巨大儿发生的危险因素及产前预测

目的研究巨大儿发生的高危因素及产前预测,以便更好地指导孕妇孕期保健,减少新生儿及孕产妇的早期及远期并发症。方法对比巨大儿组及正常体重儿组两组孕妇的孕周、宫高、腹围,B超观察胎儿双顶径、胎儿腹围。回顾性分析孕妇孕前BMI、孕期体重增加情况、是否合并GDM等。结果①孕妇孕前BMI〉24、孕期体重增）加〉18kg、合并妊娠期糖尿病、孕周大于40周巨大儿组与正常体重儿组比较差异有统计学意义,为分娩巨大儿的高危因素。②胎儿腹同大于35cm,双顶径大于9．6cm,股骨长大于7．5cm,宫高＋腹围≥140cm,这4个指标巨大儿组与正常体重组比较差异有统计学意义,可作为巨大儿预测的方法。结论应该加强孕前及孕期指导,控制体重及血糖以降低巨大儿的发生率。对孕前胎儿体重采取多方面综合评估,以期能预测巨大儿的发生,以便做好相应的应对措施。     

肿瘤坏死因子对肝损伤的影响

利用树Ｑｕ研究肿瘤坏死因子α（ＴＮＦα）在肝损害中的作用。结果显示，ＴＮＦα单独或与Ｄ－氨基半乳糖（Ｄ－ＧａｌＮ）联合作用于培养树Ｑｕ肝细胞，上清天冬氨酸氨基转移酶活性无明显变化；将ＴＮＦα处理后的树Ｑｕ血清作用于培养肝细胞，上清中ＡＳＴ活性升高，抑肽酶能抑制这种效应。在ＨＢｓＡｇ预先致敏的树Ｑｕ体内注入ＴＮＦα可导致肝、肺、肠等器官的出血、坏死。提示ＴＮＦα在肝损害中起一定作用，并在体内外存在差     

重组人粒细胞集落刺激因子对照射小鼠造血功能的影响

为研究重组人粒细胞集落刺激因子（ｒｈＧ－ＣＳＦ）对急性放射病的治疗作用，观察了不同剂量的ｒｈＧ－ＣＳＦ对６．５Ｇｙ照射小鼠造血恢复的影响，结果表明，予受照小鼠每日ｒｈＧ－ＣＳＦ１．２５、２．５０及５．００μｇ治疗后，外周血白细胞，红细胞及血小板的恢复明显加快，以５．００μｇ剂量组效果为最佳，照射后１０ｄ骨髓及脾脏ＣＦＵ－ＧＭ，暴增型红系祖细胞集落（ＢＦＵ－Ｅ）及混合型祖细胞集落（ＣＦＵ－Ｍｉｘ）含     

肽6A对大鼠血管内皮舒张因子释放的影响

本实验在离体大鼠主动脉条上，观察纤维蛋白（原）降解产物肽6A灌流对血管反应性及血管组织cGMP含量的影响，实验结果表明肽6A呈剂量依赖地显扩张离体血管，其作用在去内皮后消失；肽6A还能显提高离体血管组织cGMP含量，NO合成抑制剂L-NNA可阻断这一作用，NO前体L-精氨酸可逆转L-NNA的效应，结果提示肽6A可以通过促进血管内皮释放内皮舒张因子而扩张血管。     

Magnetic resonance imaging of bone destruction in rheumatoid arthritis: comparison with radiography

Bony changes in forty-four knees of patients with clinically established rheumatoid arthritis (RA) were examined using magnetic resonance imaging (MRI) and plain film radiography. In all cases MRI was clearly superior to radiographs, demonstrating 25 marginal erosions and 42 subchondral cysts, while the number seen on radiographs was 3 and 8, respectively. These results emphasize the problems in visualizing bone erosions in large joints using plain films. MRI is the method of choice for detecting early changes in RA, not only because of its high sensitivity, but also because of the ability of contrast-enhanced MRI to provide physiological characterization of these lesions.     

