exercise is more effective than either type of exercise alone. Eventually, a shift in the fuels being used to supply the energy demands of activity is seen as the oxidative metabolic system becomes more efficient. In general, changes become more noticeable when training is of higher volume and intensity. Types of exercise training and their effects on healthy individuals Aerobic exercise Effects of regular aerobic exercise training Regular aerobic training generally leads to improved lung function and cardiac output, allowing for the provision of more oxygen for working muscles. Fuel metabolism during acute aerobic exercise During the first 5­10 minutes of exercise, muscle glycogen is the main source of energy. As exercise continues, the bloodborne substrates, glucose and non-esterified fatty acids become increasingly important. If exercise of moderate intensity continues for several hours, the contribution of glucose diminishes and nonesterified fatty acids become the major fuel (Figure 23. During moderate intensity aerobic exercise, blood glucose levels remain virtually unchanged. Insulin secretion is reduced while the release of glucagon is promoted, encouraging a two- to fourfold increase in hepatic glucose production (controlled by the glucagon: insulin molar ratio at the portal vein) [3] to meet the needs of the exercising muscle. Glucose production and utilization fall rapidly and in parallel to baseline during the post- 358 Lifestyle Issues: Exercise Chapter 23 Table 23. If performed with sufficient intensity and frequency this type of exercise increases cardiorespiratory fitness. Anaerobic exercise Short, high intensity exercise involving anaerobic energy-producing systems. Resistance exercise involves the use of muscular strength to work against a resistive load or move a weight. Some studies have found that serum triglyceride levels decline after training [7,8]. During recovery from very intense exercise, hyperglycemia often occurs in fit individuals without diabetes, as glucose utilization decreases more quickly than glucose production [10­ 12]. In response to the hyperglycemia, plasma insulin levels increase and glycemia is restored to baseline within about 45 minutes. If moderate intensity aerobic exercise lasts for several hours without caloric intake, hepatic glucose production can no longer keep pace with increased utilization, and the blood glucose level begins to decline, eventually resulting in hypoglycemia [4]. Effects of regular training on fuel metabolism Aerobically trained athletes without diabetes have low fasting plasma insulin levels and reduced insulin responses to a glucose challenge in the face of normal glucose tolerance, and increased insulin-mediated glucose uptake under glucose clamp conditions [5]. Physical training is also known to increase muscle and hepatic 359 Part 5 Managing the Patient with Diabetes Resistance exercise Effects of regular resistance exercise training Declines in muscle strength of approximately 12­15% per decade have been reported after the age of 50 years [13,14], with muscle mass decreasing as much as 6% per decade [5,16]. With regular heavy resistance training, increases of greater than 30% in muscle strength [15,17] and gains in muscle mass ranging from 3 to 12% [18,19] have been found within the first couple of months of training, with relative increases typically being higher in elderly subjects [16,18]. Initial strength gains during the first 6 weeks are generally as a result of peripheral nervous system adaptations (improved muscle recruitment) and are not accompanied by muscle hypertrophy. Resistance training can be of additional benefit to older adults as improvements in postural stability and dynamic balance may decrease the risk of fall-related injuries [20]. When muscles are forced to perform for a given period of time at or near their maximal strength and endurance capacity (either by lifting weights or working against some other form of resistance), it will result in an increase in muscle strength, endurance and hypertrophy. Performing more repetitions (up to 2 minutes per set of each exercise) with lower resistance tends to increase endurance, while lifting heavier weights for fewer repetitions will favor strength gains [21]. During such exercise, adequate rest periods (2­5 minutes) between sets are necessary to allow regeneration of phosphocreatine stores. Glycolytic anaerobic energy production (with concomitant blood lactate accumulation) becomes more important as intensity decreases, the number of repetitions per set increases, and rest periods between sets become shorter [22]. Where multiple sets are performed, longer sets and shorter rest periods between sets are associated with greater increases in blood lactate (which can reduce muscle contractility) and declines in muscle glycogen [23,24]. The risk of microvascular complications varied inversely with self-reported activity levels at baseline. Sedentary male patients were three times more likely to die than the active ones after adjusting for age, body mass index, smoking and diabetic complications (Figure 23. A similar, although statistically non-significant, relationship was also seen in females. Women with diabetes in the study with low levels of leisure time physical activity tended to have poor glycemic control when compared with those with higher activity levels. Estimates of insulin sensitivity were also higher among more active men and