The patient had attained menopause 3 months earlier, before which

The patient had attained menopause 3 months earlier, before which she had regular cycles. There was no history of cough with expectoration, headache, arthralgia, and rash, and nor was there a history of recent travel to malaria endemic zone or exposure to any patient of tuberculosis. Examination of the patient revealed pulse rate of 118 per minute, blood pressure of 110/70 mm Hg (supine), and oral temperature of 38.3°C (101°F). She had find more moderate conjunctival pallor and scleral icterus. There was no lymphadenopathy, clubbing, eschar, or skin rashes. Oxygen saturation was 99% on room air, and there were no signs of respiratory Inhibitors,research,lifescience,medical distress in

the patient. Cardiovascular examination revealed a systolic flow murmur in the aortic area. The respiratory and nervous system examinations

were within normal limits. Her chest X-ray and abdomen ultrasound revealed no significant Inhibitors,research,lifescience,medical abnormalities except for mild hepatomegaly. Routine hematological evaluation, on admission, revealed very low hemoglobin (Hb); 22 g/L (120-160), hematocrit; 7.2% (35-45), total leukocyte count (TLC); 3×109/L (4-11), total platelet count (TPC); 64.5×109/L (150-450), absolute neutrophil count; 1.9×109/L (1.5-8×109/L), corrected reticulocyte count; 1.5% (0.5-2), Inhibitors,research,lifescience,medical red cell distribution width; 17.5% (11.5-14.5), mean corpuscular volume (MCV); 114.3 fL (80-98), mean corpuscular hemoglobin (MCH); 34.9 pg (26-32), and mean corpuscular hemoglobin Inhibitors,research,lifescience,medical concentration (MCHC); 30.6% (32-36). Peripheral smear showed pancytopenia

with a moderate degree of anisopoikilocytosis and a good number of macrocytes, macro-ovalocytes, and hypersegmented neutrophils. Bone marrow aspiration and trephine biopsy from the right posterior superior iliac Inhibitors,research,lifescience,medical spine revealed marked hypercellularity for age (70%), florid erythroid hyperplasia with an altered myeloid to erythroid ratio (1:2), megaloblastic dyspoiesis, and numerous giant metamyelocytes. Micromegakaryocytes and/or megakaryocyte clustering were not seen. Perl stain showed DNA ligase adequate marrow iron stores without any ring sideroblasts. There was no evidence of blast prominence (4%), granulomas, hemoparasites, malignancy, or increased reticulin condensation (figures 1 and ​and2).2). The bone marrow morphology was suggestive of megaloblastic anemia, which was confirmed biochemically by low levels of serum vitamin B12 (59.6 pg/mL, reference; 180- 900), low normal folic acid (3.9 ng/mL, reference; 4-24), and markedly elevated serum lactate dehydrogenase (LDH) [10,550 IU/L, reference; 225-420]. The patient’s routine liver and renal function tests were within normal limits except for mild unconjugated hyperbilirubinemia (total bilirubin; 4.8 mg/dL [0.2-1.2]/direct; 0.4 mg/dL [up to 0.3]). Her upper and lower gastrointestinal endoscopy did not show any abnormality.


some strictures which initially appear malignan


some strictures which initially appear malignant may later be found to be due to treatable causes such as chronic pancreatitis or autoimmune pancreatitis. If endoscopic ultrasound with fine-needle aspiration and on-site cytologic review is available, then this dilemma can often be solved at the time of the procedure. However, EUS is not at widespread at ERCP and many endoscopists (particularly in community settings) will Inhibitors,research,lifescience,medical have to rely on a high index of suspicion for placing a metallic stent across a presumed malignant stricture. The concern about removal of the stent in cases of benign disease would seem to be addressed by the use of a covered metallic stent. At this time there is no data specifically on the performance of covered metallic Doxorubicin research buy stents in patients undergoing neoadjuvant therapy, though the main factor which makes metallic stents preferable (i.e., Inhibitors,research,lifescience,medical larger diameter) is still present. In summary, the study by Adams et al. lends further support to the notion that SEMS are a superior device

for management of malignant obstruction in pancreatic cancer patients undergoing neoadjuvant therapy. This patient population is likely to grow as more centers embrace neoadjuvant therapy, so this kind of knowledge is critical Inhibitors,research,lifescience,medical to providing the best outcomes for patients facing this life-threatening illness. It seems increasingly clear that plastic stents are now an obsolete device for management of strictures in pancreatic cancer, and that it is time to embrace metallic stents for all patients with this disease who are not sent immediately to curative surgery, or expected to survive less than six months. Acknowledgements Disclosure: The author declares no conflict of interest.

