Serum profiles of insulin-like growth factors and their binding proteins in adults with growth hormone receptor deficiency treated with insulin like growth factor I

Six adult patients with growth hormone receptor deficiency (GHRD) (2 men, 4 women) with an identical defect in the growth hormone receptor (GHR) gene, were treated with recombinant human insulin-like growth factor I (IGF-I), 40 μgikg S.C. twice daily, for 7 days. Serum concentrations of IGF peptide and IGF binding protein-3 (IGFBP-3) were measured by specific radioimmunoassays; serum IGFBPs were also measured by Western ligand blotting. The size distribution of both IGF-I and IGF-II was measured in serum following size-exclusion fast-performance liquid chromatography. IGF-I treatment resulted in a normalization of serum IGF-I levels on days 1–7 of treatment and a decrease in serum IGF-II levels. The fall in IGF-II levels and the simultaneous rise in IGF-I levels, however, resulted in an unchanged total serum IGF level. The low IGFBP-3 values did not significantly change during treatment, whereas there was a slight increase in IGFBP-2 levels. Preliminary analysis of size-fractionated sera suggested an increase in IGF-I levels in the 40 and 150 kDa regions at the expense of IGF-II levels. The results suggest that despite the failure of IGF-I treatment to increase IGFBPs significantly, serum IGFBP concentrations were sufficient to maintain normal levels of IGF-I. 0 Laron syndrome, growth hormone receptor deficiency, insulin-like growth factors, insulin-like growth factor binding protein     

The effects of antioxidant supplementation during Percoll preparation on human sperm DNA integrity

The integrity of sperm DNA is crucial for the maintenance of genetic health. A major source of damage is reactive oxygen species (ROS) generation; therefore, antioxidants may afford protection to sperm DNA. The objectives of the study were, first, to measure the effects of antioxidant supplementation in vitro on endogenous DNA damage in spermatozoa using the single cell gel electrophoresis (comet) assay and, second, to assess the effect of antioxidant supplementation given prior to X-ray irradiation on induced DNA damage. Spermatozoa from 150 patients were prepared by Percoll centrifugation in the presence of ascorbic acid (300, 600 microM), alpha tocopherol (30, 60 microM), urate (200, 400 microM), or acetyl cysteine (5, 10 microM). DNA damage was induced by 30 Gy X-irradiation. DNA strand breakage was measured using the comet assay. Sperm DNA was protected from DNA damage by ascorbic acid (600 microM), alpha tocopherol (30 and 60 microM) and urate (400 microM). These antioxidants provided protection from subsequent DNA damage by X-ray irradiation. In contrast, acetyl cysteine or ascorbate and alpha tocopherol together induced further DNA damage. Supplementation in vitro with the antioxidants ascorbate, urate and alpha tocopherol separately has beneficial effects for sperm DNA integrity.      

氯沙坦减少高血压患者终点事件的研究(LIFE STUDY)

标　　题　应用ＡＴⅡ受体拮抗剂抗高血压治疗作　　者　ＫｊｅｌｄｓｅｎＳＥ,ＯｍｖｉｋＰ.　　参考文献　ＴｉｄｓｓｋｒＮｏｒＬａｅｇｅｆｏｒｅｎ,1996,116:504～507研究疾病　高血压病。目　　的　评估氯沙坦对心血管死亡率及非致死性心肌梗死和非脑卒中发生率的影响,同时评估该药对充血性心力衰竭或心绞痛所致的总死亡率和住院率的影响,以及长期应用氯沙坦对发生新诊断糖尿病的影响。设　　计　随机、三盲、对照研究。病人资料　8300例年龄55～80岁、收缩压在160～200ｍｍＨｇ、舒张压在95～115ｍｍＨｇ的高血压患者,ＥＣＧ上有左室…     

A monoclonal antibody with anti-Burkitt lymphoma specificity. I. Analysis of human haematopoietic and lymphoid cell lines

38-13 is a hybridoma-produced monoclonal rat IgM which appears to define a Burkitt's lymphoma-associated antigen (BLA). In this paper, we described the reactivity of 38-13 with a panel of human haematopoietic and lymphoid cell lines. In indirect immunofluorescence (IF) assays, 15 of 26 Burkitt's lymphoma (BL) lines studied were clearly stained with 38-13 (from 13 to 100% positive cells) by microscope, with varying numbers of heavily labelled cells. In these positive cell lines, fluorescence-activated cell-sorter (FACS) analysis demonstrated that BLA was actually present on all the cells. Positive BL included Epstein-Barr virus (EBV) genome-carrying lines and EBV-negative ones; thus, BLA is not related to the presence of EBV. Most of the 15 BL cells that reacted with 38-13 contained a typical t(8;14) translocation, but had variant translocations such as t(2;8) and t(8;22). The cells were derived from BL patients of different geographical origins and clinical features. Four BL lines were poorly stained and seven were negative with 38-13 in IF assays. The 32 EBV-positive lymphoblastoid cell-lines (LCL) studied were negative. In three line pairs, consisting of a tumor line and an LCL from the same patient, only the BL line was demonstrated to react with 38-13. A series of non-BL cells, including haematopoietic, lymphoid and solid tumor lines, all failed to react with 38-13. Various attempts to modulate the expression of BLA on BL cells were unsuccessful. However, it cannot be ruled out that BLA is actually a transient B-cell differentiation marker.     

Pathophysiology of oxidative stress in diabetes mellitus.

Oxidative stress is believed to play an important role, albeit not fully recognized, in the development of vascular complications in diabetes mellitus (DM) particularly type 2. In the majority of studies, attention was focused on lipid oxidation, specifically on that of low-density lipoproteins (LDLs). More recent investigations have revealed that it is not only the lipid but also the apolipoprotein moiety of LDL that becomes oxidatively modified resulting in the formation of insoluble aggregates. Consequently, it has been documented that LDL aggregation was due to the hydroxyl radical-induced dityrosine crosslinking between apo B monomers. In DM patients with atherosclerotic complications, intravascular fibrous deposits were shown to contain, in addition to oxidized LDL, a fibrin-like material (FLM). This material is immunologically identical to fibrin that is normally formed as a result of intravascular activation of the blood coagulation cascade. Although DM patients with vascular disease display increased concentration of plasma fibrinogen (Fbg), the precursor of fibrin, no markers of full blown activation of blood coagulation could be found.