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Objective To analyze the clinical and pathologieal characteristics of IgA nephmlogy secondary to primary sj(o)gren's syndrome(pSS).Method The clinical and pathological data of 8 patients with pSS and IgA in Changzheng Hospital from 2004 to 2009 were analyzed.Results The average age of seven female and one male was (44±8) years old.Five patients presented with edema and proteinuria.Eight patients presented with microhematuria.The average 24-hour proteinuria was (3±4) g.Two patients had hypertension.Serum creatinine levels of two patients were higher than normal level,the others'were normal.Light microscopy examination showed three patients were mild mesangial proliferation with Lee's classification grade Ⅰ;five patients had global sclerosis with Lee's classification grade Ⅱ,Ⅲ and Ⅳ.Positive IgA was mainly found under immunofluorescence microscopy.Electronic microscopy showed no electron-dense deposits.Conclusion IgA nephrology secondary to pSS is different from primary IgA nephrology under immunofluorescence microscopy.
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Objective To observe the efficacy of ealcitonin and bisphosphonates on renal osteopathy of maintenance hemodialysis (MHD)patients. Methods Forty-three MHD patients were raindomly divided into two groups: A group and B group. All the patients were routinely received oral calcium carbonate 1.0 g tid and calcitriol 0.25 μg qd. Calcitonin (20U) hypodermic injection was given three times a week additionally during hemodialysis in A group. Patients in B group received bisphosphonates 70 mg once a week based on the therapy of A group. Serum levels of intact parathyroid hormone (iPTH), calcium, phosphorus, alkaline phosphatase (AKP), bone mass density (BMD) of lumbar spine and femoral neck, and the degree of bone ache (visual analogue scale, VAS) were assessed before the therapy and 3, 6 and 12 months after treatment. The adverse reactions were recorded during treatment. Results The levels of AKP and iPTH in both two groups decreased significantly after treatment. The above values of pre-treatment and 12 months after treatment were as follows: AKP(U/L)of A group 244.05±41.99 and 148.35±27.71,of B group 245.60±40.86 and 143.40±28.03;PTH(ng/L) of A group 697.5±119.7 and 267.4±45.9,of B group 708.2±120.3 and 277.6±41.9 (all P<0.05). While the levels of calcium and phosphorus did not change obviously during treatment (P>0.05). BMD was not improved at 3, 6 mouths and became better at 12 mouths after treatment. As compared to pre-treatment, BMD of lumbar spine(g/cm2) in A group was 1.062±0.223 vs 1.202±0.251 ,in B group 1.033±0.152 vs 1.189±0.225; BMD of femoral neck (g/cm2)in A group was 0.993±0.108 vs 1.067±0.095,in B group 0.947±0.083 vs 1.018 ±0.217 (all P<0.05). The scores of VAS also decreased significantly at 3, 6, 12 months after treatment(P<0.05). No severe adverse reaction was found during the treatment. Conclusions Utilization of calcitonin and combination with bisphosphonates during bemodialysis can effectively preserve the BMD and prevent bone loss in MHD patients and is well tolerated. No significant difference of therapeutic effect is observed between using ealcitonin or combination with bisphosphonates.
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Objective To study the protective effects of ?-asarone against the myocardial ischemia/ reperfusion injury (MI/RI) in cultured cardiac myocytes. Methods MI/RI model was set up with Na2S2O4, which make use of rat cardiac myocytes. The viability of cardiac myocytes (using MTT method), dehydrogenase (LDH, CK) activitices in the medium were measured. Results In MI/RI model, ?-asarone can obviously advance the viability of cardiac myocytes, and decrease the dehydrogenase (LDH, CK) activitices in the medium. Conclusion ?-asarone showed protective effects against the myocardial ischemia/reperfusion injury in cultured cardiac myocytes.
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Objective To study the protective effects of ?-asarone on PC12 cells damage induced by Glutamate. Method The effects of ?-asarone on PC12 cells after Glutamate intoxication on morphology, extent of damage, livability, intracellular calcium concentration and apoptosis ratio were observed. Result Morphological changes, LDH leakage and intracellular calcium concentration increasing, and cell survival decreasing were observed in PC12 cells exposured to Glutamate. 7.5, 15, 30 ?g/mL?-asarone can increase cell survival, decrease LDH leakage. 15, 30 ?g/mL ?-asarone can reduce intracellular calcium concentration and apoptosis ratio. Conclusion ?-asarone prevents the toxicity of Glutamate, and it maybe attribute to its effect of anticalcium.
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Objective To study the effects of ?-asarone on mitochondrial membrane potential(MMP) of cardiac myocytes with ischemia reperfusion injury. Methods The cardiac myocytes model of myocardial ischemia reperfusion injury (MIRI) was induced with sodium dithionite (Na2S2O4). The primary cultured cardiac myocytes of SD neonatal rats were randomized into six groups:normal group,model control group,high-dose ?-asarone (25 ?g/mL),middle-dose ?-asarone group(12.5 ?g/mL),low-dose ?-asarone group (6.25 ?g/mL) and medium group. Mitochondrial membrane potential(MMP) of myocardial cells were measured by flow cytometry. Results Compared with the normal group,MMP in the model control group was obviously decreased(P