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21.
本文收集我院确诊为系统性红斑狼疮(SLE)的51例病人的资料,并与20例年龄、性别和身高体重配对的正常人进行对比分析。超声检出40例异常,其中办膜返流19例、心包积液7例、左室扩大8例、左房扩大5例、异常室壁增厚1例。在所查9项超声指标中,以EPSS、LVd、LVs、E、A和E/A最敏感(P<0.05)。本文认为:1.超声能显示SLE患者的明显心包、心内膜及心肌损害;2.左心舒张功能损害先于收缩功能损害:3.超声能显示亚临床型SLE患者的异常。  相似文献   
22.
采用诊断超声强度经腹部辐照宫腔.取早孕蜕膜,检测其中的免疫活性细胞,以探讨超声波对早孕蜕膜中免疫活性细胞的影响。结果表明:诊断超声强度未能影响早孕蜕膜中T淋巴细胞及其亚群的状态,却可使巨噬细胞数目减少,或许在一定程度上会削弱宫腔局部的抗感染能力。  相似文献   
23.

Background

The role of heme oxygenase-1 (HO-1) in the cardioprotection induced by delayed remote ischemic preconditioning (DRIPC) has not been investigated. Therefore, this study was designed to investigate whether HO-1 is involved in DRIPC-mediated cardioprotection in an isolated perfused rat heart model.

Materials and methods

Isolated rat hearts were subjected to 30 min ischemia followed by 60 min reperfusion. DRIPC (four cycles 5-min occlusion and 5-min reflow at the unilateral hind limb once per day for 1, 2, or 3 d before heart isolation, abbreviated as D1RIPC, D2RIPC, or D3RIPC respectively). Infarct size, myocardial troponin levels, and heart function were measured. The protein and messenger RNA levels of HO-1 were determined.

Results

DRIPC facilitated postischemic cardiac functional recovery and decreased cardiac enzyme release. The infarct size-limiting effect of DRIPC was more pronounced in the D3RIPC group (10.22 ± 2.57%) than the D1RIPC group (22.34 ± 4.02%, P < 0.001) or the D2RIPC group (14.60 ± 3.13%, P = 0.034). These effects in the D1RIPC group could be blocked by Zinc Protoporphyrin IX (ZnPP) (an HO-1 specific inhibitor). DRIPC-mediated cardioprotection was associated with enhanced HO-1 protein expression (D1RIPC, 0.11 ± 0.03; versus 0.15 ± 0.06 in the D2RIPC group, P = 0.06; versus 0.20 ± 0.04 in the D3RIPC group, P = 0.04) and messenger RNA levels of HO-1 expression.

Conclusions

Our findings suggest that HO-1 is involved in the cardioprotection induced by DRIPC, and that increase in the number of preconditioning stimuli may enhance cardioprotective effects accompanied with increased HO-1 level.  相似文献   
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Accumulating evidence has demonstrated that the sodium-potassium-chloride co-transporter 1 and potassium-chloride co-transporter 2 have a role in the modulation of pain transmission at the spinal level through chloride regulation in the pain pathway and by effecting neuronal excitability and pain sensitization. The present study aimed to investigate the analgesic effect of the speciifc sodium-potassium-chloride co-transporter 1 inhibitor bumetanide, and the change in spinal sodium-potassium-chloride co-transporter 1 and potassium-chloride co-transporter 2 expression in a rat model of incisional pain. Results showed that intrathecal bumetanide could decrease cumulative pain scores, and could increase thermal and mechanical pain thresholds in a rat model of incisional pain. Sodium-potassium-chloride co-transporter 1 expression in-creased in neurons from dorsal root ganglion and the deep laminae of the ipsilateral dorsal horn following incision. By contrast, potassium-chloride co-transporter 2 expression decreased in neurons of the deep laminae from the ipsilateral dorsal horn. These ifndings suggest that spinal sodium-potassium-chloride co-transporter 1 expression was up-regulated and spinal potassi-um-chloride co-transporter 2 expression was down-regulated following incision. Intrathecal bumetanide has analgesic effects on incisional pain through inhibition of sodium-potassi-um-chloride co-transporter 1.  相似文献   
26.
Serotonin plays an important role in mood regulation, but the involvement of serotonin pathway genes in the development of bipolar I disorder (BP-I), a mood disorder, is not clear. We selected 21 singlenucleotide polymorphisms (SNPs) within the HTR2A gene, 8 within the SLC6A4 gene and 23 within the TPH2 gene for genotyping using the GoldenGate genotyping assay. A total of 375 patients with BP-I and 475 normal controls were recruited. Two out of 21 SNPs (rs1475196 and rs9567747) in the HTR2A gene and 1/23 SNPs (rs17110566) in the TPH2 gene were significantly associated with BP-I, both genotype-wise and allele-wise. Furthermore, a specific haplotype in the HTR2A gene showed a significant association with BP-I. Our results indicate that the HTR2A and TPH2 genes in the serotonin pathway play important roles in susceptibility to BP-I.  相似文献   
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29.

Objective

To evaluated the long-term outcomes of laparoscopic unilateral adrenalectomy for primary aldosteronism (PA) caused by unilateral adrenal hyperplasia (UAH).

Methods

One hundred and sixty-four patients who underwent laparoscopic unilateral adrenalectomy for UAH from January 2004 to December 2011 were entered in this retrospective analysis. Patients demographics, perioperative parameters, and follow-up results were recorded and analyzed statistically.

Results

All 164 cases suffered hypertension with biochemical evidence of hyperaldosteronism prior to operation. Hypokalemia was observed in 52/164 (37.14 %) patients. UAH was proved by multi-slice computed tomography (MSCT). All operations were completed successfully without any conversions or complications. Postoperative pathology confirmed that 164 cases were cortical nodular hyperplasia, of which 4 cases coexist with medullary hyperplasia and 7 with micro-adenoma. At the median follow-up of 48 months, hypertension was cured in 88 (53.7 %) patients, improved in 71 (43.3 %) patients, and refractory in 5 (3.05 %) patients. Hypokalemia and hyperaldosteronism were cured in all patients except re-elevation of blood pressure and plasma aldosterone in two patients 1 month after adrenalectomy.

Conclusions

As an underestimated subtype of PA, UAH is accepted gradually. Laparoscopic unilateral adrenalectomy is nowadays the preferred approach to treat patients with PA caused by UAH. When adrenal venous sampling is not allowed, high-resolution MSCT is a reliable test for lateralization of aldosterone hypersecretion in carefully selected patients and 97 % had either cure or improvement in blood pressure control.  相似文献   
30.
This study was conducted to investigate the effects of aescin treatment in a rodent model treated with an experimentally induced varicocele. Experimental varicocele was induced by partial ligation of the left renal vein of rats. Aescin administration was performed daily for 4 weeks after the varicocele induction. Seven weeks later, a contrast‐enhanced ultrasound was performed of the rats' testis to assess testicular blood flow. The animals were sacrificed, and H&E staining was then used to evaluate testicular pathological changes and polymorphonuclear leucocytes density. Cauda epididymal sperm counts and motility were evaluated. Blood was collected for the measurement of follicle‐stimulating hormone, luteinising hormone and testosterone. Contrast‐enhanced ultrasound showed that there were significant decreases in testicular blood flow in the aescin‐treated groups compared with those in control varicocele group. Testicular oedema was detected in those rats treated with a varicocele but without aescin, while no oedema was found in the experimental group. H&E staining showed dysfunctional spermatogenesis in both cohorts; however, polymorphonuclear leucocytes density was significantly reduced in aescin‐treated groups. There was an increase in sperm counts of the aescin‐treated groups. Our study demonstrated that aescin could exert therapeutical effects on reversal of testicular lesions in varicocele rats.  相似文献   
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