Failure of (SJL/J x PL/J)F1 hybrid mice to develop immunologic tolerance to V beta 17a+ T cells results in F1 anti-SJL mixed lymphocyte reaction.

It has been reported previously that spleen cells from (SJL x PL) F1 hybrid mice are not tolerant to SJL parental cells as assessed by a one-way MLR. The possibility that the F1 anti-SJL reaction was due to the effect of lymphokines produced by the irradiated SJL T cells in response to I-Eu expressed on the F1 hybrid cells was eliminated since inclusion of anti-I-E mAb was without effect. Cell separations showed the responder cells to be plastic and nylon wool nonadherent Ia- T cells. Separation of the SJL spleen cells showed that the stimulator cells were nonadherent, passed through a nylon wool column, and were Ia-. the F1-anti-SJL MLR was blocked 70 to 90% by inclusion of mAb KJ23a in the culture medium that indicated that the stimulatory cell population was V beta 17a+ T cells. This was confirmed by the use of V beta 17a+ and V beta 17a-T cell clones as stimulators. To determine whether failure to develop tolerance to this T cell subset in F1 hybrid mice might be responsible for the F1-anti-parent MLR, (SJL x PL)F1 mice were treated at birth and 48 h thereafter with anti-I-E mAb for 7 wk. Spleen cells from antibody-treated F1 mice were nonreactive with irradiated SJL parental cells in contrast to spleen cells from control mice which indicated that V beta 17a+ T cells were eliminated by negative selection before the development of tolerance.     

Endothelial and leukocyte forms of IL-8. Conversion by thrombin and interactions with neutrophils

We have recently shown that endothelial cell-derived IL-8 inhibits neutrophil adhesion to IL1-beta-activated human umbilical vein endothelial cell monolayers. IL-8 secreted by T lymphocytes or monocytes has been characterized as a promoter of neutrophil degranulation and chemotaxis. The IL-8 isolated from each of these cell types is a mixture of two IL-8 polypeptides, one consisting of 72 amino acids (herein called [ser-IL-8]72) and the other 77 amino acids (an N-terminal extended form herein called [ala-IL-8]77). IL-8 derived from T lymphocytes and monocytes is predominantly [ser-IL-8]72, whereas endothelial-derived IL-8 is highly enriched (greater than 80%) in [ala-IL-8]77. We address the relationship and activities of these two forms of IL-8 using recombinant proteins expressed by both mammalian cells and Escherichia coli. Thrombin was found to efficiently convert [ala-IL-8]77 to [ser-IL-8]72. In contrast, urokinase and tissue-type plasminogen activator were unable to cleave [ala-IL-8]77, and trypsin generated multiple IL-8 cleavage fragments. In competitive binding assays using 125I[ala-IL-8]77 neutrophils exhibited a twofold preference for [ser-IL-8]72 over [ala-IL-8]77. Both forms of IL-8 inhibited neutrophil adhesion to IL-1-beta-activated HUVEC monolayers by up to 90%. However, [ser-IL-8]72 was approximately 10-fold more potent than [ala-IL-8]77 in these assays (ED50 approximately 0.3 nM for [ser-IL-8]72 vs approximately 3 nM for [ala-IL-8]77. Both forms of IL-8 promoted degranulation of cytochalasin B-treated neutrophils [[ser-IL-8]72 (ED50 greater than 10 nM) was two- to three-fold more potent than [ala-IL-8]77], although in this regard they were less active than FMLP. Our data suggest that [ala-IL-8]77 and [ser-IL-8]72 have qualitatively similar and potentially complex biological activities, and that full activation of IL-8 requires cleavage to the [ser-IL-8]72 form. In the case of inflamed endothelial cells this activation could be mediated by thrombin generated in the procoagulant environment associated with these cells.     

The viral envelope gene is involved in macrophage tropism of a human immunodeficiency virus type 1 strain isolated from brain tissue.

Human immunodeficiency virus type 1 (HIV-1) strains isolated from the central nervous system (CNS) may represent a subgroup that displays a host cell tropism different from those isolated from peripheral blood and lymph nodes. One CNS-derived isolate, HIV-1SF128A, which can be propagated efficiently in primary macrophage culture but not in any T-cell lines, was molecularly cloned and characterized. Recombinant viruses between HIV-1SF128A and the peripheral blood isolate HIV-1SF2 were generated in order to map the viral gene(s) responsible for the macrophage tropism. The env gene sequences of the two isolates are about 91.1% homologous, with variations scattered mainly in the hypervariable regions of gp120. Recombinant viruses that have acquired the HIV-1SF128A env gene display HIV-1SF128A tropism for macrophages. Furthermore, the gp120 variable domains, V1, V2, V4, and V5, the CD4-binding domain, and the gp41 fusion domain are not directly involved in determining macrophage tropism.     

Elastase-1-secreting acinar cell carcinoma of the pancreas. A cytologic, electron microscopic and histochemical study

A case of acinar cell carcinoma of the pancreas was diagnosed by fine needle aspiration cytology during surgery. The cytologic characteristics of this neoplasm are described. Electron microscopy disclosed numerous zymogen granules in the tumor while histochemistry demonstrated the presence of elastase-1. Serum elastase-1 levels were markedly elevated. The cytologic differential diagnosis of pancreatic tumors is discussed.     

