用免疫组织化学方法鉴别异位妊娠与正常妊娠

对57例内膜刮出组织和宫内流出组织均未检出绒毛膜绒毛。用抗血清标记绒毛滋养层的人绒毛膜促性腺激素(HCG)、人胎盘催乳素(HPL)和妊娠特异糖蛋白(SPI),结果18例被标记,37例未被标记。临床证明未被标记的37例为异位妊娠。表明用激素标记子宫内膜可提高异位妊娠的诊断率。     

Antidepressant biochemical profile of the novel bicyclic compound Wy-45,030, an ethyl cyclohexanol derivative

The novel bicyclic compound Wy-45,030 [1-2-(dimethylamino)-1-(4-methoxyphenyl)ethyl cyclohexanol, hydrochloride] exhibited a neurochemical profile predictive of antidepressant activity. Like the tricyclic antidepressants, it inhibited rat brain imipramine receptor binding and synaptosomal monoamine uptake (dopamine as well as norepinephrine and serotonin). It did not inhibit monoamine oxidase. Unlike the tricyclic antidepressants, it was not antimuscarinic in the guinea pig ileum, nor did it have any appreciable affinity for brain alpha-1 adrenergic or histamine-1 binding sites. Wy-45,030 was also without affinity for alpha-2 or beta adrenergic, benzodiazepine, serotonin-1, serotonin-2, dopamine-2, and opiate receptors. Such a profile is predictive of antidepressant activity devoid of the side-effects common to tricyclic therapy.     

Analysis of Vascular Endothelial Growth Factor (VEGF) and a receptor subtype (KDR/flk-1) in the liver of rats exposed to riddelliine: a potential role in the development of hemangiosarcoma

Riddelliine alters hepatocellular and endothelial cell kinetics and function including stimulating an increase in hepatocytic vascular endothelial growth factor (VEGF) in the absence of increased serological levels of VEGF (Nyska etal. 2002). The objective of this study was to further assess hepatic VEGF and KDR/flk-1 synthesis and expression by hepatic cells under riddelliine treatment conditions. Forty-two male F344/N rats were dosed by gavage with riddelliine (0, 1.0, and 2.5 mg/kg/day) for 6 weeks. Seven animals/group were sacrificed after 8 consecutive daily doses; remaining rats were terminated after 30 daily doses, excluding weekends. Hepatic tissues were evaluated by immunohistochemistry and in situ hybridization. The results showed that VEGF mRNA expression was observed in control and treated animals; however, qualitative differences were noted. Treated animals exhibited VEGF mRNA in clustered, focal hepatocytes and bile duct epithelium, whereas VEGF mRNA in hepatocytes from vehicle control rats was distributed evenly across all hepatocytes. Results evaluating the distribution of the VEGF cognate receptor, KDR/flk-1 showed that randomly distributed, rare sinusoidal endothelium, including those demonstrating karyomegaly and cytomegaly expressed KDR/flk-1. