细胞因子激活骨髓免疫细胞的实验研究

目的：通过对骨髓单个核细胞在体外与不同细胞因子培养,了解不同细胞因子对骨髓淋巴细胞的激活能力和对骨髓干祖细胞的损伤情况。方法：将IL-1、IL-2、γ-IFN、CD3单抗进行不同组合后,在体外与骨髓单个核细胞分成对照组、IL-2组、CD3-AK、CIK组进行培养。培养过程中观察细胞形态和数量的变化,并在培养后检测免疫活性细胞的细胞毒性和造血干细胞的保存情况。结果：培养过程中对照组细胞数量减少;IL-2组细胞数量变化不明显;CD3-AK组、CIK组细胞数量显著增多,并出现较多的集聚成簇的淋巴样细胞,培养后其细胞毒性明显强于对照组及IL-2组,但细胞数量增加和细胞毒性无明性差异,培养后各组造血干细胞保存情况约16%～87%。结论：IL-2、CD3单抗在体外与骨髓单个核细胞培养后,即能激活免疫细胞增殖,又能保留足够的造血干细胞。     

Understanding the Link Between Adolescent Same-Gender Contact and Unintended Pregnancy: The Role of Early Adversity and Sexual Risk Behavior

Past research suggests an apparent paradox: Women who engage in same-gender sexual behavior show higher rates of unintended pregnancy than women with exclusive other-gender sexual behavior. Such women also have disproportionate rates of early adversity (both harshness, such as abuse or neglect, and unpredictability, such as father absence). We used the Add Health data (N?=?5,617 cisgender women) to examine the relative contributions of early adversity, adolescent same-gender sexual behavior, and general sexual risk behavior to women’s risks for adult unintended pregnancy. Women who engaged in adolescent same-gender sexual behavior were more likely to report childhood adversity, and both childhood adversity and adolescent same-gender behavior made independent contributions to subsequent rates of unintended pregnancy. The association between adolescent same-gender sexual behavior and adult unintended pregnancy was partially attributable to the fact that women with adolescent same-gender sexual behavior engaged in greater sexual risk behavior more broadly. These findings suggest that same-gender sexual behavior in adolescence may relate to a broader set of sexual risk behaviors that augment future risk for unintended pregnancy, independent of sexual identity. We draw on life history theory to explain this pattern of results and suggest directions for future research.

     

胰弹力蛋白酶I和核糖核酸酶检测的临床价值

目的　探讨人胰弹力蛋白酶Ⅰ (Humanpancreaticelastase 1 ,HPE1 )放射免疫测定 (Radioimmunoassay ,RIA)和核糖核酸酶(Ribonuclease ,RNase)活性检测的临床价值。方法　参照Satake等建立的改良HPE1RIA和Thomas等的改良酸溶性产物法检测 82例正常成年人和 2 2 2例各类患者血清并分析结果。结果　 82例健康成人HPE1值为 2 3.8( 3.4ng L) ,RNase活性为 5 7.0 3( 1 2 .1 6 μ ml) ;急性胰腺炎和胰腺癌HPE1 值明显高于其他疾病 (P <0 .0 1 )。联合检测HPE1 、RNase活性可提高胰腺癌的检出率 ( 92 .47% )。结论　HPE1 RIA对急性胰腺炎有诊断价值 ,联合检测HPE1 、RNase活性检测对胰腺癌诊断有一定的临床价值     

Manifestations of diabeters mellitus on mouse preimplantation developement: effect of elevated concentration of metabolic intemediated

The metabolic derangements of pregnancies complicated by diabetesmellitus, specifically hyperglycaemia and hyper-ketonaemia,are known to be teratogenic during the period of organogenesisin animals. We have shown previously that poorly controled diabetesmellitus impairs in-vivo and in-vitro mouse preimplantationembryo growth, and that culturing embryos in elevated glucoseconcentrations only partially recreated this developmental dealy.To extend this observation we examined the effect on mouse preimplantationembryo growth of elevated concentrations of other metabolicintermediates, which may be deranged in diabetes mellitys, namelylipids, lactate, glycerol, amino acids, and ketones. Two-cellembryos from ovulation-induced B₆C₃F₁ mice were cultured for72 h in the presence of added lipids (250 mg/dl), lactate (5mM), glycerol (160 µM) or mixed amino acids (8.5% travosol,7 mM) and showed no significant difference in growth over 72h verus their control groups. However, growth of preimplantationembryos in acetoacetate (10 mM) or in the racemic micture ofDL--hydroxybutyrate (16 and 32mM) revealed marked retardationversus controls when assessed either by distribution of developmentalstages over time (24, 48, 72 h, P <0.001) or by the differencein the average rank of sums indicating a delay in maturation(P<0.0001). We conclude that elevated ketone concentrationsadversely affect preimplantation embryo development. These findingsextend previous studies which correlate uncontrolled diabetesmellitus as well as hyperglycaemia with abnormal organogenesis,and demonstrate tht exposure to metabolic derangements may alsohinder reproductive performane at even earlier stages in gestation.     

The nuclear jet and counterjet region of the radio galaxy Cygnus A

Very-long-baseline interferometry images of the nuclear region of the radio galaxy Cygnus A reveal a pronounced "core" and a knotty jet and counterjet. The knots are moving away from the core at apparent speeds which are subluminal for h = 1 [h = H0/100 km.s-1.Mpc-1;1 parsec (pc) = 3.09 x 10(16)m] and about c for h = 0.5. The jet is aligned with the outer, kiloparsec-scale jet to within 2 degrees. The counterjet has a total flux density at 5 GHz of about one-fifth of that of the jet. In the context of the twin relativistic jet model for active galactic nuclei, the jet in Cygnus A is oriented at an angle to our line of sight of 35-80 degrees and 55-85 degrees, and the intrinsic velocity of the jet fluid is 0.4-0.6c and 0.6-1c for h = 1 and h = 0.5, respectively.     

Ocular manifestations of genetic and development diseases

Significant advances were reported this year in the identification of the chromosomal location of mutated genes on the 13 and 6 chromosomes which cause forms of autosomal dominant Stargardt's macular dystrophy. Observations in monozygotic twins with age-related macular dystrophy were described. Mitochondrial DNA mutations in Cubans with optic and peripheral neuropathy were reported. A new autosomal dominant proximal myotonic myopathy was described. Persistence of the tunica vasculosa lentis was suggested as a helpful sign of congenital myotonic dystrophy. The panoply of ocular findings in acromesomelic dysplasia were presented. Genetic characterization of the ocular findings in Duchenne type and Becker's muscular dystrophy was reported. Finally, a new syndrome of autosomal dominant cerebellar ataxia with retinal degeneration was described.     

Microdissection and microcloning of chromosomal alterations in human breast cancer

Summary The recognition of recurring sites of chromosome changes in malignancies has greatly facilitated the identification of genes implicated in the pathogenesis of human cancers. Based especially upon recent studies [1–4], it appears increasingly likely that a subset of recurring chromosome alterations will be recognized in human breast cancer. Currently recognized chromosome changes characterizing breast carcinoma include the recognition of cytologic features of gene amplification (e.g. double minutes [dmins] and homogeneously staining regions [HSRs]) [5–8]. As these and other chromosome regions are implicated in recurring abnormalities in breast cancer, it will become increasingly important to have band-or region-specific genomic libraries and probes in order to facilitate high resolution physical mapping and ultimately to clone breast cancer related genes [9]. Toward this end an important recent development in physical mapping has been the establishment of chromosome microdissection as a rapid and reproducible approach to rapidly isolate and characterize chromosome region-specific DNA, greatly facilitating the initial steps in positional cloning of disease-related genes [10–13]. In this brief report, we will highlight the application of chromosome microdissection to the generation of region-specific probes for both fluorescent in situ hybridization (FISH) and the generation of genomic microclone libraries. Additionally, efforts using this methodology to generate a microclone library encompassing the early onset breast/ovarian cancer (BRCA1) gene will be presented.Presented by Jeffrey M. Trent at the 16th Annual San Antonio Breast Cancer Symposium, San Antonio TX, USA, November 4, 1993; Minisymposium on Molecular Genetics in Breast Cancer.