women [29]. More recently, a randomized trial showed that the onset of diabetic peripheral neuropathy can be prevented and its progression delayed over a 4-year period by regular exercise [26]. Hyperinsulinemia and hypoglycemia may occur when the peak action of a short-acting insulin analog (1), conventional soluble (regular) insulin (2) or intermediate-acting insulin (3) occurs during exercise, or if exercise itself accelerates the absorption from the injection site (4). Steady-state but elevated plasma insulin concentrations may occur if intermediate or long-acting insulin has been injected a few hours before exercise, or if the patient is using an insulin pump (5). Declining levels (6) or hypoinsulinemia (7) occur when the previous injection depots are exhausted. Hyperinsulinemia Plasma insulin concentration 4 3 5 Therapeutic range of insulin 2 1 6 7 Subject without diabetes Hypoinsulinemia Exercise Time injections, and the timing of the previous insulin injection and meal relative to the exercise can all affect the response of an individual with diabetes to physical activity (Figure 23. Accordingly, blood glucose concentrations can decline (the most common response in moderate aerobic exercise), increase (particularly in very intense exercise) or remain unchanged (Table 23. Insulin attenuates the appropriate rise in hepatic glucose production and further accelerates the exerciseinduced stimulation of glucose uptake into the contracting muscle. Regular insulin injected a few hours previously may exert its peak action during exercise. This effect is exaggerated if the previously injected limb is exercised, as insulin absorption is accelerated by exercise [30]. Moreover, the use of intermediate or long-acting insulin generally produces higher peripheral insulin levels than would be found in an individual without diabetes of similar body composition. The result is often hypoglycemia, unless the insulin dose prior to exercise is decreased or extra carbohydrate is consumed. Hyperinsulinemia can also prevent the normal increase in lipid mobilization during exercise, leading to reduced availability of non-esterified fatty acids as a fuel. Conversely, if insulin levels are too low, the inhibitory effect of insulin on hepatic glucose production and its stimulatory effect on glucose uptake are both reduced. In addition, the counterregulatory response (catecholamines, glucagon, growth hormone, cortisol) to exercise is higher than normal under conditions of insulin deficiency [30]. The overall result is markedly increased hepatic glucose production and diminished glucose utilization by the exercising muscle, thus leading to hyperglycemia. While some studies have demonstrated improvements, albeit not statistically significant, in blood glucose control as measured by decreases in HbA1c [33,34], most studies have either not shown any changes [35] or have produced increases in HbA1c [36]. The main reason for this is probably excessive reductions of insulin dose or disproportionate carbohydrate consumption before exercise in an effort to avoid hypoglycemia. It is important to note 361 Part 5 Managing the Patient with Diabetes Breakfast Snack S A Humalog Soluble insulin 250 200 150 100 Serum insulin (pmol/L) 50 * * Exercise 0 250 200 150 100 50 Exercise 0 ­30 0 60 120 Time (min) 180 240 * * Figure 23. Serum insulin concentrations during early exercise are higher after injection of the lispro (Humalog) insulin analog (A) than after conventional soluble insulin (S), whereas the opposite situation applies during delayed exercise. Soluble insulin was injected 30-min and lispro insulin 5-min after breakfast, and exercise was started either 40-min (early) or 180-min (late) after breakfast. If the rate of glucose appearance in the system is not high enough to supply the demand, blood glucose levels will drop, thereby increasing the potential for hypoglycemia [39]. Levels of insulinemia and glycemia will also affect the fuels used during aerobic activity. Hyperinsulinemia can lead to a greater reliance on exogenous glucose utilization during moderate aerobic exercise, without sparing glycogen stores [41]. In a study where insulinemia was kept constant, the contribution of carbohydrates to overall energy metabolism during exercise was greater in hyperglycemia than in euglycemia [38]. The shift towards greater carbohydrate metabolism during exercise in hyperglycemia was accompanied by a blunted cortisol and growth hormone response. Insulin, glucagon and catecholamine levels were comparable between conditions [38]. After prolonged exercise, patients may be prone to hypoglycemia for many hours, even extending overnight and to the following day. This can be explained by persistently enhanced glucose uptake by the exercised muscles to replenish the depleted glycogen stores [43]; however, after certain types of prolonged exercise, such as a marathon run, increased lipid oxidation can persist, as occurs in healthy individuals [44]. In this case, the use of glucose as a fuel and insulin sensitivity are reduced after exercise, thereby decreasing the risk of post-exercise hypoglycemia [44]. It should also be noted that individuals who experience frequent bouts of hypoglycemia (whether exerciserelated or not), may have further blunting of counter-regulatory responses to exercise, potentially creating a vicious cycle of hypoglycemic events [46­50]. Conversely, if the levels of circulating insulin are too high, muscle, adipose and hepatic cells will continue to take up glucose for 362 Lifestyle Issues: Exercise Chapter 23 of control to be able to participate effectively in competitive sports and high intensity activities, to avoid the fear of hypoglycemia during exercise. Whether or not this affects their physical and metabolic adaptations to these types of activities requires further research. More details on carbohydrate and insulin adjustments for exercise can be found later in this chapter. Fuel selection during high intensity exercise Extremely strenuous acute exercise may cause hyperglycemia even in the presence of normal or high insulin levels. High counter-regulatory hormone action (especially catecholamines) can stimulate glucose production beyond the limits of peripheral utilization [52­56]. Augmented lipid mobilization and ketogenesis in the liver increase blood ketone-body concentrations; the hypoinsulinemic individuals may thus become hyperketonemic and ketonuric after exercise. Several recent studies have shown that such high intensity exercise is effective in increasing blood glucose levels and thereby delaying or preventing hypoglycemia related to moderate exercise even when performed in extremely short bouts [57­61]. The one study completed to date involved a cross-over design with 10 weeks of heavy resistance exercise three times a week followed by a 6-week period with no resistance training, or vice versa [63]. Serum cholesterol and self-monitored glucose levels were also lower at the end of the resistance training period. While both groups showed decreases in waist circumference, reduced insulin dosage and lower selfmonitored blood glucose after the training period, these variables only reached significance in the aerobically trained group. However, HbA1c levels showed a statistically significant increase in the aerobic training group (from 8. Outcomes of these studies were generally positive, with benefits including lower HbA1c [65,67], decreased blood pressure [65,66], improved nerve conduction [65], higher cardiorespiratory fitness [67], greater muscular strength [67], higher lean body mass [65,67] and improvements in lipid profiles [67]. Resistance exercise in individuals without diabetes produces elevated epinephrine levels, which enhance hepatic glucose production, resulting in an increase in blood glucose levels [68]. After adjustment for confounding variables, participants who exercised the most had a 25­60% lower risk of subsequent diabetes compared to those who were most sedentary. This was true regardless of the presence or absence of additional risk factors for diabetes such as hypertension, parental history of diabetes and obesity in most studies. Comparable magnitudes of risk reduction are seen with walking compared to more vigorous activity when total energy expenditures are similar [77]. Among those attending a 5-year follow-up examination, 21% of the control participants (those who had declined the intervention) had developed diabetes, compared to only 11% of those receiving the intervention. They found that, 14 years after the end of the trial, incidence of diabetes remained significantly lower in those originally randomized to one of the intervention groups versus controls. Patients in the control group had one meeting per year with a physician and dietitian, at which they received standard advice on diet and exercise. The intervention group received individualized exercise plans, thrice-weekly supervised facility-based aerobic and resistance exercise, and seven 1-hour meetings with a dietitian focusing on weight reduction, reduced fat intake and reduced total caloric intake. At 4 years, 22% of the control group and only 10% of the intervention group had developed diabetes ­ a 58% risk reduction. Three years after the end of the study, participants originally randomized to the intervention group continued to have much higher levels of physical activity than those originally in the control group [90]. Incidence of diabetes in the individuals who were previously in the intervention group remained 43% lower than in those who were previously in the control group [90]. The goals of the lifestyle modification program included a 7% weight loss and at least 150 minutes of exercise per week. The lifestyle intervention included 16 lessons in the first 24 weeks, covering diet, exercise and behavior modification (delivered one-on-one by a case manager). A minimum of two supervised exercise sessions per week and at least monthly contact with the study personnel were maintained thereafter. Increased physical activity was a significant predictor of weight loss and had an important role in weight maintenance. In addition, participants who met the goal of more than 150 minutes of moderate exercise per week had a 46% reduction in diabetes risk. A 10-year follow-up of a large prospective cohort study including 347 individuals with diabetes and 1317 individuals without diabetes) found that the lowest aged-adjusted allcause death rate was among those with diabetes who walked a mile or more daily [91]. Similarly, a prospective study of 1263 men with diabetes followed over 12 years found that, compared with the least fit men (bottom 20% as determined by maximal treadmill testing), those with moderate cardiorespiratory fitness had a 60% lower risk of cardiovascular and overall mortality [79]. The effect of fitness on mortality was considerably greater than the