Comparative efficacy of tamsulosin versus nifedipine for distal ureteral calculi: a meta-analysis.

OBJECTIVE: The aim of this study was to systematically compare the therapeutic effect and safety of tamsulosin with nifedipine in medical expulsive therapy for distal ureteral calculi. METHODS: Databases, including PubMed, EMBASE, the Cochrane Library, and Clinical Trial Register Centers, were comprehensively searched. Relevant randomized controlled trials (RCTs) were selected, and quality assessment was performed according to the Cochrane Handbook. RevMan software was used to analyze the outcome measures, which consisted of expulsion rate, expulsion time, and complications. RESULTS: Twelve RCTs consisting of 4,961 patients were included (tamsulosin group, 2,489 cases; nifedipine group, 2,472 cases). Compared with nifedipine, tamsulosin significantly increased the expulsion rate (risk ratio =1.29, 95% CI [1.25, 1.33], P<0.0001) and reduced the expulsion time (standard mean difference =-0.39, 95% CI [-0.72, -0.05], P=0.02). Regarding safety, tamsulosin was associated with fewer complications than nifedipine (risk ratio =0.45, 95% CI [0.28, 0.72], P=0.0008), and further subgroup analysis showed that tamsulosin was associated with a lower risk of both mild and moderate-to-severe complications. CONCLUSION: On the bias of current evidence, tamsulosin showed an overall superiority to nifedipine for distal ureteral calculi <10 mm in aspects of expulsion rate, expulsion time, and safety. Tamsulosin was supposed to be the first drug to be recommended to patients willing to receive medical expulsive therapy.

[Effect of oxymatrine on JAK2/STAT3 signaling in renal tissues of rats with septic shock].

OBJECTIVE: To explore the effect of oxymatrine (OMT) on JAK2/STAT3 signaling in renal tissues of rats with septic shock. METHOD: The cecal ligation and puncture (CLP) was adopted to establish the rat septic shock model. Fifty-six male SD rats were randomly divided into 7 groups: the sham operation group, the model (CLP) group, CLP + OMT high, middle, low-dose (52, 26, 13 mg x kg(-1), vena caudalis bolus) groups and the positive control (CLP + dexamethasone, 10 mg x kg(-1)) group. The pathological changes in renal tissues were examined with lightmicroscope. BUN content was determined by urine enzymatic method. Expressions of tumournecrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA in renal tissues were determined by RT-PCR. Expression of JAK2 and STAT3 in renal tissues determined by Western blot. Changes in tumournecrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) contents in renal tissue were determined by radioimmunoassay. RESULT: OMT of different doses could inhibit the JAK2 and STAT3 activation in renal tissues (P<0.05), and decrease the protein expression of JAK2, STAT3, TNF-alpha and IL-1beta mRNA (P<0.05). Besides, it could reduce TNF-alpha and IL-1beta contents in renal tissue homogenate (P<0.05), serum BUN content (P<0.05), and improve such lesions as tissue hyperemia, edema and inflammatory cell infiltration, with identical results in medium and high-dose OMT groups, and the positive control group. CONCLUSION: OMT can inhibit JAK2/STAT3 signaling activity to reduce the expression of proin-flammatory factors (TNF-alpha, IL-1beta) and treat the renal injury in rats with septic shock.

[Effect of oxymatrine on NF-kappaB and other cell factors in rats lung tissue with septic shock].

OBJECTIVE: To explore the effects of oxymatrine (OMT) on NF-kappaB and other cell factors in rat lung tissue with septic shock. METHOD: Fifty-six male SD rats were randomly divided into 7 groups: sham operation group, OMT control group, model (CLP) group, CLP + OMT high, middle, low-dose group, positive control group. Changes in NF-kappaB (p65) and IkB-alpha activity in the pulmonary tissue were determined by immunohistochemical method, tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels in pulmonary tissue were determined by radioimmunoassay. RESULT: OMT could decrease significantly the NF-kappaB (p65) and IkB-alpha activity in the pulmonary tissue (P < 0.05), TNF-alpha and IL-6 levels in pulmonary tissue homogenate decreased markedly (P < 0.05). OMT could elevate the content of PaO2, SaO2, decrease the content of PaCO2, HCO3- and decrease the ratio between wet weight of the lung and dry weight of the lung and the PWI. CONCLUSION: OMT can inhibit NF-kappaB-inducing kinase (NIK), NF-kappaB activity and reduce the expression of proinflammatory factor (TNF-alpha, IL-6) and antagonize the lung injury in a rat model of septic shock.

Ghrelin blunted vascular calcification in vivo and in vitro in rats.

Ghrelin is a new peptide with regulatory actions in growth hormone secretion in the anterior pituitary gland and in energy metabolism. Currently, ghrelin has potently protective effects in cardiovascular diseases. We used an in vivo model of rat vascular calcification induced by vitamin D3 and nicotine and one of cultured rat vascular smooth muscular cells (VSMCs) calcification induced by beta-glycerophosphate to study the possible mechanism in the regulatory action of ghrelin in vascular calcification. Calcification increased total Ca2+ content and 45Ca2+ deposition in aortas and VSMCs and alkaline phosphatase (ALP) activation in plasma, aortas and VSMCs. However, calcified aortas and VSMCs showed a significant decrease in osteopontin (OPN) mRNA expression and a marked reduction of ghrelin levels in plasma and its mRNA expression in aortas. The aortic calcification was significantly attenuated by subcutaneous administration of ghrelin 30 and 300 nmol kg(-1) day(-1) for 4 weeks, and the latter dosage was more potent than the former. Ghrelin treatment at the two dosages reduced the total aorta Ca2+ content by 24.4% and 28.1%, aortic 45Ca2+ deposition by 18.4% and 24.9%, plasma ALP activity by 36.6% and 76.7%, and aortic ALP activity by 10.3% and 47.6% (all P < 0.01 or 0.05), respectively. Ghrelin at 10(-8)-10(-6) mol/L attenuated the calcification in cultured VSMCs, with decreased total Ca2+ content, 45Ca2+ deposition and ALP activity and increased OPN mRNA expression, in a concentration-dependent manner. In addition, endothelin levels in plasma and aortas and its mRNA expression in aortas significantly increased with calcification, but ghrelin treatment significantly decreased endothelin levels and mRNA expression, with the high dosage being more potent than the lower dosage. These results indicate that local ghrelin in vascular was down-regulated during vascular calcification, whereas administration of ghrelin effectively attenuated vascular and VSMCs calcification.