青海藏族青少年骨龄与生长发育关系研究

本文报告了青海省境内,世居在海拔3000-4000米地区的728名7-18岁健康藏族青少年学生的手、腕部骨骼发育情况,对骨化中心出现和骨骺愈合求出了50%出现年龄,并对骨龄与青春期身高突增的关系及与月经初衬潮的关系进行了分析。     

云南景颇族的体质特征

本文调查了云南景颇族261人（男105人,女156人）。年龄为成年人（男24－60岁,女23－55岁）。主要测量均值与现代中国汉族和云南省各少数民族比较和聚类分析的结果表明,景颇族属黄种人的东亚类型,但也有南亚类型特征表现。体质特征与傣族、哈尼族和彝族接近,与基诺族和布郎族较远。     

武汉东湖磷含量的变动及其分布

本文总结了武汉东湖水体中磷含量（均以PO4计算）的周年逐月季节和年际变动及其分布上的差异（1973－1985年）。按面积加权法计算总磷的平均含量为0．244毫克／升（1983－1985年）,总溶解磷和溶解活性磷的平均含量分别为0．121毫克／升和0．051毫克／升（1981－1984年）,总磷和总溶解磷周年中出现两次高峰含量,即春季（3－5月）和夏末秋初（8－9月）。低含量出现在水温最低的冬季（12－2月）,周年中溶解活性磷高峰含量出现在冬末春初（1－3月）,低含量多数出现在春天夏初（5－7月）。东湖水体中磷含量平面分布有明显的差异,而垂直分布表层和底层差异小,各种形态磷的组成中颗粒磷所占比较最大（1983－1984年平均值）,平均占总磷63．4％,溶解非活性磷所占比较最小,平均占总磷12．0％。     

Genetics and sequence analysis of the pcnB locus, an Escherichia coli gene involved in plasmid copy number control.

Mutations at the Escherichia coli pcnB locus reduce the copy number of ColE1-like plasmids. We isolated additional mutations in this gene and conducted a preliminary characterization of its product. F-prime elements carrying the pcnB region were constructed and used to show that the mutations were recessive. The wild-type pcnB gene was cloned into a low-copy-number plasmid, and its nucleotide sequence was determined. The sequence analysis indicated that pcnB is probably the first gene in an operon that contains one or more additional genes of unknown function. The pcnB locus should encode a polypeptide of 47,349 daltons (Da). A protein of this size was observed in minicells carrying a pcnB+ plasmid, and transposon insertions and deletions that truncated this protein generally abolished pcnB function. One exceptional transposon insertion at the promoter-distal end of the pcnB gene truncated the 47-kDa protein by about 20% but did not abolish complementation activity, indicating that the C-terminus of the PcnB product is dispensable. The deduced amino acid sequence of PcnB revealed numerous charged residues and, with 10% arginines, an overall basic character, suggesting that PcnB might interact with DNA or RNA in a structural capacity. Disruption of the pcnB gene by insertional mutagenesis caused a reduction in growth rate, indicating that PcnB has an important cellular function.     

Otolith microstructure indicating growth and mortality among plaice, Pleuronectes platessa L., post-larval sub-cohorts

Growth and mortality of post-metamorphosed plaice were studied by means of daily increments in the sagittal otoliths. The Gompertz model was the best fit to length-at-age data and there were no significant differences between length-at-age and back-calculated lengths. The microstructure pattern of the otoliths at metamorphosis was also used to estimate hatching and settlement distributions. Differential growth and mortality occurred among sub-cohorts; growth rates and mortality were higher in fish that settled earlier. In 1986, the best survival was for a sub-cohort settling in late May to early June. In contrast, in the warmer season of 1987, survival was highest for the second and third sub-cohorts settling in late April and mid May.     

Recombinant granulocyte-macrophage colony-stimulating factor increases adenylate cyclase activity in murine peritoneal macrophages

Granulocyte-macrophage colony stimulating factor (GM-CSF) is a pleiotrophic cytokine which stimulates the function and proliferation of macrophage populations. Although the effects of GM-CSF are diverse and GM-CSF has entered into clinical trials, relatively little is known about signal transduction pathways utilized by GM-CSF. In view of previous studies which have suggested that some of the effects of GM-CSF on monocyte-macrophages can be mimicked by agents which increase intracellular cAMP, we investigated the effect of rGM-CSF on adenylate cyclase (AC) activity in murine peritoneal macrophages. Adenylate cyclase activity was quantitated in macrophage membrane preparations and in intact cells. In seven separate experiments, GM-CSF (50 U/ml) increased AC activity by 61(6)% relative to macrophages treated with carrier medium alone. A dose-dependent increase in AC activity was observed (10 to 100 U/ml) which peaked within 1 to 5 min after the addition of GM-CSF and returned to basal levels by 10 to 20 min. Lineweaver-Burk analysis revealed that the Vmax of macrophage AC was increased from 0.40 to 0.52 pmoles cAMP/min by GM-CSF but the Km was unchanged. Intracellular cAMP was increased by GM-CSF to 129(27)% of control values by 1 min of treatment (n = 6). Under similar experimental conditions, GM-CSF did not increase the activity of PK C (n = 14) or phospholipase A2 (n = 3) in peritoneal macrophages. These data show that macrophage adenylate cyclase activity is rapidly stimulated by GM-CSF. Moreover, these findings support further study of the role of cAMP in transmitting the intracellular signals initiated by GM-CSF in tissue macrophages.