Discount glimepiride 4 mg visa
Evolving genetic research may offer a solution to diabetes mellitus book discount glimepiride master card the challenges of clinical development diabetic log printable purchase glimepiride online now. Genetic markers may make it possible to diabetes type 2 with hyperglycemia discount glimepiride online american express identify a patient population in advance and allow clinical trials with a smaller number of participants. Before a potential new treatment can be approved, it must be tested in clinical trials. It is often difficult to find patients to volunteer in clinical trials, and rare diseases pose an even greater challenge. Specific rare disease patient populations are very small, geographically dispersed and often include children. The biopharmaceutical sector is working with patient advocacy organizations to identify and advance better ways to connect patients to biopharmaceutical and academic researchers conducting clinical trials. Physicians and patients can find out about clinical trials being conducted all over the country in collaboration with local institutions by accessing Information on clinical trials and medicines in development is also available on While personalized medicine is just beginning to impact patients, the Personalized Medicine Coalition estimates that available personalized medicines, treatments and diagnostic products increased from 13 in 2006 to 72 by 2011. The sequencing of the human genome and the analysis of critical proteins in the blood have profoundly impacted biopharmaceutical research and are yielding important new tools for understanding and treating a wide range of conditions. These tools are proving critical for taking on rare diseases, which are often more complex than more common diseases. Researchers are increasingly able to identify much more targeted patient populations and this new knowledge is allowing clinicians to discover whether a patient is developing or will develop an illness much earlier. Rare Disease Facts and statistics Here are a few statistics and facts to illustrate the breadth of the rare disease challenge in the United States and worldwide. The designation makes the sponsor of the drug eligible for entitlements under the Orphan Drug Act of 1983. Anaplastic cancer accounts for only about 1 percent of all thyroid cancers and is a very rare disease. Symptoms include generalized weakness and wasting, which first affects the muscles of the hips, pelvic area, thighs and shoulders. The disease progresses slowly and with variability but can affect all voluntary muscles. Food and Drug Administration that is intended to expedite the development and review of drugs for serious or life-threatening conditions. The criteria for breakthrough therapy designation require preliminary clinical evidence that demonstrates the drug may have substantial improvement on at least one clinically significant endpoint over available therapy. Clostridium difficile-A bacterium that produces an irritating toxin that causes a form of colitis characterized by profuse, watery diar¬rhea with cramps and lowgrade fever. The cause of diabetes continues to be a mystery, although both genetics and environmental factors such as obesity and lack of exercise appear to play roles. It is estimated that 5 percent to 10 percent of Americans who are diagnosed with diabetes have type 1, which requires insulin treatment. Duchenne muscular dystrophy-An inherited disorder that involves rapidly worsening muscle weakness. Because of the way the disease is inherited, males are more likely to develop symptoms than are women. Fabry disease-A genetic metabolic disorder that causes build-up of certain lipids. It becomes clinically apparent in childhood and adolescence with fever, pain and small vascular tumors. It progresses to central nervous system disturbances and renal and cardiac failure in mid-life. Generally, determining factors include whether the drug will have an impact on such factors as survival, day-to-day functioning, or the likelihood that the disease, if left untreated, will progress from a less severe condition to a more serious one. Filling an unmet medical need is defined as providing a therapy where none exists or providing a therapy which may be potentially superior to existing therapy. The frequency of communication assures that questions and issues are resolved quickly, often leading to earlier drug approval and access by patients. The characteristic features of the fragile X syndrome in boys include prominent or long ears, a long face, delayed speech, large testes, hyperactivity, tactile defensiveness, gross motor delays, and autistic-like behaviors. Only about half of all females who carry the genetic mutation have symptoms themselves. Few fragile X girls have autistic symptoms, although they tend to be shy and quiet. The spinal cord becomes thinner and nerve cells lose some of their myelin sheath-the insular covering on all nerve cells that helps conduct nerve impulses. The condition, although rare, is the most prevalent inherited ataxia, affecting about 1 in every 50,000 people in the United States. The condition is characterized by blood that clots normally, but the clots are unstable, so bleeding recurs. Gaucher disease-An inherited disease caused by a lack or deficiency of an enzyme (glucocerebrosidase). The tumor grows so fast that it increases pressure in the brain, producing headaches, slowed thinking, and if severe enough, sleepiness and coma. Gliomas make up about 60 percent of all primary brain tumors and are frequently malignant. It is caused by low levels or improper functioning of a protein called C1 inhibitor, which affects the blood vessels. People with hereditary angioedema can develop rapid swelling of the hands, feet, limbs, face, intestinal tract, or airway (larynx or trachea). Hpv (human papillomavirus)-Viral agent of warts, believed to be contagious and usually harm-less, but it can lead to cervical cancer. Symptoms of hypophosphatasia in infants include poor feeding, failure to gain weight, failure to thrive, delayed development, loss of teeth, and bone pain. The reduced number of platelets may result in abnormal bleeding into the skin (purpura) and other parts of the body. The result is often muscle weakness, fa- tigue, and problems with the heart, eyes, and various other systems. Juvenile rheumatoid arthritis-Refers to arthritis or an arthritis-related condition (rheumatic disease) that occurs by age 15 or younger. A variety of other eye-related abnormalities including roving eye movements, deep-set eyes, and sensitivity to bright light also occur with this disease. Abnormally high uric acid levels can cause sodium urate crystals to form in the joints, kidneys, central nervous system, and other tissues of the body, leading to gout-like swelling in the joints and severe kidney problems. This leaves the patient highly susceptible to serious infections, anemia and bleeding episodes. B and T-cell lymphomas are caused by proliferation of the two principal types of white blood cells, called B- and T-lymphocytes. Mycosis fungoides is a type of lymphoma that primarily affects the skin of the buttocks, back or shoulders but can also occur in other sites. Mucositis can occur anywhere along the digestive tract from the mouth to the anus.
Purchase cheap glimepiride on-line
Note 2: There are two main methods of describing concentrations: by weight diabetic diet regimen purchase 1mg glimepiride otc, and by molecular count diabetes definition guidelines buy generic glimepiride pills. Code 1 2 7 8 9 Description Milligrams/deciliter (mg/dL) Micromoles/liter (umol/L) Test ordered metabolic disease symposium glimepiride 2mg low cost, results not in chart Not applicable: Information not collected for this case (If this item is required by your standard setter, use of code 8 will result in an edit error. However, code 7 when the physician statement of fibrosis score is not based on histologic examination of the liver. Information collected after the start of treatment may not be used to code this data item. Patients with primary sclerosing cholangitis are advised to receive neoadjuvant chemoradiation and liver transplantation. Periductal infiltrating type (20%): spreads along the duct in a diffuse manner that may be associated with poorer prognosis. The periductal infiltrating type of cholangiocarcinoma demonstrates a diffuse longitudinal growth pattern along the bile duct. Coding Instructions and Codes Note: A schema discriminator is used to discriminate for primary site C240 (extrahepatic bile ducts) for the subsite in which the tumor arose. Their presence in the same or different lobes of lung from the primary tumor affects the T and M categories. Coding guidelines Record the presence of separate tumor nodules within the same ipsilateral lobe and/or different lobes of the same lung which are considered a single primary. Histology may be determined clinically (presumed to be the same based on imaging or physician judgement) or microscopically confirmed. They are · · · second primary tumors, also called synchronous primary tumors (not the same histology as the primary tumor) multifocal lung adenocarcinoma with ground glass/lepidic features diffuse pneumonic adenocarcinoma Note 5: "Synchronous" describes the appearance in time compared to the primary tumor. If separate nodules are described as "metachronous," the nodules may be evidence of progression of disease in which case they would not be coded here. Note 6: If there are multiple tumor nodules or foci and the terminology used is not readily identifiable as one of the situations described in Note 4, consult with the pathologist or clinician. Note 7: Code 0 if relevant imaging or resection is performed and there is no mention of separate tumor nodules. Definition Invasion of one or more layers of the pleura covering the lung (visceral pleura), such as invasion beyond the elastic layer of the pleura. Elastic stains may also be helpful in cases where the visceral and parietal pleura are adherent, making it difficult to identify the boundary between the visceral pleural surface and the parietal pleura. Do not code separate pleural tumor foci or nodules in this field (discontinuous pleural metastasis). Note 3: If imaging indicates a pleural effusion but pleural fluid cytology is described as negative for malignant cells, assign code 1. Record the percentage value of tumor necrosis post neo-adjuvant chemotherapy as stated by the pathologist in the pathology report. This field does not include distant or discontinuous metastases to the skeletal system. Do not record secondary or acquired mutations that may have developed because of long-term imatinib treatment. These cells usually are found in the subcapsular nodal sinuses but may be seen within the nodal parenchyma. Definition Profound immune suppression may greatly increase the risk of developing Merkel cell carcinoma. Immune suppression may be deliberately induced with drugs, as in preparation for bone marrow or other organ transplantation, to prevent rejection of the donor tissue. Do not assume that a patient is immune suppressed just because the patient has one of the conditions listed below in the table. Note 3: Code 9 if conditions in the table below were not active within 2 years of (or resolved more than 2 years prior to) diagnosis, or if it is unknown when they existed. The tumor thickness (depth) is usually measured from the top of the tumor to the deepest tumor cells. If the tumor is ulcerated (the skin is broken), it is measured from the base of the ulcer to the deepest tumor cells. In the absence of this label, a measurement described as taken from the cut surface of the specimen may be coded. And in the absence of either of these labels, the third dimension in a statement of tumor size can be used to code this field. If the tumor is excised post-neoadjuvant treatment, tumor measurements cannot be compared before and after treatment to determine which would indicate the greater involvement. Measurement given in hundredths of millimeters should be rounded to the nearest tenth. Primary tumor ulceration has been shown to be a dominant independent prognostic factor, and if present, changes the pT stage from T1a to T1b, T2a to T2b, etc. Note 4: Code 9 if there is microscopic examination and there is no mention of ulceration. The lab value may be recorded in a lab report, history and physical, or clinical statement in the pathology report. The Allred Score is calculated by adding the Proportion Score and the Intensity Score, as defined in the tables below. The Allred score combines the percentage of positive cells (proportion score) and the intensity score of the reaction product in most of the carcinoma. Code 0 1 2 3 4 7 8 9 Description Negative (Score 0) Negative (Score 1+) Equivocal (Score 2+) Stated as equivocal Positive (Score 3+) Stated as positive Stated as negative, but score not stated Test ordered, results not in chart Not applicable: Information not collected for this case (If this item is required by your standard setter, use of code 8 will result in an edit error. Note 7: If the test results are presented to the hundredth decimal, ignore the hundredth decimal. Recent studies indicate that these tests may also be helpful in planning treatment and predicting recurrence in node positive women with small tumors. For the Breast cases, there are 2 data items that record information on Multigene testing. It tests a sample of the tumor (removed during a biopsy or surgery) for a group of 50 genes. Coding Instructions and Codes Note 1: Physician statement of the Multigene Signature Method can be used to code this data item. Note 3: Record only the results of an Oncotype Dx-Invasive recurrence score in this data item. Note 3: Record only the results of an Oncotype Dx Risk Level-Invasive in this data item. As of early 2017 there are no established standards for interpretation of results or for cutoffs for positive and negative. If the pathology report indicates that axillary nodes are positive, but size of the metastases is not stated, assume the metastases are greater than 0.
Glimepiride 1 mg lowest price
For its part diabetes insipidus natremia buy glimepiride 4 mg low price, Myriad provides a wide variety of payment options as noted on its "Reimbursement Assistance Program" website diabetes symptoms ketones discount glimepiride, both insurance-based and cash-based diabetes medications reference chart effective 4 mg glimepiride. Genetic testing and pharmacogenomics: issues for determining the impact of healthcare delivery and costs. A-31 of agreements and more consistent coverage and reimbursement have reduced the number of self-pay patients to single-digit percentages of its clientele. Myriad has established contracts or payment agreements with over 300 carriers and has received reimbursement from over 2500 health plans. The price comparison we made is compatible with a scenario in which Myriad, as a monopolist, maximizes its profit through price discrimination in which it charges the highest price to those women who most value the test. Myriad is not alone in building a dedicated testing facility around its gene patents. The target population is the general population rather than those with family history. The website now asks prospective customers to call for individualized pricing, but Steven Pinker reported it to be $99,000 in his January 2009 article in the New York Times Magazine. It changed this policy and decided to enforce its patent rights, and the policy change became public in July 2008 when it was widely covered in the Australian public media. The incentive to advertise the service and broaden the market is stronger for a monopoly provider than in a shared market because a monopolist will gain the full benefit of market expansion. In a competitive market, advertising may increase market share of a given provider, or it can expand the size of the market, but the expansion effect spills over to benefit competitors as well, and so the incentive to advertise is weaker. Once a market is saturated, a monopolist no longer gains from advertising to expand market (but may advertise for other reasons). For the same reason, communication and marketing incentives are also strong to educate health professionals who order the tests, because any increase in orders results in higher volume of testing for Myriad. Again, this increase is not shared with other providers; Myriad gets the full benefit of any market expansion. Myriad makes money off of any test, regardless of whether the person is actually at risk. Medical societies establish guidelines for their membership which, in turn, form the basis for payer coverage criteria. Insurers and other payers work not to reimburse for tests when patients do not meet clinical appropriateness criteria. The story was also covered in most of the major dailies in Melbourne, Sydney, Canberra, and elsewhere in Australia. The proposed new Board member declined to serve, leading to a proposal for an interim board appointment. The limited pre-test counseling resource is used to fulfill specific payer criteria for high-risk patients eligible for coverage and reimbursement. Low-risk candidates can clog the pre-test filters of counseling and coverage determination, occupying them with cases that would not ultimately lead to testing, or if tested, would not be reimbursed by third parties. In the context of breast cancer testing, Myriad has a strong incentive to "get the word out" about genetic testing for inherited risk of breast cancer. The social benefit from this incentive is more public knowledge of test availability. Building Genetic Medicine: Breast Cancer, Technology, and the Comparative Politics of Health Care. Genetic testing for breast and ovarian cancer susceptibility: evaluating direct-toconsumer marketing-Atlanta, Denver, Raleigh-Durham, and Seattle, 2003. They surveyed health professionals and consumers and assessed impact on health systems in the advertising market (Denver Kaiser Permanente) and in a comparison city (Detroit) and health system (Henry Ford) not exposed to the advertisements. There was no increase in actual testing among women with low risk in the population studied. Physician surveys showed a modest effect on physicians, with 3 percent reporting significant patient anxiety, 19 percent reporting significant increase in time spent explaining and another 23 percent a little extra time, and 7 percent reporting significant and 8 percent a little strain on the doctorpatient relationship. Consumers reporting "any anxiety" varied from 28 percent (low family risk) to 55 percent (high risk). Anxiety was most pronounced among Latina/Hispanic women (65 percent), and much more common in low-income (62 percent among those making less than $30,000) than high-income women (30 percent among those making over $80,000). Physicians were asked to assess the effect overall on their practice, and 6 percent were positive or very positive, 14 percent were negative or very negative, and 79 percent reported no effect. A comparison between the experience of physicians and women in Kaiser Permanente to other parts of the health system in Denver at the same time would have been immensely useful, as the Kaiser Permanente system is much more organized for genetic services than general medical care. The Mouchawar studies are illuminating as a "best case" of a health system prepared for a surge and with practice guidelines in place; it is very unlikely to represent the effects of the ad campaign elsewhere in Denver (or anywhere else) with a less organized and prepared genetic services program and with physicians less educated about how to triage testing. Impact of direct-to-consumer advertising for hereditary breast cancer testing on genetic services at a managed care organization: a naturally occurring experiment. Assessing controversial direct-toconsumer advertising for hereditary breast cancer testing: reactions from women and their physicians in a managed care organization. We have not found similar marketing campaigns launched by Myriad or other groups on behalf of other tests. The growing number of physicians ordering genetic tests, the greater availability of third party coverage, the accumulating experience in using genetic tests to manage hereditary cancer risk, and the greater consumer awareness about genetic testing all suggest the 2003 surveys may not predict current or future behavior. Moreover, the increasing conspicuousness and commercial interest in personal genomics may also change perceptions and behaviors. This benefits the company, but it also benefits patients to the degree it relieves them of the hassle and paperwork of dealing with health plans and insurers, and it benefits providers by relieving them of those duties as well as legal liability for test inaccuracies. The countervailing force here is that Myriad as a sole-source provider requires providers to send samples, track paperwork, and bill for services providers might otherwise handle at their own institution through internal billing and administrative procedures. Myriad Genetics Launches Awareness Advertising Campaign to Educate Women About Hereditary Risks of Breast and Ovarian Cancers. It thus appears there is some advantage to consolidating testing at a few laboratories that can attain sufficient volume to justify sunk costs in developing the test and resources to ensure quality and reduce legal liability for errors. Myriad would have grounds for infringement liability only if the invention (making and using the patented sequences and methods) were performed abroad in a jurisdiction where those activities are claimed in patents, and Myriad would have to sue in those jurisdictions. Laboratories in countries with diagnostic use exemptions would not face infringement liability. Regarding third-party payers, at least one study noted in the Lewin Group report showed that as of late 1995, "only 4% of insurance providers. The same study cited by the Lewin Group had two other findings of relevance to patented gene tests. Second, the proclivity to offer coverage was sharply dependent on cost: 25% were willing to cover it if the testing cost were $250, but only 14% would cover if the cost rose to $1,000 (it was $2400 at the time). Taken at face value, the figures imply that even if gene patents confer a premium of $750 this would only reduce the likelihood of third party coverage by 11 percentage points. However, the low response rate (22%) and early timing of this study limit the current usefulness of this study. Finally, the enactment of the Genetic Information Nondiscrimination Act of 2008, and its implementation in 2009 and 2010, may reduce fears of discrimination in employment and health insurance. In the most recent study to address reimbursement for genetic testing, 56% of non-testers from a sample who had received genetic counseling services and declined testing said they could not afford all costs of the test or their share not covered by insurance, yet more than half also reported income of over $70,000 192 193 the Lewin Group. Writing effective insurance justification letters for cancer genetic testing: a streamlined approach.
