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A microcentrifuge (max speed ~20,000 rpm or 11,500 В g) with a 10­15 cm rotor that accepts standard microfuge tubes is essential to facilitate ultrafiltration. Sample preparation can be done in almost any moderately equipped laboratory with access to a cold room or walk-in refrigerator. Most centrifugation steps should be done at 4 C, so a refrigerated microcentrifuge or a regular microcentrifuge placed in a cold room should be sufficient. A tabletop microcentrifuge or microfuge (with a maximum speed ~20,000 rpm or 11,500 В g) equipped with a 10­15 cm rotor that accepts standard microfuge tubes. It is assumed that the biological samples have already been collected, sub-aliquoted into cryovials, and stored at А20 C or at А80 C. Regardless of whether the sample is a tissue or a biofluid, it is important to remember that most biological samples collected for metabolomics are metabolically "alive. If not properly accounted for, this underlying metabolic activity can produce deceptive results and large variations in metabolite composition and concentrations. Metabolic quenching is the rapid arresting of all metabolic activities via physical or chemical means [10]. The best route to metabolic quenching for tissues is rapid freezing (using liquid nitrogen). For blood, rapid removal of the red and white blood cells to produce plasma or serum must be done prior to freezing (to avoid any red blood cell lysis upon thawing). Dispose the glycerol containing filtrate into the sink and repeat step 1 four more times. Dry the Amicon ultrafilter with a tissue (Kimwipe or other brand), and place it into a new 1. Centrifuge the sample at 9400 В g for 3 min at 4 C to remove any particulate material (see Note 6). Place the microcentrifuge tube into a suitably equipped shaker to shake the tube at between 150 and 200 rpm for 25 min at 4 C. Sonicate (using an ultrasonic bath sonicator with the frequency of 40 kHz) the microcentrifuge tube containing the fecal water for 15 min at 4 C to solubilize the fecal material. Weigh about 2 g of a frozen tissue sample, and grind it with a 200­300 mL pestle and mortar with about 100 mL liquid nitrogen (see Note 10). Separate upper polar phase and lower nonpolar phase carefully using a Pasteur pipette (see Note 14). Transfer the upper polar phase into a pre-weighed 15 mL Falcon tube (initial weight). Purge the upper polar phase comprising of water-soluble metabolites from the tissue under nitrogen gas for 90­120 min. Weigh the Falcon tube with the lyophilized (to determine the final dry weight of the sample). Transfer a precisely weighed amount (typically in the range of 10­15 mg for the best results) of the lyophilized sample into a 1. With tissue samples it is important to be able to report metabolite concentrations relative to the dry weight of the sample. Use a Pasteur pipette to carefully transfer the biofluid or tissue extracts prepared in Subheading 3. Ensure that the sample and magnet are properly matched, locked, and tuned (see Note 18). Set the number of data points for the acquisition to be 64 k or 128 k so that the digital resolution will be santanu. Typically, 64­128 transients are sufficient for most biological samples, although this may vary with the concentration of the metabolites in the sample, the sample type, or instrument specification, such as type of probe installed and the magnet field strength. Here we will describe two common routes, one uses a commercial software package called Chenomx and the other uses an open-access webserver called Bayesil [8]. Send the processed spectrum to the Chenomx Profiler to identify metabolites and determine their concentrations. The black line represents the actual serum spectrum while the red line the fitted spectrum. The first strategy is a targeted profiling, where the spectrum is searched for the known metabolites. The second strategy is an untargeted profiling, where the metabolite list is searched for the peaks of interest. Right-click on an unassigned peak to search for possible candidates for this peak in the library.


