Benign glandular inclusions in inguinal and abdominopelvic lymph nodes in gynecologic pathology

From 4 cases recently seen at the Institut Gustave-Roussy, this report describes the pathological and evolutive features of benign glandular inclusions in inguinal, pelvic or abdominal lymph nodes. These lesions are defined by the presence of tubular formations in lymph nodes, lined by a single layer of epithelium which is cuboidal or columnar and resembled that of tubal epithelium with ciliated, secretory and intercalary cells. In most cases, benign glandular inclusions in lymph nodes still quiescent. In rare instances, they may proliferate and become papillary. The association of proliferating glandular inclusions in lymph nodes with borderline tumor of the ovary raises the problem of their primary or metastatic origin. However, their pathological features argues for a primary origin in lymph nodes. Thus, we think that a metastatic potential of borderline tumors of the ovary is not supported by any convincing argument.     

Ligands that activate protein kinase-C differ in their ability to regulate basic fibroblast growth factor and insulin-like growth factor-I messenger ribonucleic acid levels

In this study, rat dermal fibroblasts were used as a model system to examine the ability of ligands that are known to activate protein kinase-C to regulate the levels of the mRNAs encoding basic fibroblast growth factor (bFGF) and insulin-like growth factor-I (IGF-I), two growth factors that are thought to be important in processes such as tissue repair and regeneration and wound healing. Treatment of fibroblasts with the phorbol ester phorbol 12-myristate 13-acetate (PMA), thrombin, bradykinin, serotonin, angiotensin-II, or bombesin increased protein kinase-C activity to a similar degree. Treatment of fibroblasts with 1 microM serotonin transiently increased bFGF mRNA levels about 3-fold compared to the level in control cells maintained in serum-free medium with 0.25% BSA and decreased IGF-I mRNA levels by approximately 50% compared to the level in control cells. This is similar to the previously described changes induced by bradykinin in these cells, but different from the more marked and sustained changes induced by thrombin and PMA. In contrast, angiotensin-II and bombesin had no effect on bFGF or IGF-I mRNA levels. The effects of serotonin, bradykinin, and PMA on bFGF and IGF-I mRNA levels were abrogated by preincubation of cells in 250 nM PMA to down-regulate protein kinase-C. In contrast, the effect of thrombin on bFGF mRNA levels was only partially inhibited by down-regulation of protein kinase-C, while its effect on IGF-I mRNA levels was unaffected. The activation of signaling pathways by the different ligands was further investigated to begin to determine the mechanism for the differences in the effects of thrombin vs. serotonin and bradykinin and in the effects of these three ligands vs. angiotensin-II and bombesin. All of the ligands activated phospholipase-D to a similar degree, suggesting that activation of this enzyme was not responsible for the differential effects of the ligands. In contrast, thrombin, serotonin, and bradykinin had marked effects on the hydrolysis of phosphatidylcholine and phosphatidylinositol, whereas bombesin and angiotensin-II had a small effect on phosphatidylcholine hydrolysis and no effect on phosphatidylinositol hydrolysis.(ABSTRACT TRUNCATED AT 400 WORDS)     

顺丁橡胶生产过程"门尼升值"的原因研究

研究了顺丁橡胶生产过程中门尼升值的原因。结果表明，顺丁橡胶生产后处理的膨胀干燥过程存在门尼升值现象。不同内在质量的顺丁橡胶门尼升值不同，正常条件下门尼升值发生于门尼粘度的测试过程。     

三塘湖盆地上古生界烃源岩镜质组反射率异常研究

镜质组反射率是评价有机质成熟度的重要指标 ,然而由于地质因素和测试技术的原因 ,镜质组反射率测量值常与预计值有一定的偏差。在三塘湖盆地上古生界烃源岩中 ,可以观察到镜质组反射率的局部增强和镜质组反射率的抑制。局部增强多分布在上二叠统的烃源岩中 ,主要与火山活动有关。这种反射率的增强在平面上分布广泛 ,但纵向上影响范围较小。反射率的抑制是在上古生界烃源岩含有较高含量的腐泥组分背景下产生的。用氢指数模板方法对抑制进行了校正 ,抑制的幅度最大可达 0 .3%     