Buy glimepiride 1mg low price
As part of the sensitivity analysis diabetes mellitus tipe 2 adalah safe glimepiride 2 mg, the reported maximum or minimum well arsenic concentrations were also applied to diabetes urine test strips purchase glimepiride on line the models diabetes quality improvement project buy cheapest glimepiride and glimepiride. Risk Assessment Methodology 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 the cancer risk assessment for U. Dose-Response Estimation Based on Taiwan Cancer Mortality Data 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 4 A "Poisson model" was used to fit the cancer mortality data for the Taiwanese population. Cancer mortality data for the southwest Taiwan reference groups also were included in the preferred version of the model; estimates were derived without the reference population and with cancer mortality statistics from all regions of Taiwan. In the Poisson model, which is widely applied in the analysis of epidemiology data, cancer deaths are assumed to be "rare" events and Poisson-distributed within each age-dose group. Because data are given in 5-year age intervals, the parameter is related to hazard rate h which is equal to /5. In this model, the exponential term represents "h0(t)"in Equation 5-1, the age-dependent risk of cancer at the "background" doses of arsenic (zero from drinking water and 10 g/day from diet in the preferred model). The last term in the equation captures the dependency of risk on the daily ingestion dose of arsenic. Cancer mortality data were stratified across 13 5-year age groups and 43 villages (42 exposed villages plus the reference population). This stratification yielded 559 data points per cancer endpoint for model fitting. Mid-range values for the age ranges were standardized to their mean values and treated as nuisance parameters. In the primary (baseline) risk model, the estimated nonwater arsenic intake was 10 g/day for both the exposed and reference populations. The total arsenic dose received by the population of any village was estimated as the sum of the nonwater dietary intake plus the median arsenic well water concentration for the village (baseline model), multiplied by the estimated water Taiwanese consumption rates (3. The southwest Taiwanese population outside of the arseniasis-endemic area (Morales et al. Replicated results (estimated age and dose coefficients) were identical to Solver estimates to the third decimal place for all endpoints. The confidence limits were calculated using the likelihood profile method (Venson and Moolgavkar, 1988). In this approach, the value of the dose parameter, b, was varied from its estimated mean value. Confidence limit calculations using other methods (empirical Bayesian simulation 5 and "bootstrap-t") gave comparable results (within a few percent of the values estimated by profile likelihood). The dose is then adjusted until the estimated extra incidence risk from arsenic-associated cancer risk equals 0. Confidence limits were then estimated assuming the posterior probability of b was normally distributed. Estimated lifetime incidence risks corresponding to 10 g/L arsenic in drinking water follow similar patterns for the various endpoints. Estimated drinking water concentrations associated with 10-4 lifetime incidence range from 0. In this analysis, total cancer risk (lung plus bladder) for males and females is calculated by combining the risk for the individual tumor types. If this is the case, the 95% upper bound, U, for the combined cancer potency can be calculated as: U = (m1 + m2) + (u1 - m1) 2 + (u 2 - m2) 2 (Equation 5-5) where mi and ui, i = 1,2, are respectively mean and 95% upper bound cancer potency for the two tumor types. The estimated drinking water unit risk for combined male lung and bladder cancer is 4. The drinking water concentrations corresponding to 10-4 combined cancer risks for males and females are 0. Cancer Slope Factor, per mg/kg-day 30 25 20 15 10 5 0 Male Lung Male Bladder Male Combined Female Lung Female Bladder Female Combined Figure 5-1. Thus, the detailed comparisons in this section are limited to assessments that also address lung and bladder cancer. In the analyses that follow, some of the risk comparisons are based on mortality estimates that have been converted to incidence using recent U. This conversion introduces additional uncertainty into the comparisons; different results would have been obtained had the incidence been modeled directly rather than estimated after the fact. In addition, these values do not account for differences in drinking water consumption between the U. This finding is not surprising because the results are estimated for the same cohort in both cases, and because the case mortality for lung cancer is so high (nearly 100%). In addition to the differences in modeling approaches outlined above, another possible reason for this difference is that the Chen et al. Only four exposure categories were analyzed (less than 10 g/L, 1050, 50-100, and more than 100 g/L in water; nonwater exposures were not evaluated). Changes in the assumptions related to nonwater arsenic intake also would be expected to have small to moderate effects on the results within the range in question. In this assessment, both the reference and exposed populations are assumed to receive 10 g/day nonwater arsenic intake (see Section 5. The Agency felt that the currently available data were insufficient to support detailed probabilistic uncertainty and variability estimation. Sensitivity cases were run in which the nonwater arsenic intake in the exposed populations was varied from its default value of 10 g/day to 0, 100, and 200 g/day. An additional case was run in which both the exposed and reference populations were assumed to receive 0, 30, and 50 g/day nonwater arsenic exposure. Because the Poisson risk model for female bladder cancer is particularly sensitive to changes in assumptions related to nonwater arsenic intakes (see below), nonwater arsenic intake was limited to below 50 g/day in reference populations. Varying assumptions related to drinking water intake by the exposed Taiwanese population. Cases were run in which the male drinking water consumption was varied from its baseline value of 3. Female drinking water intake in the Taiwanese population was varied from its baseline value of 2. Varying the arsenic well concentrations used to fit the dose-response model for the Taiwanese population. The baseline risk model used the median village arsenic concentrations as the exposure metric. In the sensitivity analysis, cases also were run using the minimum and maximum well concentrations in each village. Including different Taiwanese reference populations in the dose-response assessment. The baseline (southwest Taiwan) reference population was replaced by data from all Taiwan. Table 5-10 shows the estimated (incidence) risks associated with a drinking water concentration of 10 g/L for the U. Table 5-11 shows the proportional changes in estimated risks in relations to the baseline estimate.
