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971.
972.
A patient with Hodgkin’s disease received a fractionated 3, 740 rad dosage over 4 weeks to a portal that included both kidneys. Three months later a computed tomographic scan obtained 2 hours after intravenous contrast injection demonstrated sharply demarcated, dense, persistent nephrograms corresponding to the irradiated areas. These changes are ascribed to acute radiation nephritis, reflecting tubular stasis and ischemia.  相似文献   
973.
This investigation was undertaken to determine whether human skeletal muscle buffer capacity (BCm) is affected by training. Eight untrained males participated in 8 weeks of sprint training on bicycle ergometers. Muscle biopsy samples were taken from the vastus lateralis before and at several times following an incremental bicycle ergometer test (0 min, 5 min, 15 min). These subjects were tested before (PRE) and following (POST) the training period. Seven endurance-trained cyclists (ET) were also tested for the purpose of comparing the BCm of ET to that of PRE and POST. Biopsy samples were quick-frozen in liquid nitrogen and later analyzed for lactate concentration (HLam), homogenate pH (pHm), and creatine phosphate concentration. BCm was calculated from the change in HLam and pHm observed from rest to exhaustion and was expressed as mmol X kg-1 X pH-1 (Slykes). There was no significant difference in resting HLam or resting pHm among the groups. There was a significant difference in HLam at exhaustion between PRE (21.41 +/- 1.65 mmol X kg-1), POST (25.61 +/- 2.38 mmol X kg-1), and ET (11.16 +/- 0.31 mmol X kg-1) but no significant difference in pHm at exhaustion between PRE (6.65 +/- 0.03 pH units) and POST (6.69 +/- 0.06 pH units). pHm at exhaustion for the ET group was significantly higher than the others at 6.91 +/- 0.02 pH units. A significant difference between PRE and POST BCm was found (PRE: 44.68 +/- 3.03 S1; POST: 61.04 +/- 4.11 S1) while ET BCm (47.21 +/- 7.26 S1) was not significantly different from PRE. These data indicate that muscle buffer capacity is increased with highly intense sprint training but provide no evidence to suggest that muscle buffer capacity is affected by endurance training.  相似文献   
974.
975.
976.
胃癌组织p16基因蛋白表达的意义   总被引:9,自引:4,他引:5  
目的 检测 p1 6基因蛋白在胃癌组织、癌旁组织中的表达及其分布特点 ,分析其与胃癌临床病理学特征及预后的关系 .方法 采用 S- P免疫组织化学法对 53例胃癌组织及 35例癌旁组织进行 p1 6蛋白的定位观察 .结果 各病理类型胃癌组织、癌旁组织均有 p1 6基因蛋白表达 .阳性率分别为 62 .3% (33/53)和 88.6% (31 /35) ,阳性细胞的棕黄色颗粒主要位于细胞核 .胃癌 p1 6基因蛋白表达与性别、年龄、肿瘤部位在统计学上无差异 (P>0 .0 5) ;而与组织学类型、病理分级、淋巴结转移、临床病理分期在统计学上有差异 (P<0 .0 5) .p1 6蛋白阳性者 5年生存率 51 .0 %高于 p1 6蛋白阴性者 2 0 .0 % (P<0 .0 5) .结论  p1 6基因缺失和表达水平的改变与胃癌发生、发展密切相关 ,检测 p1 6基因蛋白表达可作为辅助临床判断胃癌的生物学行为及推测预后的指标  相似文献   
977.
To determine whether the mouse loses bone with aging and whether the changes mimic those observed in human aging, we examined the changes in the tibial metaphysis and diaphysis in the male C57BL/6J mouse over its life span using microcomputed tomography (microCT). Cancellous bone volume fraction (BV/TV) decreased 60% between 6 weeks and 24 months of age. Loss was characterized by decreased trabecular number (Tb.N), increased trabecular spacing (Tb.Sp), and decreased connectivity. Anisotropy decreased while the structure model index increased with age. Cortical bone thickness increased between 6 weeks and 6 months of age and then decreased continuously to 24 months (-12%). Cortical bone area (Ct.Ar) remained constant between 6 and 24 months. Fat-free weight reached a peak at 12 months and gradually declined to 24 months. Total mass lost between 12 and 24 months reached 10%. Overall, the age-related changes in skeletal mass and architecture in the mouse were remarkably similar to those seen in human aging. Furthermore, the rapid early loss of cancellous bone suggests that bone loss is not just associated with old age in the mouse but rather occurs as a continuum from early growth. We conclude that the C57BL/6J male mouse maybe a useful model to study at least some aspects of age-related bone loss in humans.  相似文献   
978.
Somatostatin (SRIF) in the central nervous system is mostly concentrated in the median eminence (ME). Immunocytochemical methods have revealed high densities of SRIF-positive perikarya between the preoptic area and the periventricular nucleus of the hypothalamus (NPE). The aim of the present study was to define more precisely the specific pathways of SRIF neurons from NPE to the ME. SRIF levels were measured by radioimmunoassay, following various hypothalamic transections. Frontal periventricular sections decreased SRIF-ME content by 70% (P less than 0.01), when located at the anterior end of the ME but no diminution was observed when the cuts were located anteriorly or posteriorly. Parasaggital transections decreased SRIF-ME levels by 50% (P less than 0.05) when located at the outer border of the ventromedial and premammillary nucleus, but the decrease was not significant when cuts were located anteriorly. Taken together, our data indicate that most SRIF-containing neurons, originating in the NPE, do not reach the ME directly along the border of the 3rd ventricle; instead they form a loop across the medial forebrain bundle before re-entering the mediobasal hypothalamus at the ME level.  相似文献   
979.
980.
PURPOSE: To delineate gene expression patterns and profile changes in metastatic tumor biopsies at baseline and 1 month after treatment with the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor erlotinib in patients with metastatic breast cancer. EXPERIMENTAL DESIGN: Patients were treated with 150 mg of oral erlotinib daily. Gene expression profiles were measured with Affymetrix U133A GeneChip and immunohistochemistry was used to validate microarray findings. RESULTS: Estrogen receptor (ER) status by immunohistochemistry is nearly coincided with the two major expression clusters determined by expression of genes using unsupervised hierarchical clustering analysis. One of 10 patients had an EGFR-positive tumor detected by both microarray and immunohistochemistry. In this tumor, tissue inhibitor of metalloproteinases-3 and collagen type 1 alpha 2, which are the EGF-down-regulated growth repressors, were significantly increased by erlotinib. Gene changes in EGFR-negative tumors are those of G-protein-linked and cell surface receptor-linked signaling. Gene ontology comparison analysis pretreatment and posttreatment in EGFR-negative tumors revealed biological process categories that have more genes differentially expressed than expected by chance. Among 495 gene ontology categories, the significant differed gene ontology groups include G-protein-coupled receptor protein signaling (34 genes, P = 0.002) and cell surface receptor-linked signal transduction (74 genes, P = 0.007). CONCLUSIONS: ER status reflects the major difference in gene expression pattern in metastatic breast cancer. Erlotinib had effects on genes of EGFR signaling pathway in the EGFR-positive tumor and on gene ontology biological process categories or genes that have function in signal transduction in EGFR-negative tumors.  相似文献   
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