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Metabolites with consistent and significant changes in ion signal in untargeted metabolomics are plotted in a heat map. Centrifuge column at 1000 В g at room temperature for 2 min to remove storage solution. Repeat this step two additional times, discarding buffer from the collection tube. After the spin desalting column is conditioned, pellet particulates in the cell lysates by centrifugation at 18,800 В g at 4 C for 10 min. Transfer the supernatant (total clarified cell lysate) to the conditioned spin desalting column. Add more protease and phosphatase inhibitor cocktail to sample (1:100), aliquot to 1 mg per tube. Add 10 L of 1 M MnCl2 to each sample, and mix and rotate for 5 min at room temperature. Cool samples to room temperature, add 40 L of cysteine alkylation solution containing 1 M iodoacetamide (see Subheading 2. Transfer the solution containing the labeled, reduced, and alkylated proteins to the spin desalting column. Transfer desalted proteins to a new microcentrifuge tube, and add 10 L of trypsin (2 g/L) to each sample, and incubate with shaking at 37 C overnight. To obtain the streptavidin beads for labeled peptide capture, mix the slurry of 50% high-capacity streptavidin agarose resin santanu. You should be able to see the white beads in pipette tips and verify that similar bead bed volumes (25 L) are used for all experiments. Add to each digest and incubate with constant mixing on a rotator at room temperature for 1 h. For each wash, vortex briefly after adding buffer, centrifuge samples at 1000 В g for 1 min to pellet resin, and discard supernatant. This step may be facilitated by transferring resin to an optional spin desalting column. Repeat this step two additional times, combining all elutions in the same tube and freezing the samples. Sixteen tandem mass spectra were collected in a datadependent manner following each survey scan. Up to three missed cleavage sites were allowed due to probe labeling of lysine residues. The match between runs function was applied with the retention time window size set to 4 min. This approach assumes a common background and is therefore appropriate for cell line comparisons, such as these. Data are then assessed for missing values; filters can be applied to select different groups of analytes. Inconsistently detected analytes can be removed, based on filtering criteria either for the number of observations or for Ё signal intensity. Analytes observed in only naive or only drugresistant cells can be separated from the rest of the analysis but are definitely considered as differentially expressed and significant; targeted measurements may be necessary to detect these across all samples for confirmation. Log2 ratios were calculated using the average log2 value of signal intensity for all biological replicates. T-test P values, Hellinger distance, and Bhattacharya distances were all calculated in order to assess the significance Ё of differences between naive and drug-resistant cells. Known metabolites with significant differences were entered by name into MetaboAnalyst to determine pathways that were modulated in drug resistance (see. Default parameters were used except for the following filters and adjustments: Filter data, 80% present. Our overall goal is to develop a comprehensive list of metabolites and proteins that can serve as santanu. Ё Future plans include analysis of drug response in the naive and drug-resistant cell lines to other agents and combination treatments as well as technical development of strategies for ex vivo analysis of patient specimens [54] using very limited numbers of myeloma cells obtained by bone marrow aspiration. We typically use Bradford assays with the Pierce Coomassie Plus reagent, but the use of other techniques. Expansion of this dataset with expression proteomics may be recommended to gain additional data, specifically measurements for other related proteins, which can then further fill in the pathway maps. The comparison of the two datasets also enables determination of changes in protein expression as opposed to changes in probe uptake.

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It is known that preantral folliculogenesis is regulated by autocrine and paracrine factors in an orchestrated mechanism that defines the course of activation and follicular growth or death. To this end, fragments of collared peccaries (Pecari tajacu) ovarian cortex were cultured for 1 or 6 days, at 38. Fragments from non-cultured ovarian tissue as well as from those cultured for 1 or 6 days in a specific medium were processed for classical histology to evaluate follicular integrity and to calculate the percentages of normal follicles, and percentage of follicular activation. With regard to activation, fresh ovarian tissues predominantly contained primordial follicles, and after 1 or 6 days of culture, a significant decrease of primordial follicles and concomitant increase of growing follicles was verified in all the treatments, denoting activation follicular. Estimating the estrus cycle phase in bitches using different diagnostic methods: preliminary results F. During the estrous cycle, the bitch undergoes behavioral and cytological changes that are physiological and coordinated by sex hormones. In this context, different methods are used to identify the phase of the estrous cycle in order to determine the ideal moment for mating or artificial insemination. In this way, this work aimed to compare the efficacy of different diagnostic methods (behavioral examination, vaginal cytology, vaginal endoscopy) in the identification of the phase of the estrous cycle in bitches. For this purpose, adult, cyclic bitches (n = 10) from different breeds attended at the Metropolitan Veterinary Hospital of Caucaia, Cearб from April to June 2018 were used. The behavioral response of the bitches to a male with a proven libido was evaluated. The correlation between receptivity and estrous cycle phases was measured as follows: (A) attractive + non-receptive females (proestrus), (B) attractive + receptive females (estrus), (C) unattractive + non-receptive females (metestrus/anestrous). The percentage of cells for basal cells, intermediate cells, superficial (nucleated) cells, and cornified cells was analyzed. The presence of blood cells (erythrocytes or neutrophils) and bacteria in the smear were also analyzed. In the vaginal endoscopy, mucosal staining (pale or reddish), pleating (absent or present) and secretion (absent, present, serous secretion, mucous secretion or serosanguinolent secretion) were analyzed. The reliability of the methods was compared to the serum progesterone assay results. No correlation was observed between the behavioral evaluation and serum progesterone assay, so this method is unreliable to estimate the phase of the estrous cycle in bitches. The correlation between vaginal endoscopy and serum progesterone assay in the determination of estrus cycle phase in bitches was 40% (4/10). This method has proven to be the most effective, however, although it is a simple, easy to perform exam, the high cost of the device often limits its routine use. No correlation was observed between vaginal cytology and serum progesterone assay. Vaginal cytology proved ineffective in predicting the phase of the estrous cycle in bitches, probably because a single collection was performed and not a follow-up with serial collections through the estrous cycle. The vaginal endoscopy was considered the most effective method to estimate the phase of the estrous cycle in bitches. The follicles visualized under an optical microscope were classified morphologically by the stage of development and as normal or degenerate. The data were analyzed considering the normality of its distribution, using the Shapiro-Wilk test. The results were expressed by means ± standard errors considering the significance level of P <0. There was no difference between the genotypes in the oocyte size of the primary and antral follicles. The nuclei of oocytes from antral follicles were not analyzed due to low frequency. There was no difference between genotypes regarding oocyte nucleolus size independent of the follicular development stage. The high rate of double ovulations may be due to the strong ancestry in forming breeds showing a high rate of double ovulation (2, 8, 9). However, since the mechanisms involved in the transition from anestrus to proestrus have not yet been fully elucidated in this species (2), the manipulation of the estrous cycle is challenging.

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A to B) Prescriptions should include the signature, bleep and date as well as the time and date infusion started Box 32. Novorapid) · For a twice daily fixed mixture regime divide 60: 40 morning: evening. Give 36 units am; 14 units pm (b) Estimation of insulin dose when no insulin infusion has been used Calculate the total daily insulin dose insulin according to diabetes type · Known type 2 diabetes 0. This insulin infusion can be piggy-backed into the infusion of dextrose using a three-way connector and a non-return valve. All patients should commence on algorithm A and uptitrate to achieve target glucose range (Table 32. The recommendation is that once intravenous insulin has been commenced the blood glucose level should be maintained at 140­180 mg/dL (7. There is recognition that lower targets may be beneficial in specified groups but there is insufficient evidence to make firm recommendations. It is recommended that target glucose should not fall below a level of 110 mg/dL (6. Transition from intravenous to subcutaneous insulin Conversion to subcutaneous insulin should be delayed until patients are able to eat and drink normally without nausea or emesis. It is therefore good practice to continue the infusion of insulin for 1 hour after the subcutaneous insulin has been administered to allow time for the insulin to be absorbed. Estimation of insulin doses can also be made 521 Part 6 Treatment of Diabetes Table 32. Cause of in-hospital hypoglycemia Example Primary reason for hospital stay Medical causes: hepatic failure, cardiogenic shock, severe sepsis Surgical causes: nil by mouth for operation or procedure Change of meal times, missed meals, poor access to snacks Poorly written medication charts. Avoiding and treating in-hospital hypoglycemia There is an increasing body of evidence supporting the widespread occurrence of hypoglycemia in hospitals and poor knowledge of how to detect and manage it. Acute hypoglycemia is associated with significant morbidity and more rarely mortality as it causes an intense hemodynamic response that can lead to potentially fatal cardiac arrhythmias, myocardial ischemia, cerebrovascular accidents, coma and death. In-hospital hypoglycemia is defined as a blood glucose level equal or below 72 mg/dL (4. They contain all the equipment required to treat hypoglycemia, from cartons of fruit juice to intravenous 20% glucose. There are general guidelines for the treatment of in-hospital hypoglycemia and these should be available in each ward and outpatient setting; however, each patient developing in-hospital hypoglycemia should be assessed as an individual and diabetes teams should agree local guidance for self-management. Certain conditions such as renal impairment or heart failure may require tailored treatment to avoid fluid overload. Many people with diabetes carry their own treatment supplies for hypoglycemic events and should be supported to self-manage when capable and appropriate. This information regarding capacity to self-manage should be recorded in the patient notes at the time of the admission assessment. If the patient is not capable and/or uncooperative but is able to swallow, give either 1. If the blood glucose levels are still less than 4 mmol/L, GlucoGel treatment can be repeated up to three times. Once the blood glucose is above 4 mmol/L and patient has recovered, a long-acting carbohydrate snack should be offered. Once the blood glucose is above 4 mmol/L and patient has recovered, a long-acting carbohydrate such as 200 mL milk (not soya) can be given and the feed. Insulin should not be omitted and regular continued capillary blood glucose level monitoring should be recorded for 24­48 hours. Causes of in-hospital hypoglycemia There are many reasons why hypoglycemia is more likely to be to occur during hospitalization but most of these relate to insulin administration and prescribing errors and inappropriate food administration (Table 32. Prevention of recurrent in-hospital hypoglycemia When hypoglycemia has been successfully treated it is important that the reason for hypoglycemia is ascertained and the treatment documented in the patient notes. Measures such as medication adjustment or timing of meals should be introduced to prevent further episodes of hypoglycemia. Moderate Patient conscious but confused/disorientated or aggressive and able to swallow. Give 20 g of long acting carbohydrate eg 2 biscuits or a slice of bread or next meal if due. Hypoglycemia is defined as blood glucose of <4 mmol/L (if not <4 mmol/L but symptomatic, give a small carbohydrate snack for symptom relief). Surgery in patients with diabetes Patients with diabetes have poorer health than those without diabetes so this means they are more likely to undergo surgery.

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Diabetic nephropathy is associated with gene expression levels of oxidative phosphorylation and related pathways. Glyceraldehyde-3phosphate dehydrogenase: nuclear translocation participates in neuronal and nonneuronal cell death. Effect of intensive therapy on the development and progression of diabetic nephropathy in the Diabetes Control and Complications Trial. The effect of intensive diabetes therapy on the development and progression of neuropathy. Replication timing and epigenetic reprogramming of gene expression: a two-way relationship? Hyperglycemia induces a dynamic cooperativity of histone methylase and demethylase enzymes associated with gene-activating epigenetic marks that co-exist on the lysine tail. Lymphocytes from patients with type 1 diabetes display a distinct profile of chromatin histone H3 lysine 9 dimethylation: an epigenetic study in diabetes. Role of the lysine-specific demethylase 1 in the proinflammatory phenotype of vascular smooth muscle cells of diabetic mice. Epigenetic histone H3 lysine 9 methylation in metabolic memory and inflammatory phenotype of vascular smooth muscle cells in diabetes. Association between sorbitol dehydrogenase gene polymorphisms and type 2 diabetic retinopathy. Promoter polymorphism of the erythropoietin gene in severe diabetic eye and kidney complications. Assessment of 115 candidate genes for diabetic nephropathy by transmission/disequilibrium test. Clustering of long-term complications in families with diabetes in the diabetes control and complications trial. Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group. Multiple superoxide dismutase 1/splicing factor serine alanine 15 variants are associated with the development and progression of diabetic nephropathy: the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Genetics study. Decreasing intracellular superoxide corrects defective ischemia-induced new vessel formation in diabetic mice. Improving microvascular outcomes in patients with diabetes through management of hypertension. Permissive role of hypertension in the development of proteinuria and progression of renal disease in insulin-dependent diabetic patients. Mechanical forces in diabetic kidney disease: a trigger for impaired glucose metabolism. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Regulation of intracellular glucose and polyol pathway by thiamine and benfotiamine in vascular cells cultured in high glucose. Benfotiamine counteracts glucose toxicity effects on endothelial progenitor cell differentiation via Akt/FoxO signaling. Oral benfotiamine plus alpha-lipoic acid normalises complication-causing pathways in type 1 diabetes. High-dose thiamine therapy for patients with type 2 diabetes andmicroalbuminuria: a randomised, double-blind placebo-controlled pilot study. High prevalence of low plasma thiamine concentration in diabetes linked to a marker of vascular disease. Therapeutic approach for diabetic nephropathy using gene delivery of translocase of inner mitochondrial membrane 44 by reducing mitochondrial superoxide production. Overexpression of mitochondrial superoxide dismutase in mice protects the retina from diabetes-induced oxidative stress. Acceleration of diabetic renal injury in the superoxide dismutase knockout mouse: effects of tempol.

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Cocaine is a sympathomimetic that inhibits reuptake of norepinephrine and dopamine at sympathetic nerve terminals. Amfetamine and ecstasy potentiate the release of norepinephrine, dopamine and serotonin from the central and autonomic nervous systems. Cocaine toxicity may be potentiated by cannabis, while amfetamine toxicity is enhanced by alcohol. Drug-induced sympathetic activation leads to tachycardia, vasoconstriction and hypertension. Myocardial ischemia and infarction, supraventricular and ventricular tachyarrhythmias, and severe hypotension can all occur. The sympathetic activation produced by these drugs antagonizes the action of insulin and cocaine use has been identified as an independent risk factor for diabetic ketoacidosis [103]. The risk of diabetic ketoacidosis may be increased by the omission of insulin before discos and parties to avoid the potential risk and embarrassment of hypoglycemia. Ecstasy is also associated with severe hyponatremia, secondary to inappropriate secretion of antidiuretic hormone, which may complicate the management of diabetic ketoacidosis [95]. Cannabis Cannabis is not known to affect glucose metabolism but its effects on the central nervous system may increase appetite and impair recognition of hypoglycemia. Use of cannabis in low doses is associated with sympathetic activation and tachycardia; at high doses, parasympathetic activation may predominate, resulting in bradycardia and hypotension. In the absence of any structural heart disease, these effects are usually well tolerated. Intravenous drug abuse Recreational drug use often disrupts normal lifestyle and a person with diabetes may abandon the daily routine of regular meals and insulin injections. Recreational drug use may also be only one aspect of a chaotic lifestyle associated with other high-risk behaviors. This can result from the use of any recreational drug, but intravenous drug abuse (particularly of opiates, but also amfetamines) is particular damaging and is strongly associated with poor social support, criminality and mental illness. Intravenous drug use is uncommon in people with diabetes (as it is in the Hypoglycemia While the association between recreational drug use and diabetic ketoacidosis is well established, there are few data suggesting any association with hypoglycemia. Such drugs, however, are often taken in conjunction with alcohol and may be associated with poor oral intake of carbohydrate both of which will increase the risk of hypoglycemia. Moreover, amfetamine-like stimulants can induce frenetic behavior at night clubs and raves which can induce hypoglycemia in people treated with insulin [104]. Furthermore, the sympathomimetic effects of cocaine and amfetamine-type stimulants may mimic the autonomic signs and symptoms of hypoglycemia. Advice on recreational drug use in diabetes Illicit drugs cause significant morbidity and are hazardous for people with diabetes. When exposed to recreational drugs and alcohol, modest reductions in insulin dosage and regular consumption of carbohydratebased snacks or non-alcoholic sugary drinks are required, particularly if strenuous dancing is to be undertaken. Travel Diabetes must not be regarded as a bar to short or long-distance travel, although careful planning may be required to avoid metabolic disturbances and other problems of diabetes that could have particularly serious consequences away from home. Diet and an adequate fluid intake may be disrupted while traveling or staying abroad, and local differences in climate, food, endemic diseases and medical facilities may compromise diabetes control. Blood glucose levels should be monitored frequently during travel and holidays, and people with diabetes must be able to take a pragmatic approach to deal with contingencies. Occasionally, specific diabetic complications or other medical disorders such as uncontrolled hypertension or ischemic heart disease can jeopardize health and safety during travel and periods away from home. Insurance and medical care abroad Comprehensive medical insurance is essential to cover accidents and illness that require medical assistance, and loss of medical equipment and drugs. The insurance policy must cover diabetes and other pre-existing medical conditions, as claims relating to these may otherwise be rejected. Most travel policies contain exclusions, which frequently include diabetes; a person with diabetes may not be covered for conditions such as a stroke or myocardial infarction for which diabetes is a recognized risk factor. When appropriate, insurance must be adequate to cover any dangerous sporting activities (when hypoglycemia could be particularly hazardous), and the costs of emergency air transport home in the event of a serious accident or illness. A list of insurers who do not load premiums against people with diabetes can be obtained from national diabetes associations. Irrespective of medical insurance cover, it should be appreciated that emergency medical care available in some countries is suboptimal or even potentially dangerous for a diabetes-related emergency. In some parts of the world, insulin is not readily obtainable and intravenous fluids are in short supply. These considerations may influence the choice of holiday destination for people with diabetes.

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Fournier gangrene (gangrene of the perineum and genitalia) is associated with diabetes in almost 50% of cases [11]. The rare and often fatal facial and/or maxillary sinus fungal infection mucormycosis is most often associated with diabetes [12]. Abdominal pain and vomiting may be sufficiently severe as to mimic an acute surgical problem. It is critically important to recognize this, as the administration of an anesthetic is almost invariable fatal. Clinical signs include dehydration, deep, sighing respirations (air hunger or Kussmaul respiration) and a sweet-smelling fetor (like nail varnish remover) caused by the ketones on the breath. As the ability to detect the smell of ketones is genetically determined, and approximately one-third of people are unable to do this, it is important that individual doctors are aware if they are not equipped with this additional diagnostic tool. If the condition has progressed to the stage of coma, the associated signs of dehydration must lead to urgent checking of blood glucose, urinary ketones and arterial blood pH in order to expedite definitive treatment. Blurred vision Major changes in plasma glucose will be followed over a period of days and weeks by blurring of vision. It is most important to explain to the patient that the visual blurring will become worse following the relatively rapid correction of gross hyperglycemia. This explanation is vital to avoid the supposition that diabetic blindness is already progressing with consequent unnecessary worry. It is also important to prevent the unnecessary purchase of spectacles that will be redundant after the hyperglycemia is treated. It is reasonably assumed that shifts in osmotic pressure between plasma and inside the eyeball accounts for the visual change. Detailed tests, however, have not to date tied down any identifiable refractive change [7]. Infections Exposure of leukocytes to glucose concentrations above 11 mmol/L produces paralysis of phagocytic and other functions [8]. This effect, together with other possible effects upon immune function, explains the impaired ability to fight off bacterial and fungal infections. Susceptibility to viral infections appears to be little changed although clear data are lacking. In the meantime, the dysregulated secretion of counter-regulatory hormones (glucagon, growth hormone and catecholamines) enhances the breakdown of triglyceride into free fatty acids and increases the rate of gluconeogenesis, which is the main cause for the high blood glucose level in diabetic ketoacidosis. Beta-oxidation of these free fatty acids leads to formation of ketone bodies (-hydroxybutyrate, acetoacetate and acetone). Acetone is volatile and is released from the lungs, giving the characteristic sweet smell to the breath. Metabolic acidosis ensues when the ketone bodies are released into circulation and deplete the acid buffers. The hyperglycemia-induced osmotic diuresis further depletes sodium, potassium, phosphates and water. Patients are often profoundly dehydrated and have a significantly depleted total body potassium at presentation. Sometimes, a normal or even elevated serum potassium level is seen as a result of the extracellular shift of potassium with severe acidosis. Great care must be taken to monitor serum potassium levels repeatedly once insulin treatment is started as the concentration can drop precipitously. This presentation is complicated by stress hyperglycemia resulting from the catecholamine and cortisol elevations. Although this may cause problems for the purist wishing to evaluate an effect of diabetes per se, from the perspective of the patient with a life-threatening condition exacerbated by dysglycemia, exact definitions of diabetes are not relevant. The 3-year death rate in those with normal glucose levels was 24% in the same study. The effect of reasonable glycemic management (blood glucose <10 mmol/L) for those with no prior insulin therapy and stratified as having low coronary risk factors produced a 52% improvement in mortality [18]. Good clinical practice demands measurement of plasma glucose on diagnosis of an acute coronary syndrome. If plasma glucose is raised (7 mmol/L may be quoted, but in the individual case interpretation depends upon time since last meal), then both fasting plasma glucose and HbA1c should be measured.

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There is little information in the literature about the potentiation of activity between a biocide and an antibiotic and such a study is important and provides interesting application/effect of triclosan. On pages 37-38, the text of the opinion (section 12) has been modified to clarify the use of in situ data in relation to in vitro investigations. The conclusion of the opinion has been clarified to reflect comments received suggesting additional clarity. For reasons of clarity, a brief rationale underpinning its evaluation of each comment is provided for each comment. Regarding the comment on stability and solubility of triclosan, the normal storage conditions are not defined in the submission. Regarding the comment on evidence of the potential of triclosan to induce or transmit antibacterial resistance stating that since 2006 "there do not appear to be any compelling reasons or scientific data to support different conclusions regarding the potential for triclosan to induce or transmit antibacterial resistance. In fact, there are several studies that provide support for a lack of antibacterial resistance in situ (Cole et al. In addition, the methodologies used in these studies differ, notably in the measurement of resistance and although useful, the data provided by these studies showing a lack of correlation between triclosan usage and selection of triclosan resistance are limited. The in situ studies focused on measuring triclosan resistance and antibiotic resistance following triclosan exposure. The six in situ studies reported in this opinion showed no increase in bacterial resistance following exposure to triclosan. The points regarding dental plaque and gingival health and the lack of resistance found in a number of environmental isolates are already covered by the opinion. While the Walker study and the other studies cited were state-of-the art at the time they were performed, they did not have the modern tools. Through the use of different methodologies and analysis of data, these studies did not find a correlation between triclosan exposure and emerging resistance. This contrasts with studies performed in vitro and emphasizes the need for translational research. The development of bacterial resistance through well-defined mechanisms, notably following triclosan exposure, has been very well-described. These studies have however not looked at the phenotypic expression of these mechanisms, nor at the maintenance of the gene pool and transfer of resistance determinants. With this in mind, the information obtained in situ is limited, and it is premature at this point to conclude that triclosan is not of any concern. It must be emphasized that, although this opinion focuses on triclosan, the conclusion and observation drawn in this document are also valid for other biocides. Regarding the comment that the statement that environmental concentrations in selected geographical regions are high enough that "triggering of bacterial resistance could also occur in the environment" is speculative and not supported by the studies conducted by Ledder et al. Where a selective pressure exerted by a biocide is present, then alteration of a microcosm is to be expected. Hence prudent use is mentioned in the conclusion of the opinion: When used appropriately, biocides, including triclosan, have an important role to play in disinfection, antisepsis and preservation. This opinion is based on the weight and quality of the available scientific evidence regardless of its source. There were indeed no differences in susceptibility of the clinical isolates to various biocides over time. This study confirmed that antibiotic resistant bacterial isolates might not necessarily be less susceptible to a range of biocides. Comemnts on ecotoxicity were not considered as they are out of the scope of this opinion. Baumannii was susceptible to triclosan with only 3% showing reduced susceptibility (max. They further observed that all triclosan resistant isolates were also resistant to important chemotherapeutic antibiotics while the susceptible isolates showed a resistance percentage between 40% and 55%. Concerning comments on the link between triclosan exposure and resistance to important antibiotics in vitro this has been made clear in the opinion. The role of biocides, including triclosan, in emerging resistance to clinically effective antibiotics and their impact in clinical settings needs to be clarified. This confirms that there was no correlation between antibiotic susceptibility profile and biocide susceptibility. Scientific Committee members Jьrgen Angerer, Ulrike Bernauer, Claire Chambers, Qasim Chaudhry, Gisela Degen, Gerhard Eisenbrand, Thomas Platzek, Suresh Chandra Rastogi, Vera Rogiers, Christophe Rousselle, Tore Sanner, Kai Savolainen, Jacqueline Van Engelen, Maria Pilar Vinardell, Rosemary Waring, Ian R.