Clinical Significance of the Epidermal Growth Factor Receptor and HER2 Receptor in Resectable Gastric Cancer

Background: Epidermal growth factor receptor (EGFR or HER1) and its homolog c-erbB-2 (HER2) are membrane receptors. Both EGFR and HER2 genes are overexpressed in a variety of solid human cancers and are related to poor prognosis of the patients. The objective of this work was to evaluate the EGFR and HER2 contents in resectable gastric cancer, their possible relationship with clinicopathologic parameters of tumors, and their prognostic significance.Methods: This was a prospective analysis of 63 patients with resectable gastric carcinomas, with a mean follow-up period of 40.7 months. Membranous EGFR levels were examined by radioligand binding assays, and cytosolic HER2 levels were examined by means of an immunoenzymatic assay.Results: There was a wide variability of EGFR (1–1,239 fmol/mg of protein) and HER2 (7–20,863 NHU/mg of protein) levels in tumors. There was no significant correlation between these levels and patient or tumor characteristics. However, high levels of EGFR and HER2 were significantly associated with a shorter overall survival period (P = .03 and P = .02, respectively).Conclusions: There is a wide variability in membranous EGFR levels and in cytosolic HER2 levels in gastric cancer, which seems to be related to the biological heterogeneity of these tumors. In addition, high tumor EGFR and HER2 levels were associated with an unfavorable outcome in patients with resectable gastric cancer.     

Prognostic Significance of Vascular Endothelial Growth Factor,Basic Fibroblast Growth Factor,and Angiogenin in Patients With Resectable Hepatocellular Carcinoma After Surgery

Background: Hepatocellular carcinoma (HCC) is a hypervascular malignancy. Vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and angiogenin (ANG) are important angiogenic factors of neoangiogenesis. This study investigated the predictive value of serum VEGF, bFGF, and ANG in tumor recurrence, disease-free survival (DFS), and overall survival (OS) in HCC patients.Methods: Preoperative serum VEGF, bFGF, and ANG were measured in 98 patients with resectable HCC and in 15 healthy controls. The median follow-up time was 43 months.Results: Preoperative serum VEGF was increased in patients with resectable HCC compared with healthy controls (P < .05). Increased serum VEGF was correlated with tumor recurrence (P = .001). Univariate analysis showed that serum VEGF, tumor-node-metastasis stage, tumor size and number, macroscopic portal vein invasion, and microscopic vascular invasion were correlated with OS and DFS. Serum bFGF and ANG were not associated with survival. Multivariate analysis showed that serum VEGF was the most significant predictor of DFS (relative risk, 2.35; 95% confidence interval, 1.26–4.39; P = .007) and OS (relative risk, 3.44; 95% confidence interval, 1.81–6.57; P < .001) in HCC patients after surgical resection.Conclusions:Preoperative serum VEGF is a significant independent predictor of tumor recurrence, DFS, and OS in patients with resectable HCC.     

The impairment of hepatocytes and sinusoidal endothelial cells during cold preservation in rat fatty liver induced by alcohol and the beneficial effect of hepatocyte growth factor

A fatty liver resulting from alcohol intake is often unattractive for grafting. In this study, we investigated the impairment of hepatocytes and sinusoidal endothelial cells (SECs) during cold preservation of alcohol-induced fatty liver and examined the efficacy of human recombinant hepatocyte growth factor (hrHGF). Rats were fed an alcohol diet. We performed histological examinations of the hepatocytes and observed the ultrastructural alteration of the SECs. Additionally, we measured hepatic transaminase and peroxidative lipids for hepatocellular injury and the hyaluronic acid uptake rate (HUR) to determine SEC injury. We added hrHGF to University of Wisconsin (UW) solution to assess the protective effect of the agent. Numerous fatty deposits were observed in ethanol-induced fatty livers. These grew with the duration of cold storage. Hepatic transaminases of the effluents increased during cold preservation in the livers of alcohol-treated rats. Additionally, peroxidative lipids in the effluents increased during cold preservation in the livers of alcohol-treated rats, whereas they were undetectable in non-alcohol-treated rat livers. The sinusoidal endothelium had severely deteriorated in the livers of alcohol-treated rats. Further, the HUR decreased with ethanol treatment and/or cold preservation. The addition of hrHGF suppressed the increase of hepatic transaminase in the effluent of cold-preserved alcohol-treated livers. Peroxidative lipids in the same effluents were undetectable. In fatty livers, both hepatocytes and SECs received severe damage during cold preservation. Furthermore, we demonstrated that hepatocellular injury was significantly inhibited by hrHGF.     