the Editor, We would like to thank Dr. Kapetanakis and his Inhibitors,research,lifescience,medical colleagues for their interest in our article Inhibitors,research,lifescience,medical (1). We specifically appreciate the attention they brought to the importance of environmental factors, particularly Helicobacter pylori (H. pylori) infection, in the development of sporadic colorectal carcinoma (CRC). While the focus of our article was on the pathologic aspects (2), we would like to take this opportunity to extend our discussion to H. pylori as a STK38 potential etiopathogenetic factor in colorectal tumorigenesis. As mentioned by Dr. Kapetanakis and his colleagues, the development of sporadic CRC is associated with a variety of environmental factors including diet and lifestyle. Given that the colon harbors the largest number of microorganisms in the body, it is natural to assume that certain microbial species may play a role in colorectal tumorigenesis. The first reports connecting intestinal microflora with CRC were published back in the early 1950s. Streptococcus bovis septicemia was reported to be associated with carcinoma of the sigmoid colon (3). This association was subsequently supported by several publications (4-6). Animal studies have shown that S.

Colaco et al report that proton therapy reduced bone marrow expo

Colaco et al. report that proton therapy reduced bone marrow exposure and small bowel exposure, compared to both IMRT and 3D-CRT. Proton therapy also reduced bladder exposure, compared to 3D-CRT, but not compared to IMRT. Their findings are similar to that reported by previous studies on proton therapy for rectal cancer, which also showed that proton

therapy reduced normal tissue exposure compared to 3D-CRT and IMRT (2-4). However, all of these studies have Inhibitors,research,lifescience,medical been dosimetric analyses and not clinical evaluations. While proton therapy does appear to reduce normal tissue exposure, it remains unknown whether this reduction will lead to differences in acute and late toxicity. Clinical studies, ideally prospective trials, will be necessary to evaluate the role of proton therapy in the neoadjuvant treatment of rectal cancer. However, it will be difficult Inhibitors,research,lifescience,medical to design such studies. Treatment-related toxicity in rectal cancer patients is multifactorial, arising from the combination of chemotherapy, radiation therapy and surgery. Hence, it may be difficult to discern the contribution of radiation therapy

to toxicity. If the use of proton therapy leads to only a modest-sized reduction in toxicity, then a large sample size will be required to demonstrate the benefit of proton therapy. Furthermore, long follow-up will be required to Inhibitors,research,lifescience,medical evaluate late toxicity. Similar challenges have made it difficult to evaluate the role of IMRT for rectal cancer. While multiple Inhibitors,research,lifescience,medical dosimetric studies have shown that IMRT reduces normal tissue exposure, only a limited number of retrospective studies have shown reductions in acute toxicity; furthermore, a prospective study did not show a significant BKM120 difference in acute toxicity with the use of IMRT compared to conventional radiotherapy (5-8). Proton therapy for rectal cancer may be associated with certain technical challenges. For example, proton range is highly dependent on the stopping power of different

substances; proton range is much higher in air than in tissue. Changes in rectal gas volume may therefore affect proton range, leading to either undercoverage Inhibitors,research,lifescience,medical of the target or overexposure of normal tissues. In Colaco et al.’s study, Hounsfield units were overridden out for air in the rectum. Hence, this study did not account for uncertainties arising from rectal gas. Further studies are needed on such technical factors. Proton therapy may have a potential role in some specific clinical situations. Proton therapy may reduce the risk of second malignancies in patients undergoing radiation therapy for rectal cancer at a young age. Proton therapy may also have a role in reirradiation for rectal cancer, in patients previously treated with pelvic radiation therapy. While it is difficult to develop clinical trials for such uncommon indications, retrospective studies may help us better understand the role of proton therapy in these situations.

Thus, decision makers are active partners in the design of the

Thus, decision makers are active partners in the design of the pragmatic trials.6,7 The tree or the forest? The distinction

between an explanatory and a pragmatic trial in real life is not that easy. Most trials have both explanatory and pragmatic aspects. Gartlehner et al proposed a set of seven domains to evaluate the explanatory or pragmatic nature of a trial.8 Although they acknowledged that efficacy (explanatory) and effectiveness (pragmatic) exist in a continuum, they used a binary system (yes/no) in the evaluation of these domains. Thorpe et al, a few years later, introduced the pragmatic-explanatory continuum indicator summary (PRECIS) tool.9 PRECIS #KU-57788 manufacturer keyword# was created to enable investigators to design trials acknowledging the explanatory/pragmatic continuum in 10 domains: Eligibility criteria Flexibility of the experimental intervention Practitioner expertise (experimental) Flexibility of the comparison intervention Practitioner Inhibitors,research,lifescience,medical expertise (comparison) Follow-up intensity Outcomes Participant compliance Practitioner adherence Primary outcomes. To illustrate, a very pragmatic trial

across these 10 domains would be: There are no inclusion or exclusion criteria Practitioners are not constricted by guidelines on howapply the experimental intervention The experimental intervention Inhibitors,research,lifescience,medical is applied by all practitioners, thus covering Inhibitors,research,lifescience,medical the full spectrum of clinical settings The best alternative treatments are used for comparison with no restrictions on their application The comparative treatment is applied by all practitioners, covering the full spectrum of clinical settings No formal follow-up sections The primary outcome is a clinical meaningful one that does not require extensive training to assess There are no plans to improve or alter compliance for the experimental or the comparative treatment No special strategy to motivate

Inhibitors,research,lifescience,medical practitioner’s adherence to the trial’s protocol The analysis includes all participants in an intentionto-treat fashion. The idea of the explanatory continuum is very intriguing, although rather challenging to apply and quantify. Some modifications of the PRECIS tool have been developed. Koppenaal et al, for example, adapted the PRECIS Terminal deoxynucleotidyl transferase tool in the assessment of systematic reviews, introducing a scale from 1 to 5 for the 10 domains (1 is for explanatory and 5 for the pragmatic end).10 Using the ordinal scale system, they demonstrated how their modification (named the PR-tool) could quantify the continuum per domain and study, thus giving an overall summary for systematic reviews. The study by Tosh et al11 in this issue of Dialogues in Clinical Neuroscience adapts PRECIS into the Pragmascope tool to help the appraisal of RCTs by mental health researchers.

Hypothermia may then be applied immediately after exercise, while

Hypothermia may then be applied immediately after exercise, while high dosages of anti-inflammatory nutrients such as green tea extract may be taken as additional support on these exercise days. If available, massage treatments could then be added on ‘non exercise days’ in order to complement the overall antifibrotic treatment. However, any exercise regimen should be accompanied by regular assessment of antioxidant stress levels as well as the on-going development of fibrotic tissue changes (see below). General considerations for clinical treatment Fibrosis in

DMD is a complex cascade Inhibitors,research,lifescience,medical involving mechanical, humoral and cellular factors. Originating from wounded myofibres, muscle cell necrosis and inflammatory processes are present in DMD. Muscular recovery is limited due to the limited number and capacity of satellite cells.

Inhibitors,research,lifescience,medical Hence, a proactive and multimodal approach is necessary in order to activate protective mechanisms and to hinder catabolic and tissue degrading pathways. Fibrotic changes in muscle are not confined to DMD muscle. Back in the 1980s, Michelsson developed an animal model to study the effects that develop after forceful exercise of immobilised limbs. He concluded that autoinflammatory processes lead to myositis and secondarily Inhibitors,research,lifescience,medical to fibrosis and even calcification with heterotopic bone formation (73). Two main points can be extracted for DMD. First of all, Inhibitors,research,lifescience,medical immobilisation is not advisable and second forceful overstrain should be avoided. Corticosteroids are frequently used in myofascial inflammation. Corticosteroids generally reduce gene expression and inhibit the proliferation and activity of myofibroblasts, Inhibitors,research,lifescience,medical which mainly leads to suppression of collagen production. Additionally myofibroblast migration, which is fundamental in fibrosis, is delayed after corticosteroid injection. These corticoid-associated disturbances on tendon cell metabolism

may affect the structural for integrity of the tendon and weaken its mechanical properties. There are many side effects of corticosteroids, which include a risk of diabetes, disturbance of hormonal glands and metabolism, suppression of angioneogenesis, immune learn more function and coagulation. Hence, therapeutic protocols that lower the use of corticosteroids are desirable. Stiffening of pulmonary and pericardial connective tissues Mortality in DMD patients is often due to respiratory or cardiac problems. In both body areas – the pulmonary and the pericardial connective tissues – the fibrotic changes in muscular dystrophy tend to be very severely expressed and they tend to influence strongly muscular function (74, 75). An increased stiffening of related tissues can impair muscular function.