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In spite of the availability of advanced injection devices, some patients feel it a burden to take these additional injections 2­4 times a day. For reasons of biochemical compatibility, it is unfortunately not possible to mix insulin and pramlintide in the same pen. Conclusions and perspectives Overall, pramlintide has proven effective in terms of reducing glycemia and weight, but must now prove efficacy against new drugs such as incretin mimetics. Conversely, pramlintide appears to be a safe antidiabetic drug, which can be used in combination with classic antidiabetic agents. Similar elimination rates of glucagon-like peptide-1 in obese type 2 diabetic patients and healthy subjects. Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type 2 diabetes mellitus. Four weeks of near-normalisation of blood glucose improves the insulin response to glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide in patients with type 2 diabetes. The pathophysiology of diabetes involves a defective amplification of the late-phase insulin response to glucose by glucose-dependent insulinotropic polypeptide ­ regardless of etiology and phenotype. Reduced incretin effect in dexamethasone-induced insulin resistance and glucose intolerance in diabetic offspring. Role of incretin hormones in the regulation of insulin secretion in diabetic and nondiabetic humans. Pancreatic beta-cells are rendered glucose-competent by the insulinotropic hormone glucagon-like peptide-1(7-37). Glucagon-like peptide 1 (7-36) amide stimulates exocytosis in human pancreatic beta-cells by both proximal and distal regulatory steps in stimulus-secretion coupling. Beta-cell Pdx1 expression is essential for the glucoregulatory, proliferative, and cytoprotective actions of glucagon-like peptide-1. Exendin-4 stimulates both beta-cell replication and neogenesis, resulting in increased beta-cell mass and improved glucose tolerance in diabetic rats. Glucagon-like peptide 1 inhibits cell apoptosis and improves glucose responsiveness of freshly isolated human islets. Receptor gene expression of glucagon-like peptide1, but not glucose-dependent insulinotropic polypeptide, in rat nodose ganglion cells. Determinants of the impaired secretion of glucagon-like peptide-1 in type 2 diabetic patients. Lack of suppression of glucagon contributes to postprandial hyperglycemia in subjects with type 2 diabetes mellitus. Glucagon-like peptide-1, but not glucose-dependent insulinotropic peptide, inhibits glucagon secretion via somatostatin (receptor subtype 2) in the perfused rat pancreas. Glucagon-like peptide 1 inhibition of gastric emptying outweighs its insulinotropic effects in healthy humans. Glucagon-like peptide-1 promotes satiety and reduces food intake in patients with diabetes mellitus type 2. A meta-analysis of the effect of glucagon-like peptide-1 (7-36) amide on ad libitum energy intake in humans. Tissue distribution of messenger ribonucleic acid encoding the rat glucagon-like peptide-1 receptor. Cardioprotective and vasodilatory actions of glucagon-like peptide 1 receptor are mediated through both glucagon-like peptide 1 receptor-dependent and -independent pathways. Direct effects of glucagon-like peptide-1 on myocardial contractility and glucose uptake in normal and postischemic isolated rat hearts. Glucagonlike peptide 1 can directly protect the heart against ischemia/reperfusion injury. Effects of glucagon-like peptide-1 in patients with acute myocardial infarction and left ventricular dysfunction after successful reperfusion. Recombinant glucagon-like peptide-1 increases myocardial glucose uptake and improves left ventricular performance in conscious dogs with pacing-induced dilated cardiomyopathy. Glucagon-like peptide-1 infusion improves left ventricular ejection fraction and functional status in patients with chronic heart failure. Effects of glucagon-like peptide-1 on endothelial function in type 2 diabetes patients with stable coronary artery disease. Exenatide effects on diabetes, obesity, cardiovascular risk factors and hepatic biomarkers in patients with type 2 diabetes treated for at least 3 years.