effect of body mass index. Greater habitual exercise was also associated with a lower subsequent risk of cardiovascular disease among women in the Nurses Health Study [94]. Effects of regular aerobic exercise training in type 2 diabetes Exercise-induced stimulation of glucose uptake may involve many factors (Figure 23. Decreases in visceral fat result in decreased concentrations of tumor necrosis factor [105] and free fatty acids [106], leading to decreased insulin resistance. Inflammatory markers present in the bloodstream predict the onset of cardiovascular disease and related complications. For instance, in elderly patients with relatively advanced atherosclerosis, exercise training may be less effective in retarding atherogenesis [113]. The prophylactic value of exercise against atherosclerosis might be greater in younger healthier individuals who have not yet developed disease. During moderate intensity exercise, peripheral glucose uptake usually rises more than hepatic glucose production, and the blood glucose concentration tends to decline [116]. It has been shown that moderate intensity exercise decreases glycogen content similarly in individuals with and without diabetes [118]; however, glycogen and plasma glucose decreases more in obese individuals with diabetes compared with those without diabetes whether obese or lean [118]. The effects of moderate exercise on glucose tolerance and insulin sensitivity are similar whether the activity is performed in single versus multiple bouts of the same total duration [119]. Moderate aerobic exercise has also been shown to attenuate the increase in circulating triglyceride levels following ingestion of a high fat meal [120]. Resistance exercise Effects of regular resistance exercise training in type 2 diabetes the age-related decline of muscle mass may cause reduced insulin sensitivity. Resistance training has been shown to improve insulin sensitivity and glucose metabolism in both men and women [124­130] and has also been associated with modest improvements in lipid profiles [63,67,128]. In longitudinal 366 Lifestyle Issues: Exercise Chapter 23 studies involving healthy untrained adults, insulin responses to an oral glucose challenge are lower in both healthy younger [124,131] and older [131,132] individuals after resistance training. Resistance exercise, and its resulting increase in lean body mass, has also been associated with greater resting energy expenditure in older adults [133]. Overall, participants in exercise intervention groups had HbA1c levels that were 0. Post-intervention body weight did not differ between exercise and control participants, suggesting that exercise is beneficial in its own right, not merely as an avenue to reduce body weight. Snowling & Hopkins [137] found in a more recent meta-analysis that the two types of exercise had similar effects on glucose control. Participants (aged 60­70 years) were randomized into an exercising intervention group (three times per week) or a nonexercising control group for 1 year. The exercise group showed a significant decrease in body mass index, fasting glucose, HbA1c and improved lipid profile. In addition, those in the exercise group using medication showed a decreasing trend in medication use whereas the control group showed an increasing trend. Intervention groups performed exercise three times per week for 6 months in community facilities, supervised by personal trainers. Improvements in glycemic control were found in all exercise groups, and the improvements in the combined aerobic and resistance exercise group were significantly greater than with either aerobic training or resistance training alone. In contrast to this, a smaller study with participants randomized to combined exercise, aerobic exercise or non-exercise control did not find significant differences between the two exercising groups [141]. The group receiving the combined aerobic and resistance exercise training had significantly more favorable results for glycemic control, lipids, body composition, blood pressure and estimated cardiovascular risk than the group receiving exercise counseling alone. All three exercise modalities showed clinically significant reductions in HbA1c, while the combined training showed an additive and large beneficial effect on insulin sensitivity. Study outcomes have been consistent, showing increases in aerobic fitness and muscular fitness [114,115,134] as well as improvements in body composition [139,140] and cardiovascular disease risk profile [19,114,115,139,140]. Exercise does not need to be strenuous, and even regular walking has beneficial effects [79,94]. Specific recommendations and guidelines for exercise in individuals with diabetes have been published by the American Diabetes Association [143,144] and the American College of Sports Medicine [145]. Advice should be tailored to individuals, taking 367 Part 5 Managing the Patient with Diabetes No. Resistance component consisted of 3 sets of 10­15 reps Control group: No significant change from baseline Intervention group: 8. Aerobic training Reference Frequency Intensity Duration Resistance training Frequency No. Relative contraindications · If receiving insulin treatment: sports in which hypoglycemia would be dangerous.

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Atypical small acinar proliferation in the prostate: clinical significance in 2006.

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