Approximately 50% of patients with node-positive colorectal cance

Approximately 50% of patients with node-positive colorectal cancer (CRC) will eventually develop liver metastases during their Selleckchem ALK inhibitor disease process (1,2). The median survival of patients with CRHM without

any treatment is 8 to 10 months, and 5-year survival is less than 5% (3,4). With the use of modern combination systemic therapy regimens, median overall survival has increased to 20-24 months (5-8). For selected patients, who undergo surgical resection, a 5-year survival as high as 58% has been reported (9-11). Thus, surgical resection is the gold standard for treatment for patients Inhibitors,research,lifescience,medical with CRHM and the only potentially curative therapy. Unfortunately, approximately 80-90% of patients with CRHM are not candidates for surgical resection with intent to cure due to various limitations, including: the presence of extra-hepatic metastases, Inhibitors,research,lifescience,medical unfavorable anatomic location of tumor(s), estimated insufficient post-resection functional hepatic reserve (<25-30%), or prohibitive medical co-morbidities. In addition, modern chemotherapy regimens involving oxaliplatin may limit the functional capacity of the liver remnant

due to hepatotoxicity (12,13) (Figure 1). Thus, for the majority of patients, only non-surgical treatment options are available and these can be broadly categorized as systemic therapies or regional hepatic therapies (RHT). Systemic Inhibitors,research,lifescience,medical therapies include chemotherapy and/or biologic agents alone or in combination with other modalities, which are intended to downstage initially

unresectable metastases, reduce or stabilize the disease Inhibitors,research,lifescience,medical burden in the liver for previously chemotherapy naïve patients at high risk for progression, or as sole treatment for clearly advanced unresectable disease. Figure 1 *Systemic therapy may be given prior to and/or following liver directed treatment. RHT can be further Inhibitors,research,lifescience,medical grouped into catheter based treatments such as trans-arterial chemo-embolization (TACE, DEBS, etc), radio-embolization (Ytrrium-90) or immune therapies, such as those offered at our center; regionally infused genetically modified T cells. The other RHT are the local tumor-ablative therapies such as radiofrequency ablation (RFA), microwave ablation (MWA). In recent years, local ablative therapies have become one of the most widely employed modalities to treat initially unresectable CRHM. RFA and MWA are “hot” thermal tumor-ablation Tryptophan synthase treatments that can be used as a component of the initial resection, as components of staged resection, with or without systemic therapy or as standalone treatment strategies for patients with CRHM whom are not initially candidates for resection or are ultimately determined to be unresectable. RFA and MWA are important components of the armamentarium for treating CRHM when surgical resection with negative margins, the gold standard, is not possible due to oncologic, physiologic, or anatomic reasons.

34 Thus, the NMDA antagonist PPI model docs not appear to be anot

34 Thus, the NMDA antagonist PPI model docs not appear to be another instance of receptor tautology and may, therefore, provide a pathway to identification of novel molecular targets for treatments of schizophrenia. PPI in the post-MATRICS era By virtue of the MATRICS program, the new focus of drug discovery in schizophrenia is on the identification

of potential procognitive cotreatments. In contrast, the work discussed above addressed the effects of antipsychotic treatments on PPI in animal models. In the post-MATRICS era, the question arises as to the possible utility of PPI models in the discovery process for procognitive cotreatments. The previous work in rodents indicated that the dopamine PPI model is reliably predictive Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical of existing antipsychotics, while

the NMDA PPI model is insensitive to first-generation antipsychotics, but responsive to clozapine and some other second-generation compounds. Since the anticipated application is for cotreatments to be used in patients already stably treated with antipsychotic drugs, any animal model that is responsive to first-generation antipsychotics is likely to be uninformative. Given that the patients will already be treated with antipsychotics having antagonist actions at dopamine D2 receptors, dopamine agonist models are inappropriate. In Inhibitors,research,lifescience,medical contrast, the PPI models based on the effects of NMDA antagonists may be of considerable value in this context. Antipsychotic effects on PPI and cognition in patients The fundamental difficulty in evaluating

the potential applicability of any animal model for the Inhibitors,research,lifescience,medical I-BET151 nmr prediction of procognitive agents in schizophrenia is the absence of any established positive control compound. That is, in the absence of any path to registration of procognitive treatments that do not also treat positive symptoms of schizophrenia, virtually no studies have been done in this specific area. What we do have some information about, however, arc comparisons of different classes of antipsychotic drugs on both cognition and PPI in patients with schizophrenia. As summarized recently by Hagan and Jones,35 it is clear Inhibitors,research,lifescience,medical that first-generation antipsychotics, which are principally dopamine D2 antagonists, have no beneficial effects on cognition. Similarly, as evident from the many early demonstrations of deficient PPI in antipsychotic-treated patients, first-generation compounds do not normalize PPI in schizophrenia.21,36 With respect to second-generation antipsychotics, and in particular Mephenoxalone clozapine, the evidence is less clear, but indicates that clozapine and some other multireceptor antagonist antipsychotics may have some salutary influences on cognition37 and appear to be associated with relatively normal PPI.36 Of particular interest in this regard is a crosssectional study indicating that clozapine treatment, relative to typical antipsychotic treatments, is associated with reduced PPI deficits in patients with schizophrenia.

ACE is Involved in the so-called reninangiotensin cascade of wate

ACE is Involved in the so-called reninangiotensin cascade of water regulation, which in turn affects blood volume and blood pressure.

A recent study observed an association between the combined dex/CRH test and brain-derived neurotrophic factor (BDNF) in depressed patients, which has been interpreted as evidence for an involvement of a reduced neuroplasticity in the development of disturbed HPA axis regulation.23 Inhibitors,research,lifescience,medical Taken together, there are only a limited number of studies examining the association between candidate genes and the stress response. Besides genes involved in the sympathetic (ACE) or HPA axis-mediated (GR) stress response, further genes constituting different biological systems implicated in emotional regulation26 and neuroplasticity (BDNF) have been examined. However, the results show only moderate effect sizes, although heritability estimates suggest a strong involvement

of genetic factors. Further evidence Inhibitors,research,lifescience,medical for genes involved in the regulation of the stress response could be provided by clinical studies investigating genetic vulnerability factors for stress-related disorders. These genetic risk factors are assumed to be responsible for an inappropriate response to repeated and/or continuous stress and thus for mediating the vulnerability for stress-related disorders. Genetics of stress-related Inhibitors,research,lifescience,medical disorders A large number of diseases can be understood as stress-related disorders, and most of them are characterized by an at least moderate Inhibitors,research,lifescience,medical heritability. In this review, we focus on the most prevalent stress-related disorders, hypertension and coronary artery disease, as examples of cardio-vascular disorders, and on bipolar disorder and unipolar depression as examples of psychiatric disorders. Cardiovascular disorders are the leading cause of mortality in the Western world, and are projected to become the

leading cause of disease Inhibitors,research,lifescience,medical burden worldwide in 2020.32 Essential hypertension is the most common cardiovascular disorder, with a lifetime Ketanserin prevalence of above 50% in most western communities, affecting approximately f billion individuals worldwide33; heritability estimates around 30% have been reported.34 Myocardial Dinaciclib cell line infarction is a serious outcome of coronary artery disease. Twin studies suggest that the risk for myocardial infarction is fairly heritable, with a heredity estimate of 60% in females and 26% in males.35 A large number of case-control association studies in essential hypertension are available (Table IIa) focussing on a number of candidate gene systems. The majority of findings have been obtained with candidates from the sympathetic system, including adrenergic genes, genes of the renin-angiotensin-aldosterone system (RAAS), and genes involved in vascular regulation.

The patients’ weights were measured by Seca scale with 0 1 kg acc

The patients’ weights were measured by Seca scale with 0.1 kg accuracy. Also, using a questionnaire, data were collected on age, literacy level, occupation, type of therapy for diabetes, and type of delivery using medical history and interview with the patients. Laboratory Measurements After

an overnight fasting, samples of 6 ml peripheral blood were taken from all of the patients at most 10 days after the delivery, and were used to determine plasma glycosylated hemoglobin A1C (HBA1C) test by immunoassay method. Also, blood samples were used to prepare serums, which were #PLX-4720 order keyword# kept frozen at -80°C until analysis. Fasting blood samples were also obtained on follow ups and were used to prepare serums, which were kept similarly. The serum samples were used to measure 25(OH) vitamin D3, paratormone (PTH), calcium and phosphorus. The serum 25(OH) vitamin D3 was measured by ELISA and kit of immunodiagnostic systems Ltd (Nyco card equipment, Nyco corporation, Norway). The sensitivity