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Brewin (75), for example, has suggested that flashbacks are clearer than other trauma memories, albeit more 114 Verfaellie and Vasterling fragmented and less easy to retrieve in a well-regulated manner. Supporting this notion, Hellawell and Brewin (72,76) found that "flashback" reexperiencing episodes, as compared to "normal" trauma memories, were associated with more autonomic and motor behaviors and greater sensory detail; they were experienced more often in the present tense and were characterized more often by primary emotions such as horror, fear, and helplessness. In examining nonflashback intrusions, Rubin, Feldman, and Beckham (61), however, found no evidence that trauma memories differed from nontrauma memories in coherence, although reliving phenomena increased as memories were more related to the trauma. Indeed, recurrent involuntary trauma memories appear to share many of the same characteristics. Characterizing the New Learning Impairments the results of neuropsychological studies examining the presence and nature of difficulties in new learning remain unclear. Several of these observed that memory impairments tend to be selective to the verbal domain (80), but others have documented impairments in visual memory as well (28,81­83). Different conclusions also have been drawn with regard to the nature of the impairment, with studies variably highlighting problems with the initial registration of information (28,84,85), with both immediate and delayed memory (86­88), and with sensitivity to interference (28,89,90). These studies raise the question of whether impaired memory, when observed, may be due to comorbid conditions such as substance abuse or depression (95). A meta-analysis by Brewin, Kleiner, Vasterling, and Field (78) helps to clarify the role of several of these variables. Although the magnitude of memory impairment is greater when the comparison group consists of individuals without trauma exposure, a significant impairment remains when a trauma-matched control group is used, which is on the order of one-third of a standard deviation. To the extent that continued stress exposure may lead to a progressive course of the disorder, cognitive deficits might be more obvious over time; indeed, in at least one study, memory impairment was absent on most measures of memory in recent adult trauma survivors with post-traumatic stress symptoms (98). The frontal lobes, by contrast, are critical for strategic aspects of encoding and retrieval. Specifically, it has been suggested that a disruption of strategic encoding processes, leading to impoverished encoding, may underlie enhanced susceptibility to interference (79). A similar sensitivity to interference is often seen in patients with structural lesions to the frontal lobes (102,103). Further, since strategic encoding processes are more critical for encoding of unrelated compared to related word lists, the fact that memory impairment is seen more consistently on the Rey Auditory Verbal Learning test (which is composed of unrelated words) than on the California Verbal Learning Test (which is composed of categorized words) is consistent with this interpretation (79). It should be noted that such frontal encoding deficits are not simply a consequence of poor attention as memory impairments persist even when attention is controlled for (84,87). Frontal functions are also critical for monitoring the appropriateness of a retrieved memory. Examining the relationship between monitoring errors and aspects of psychopathology, we found that intrusions and false alarms were positively correlated with reexperiencing symptoms and negatively correlated with avoidance and emotional numbing symptoms (28). One explanation of these findings is in terms of a failure to inhibit task-irrelevant processes, reflecting a faulty gating mechanism for the controlled processing of task-relevant information (28). Another explanation is that hyperarousal and associated frontal system disruption may interfere with the controlled aspects of memory. The relationship between symptom severity and memory performance, however, is likely multidetermined as another study found that memory performance correlated not with current symptoms but rather with reported worst-episode symptoms (104). Of note, in a recent study that specifically targeted the role of the hippocampus in configural processing, the ability to perform a configural task was significantly correlated with hippocampal volume (119). It has been suggested that the ability of the hippocampus to process and encode the configural relationships among multiple elements is critical for the contextual regulation of emotional responses (121). Perhaps more important, given the intricate link among these regions, functional imaging studies that examine not only distinct patterns of activation in each of these regions but also the functional connectivity among these regions will be critical. In the last few years, several prospective studies in humans have documented similar adverse effects on memory of acute stress associated with military exercises (125) or special operations (126). In the first prospective study of Army soldiers deployed to Iraq, significant pre- to post-deployment declines were observed in both verbal and visuospatial memory (127). To address this question, a number of studies have compared memory for neutral and trauma-related words in the context of list-learning tasks. These findings suggest a processing bias that may favor both attending and responding to trauma-related information and that may have an impact on memory, especially under conditions that require self-initiated retrieval. In one of the recall studies mentioned (133), an independent probe indicated that traumarelated words did not receive preferential attention, and yet they were better recalled. On a cognitive level, this "memory bias" may be due to the fact that traumarelated information is encoded more richly and, to the extent that it evokes memories of the traumatic event, is assimilated within an already existing emotional memory network, thus making it easier to retrieve later. On a neurobiological level, emotional arousal activates b-adrenergic receptors in the amygdala, and amygdala activation in turn modulates hippocampally mediated consolidation (142). It is possible that increased amygdala responsivity plays a similar role in the enhanced encoding of trauma-related information.


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