Plasma beta-endorphin level in cases of luteal phase defect

OBJECTIVE: To evaluate beta-endorphin secretion in euprolactinemic cases of luteal phase defect (LPD). DESIGN: Serial blood samples from the 18th to the 26th day of the menstrual cycle were assayed for beta-endorphin, progesterone (P), estradiol (E2), and prolactin (PRL) in cases of LPD and controls. Diagnosis of LPD was based on determinations of serum P and premenstrual endometrial biopsy. SETTING: From Cairo University Hospitals. PATIENT, PARTICIPANTS: Twenty-six women with LPD and 8 normal fertile women (controls) were chosen. INTERVENTIONS: None. MAIN OUTCOME MEASURES: beta-Endorphin, P, E2, and PRL concentrations were determined by the corresponding 125I radioimmunoassay. RESULTS: Plasma beta-endorphin level in cases of LPD varied from 2.58 to 9.14 pmol/L, whereas the level of controls varied from 2.41 to 5.57 pmol/L. The mean value of plasma beta-endorphin in cases of LPD was significantly higher than that of controls by 146% (P less than 0.0005). In spite of the significant decrease of serum P in cases of LPD, serum E2 level did not differ significantly from that of controls. CONCLUSION: The possible sources of beta-endorphin rise and its implication in the etiology of LPD are explained.     

Comparative value of prostaglandin E1 and papaverine in treatment of erectile failure: double-blind crossover study among Egyptian patients.

In a double-blind, crossover designation penile intracavernous prostaglandin E1 and papaverine hydrochloride were compared in regard to effectiveness and safety in 52 patients investigated and treated for sexual erectile dysfunction. In evidence of the reliable effectiveness, prostaglandin E1 (20 micrograms/ml.) induced significant positive erectile response in 42 of 52 patients (81%). This rate reached 100% with neurogenic, hyperprolactinemic and/or psychogenic impotence. However, with papaverine hydrochloride (30 mg./ml.) and exclusively in cases of vasculogenic (most probably arteriogenic) impotence, negative erectile response was revealed as absent erection in 6 of 52 patients (11.5%) and nonrigid tumescence in 13 (25%) versus 2 (3.8%) and 8 (15.4%), respectively, with prostaglandin E1. Moreover, with prostaglandin E1 the regional pain was tolerable and transient, and the positive erectile response was not attended by priapism even in patients who formerly had priapism with papaverine hydrochloride. However, presently with prostaglandin E1 the relatively higher cost and shorter expiration period would probably limit its diagnostic and therapeutic use in Egypt, and probably in other developing countries.     

Disturbances of Haemostasis in Diabetes Mellitus

Diabetes mellitus is associated with disturbances in haemostasis that could contribute to the development of thrombotic complications.The present study was undertaken to determine the behavior of coagulation variables and fibrinolytic system in diabetes mellitus. Forty five diabetic patients and forty five matched controls were evaluated by doing the following haemostatic parameter, prothrombin time, partial thromboplastin time, thrombin time, coagulation factors assay II, VII, IX, & plasma fibrinogen, ADP-induced platelet aggregation, protein C, a₂- antiplasmin, PAI and FDPs. Generally diabetic patients have high levels of fibrinogen, a₂- antiplasmin, & PAI and lower level of protein C. Other haemostatic parameters did not show statistically significant difference between diabetic patients and control group. Significantally elevated levels of PAI, a₂- antiplasmin together with low protein C level in diabetic patients may result in the disturbance of haemostatic balance favoring thrombotic events. Conclusion: High levels of plasma fibrinogen, a₂A- antiplasmin with low plasma protein C activity could lead to a prothrombotic tendency in insulin dependent diabetic patients. Moreover, in non-insulin dependent diabetic patients, the above mentioned parameters together with high levels of ADP-induced platelet aggregation and plasminogen activator inhibitor may increase the risk of thrombotic complications. Obesity can be considered as an additional risk factor for development of thrombosis in diabetic patients.     

Sputum microbiome profiles identify severe asthma phenotypes of relative stability at 12 to 18 months

1. Download : Download high-res image (203KB)
2. Download : Download full-size image

     

Steroidal Sapogenins from Tacca leontopetaloides

Diosgenin and its ring-F-hydroxylated derivatives isonarthogenin {spirost-5-ene-3,27-diol {3beta, 22 R, 25 S)} and isonuatigenin {spirost-5-ene-3,25-diol (3beta, 22 R, 25 S)}, together with the 22,25-epoxyfurost-5-ene isomer nuatigenin {furost-5-ene-3,26-diol-22,25-epoxy (3beta, 22 R, 25 S)}, were identified as the major steroidal sapogenins of the acid hydrolysate of an extract of leaves of TACCA LEONTOPETALOIDES by IR, (1)H-NMR, (13)C-NMR, and mass spectroscopy. A diosgenin ester was isolated which apparently arose by ring closure of a glycosylated furostene during hydrolysis.     

The ALK inhibitor ASP3026 eradicates NPM-ALK+ T-cell anaplastic large-cell lymphoma in vitro and in a systemic xenograft lymphoma model

NPM-ALK⁺ T-cell anaplastic large-cell lymphoma (ALCL) is an aggressive type of cancer. Standard treatment of NPM-ALK⁺ ALCL is CHOP polychemotherapy. Although patients initially respond favorably to CHOP, resistance, relapse, and death frequently occur. Recently, selective targeting of ALK has emerged as an alternative therapeutic strategy. ASP3026 is a second-generation ALK inhibitor that can overcome crizotinib resistance in non-small cell lung cancer, and is currently being evaluated in clinical trials of patients with ALK⁺ solid tumors. However, NPM-ALK⁺ ALCL patients are not included in these trials. We studied the effects of ASP3026 on NPM-ALK⁺ ALCL cell lines in vitro and on systemic lymphoma growth in vivo. ASP3026 decreased the viability, proliferation, and colony formation, as well as induced apoptotic cell death of NPM-ALK⁺ ALCL cells. In addition, ASP3026 significantly reduced the proliferation of 293T cells transfected with NPM-ALK mutants that are resistant to crizotinib and downregulated tyrosine phosphorylation of these mutants. Moreover, ASP3026 abrogated systemic NPM-ALK⁺ ALCL growth in mice. Importantly, the survival of ASP3026-treated mice was superior to that of control and CHOP-treated mice. Our data suggest that ASP3026 is an effective treatment for NPM-ALK⁺ ALCL, and support the enrollment of patients with this lymphoma in the ongoing clinical trials.