Inhibitors,research,lifescience,medical of the test was 2 nmol/ml. Serum paratormone was also measured by ELISA and immunodiagnostic systems Ltd (IDS Ltd), which had a sensitivity of 0.6 picomol/l. The serum calcium and phosphorus were respectively measured by calorimetric method by AutoAnalyzer (Echoplus Corporation, Italy), Biosystems kit (Spain), and ELISA method. Dose and Follow-Up The administered Inhibitors,research,lifescience,medical vitamin D was vitamin D3, which were kept from light, frozen, and stored at 15 to 30oC during the study. Patients’ Inhibitors,research,lifescience,medical vitamin D status was determined by measuring serum 25(OH) vitamin D3 concentration. Serum concentrations of lower than 12.5 nmol/l was considered severe deficiency, 12.5 to 24.9 nmol/l was taken as moderate deficiency, 25 to 34.9 nmol/l as mild deficiency, and concentrations higher than 35 nmol/l was regarded as optimal.12 Statistical Analysis The data were

analyzed by the SPSS package Version 11 (SPSS Inc., Chicago, IL, USA). Kolmogro-Smirnov test was used to determine the distribution of quantitative data. Between-group Inhibitors,research,lifescience,medical comparisons were made using t or Wilcoxon tests, and within-group comparisons were made using paired t-test 17-DMAG (Alvespimycin) HCl or Mann-Whitney U-tests. Between-group and within-group comparisons of qualitative data were performed Chi-Square or McNemar tests. A P value of ≤0.05 was considered statistically significant. Results Forty five patients including 24 with the age of 30.7±6.2 years in the IG and 21 with the age of 29.5±4.0 years in the CG completed the study. There was no significant difference between the body mass index (BMI) for the subjects in the IG (28.9±4.8 kg/m2) and CG (27.9±3.6 kg/m2) (table 1). Moreover, there was no significant difference between the two groups in terms of plasma HA1C, literacy level, type of treatment for GDM, or type of delivery.


In the EPO group, there was a reduction in left ven


In the EPO group, there was a reduction in left ventricular end-systolic and end-diastolic diameters (LVESD and LVEDD, respectively), as compared to the control group. Conclusion: Our results indicated that perioperative exogenous EPO infusion could not improve the ventricular function and wall motion index in the immediate post-CABG weeks. Nevertheless, a reduction in LVEDD and LVESD at 4 days and 30 days after CABG in the EPO group, by comparison with the control group, suggested that EPO correlated with a reduction in the remodeling of myocytes and reperfusion injuries Inhibitors,research,lifescience,medical early after CABG. Trial Registration Number: 138809102799N1 Keywords: Erythropoietin, Ischemia, Reperfusion injury, selleck chemicals llc Coronary artery bypass graft Introduction Erythropoietin (EPO) is a glycoprotein hormone produced by the kidney and plays a key role in hematopoiesis.1

In addition to these hematopoietic effects, EPO exerts non-hematopoietic effects on some tissues like the brain,2 kidney,3 retina,4 and muscles.5 Inhibitors,research,lifescience,medical Moreover, both ventricular myocytes and endothelial cells have EPO receptors.6 EPO wields its protective effects on myocardial cells via different Inhibitors,research,lifescience,medical pathways, including stimulation of neovascularization, activation of the PI3K and 2.1 ERK pathways,7,8 and synthesis stimulation of endothelial progenitor cells from the bone marrow.9,10 Coronary artery bypass graft surgery (CABG), an Inhibitors,research,lifescience,medical important treatment modality in ischemic patients, increases myocardial perfusion and ejection fraction (EF) in patients with coronary artery diseases.11 Although the rapid reperfusion by CABG significantly reduces mortality and morbidity,12 this reperfusion paradoxically may contribute to myocardial stunning injuries and/or death after CABG.13,14 Therefore, new treatment modalities should focus on decreasing damage after reperfusion. In addition to the protective effect of EPO on myocardial ischemia, studies on animal Inhibitors,research,lifescience,medical models have shown that EPO can also reduce reperfusion tissue injuries.15-17 Studies on human models have, however, proved somewhat controversial.18,19

While some authors have reported that EPO can reduce ischemia-reperfusion injuries in the myocardium and posited the possible mechanism for this action,20,21 others such as Mocini et al.19 in a different model, SB-3CT performed on patients having undergone CABG, have maintained that EPO has no association with a reduction in the levels of myocardial biomarkers (troponin I and CKMB) after CABG. The latter group of authors justify their conclusions by arguing that EPO induces tissue protection with anti-apoptotic mechanism. Nonetheless, these authors assessed the effects of EPO by two indicators of necrosis, namely troponin I and CKMB. The left ventricular (LV) function is usually described in terms of the EF.