Roles of connective tissue growth factor and prostanoids in early streptozotocin-induced diabetic rat kidney: the effect of aspirin treatment

Background. Connective tissue growth factor (CTGF) is a cysteine-rich growth factor induced by transforming growth factor-β (TGF-β) and is thought to play a critical role in TGF-β-stimulated extracellular matrix accumulation. To explore its involvement in early diabetic nephropathy, we investigated the time course of CTGF gene expression and its regulation in streptozotocin (STZ)-induced diabetic rat kidney. Methods. Northern blot analysis for CTGF, TGF-β, and fibronectin expression was performed in the glomeruli of STZ-induced diabetic rats from 3 days to 12 weeks after the induction of diabetes, together with histological examination. To investigate the role of prostanoids in this process, aspirin was administered in one group of diabetic rats. Furthermore, CTGF expression was analyzed in rat mesangial cells cultured under high-glucose conditions. Results. Glomerular expression of CTGF and TGF-β1 mRNA was coordinately upregulated as early as day 3, followed by fibronectin induction and mesangial matrix accumulation. Chronic aspirin treatment in diabetic rats significantly attenuated mesangial expansion, and effectively suppressed CTGF induction, as well as inhibiting the upregulation of TGF-β1 and fibronectin expression. In cultured mesangial cells, aspirin treatment abolished high glucose-stimulated CTGF upregulation. Conclusions. These results indicate that CTGF expressed in the glomeruli is upregulated in the early stage of STZ-induced diabetic nephropathy in rats, and could be a critical mediator of the development of diabetic glomerulosclerosis. In addition, the modulatory effects of aspirin during this process suggest a role of the cyclooxygenase pathway in the progression of diabetic nephropathy. Received: March 5, 2002 / Accepted: December 6, 2002 Acknowledgments We thank Ms. A. Wada, Ms. J. Nakamura, and Ms. Y. Oki for technical assistance, and Ms. S. Doi and Ms. A. Sonoda for secretarial assistance. This work was supported in part by research grants from the Japanese Ministry of Education, Science, Sports and Culture; the Japanese Ministry of Health and Welfare; “Research for the Future (RFTF)” of the Japan Society for the Promotion of Science; the Ono Foundation for Medical Research; the Smoking Research Foundation; and the Salt Science Research Foundation. Correspondence to:M. Mukoyama     

Inflammatory Mediators as Essential Elements in Bone Remodeling

Inflammatory disorders such as rheumatoid arthritis (RA), may have profound effects on skeletal homeostasis. In contrast to physiologic remodeling in which mechanical influences and/or systemic endocrine hormones initiate the remodeling process, in disorders such as RA the recruitment of macrophage lineage cells to sites of inflammation and the action of local osteoclastogenic cytokines associated with the inflammatory process initiate the remodeling process. In both physiologic and pathologic remodeling, osteoclasts appear to be the principal cell type responsible for the bone resorption. In addition, many of the same cytokines and mediators are involved in physiologic and pathologic bone remodeling. These observations have important implications with respect to the development of therapeutic strategies to prevent bone loss in inflammatory conditions. Abbreviations: rheumatoid arthritis (RA), interleukin-1 and (IL-1 and ), interleukin-6 (IL-6), interleukin-11 (IL-11), interleukin-15 (IL-15), interleukin-17 (IL-17), macrophage-colony stimulating factor (M-CSF), tumor necrosis factor- (TNF-), parathyroid hormone related peptide (PTHrP), receptor activator of NF- (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG)