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71.
目的探讨骨形成蛋白-2(BMP-2),成纤维细胞生长因子-2(FGF-2)单独及联合作用对毛乳头细胞增殖和毛发诱导能力的影响。方法采用显微机械法分离大鼠触须毛乳头并培养,行免疫荧光鉴定。CCK-8法检测毛乳头细胞的增殖活性。毛发诱导能力通过检测碱性磷酸酶(ALP)活性确定。采用ELISA法检测胰岛素样生长因子-1(IGF-1)的含量。结果毛乳头细胞的ALP免疫荧光染色阳性,确定培养的细胞是毛乳头细胞。BMP-2对毛乳头细胞增殖无影响,但可提高毛乳头细胞的ALP活性并呈剂量依赖性。FGF-2促进毛乳头细胞增殖,但会降低毛乳头细胞的ALP活性并呈剂量依赖性。联合BMP-2和FGF-2既可以促进毛乳头细胞的增殖,又可以增强ALP活性,并呈时间依赖性。BMP-2可上调毛乳头细胞培养上清液中IGF-1的含量,并呈剂量依赖性。结论 BMP-2可能通过促进毛乳头细胞分泌IGF-1以保持毛乳头细胞的毛发诱导能力,按适当浓度比例联合BMP-2和FGF-2可形成互补作用,既促进毛乳头细胞的增殖,又可以保持其毛发诱导能力。  相似文献   
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Although cardiac injury is known to be the leading cause of death in electrocution, the differential diagnosis can be challenging in forensic practice since the exact mechanism is poorly understood and there is lack of reliable markers. Thus, death due to electrocution may be classified as a negative autopsy. The serum levels of and myocardial immunostaining loss for cardiac troponins and heart-type fatty acid binding protein (H-FABP) are highly sensitive and specific biomarkers of ischemic myocardial damage and may have a diagnostic value in determining the myocardial injury or the cause of death due to electrocution. Due to this reason, a rat model is prepared to investigate these issues. Thirty-two Wistar albino female rats were included and randomly divided into four groups of eight subjects. Group A was the control group, and Group B, C, and D were exposed to electrical current of 110 volt (V), 220 V, and 600 V, respectively. Blood samples and the hearts were collected from the rats for biochemical and immunostaining analyses.It is found that increased serum H-FABP levels were significantly associated with the higher voltage immediately after electrocution. However, serum cardiac troponin I (cTnI) levels did not show significant changes associated with the higher voltage in the early period of electrocution. As for histopathological examinations, the only significant difference in myocardial immunostaining loss was for H-FABP in Group B.Serum H-FABP levels may have a diagnostic value in the early postmortem period immediately after electrocution. Besides, it seems that serum H-FABP levels may be a better indicator than those of cTnI to reflect the myocardial damage in the early period of the electrocution.  相似文献   
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对称性肢端角化病皮损中PrxI和CLASP1的表达   总被引:1,自引:0,他引:1  
目的:检测对称性肢端角化病(SAK)皮损中过氧化物还原酶I(Prx I)和胞质链接相关蛋白1(CLASP1)的表达水平。方法:用RT-PCR和免疫组化方法检测9例SAK患者腕部皮损及其周围皮肤和9名正常人腕部皮肤中的Prx I和CLASP1 mRNA及蛋白质的表达。结果:SAK皮损中Prx I和CLASP1 mRNA水平为(0.94±0.66)和(0.95±0.76),明显高于皮损周围(0.51±0.20,0.56±0.31)和正常皮肤(0.45±0.26,0.47±0.33)。SAK皮损中Prx I阳性细胞弥漫分布于表皮基底层和棘层,而CLASP1阳性染色主要位于棘层,二者的阳性染色范围及程度明显高于皮损周围和正常人皮肤。结论:SAK皮损中Prx I和CLASP1表达上调,可能参与表皮角质形成细胞过度增殖和异常分化。  相似文献   
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Introduction

Non-androgenic growth factors are involved in the growth regulation of prostate cancer (PCa).

Objective

This is the first Brazilian study to correlate, in a population of patients operated for PCa, PSA, total testosterone, insulin-like growth factor-I (IGF-I) and insulin-like growth factor-binding protein-3 (IGFBP-3) with Gleason score and to compare with a control group with benign prostate hyperplasia (BPH).

Materials and Methods

This retrospective single-center study included 49 men with previously diagnosed PCa and 45 with previously diagnosed BPH. PSA, testosterone, IGF-I, IGFBP-3 were determined in both groups.

Results

PSA and IGFBP-3 levels were significantly higher in the PCa group as compared to the BPH group (p<0.001 and p=0.004, respectively). There was a significant difference when we compared the PSA before surgery (p<0.001) and at the inclusion in the study (p<0.001) and IGFBP3 (0.016) among patients with Gleason <7, ≥7 and BPH. In the PCa group, PSA, testosterone, IGF-I and IGFBP-3 levels were comparable between Gleason <7 and ≥7.

Conclusions

Our data suggest that in localized PCa, the quantification of PSA and, not of IGF-1, may provide independent significant information in the aggressiveness. IGFBP-3 could be a biochemical marker of disease control in PCa patients.  相似文献   
79.
ObjectivesThe goals of the study were to describe the MR imaging features of endometriosis of the urinary tract and identify those that suggest intrinsic involvement of ureteric wall.Materials and methodsThirty-five women with proven urinary tract endometriosis and who had preoperative MR imaging between 2001 and 2011 were included retrospectively. MR images were intrepreted by one junior and one senior radiologists. To characterize the intrinsic parietal involvement, the ureteric circumference involved by the lesion of endometriosis was noted.ResultsThirty-eight ureteric and 13 bladder lesions were analyzed. They were found in association in nine women. Ureteric lesions were bilateral in seven women. Of the 38 ureteric lesions, 27 were extrinsic and 11 intrinsic at histopathological analysis. Sixteen women with extrinsic lesions and 10 with intrinsic ones were correctly identified on MR imaging. When the ureter was included less than 360° in the lesion, extrinsic involvement was confirmed in 80% of cases.ConclusionMR imaging appears to be more sensitive (91%vs 82%) but less specific (59% vs 67%) than surgery for the diagnosis of intrinsic form of ureteric location.  相似文献   
80.
Identifying disease and making sophisticated diagnoses at a specialist level is dependent on opportunity. Effective and accurate diagnosis starts with persons presenting to medical concern, their subsequent funneling, levels of awareness and expertise encountered, and available technology. In this article we describe a young woman (index case) with classic features of restrictive cardiomyopathy (RCM) who was referred to us with hypertrophic cardiomyopathy (HCM). Cascade screening identified the same disease in four relatives, in whom the diagnosis for some has changed from tuberculosis (TB) as a cause for pleural effusions, to cor pulmonale, constrictive pericarditis (CP) and RCM as the cause of sarcoidosis or amyloidosis. At the same time, an unrelated young boy presented with a disease profile similar to our index case, but without a history of disease in any other first-degree relative.In view of the associated focal hypertrophy, we speculated that it could be caused by a mutation in troponin I [I type 3 (TNNI3; Genbank accession no. X90780.1)], which has been implicated in cases of unexplained RCM and/or HCM with ‘restrictive features’.1-3 Mutations in this gene have been described to cause RCM, HCM and dilated cardiomyopathy and specific mutations have on occasion been associated with more than one of these phenotypes.4 We focused on screening TNNI3 in a South African panel of HCM-affected probands for mutations, which included these two probands, using a high-resolution melt (HRM) approach.  相似文献   
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