Analysis of simian hemorrhagic fever virus (SHFV) subgenomic RNAs, junction sequences, and 5' leader

Full-length simian hemorrhagic fever virus (SHFV) genome RNA (about 15 kb in length) and six subgenomic RNAs, ranging in size from 0.65 to 4.7 kb, were detected by Northern blot hybridization in MA104 cytoplasmic extracts with a 3' genomic antisense probe. The 5' regions of the two smallest subgenomic RNAs (RNAs 6 and 7) were cloned and sequenced. Sequence analysis indicated that these two RNAs contained a common 5' leader sequence joined to the subgenomic RNA bodies via a highly conserved junction sequence; the junction sequence of RNA 7 was 5'-TTAACC-3', while that of RNA 6 was 5'-TCAACC-3'. The complete 5' leader sequence (208 nt) was obtained from genomic RNA. The genomic 5' junction sequence is identical to that of RNA 7. Northern blot hybridization with an antisense 5' leader probe confirmed the presence of the complete leader sequence in all six species of subgenomic RNA. In its virion morphology, genome size, gene order, and replication strategy, SHFV is most similar to viruses such as equine arteritis virus, lactate dehydrogenase-elevating virus, and Lelystad virus/porcine respiratory and reproductive syndrome virus.     

Perfection of methodical approaches to designing vaccines against tick-borne encephalitis

Nine female patients with a urethral diverticulum were admitted to our center over a six period: The clinical symptomatology was not specific. The diagnosis has been performed by voiding and retrograde cysto-uretrogram. The surgical treatment consisted in the excision of the diverticula, with the patient in the supine position. No perioperative morbidity was observed.     

Effect of furosemide and intravenous normal saline fluid load upon the renal resistive index in nonobstructed kidneys in children

Recent literature has shown that relative to baseline the renal resistive index remains unchanged in nonobstructed kidneys and increases in obstructed kidneys after administration of furosemide. To our knowledge the effect upon the renal resistive index of furosemide administered in conjunction with intravenous normal saline fluid load has not been reported. We evaluated the renal resistive index in 13 nonobstructed kidneys in 8 children 6 to 18 years old before and after furosemide and intravenous normal saline fluid load. The mean resistive index decreased from baseline (mean decrease was 0.06 +/- 0.06 standard deviation), with the observation of a resistive index decrease significant to p < 0.005). It appears likely that the combination of an intravenous normal saline fluid load and furosemide caused the resistive index decrease, since a decrease was not observed with furosemide alone; however, these results cannot exclude the possibility that the resistive index decrease was due to the intravenous normal saline fluid load alone. Nonetheless, these data are important since they may provide the foundation for the development of a pharmacologically challenged Doppler sonographic examination using furosemide and intravenous normal saline fluid load to evaluate better potentially obstructed kidneys.     

Envelope glycoprotein gp120 of human immunodeficiency virus type 1 alters ion transport in astrocytes: implications for AIDS dementia complex

Infection by human immunodeficiency virus type 1 (HIV-1) is often complicated by a variety of neurological abnormalities. The most common clinical syndrome, termed acquired immunodeficiency syndrome (AIDS) dementia complex, presents as a subcortical dementia with cognitive, motor, and behavioral disturbances and is unique to HIV-1 infection. The pathogenesis of this syndrome is poorly understood but is believed to involve interactions among virally infected macrophages/microglia, astrocytes, and neurons. In this study, we show that exposure of primary rat and human astrocytes to heat-activated HIV-1 virions, or to eukaryotically expressed HIV-1 and HIV-2 envelope glycoproteins (gp120) stimulates amiloride-sensitive Na+/H+ antiport, potassium conductance, and glutamate efflux. These effects are blocked specifically by amiloride, an inhibitor of Na+/H+ antiport and by the selective removal of gp120 with immobilized monoclonal antibody. As a result of modulation of astrocytic function by gp120, the ensuing neuronal depolarization and glutamate exposure could activate both voltage-gated and N-methyl-D-aspartate-regulated Ca2+ channels, leading to increases in intraneuronal Ca2+ and neuronal death. These findings implicate the astrocyte directly in the pathogenesis of AIDS dementia complex.