Investigation the effect of propranolol, metoprolol and carvedilol on spermatogenesis in rat testis

Background: Coronary arterial diseases are one of the increasing disease around the worldwide. Because of common using of the beta blockers, we aimed to investigate the effect of different beta-adrenergic receptor blockers on spermatogenesis in male rats.Methods: Adult male Sprague Dawley rats were obtained. Totally 32 rats homogenized according to their weight and divided into four groups that each one includes eight rats. Three of groups were determined as drug groups and remained groups were determined as a control group. Propranolol 40mg/kg, Metoprolol succinate 60mg/kg, Carvedilol 30mg/kg dosage was given by oral gavage within the saline solution, and the only saline solution was given to control group for 21 days, respectively. After 21 days rats were sacrificed, and testis were extracted. Then, histopathologic evaluation was performed.Results: There was statistical significance both right and left testis volume of experimental between control and carvedilol groups (p<0.05). There was statistical histopathological significance between control and carvedilol (p<0.05), control and propranolol (p<0.05), metoprolol succinate and propranolol (p<0.05), metoprolol succinate and carvedilol groups (p<0.05), respectively.Conclusions: Beta-adrenergic receptor blockers have adverse effects on spermatogenesis. Especially propranolol and carvedilol that were non-selective, effects spermatogenesis worse than selective beta blockers such as metoprolol succinate. Extensive use of these drugs may affect spermatogenesis in male, so male patients who have a complaint of infertility should be questioned regarding the use of beta blockers

Effect of pathologic fractures on survival in multiple myeloma patients: a case control study

<p>Abstract</p> <p>Background</p> <p>Multiple Myeloma (MM) is a B cell neoplasm characterized by the clonal proliferation of plasma cells. Skeletal complications are found in up to 80% of myeloma patients at presentation and are major cause of morbidity.</p> <p>Methods</p> <p>49 patients were enrolled with MM admitted to Black Sea Technical University Hospital between 2002–2005. Pathologic fractures (PFs) were determined and the patients with or without PF were followed up minumum 3 years for survival analysis.</p> <p>Results</p> <p>PF was observed in 24 patients (49%) and not observed in 25 patients (51%). The risk of death was increased in the patients with PF compared with patients who had no fractures. While overall survival was 17.6 months in the patients with PFs, it was 57.3 months in the patients with no PFs.</p> <p>Conclusion</p> <p>These findings suggest that PFs may induce reduced survival and increased mortality in the MM patients, however, larger sample size is essential to draw clearer conclusions added to these data.</p

The oral HDAC inhibitor pracinostat (SB939) is efficacious and synergistic with the JAK2 inhibitor pacritinib (SB1518) in preclinical models of AML

Acute myeloid leukemia (AML) is currently treated with aggressive chemotherapy that is not well tolerated in many elderly patients, hence the unmet medical need for effective therapies with less toxicity and better tolerability. Inhibitors of FMS-like tyrosine kinase 3 (FLT3), JAK2 and histone deacetylase inhibitors (HDACi) have been tested in clinical studies, but showed only moderate single-agent activity. High efficacy of the HDACi pracinostat treating AML and synergy with the JAK2/FLT3 inhibitor pacritinib is demonstrated. Both compounds inhibit JAK-signal transducer and activator of transcription (STAT) signaling in AML cells with JAK2V617F mutations, but also diminish FLT3 signaling, particularly in FLT3-ITD (internal tandem duplication) cell lines. In vitro, this combination led to decreased cell proliferation and increased apoptosis. The synergy translated in vivo in two different AML models, the SET-2 megakaryoblastic AML mouse model carrying a JAK2V617F mutation, and the MOLM-13 model of FLT3-ITD-driven AML. Pracinostat and pacritinib in combination showed synergy on tumor growth, reduction of metastases and synergistically decreased JAK2 or FLT signaling, depending on the cellular context. In addition, several plasma cytokines/growth factors/chemokines triggered by the tumor growth were normalized, providing a rationale for combination therapy with an HDACi and a JAK2/FLT3 inhibitor for the treatment of AML patients, particularly those with FLT3 or JAK2 mutations

Eosinophilic pancreatitis mimicking pancreatic neoplasia

Eosinophilic pancreatitis (EP) is a rare disease. It typically occurs in the setting of either eosinophilic gastroenteritis or the hypereosinophilic syndrome. Isolated eosinophilic infiltration of the pancreas is less common. EP usually presents as a pancreatic tumour with abdominal pain and/or obstructive jaundice. The diagnosis is often not made until after pancreatic resection under suspicion of a pancreatic tumour

Brenner tumor of the ovary revealed by cyst aspiration in a patient undergoing in vitro fertilization

unsal, mesut a/0000-0002-2766-5999;WOS: 000319311200018PubMed: 23477702[No abstract available