Purchase 4mg glimepiride mastercard
Heart rate should be monitored at regular intervals consistent with usual clinical practice diabetes test target buy glimepiride 4 mg cheap. Some of these events were reported in patients without known underlying renal disease diabetes mellitus history discount glimepiride online american express. A majority of the reported events occurred in patients who had experienced nausea diabetes test hc1 effective 4 mg glimepiride, vomiting, or diarrhea leading to volume depletion. Some of the reported events occurred in patients receiving one or more medications known to affect renal function or volume status. Altered renal function has been reversed in many of the reported cases with supportive treatment and discontinuation of potentially causative agents, including liraglutide. All patients received study drug in addition to a reduced-calorie diet and increased physical activity counseling. In one of the 56-week trials, a subset of patients (with abnormal glucose measurements at randomization) [see Clinical Studies (14. Four of these papillary thyroid carcinomas were less than 1 cm in greatest diameter and 4 were diagnosed in surgical pathology specimens after thyroidectomy prompted by findings identified prior to treatment. The proportion of patients with calcitonin greater than or equal to 2 times the upper limit of normal at the end of the trial was 1. See text below for further information regarding hypoglycemia in patients with and without type 2 diabetes. Hypoglycemia Adult Patients with Type 2 Diabetes In a clinical trial in adult patients with type 2 diabetes mellitus and overweight (excess weight) or obesity, severe hypoglycemia (defined as requiring the assistance of another person) occurred in 3 (0. In this trial, among patients taking a sulfonylurea, hypoglycemia defined as a plasma glucose less than 54 mg/dL with or without symptoms occurred in 31 (28. The doses of sulfonylureas were reduced by 50% at the beginning of the trial per protocol. Among patients not taking a sulfonylurea, blood glucose less than 54 mg/dL with or without symptoms occurred in 22 (7. No meaningful difference in hypoglycemia, defined as blood glucose less than 54 mg/dL with or without symptoms, was reported between groups. Spontaneously reported symptomatic episodes of unconfirmed hypoglycemia were reported by 46 (1. Fasting plasma glucose values obtained at routine clinic visits less than 54 mg/dL, irrespective of hypoglycemic symptoms, occurred in 2 (0. Pediatric Patients without Type 2 Diabetes In a 56-week placebo-controlled clinical trial of pediatric patients without type 2 diabetes mellitus in which blood glucose meters were provided, 19 (15. Four (4) events of hypoglycemia defined as a plasma glucose less than 54 mg/ dL occurred in 2 (1. Most episodes of gastrointestinal events were mild or moderate and did not lead to discontinuation of therapy (6. There have been reports of gastrointestinal adverse reactions, such as nausea, vomiting, and diarrhea, associated with volume depletion and renal impairment. Most adverse reactions leading to discontinuation were due to vomiting and nausea (4. Immunogenicity the detection of antibody formation is highly dependent on the sensitivity and specificity of the assay. Antibodies that had a neutralizing effect on liraglutide in an in vitro assay occurred in 18 (1. Presence of antibodies may be associated with a higher incidence of injection site reactions and reports of low blood glucose. In clinical trials, these events were usually classified as mild and resolved while patients continued on treatment. Cases of anaphylactic reactions with additional symptoms such as hypotension, palpitations, dyspnea, and edema have been reported with marketed use of liraglutide. In clinical pharmacology trials, liraglutide did not affect the absorption of the tested orally administered medications to any clinically relevant degree. There are no available data with liraglutide in pregnant women to inform a drug associated risk for major birth defects and miscarriage. Animal reproduction studies identified increased adverse embryofetal developmental outcomes from exposure during pregnancy. Clinical Considerations Disease-associated maternal and/or embryofetal risk A minimum weight gain, and no weight loss, is recommended for all pregnant women, including those who are already overweight or obese, due to the necessary weight gain that occurs in maternal tissues during pregnancy. The number of early embryonic deaths in the 1 mg/kg/ day group increased slightly. Fetal abnormalities and variations in kidneys and blood vessels, irregular ossification of the skull, and a more complete state of ossification occurred at all doses. The incidence of fetal malformations in liraglutide-treated groups exceeding concurrent and historical controls were misshapen oropharynx and/or narrowed opening into larynx at 0. Liraglutide decreased fetal weight and dose-dependently increased the incidence of total major fetal abnormalities at all doses. Irregular ossification and/or skeletal abnormalities occurred in the skull and jaw, vertebrae and ribs, sternum, pelvis, tail, and scapula; and dose-dependent minor skeletal variations were observed. Bilobed or bifurcated gallbladder was seen in all treatment groups, but not in the control group. Group mean body weight of neonatal rats from liraglutide-treated dams was lower than neonatal rats from control group dams. Bloody scabs and agitated behavior occurred in male rats descended from dams treated with 1 mg/kg/day liraglutide. Group mean body weight from birth to postpartum day 14 trended lower in F2 generation rats descended from liraglutide-treated rats compared to F2 generation rats descended from controls, but differences did not reach statistical significance for any group. Data In lactating rats, liraglutide was present unchanged in milk at concentrations approximately 50% of maternal plasma concentrations. No overall differences in safety or effectiveness were observed between these patients and younger patients, but greater sensitivity of some older individuals cannot be ruled out. However, there have been postmarketing reports of acute renal failure and worsening of chronic renal failure with liraglutide, which may sometimes require hemodialysis [see Warnings and Precautions (5. Liraglutide is made by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor. The molecular formula of liraglutide is C172H265N43O51 and the molecular weight is 3751. The structural formula (Figure 1) is: His C-16 fatty acid (palmitoyl) Glu Lys Ala Ala Gln Gly Glu Leu Tyr Ala Glu Gly Thr Phe Thr Ser Asp Val Ser Ser Glu Phe Ile Ala Trp Leu Val Arg Gly Lys Arg Gly Figure 1. In animal studies, peripheral administration of liraglutide resulted in the presence of liraglutide in specific brain regions regulating appetite, including the hypothalamus. Although liraglutide activated neurons in brain regions known to regulate appetite, specific brain regions mediating the effects of liraglutide on appetite were not identified in rats. Liraglutide exposures were considered similar among three subcutaneous injection sites (upper arm, abdomen, and thigh). Absolute bioavailability of liraglutide following subcutaneous administration is approximately 55%. Distribution - the mean apparent volume of distribution after subcutaneous administration of liraglutide 3 mg is 20-25 L (for a person weighing approximately 100 kg). The mean volume of distribution after intravenous administration of liraglutide is 0.
Buy generic glimepiride 2mg
The urban as Indigenous (Bang diabetes test how long does it take purchase glimepiride with amex, 2009; Belin diabetes foot problems cheap glimepiride 2mg mastercard, 1999; Friedel blood sugar symptoms cheap 2 mg glimepiride fast delivery, 2011; Goeman, 2008; Intertribal Friendship House & Lobo, 2002) Indigenous storied land as disrupting settler maps (Goeman, 2008) Decolonization is not a metaphor 31 Novels, poetry, and essays by Greg Sarris, Craig Womack, Joy Harjo, Gerald Vizenor To Remain an Indian (Lomawaima & McCarty, 2006) Shadow Curriculum (Richardson, 2011) Red Pedagogy (Grande, 2004) Land Education (McCoy, Tuck, McKenzie, forthcoming) More on incommensurability Incommensurability is an acknowledgement that decolonization will require a change in the order of the world (Fanon, 1963). This is not to say that Indigenous peoples or Black and brown peoples take positions of dominance over white settlers; the goal is not for everyone to merely swap spots on the settler-colonial triad, to take another turn on the merry-go-round. The goal is to break the relentless structuring of the triad - a break and not a compromise (Memmi, 1991). Breaking the settler colonial triad, in direct terms, means repatriating land to sovereign Native tribes and nations, abolition of slavery in its contemporary forms, and the dismantling of the imperial metropole. However, decolonial struggles here/there are not parallel, not shared equally, nor do they bring neat closure to the concerns of all involved - particularly not for settlers. Settler sovereignty over these very pieces of earth, air, and water is what makes possible these imperialisms. The same yellow pollen in the water of the Laguna Pueblo reservation in New Mexico, Leslie Marmon Silko reminds us, is the same uranium that annihilated over 200,000 strangers in 2 flashes. Through the voice of her character Betonie, Silko writes, "Thirty thousand years ago they were not strangers. You saw what the evil had done; you saw the witchery ranging as wide as the world" (Silko, 1982, p. Only curricular materials affirming the settler innocence, ingenuity, and right to America may be taught. In "No", her response to the 2003 United States invasion of Iraq, Mvskoke/Creek poet Joy Harjo (2004) writes, "Yes, that was me you saw shaking with bravery, with a government issued rifle on my back. The first Black American President said without blinking, "There was a point before folks had left, before we had gotten everybody back on the helicopter and were flying back to base, where they said Geronimo has been killed, and Geronimo was the code 32 E. Geronimo is settler nickname for the Bedonkohe Apache warrior who fought Mexican and then U. The technologies of the permanent settler war are reserviced for foreign wars, including boarding schools, colonial schools, urban schools run by military personnel. South African apartheid townships, the kill-zones in what became the Philippine colony, then nation-state, the checkerboarding of Palestinian land with checkpoints, were modeled after U. The admiration is sometimes mutual, the doctors and administrators of forced sterilizations of black, Native, disabled, poor, and mostly female people - the Sterilization Act accompanied the Racial Integrity Act and the Pocohontas Exception - praised the Nazi eugenics program. The management technologies of North American settler colonialism have provided the tools for internal colonialisms elsewhere. The prominence of "flat world" perspectives asserts that technology has afforded a diminished significance of place and borders. The collapsing of levies heralded the selective collapsibility of native-slave, again, for the purpose of reinvasion, resettlement, reinhabitation. It necessitates the manufacturing of crime at rates higher than anywhere in the world. Plantation owners lived in houses like pyramids and chattel slavery took an extreme form here, even for the South, beginning with enslaved Chitimachas, Choctaw, Natchez, Chaoьachas, Natchez, Westo, Yamasee, Euchee, Yazoo and Tawasa peoples, then later replaced by enslaved West Africans. This "most Southern on earth"(Cobb, 1992) was a place of ultimate terror for Black people even under slavery (the worst place to be sold off too, the place of no return, the place of premature death). Black and Native people alike were induced to raid and enslave Native tribes, as a bargain for their own freedom or to defer their own enslavibility by the British, French, and then American settlers. The Delta is now more segregated than it was during Jim Crow in 1950 (Aiken, 1990). The rising number of impoverished, all black townships is the result of mechanization of 25 Source: Chang (2012). Yang agriculture and a fundamental settler covenant that keeps black people landless. Angola Farm is perhaps the more notorious of the two State Penitentiaries along the Mississippi River. Both State Penitentiaries (Mississippi and Louisana, respectively), both former slave plantations, both turned convict-leasing farms almost immediately after the Civil War by genius land speculators-cum-prison wardens. The stench from it hangs like a pall over the whole area" John Spivak, Georgia N, 1932. To mobilize labor on land by landless people whose crime was mobility on land they did not own. The largest human trafficker in the world is the carceral state within Decolonization is not a metaphor 35 the United States, not some secret Thai triad or Russian mafia or Chinese smuggler. Geopolitics and biopolitics are completely knotted together in a settler colonial context. Despite the rise of publicly traded prisons, Farms are not fundamentally capitalist ventures; at their core, they are colonial contract institutions much like Spanish Missions, Indian Boarding Schools, and ghetto school systems26. The labor to cage black bodies is paid for by the state and then land is granted, worked by convict labor, to generate additional profits for the prison proprietors. However, it is the management of excess presence on the land, not the forced labor, that is the main object of slavery under settler colonialism. Conclusion An ethic of incommensurability, which guides moves that unsettle innocence, stands in contrast to aims of reconciliation, which motivate settler moves to innocence. Reconciliation is about rescuing settler normalcy, about rescuing a settler future. Incommensurability acknowledges that these questions need not, and perhaps cannot, be answered in order for decolonization to exist as a framework. We want to say, first, that decolonization is not obliged to answer those questions decolonization is not accountable to settlers, or settler futurity. Still, we acknowledge the questions of those wary participants in Occupy Oakland and other settlers who want to know what decolonization will require of them. The answers will not emerge from friendly understanding, and indeed require a dangerous understanding of uncommonality that un-coalesces coalition politics moves that may feel very unfriendly. But we will find out the answers as we get there, "in the 26 As we write today, Louisiana has moved to privatize all of its public schools. Yang exact measure that we can discern the movements which give [decolonization] historical form and content" (Fanon, 1963, p. To fully enact an ethic of incommensurability means relinquishing settler futurity, abandoning the hope that settlers may one day be commensurable to Native peoples. The Native futures, the lives to be lived once the settler nation is gone - these are the unwritten possibilities made possible by an ethic of incommensurability. Decolonizing feminism: Challenging connections between settler colonialism and heteropatriarchy. The contemporary reality of Canadian imperialism, settler colonialism, and the hybrid colonial state. The most southern place on earth: the Mississippi Delta and the roots of regional identity.
Purchase cheapest glimepiride
The results from the Co-Carcinogenesis category all relate to diabetes diet lemonade buy generic glimepiride 2mg on-line promotion of benzo[a]pyrene (B[a]P)-mediated carcinogenesis via exposure to diabetes in dogs red eyes discount glimepiride 1 mg with mastercard 1 diabetes glucose chart buy 1 mg glimepiride fast delivery. When the arsenite treatment was preceded by exposure to 100 nM B[a]P for 24 hours, there was a synergistic interaction. Results indicate that the transformation rate increased more than 500 and 200 times when compared to arsenite and B[a]P treatments alone, respectively. The data found in Table C-3 under Cytotoxicity are sometimes important to help determine the possible relevance to human health of findings related to other key events. For example, a large arsenic-induced increase in the expression of some protein that is important in signal transduction is much more likely to have such relevance if it occurs at concentrations having little or no cytotoxicity than if it occurs only when most cells are dying. Sometimes the different assays yield more similar results when treatments last at least 48 hours (Komissarova et al. Effects of modulators on arsenic-induced cytotoxicity were tested in many experiments. Also, from the numerous dose-response curves published in those papers, it is apparent that cytotoxicity generally has a threshold below which there is no apparent effect. The decrease in expression was 45% at that concentration and 60% at concentrations of 0. When a reduction in the effects was seen, it was taken as evidence that oxidative stress was the cause of the original effects observed, as, for example, in the study by Sasaki et al. The order of effectiveness of the different arsenicals differed in the two cell lines used and for the different types of damage. Consistent with these effects, increased levels of nitric oxide, superoxide ions, hydrogen peroxide, and the cellular free iron pool were consistently detected in both cell lines after treatments by all three trivalent arsenicals. Almost all of the data in Table C-3 for Gene Mutations show no induction of mutations by arsenic. Hypermethylation in this cell line was demonstrated within a 341-base-pair fragment of the promoter region of p53 (Mass and Wang, 1997; Zhong and Mass, 2001). Some loci were affected only after 25 days of exposure, while others were affected after 75 days of exposure. This discussion provides highlights from that table and Appendix D, which is devoted entirely to the immunotoxicity of inorganic arsenic. Appendix D discusses some aspects of the immunotoxicity of inorganic arsenic in much more detail, including more emphasis on human studies and in vivo experiments on laboratory animals, as well as on some older in vitro studies. Effects thought to be related to Immune System Response were grouped under that heading in Table C-3 even if they dealt mainly with other key events. For example, several findings related to Apoptosis, Cytotoxicity, or Signal Transduction are included in this section of Table C-3. Regarding Inhibition of Differentiation, in experiments done on spontaneously immortalized human keratinocytes and on normal human epidermal cells derived from foreskin, sodium arsenite was shown to delay differentiation and preserve the proliferative potential of keratinocytes (Patterson et al. Interference With Hormone Function was demonstrated in experiments by Bodwell et al. More detailed information on interference with hormone function can be found in Table C-3. After 26 weeks, this experiment showed much anchorage-independent growth but not yet enhanced tumorigenicity. Table C-3 summarizes many findings related to the Signal Transduction category, even though considerable data found under Aberrant Gene or Protein Expression could have been placed into this category. Details presented in Table C-3 show that the responses of those three arsenicals were different and that, in some cases, the direction of the response reversed as the concentration increased. In some cases a reduction from an increase was observed, which is interesting because various responses for some endpoints described above showed a reversal in which the lowest doses caused a bigger effect. Additionally, several experiments in this category related to different ways in which arsenic affects signal transduction to either increase or decrease apoptosis. By decreasing apoptosis, such an effect might permit the survival of cells containing damage that could eventually lead to a cancer. The Ca2+ concentration in cells was substantially increased (and by rather similar amounts) by exposure to either 0. Arsenic is a multisite carcinogen, with numerous studies finding an association between arsenic and increased incidences of a number of different types of cancers. The carcinogenic effect of arsenic has been reported for populations in many different countries. While the studies detailed in this document provide evidence for cancer after oral exposure to arsenic, arsenic also has been associated with cancer after inhalation exposure (U. Synthesis of Human, Animal, and Other Supporting Evidence 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 Numerous epidemiologic investigations, each conducted differently and containing its own biases. This is because between 1910 and 1920, water supplies were changed from shallow surface water wells to artesian wells, which were subsequently found to contain high levels of arsenic in various regions. Studies in these arsenic-endemic regions of Taiwan have found increases in all of the aforementioned cancer types. The link between these cancers and arsenic exposure in drinking water also have been observed in other parts of the world, including Japan, Chile, and Argentina. Most of the epidemiology studies examining the relationship between arsenic exposure from drinking water and cancers are ecological in nature and are therefore subject to the limitations inherent in such studies. Strengths of the data include the size of the population, the reliability of the population and mortality counts, the stability of residential patterns, the homogenous lifestyle as confirmed by surveys, the long-term exposures, the extensive follow-up (almost 900,000 person-years), the large number of exposed villages (42), and the large number of cancer deaths (1152 recorded from 1973 to 1986). In addition, cancer cases were pathologically confirmed in some of the Taiwanese studies. Although dose-response relationships have been observed for the majority of cancers noted in areas with high levels of arsenic in their drinking water, results for low-level arsenic epidemiologic investigations (primarily from the United States and Europe) have been equivocal with regard to the relationship between these cancers and arsenic exposure. This could be due to the fact that none of the studies accounted for arsenic exposure through food sources. Therefore, as the exposure of arsenic from drinking water decreases and the relative contribution from food increases, misclassification of exposure groups can become significant. At the lower concentrations, dietary intake could easily create total arsenic intake levels to be similar between the referent group and what is considered the exposure group. Cantor and Lubin (2007) also conclude that misclassification occurs because exposure is not necessarily assessed during disease-relevant exposure periods. In regards to cancer, there is a long latency period, which appears to vary depending on the type of cancer and exposure. This means that exposure to arsenic sources during the decades prior to cancer outcome is necessary. Therefore, studies with low levels of exposure that are ecological in nature (no individual exposure) are more prone to misclassification, which means they are biased toward the null hypothesis. In addition, studies that attempted to individualize exposure by examining toenail arsenic levels are looking at only the prior year of exposure (Cantor and Lubin, 2007) and may miss the important exposure period. Despite all these numerous limitations in low-level exposure studies, significant associations have been observed for cancers of the prostate (Hinwood et al. There are very few animal data demonstrating the carcinogenic potential of arsenic. Since it has been noted that humans who are better methylators are at lower risk (Yu et al. As stated before, arsenic has been associated with cancers of the skin, lung, kidney, bladder, and liver.
Cheap generic glimepiride uk
Subsequent classes will cover population genetics and the modern evolutionary synthesis blood glucose quiz generic glimepiride 1 mg online, chromosomal theory and the central dogma of molecular biology as well as phylogenetics diabetes type 2 pregnancy order glimepiride 2mg with mastercard, diversity diabetes test breakthrough cost of glimepiride, and common descent. Molecular genetics will be introduced in the context of bacterial gene regulation and gene regulatory networks. The course will end with a discussion on genomics, post-genomics, and epi-genomics. Student assignments will include an essay about a specific topic on breeding and heredity, a presentation about traits or diseases associated with cytogenetic abnormalities or the research of a modern synthesis contributor, and a descriptive report about a disease-causing gene and its genomic setting. At the end of the course, students will understand how the paradigms of evolution and genetics have advanced since Darwin and will be able to discuss our modern-omicsoriented understanding of heritable disease and evolution in its historical context. The first semester will introduce basic concepts of genetics, cytogenetics, and molecular genetics. The second semester will include presentations on clinical topics emphasizing the diagnosis and management of patients with genetic disorders. This course should impart basic principles of genetics as applied to medicine and provide an approach to a patient with a suspected genetic disorder. This course is designed for Fellows and genetic counseling students who are preparing for subspecialty examinations of the American Board of Medical Genetics and others who wish to learn about the expanding role of genetics in medicine. Learning objectives-Fall: Appreciate organization of the human genome and tools used to investigate it Acquire skills to determine the most likely mode of inheritance of a trait, to interpret the results of linkage and association studies Learning objectives-Spring: Appreciate the impact genetic disorders have on the various organ systems Acquire skills to develop a differential diagnosis and appropriate work-up for a given phenotype Prerequisites: graduate-level training or experience in the biomedical sciences or consent of the course instructor. The course will begin with lectures on the methodology and model systems of developmental biology, a review of preimplantation development and gastrulation, and embryogenesis/ organogenesis. Learning objectives: Connect conceptually the apparently distinct disciplines of embryology, developmental biology, and clinical medicine to appreciate mechanisms of normal and abnormal development Appreciate the role of evolution for understanding the mechanistic basis of malformations and as a basis for the study of these disorders in animal models Develop skills of integrating data from clinical, anatomic and molecular studies to form a comprehensive description of malformations Prerequisites: permission of the course instructor. This class offers a dynamic forum for discussion, focusing on genetics counseling research, policy and education, and their impact on clinical practice. A diverse group of professionals present topics well suited for class discussions. Student-led case presentations and discussions highlight pertinent psychological, social, and ethical issues in genetic counseling. Clients who have had personal experiences with a genetic condition or risk expose students to a variety of attitudes, reactions, and experiences. Students enrolled in related graduate programs are encouraged to enroll to maximize the opportunity for exchange among disciplines. This course presents an opportunity to college graduates interested in genetic counseling to learn about the theoretical and practical aspects of the profession. The course is designed as part of the required curriculum for Clinical Genetics residents and Fellows preparing for the Clinical Molecular Genetics Boards given by the American Board of Medical Genetics. Topics include Smith-Lemli-Opitz syndrome, Rasopathies, neurocutaneous syndromes, muscular dystrophies, cohesinopathies, connective tissue disorders, ciliopathies, and psychosocial and genetic counseling issues in the era of genomic medicine. The course is designed as part of the required curriculum for residents, Fellows, and students preparing for the Genetics Certification Boards given by the American Board of Medical Genetics and the American Board of Genetic Counseling. Topics to be covered include statistical and mathematical subjects in clinical genetics and population genetics, clinical cytogenetics, dysmorphology, ophthalmologic genetics, and general treatment and management of genetic diseases. Learning objectives: Review the fundamentals of genetics and a variety of genetic disorders in preparation for the American Board of Medical Genetics certification examination Acquire skills to recognize and eliminate distractors on the certification exam Prerequisite: Board candidate for any subspecialty exam of the American Board of Medical Genetics. Prevention and treatment strategies that take individual variability into account are not new concepts. This course will explore the possibilities, promises, and pitfalls of precision medicine, using real-world examples, and is intended to bridge the gap between basic biomedical research and its practical clinical applications. The course will begin with a detailed overview of the basic tissues: epithelial; connective; muscle; and, nervous tissues. The four basic tissues will then be applied to organ systems, and a discussion of some clinical pathologies will follow. The course will also cover cell functions within the different tissues as well as tissue preparations and types of stains to highlight different characteristics of tissue. Learning objectives: Define and describe histological characteristics of different cell types Identify different tissue types and organization within organs Understand functions of cell types within the tissue Gain general knowledge of tissue preparation and commonly used staining techniques Understand how the different cell types and basic tissues come together to function as a whole organ Prerequisites: knowledge of biology and/or cell biology. This introductory course is aimed to bridge the gap between traditional Chinese medicine and modern science. The course is designed to cover fundamental concepts of molecular biology, genetics, and basic biochemical principles and to use these principles to analyze commonly occurring health-related problems. Presentation, analysis, and group discussions of clinical cases selected to exemplify the subject topic will be integral part of the lectures. An historical perspective of how molecular medical knowledge and recent technological developments that have been instrumental in medical treatments will be also presented. The course differs significantly from a comprehensive biochemistry or biology course and is aimed at students in the health sciences or prospective medical students. Learning objectives: Identify interactions between metabolic pathways and human diseases Describe recent advances in medical applications of biotechnology and genetics Discuss health issues in relation to molecular mechanisms of the cell Prepare an original presentation about a disease of interest to the class Prerequisites: college-level knowledge of biology and/or chemistry. It interacts with the systems of the body (digestive, nervous, renal, reproductive, cardiovascular, respiratory, skeletal, and metabolic) to provide a homeostatic environment. The objective of this course is to provide students with an overview of endocrine physiology and pathophysiology. The course will describe how the endocrine system is integrated with the other physiological systems, along with the biochemistry of hormone synthesis and actions. Problem solving with endocrine disorders will form a basis for understanding the principles of hormone function. Students seeking basic knowledge on the principles of endocrinology to apply in their research or clinical training will find this course useful. Learning objectives: Identify and describe the key hormones and their roles in metabolism, digestion, reproduction, and growth Understand regulation of hormonal control, including the principles of feedback control and hormone-receptor interactions Problem solve the biological basis of endocrine disorders and treatments Develop the scientific background needed to understand the literature about endocrine function and pathology Prerequisites: general biology and chemistry required; prior coursework in introductory biochemistry and human physiology recommended. Topics studied in the fall semester are: molecular basis of physiology; the nervous system; and, cardiovascular system. Topics studied in the spring semester are: respiratory; renal; gastrointestinal; endocrine; and, reproductive physiology. The course sequence is intended as a bridge to advanced studies in pathophysiology and medicine. Diagnoses, symptomology, and treatment strategies will be presented by guest lecturers with clinical and research expertise in specific disease pathologies. The course will be comprised of a combination of lectures and discussions, with reading assignments, an exam, a writing assignment, and a group presentation assignment. Learning objectives: Identify the most common gastrointestinal/metabolic diseases Explain diagnostic criteria and symptoms associated with each disease/disorder; describe treatment strategies for each disorder Describe and discuss the underlying physiological, cellular, and molecular mechanisms associated with each disease Demonstrate an understanding of the relationship between pathology and the underlying physiological, molecular, and cellular mechanisms for each disease Analyze and critique research publications and data investigating the pathophysiological mechanisms for a selected disease Prerequisites: undergraduate coursework in cell biology, genetics, physiology, or college degree in biomedical sciences. Additional topics will include cancer genomics, epithelial to mesenchymal transition, adhesion, angiogenesis, targeted therapies, and animal models. This course will also have a journal-club component, which will enable students to read and discuss scientific journal articles related to the course. Selected topics of topographic anatomy will be also examined, including head/neck and pelvis.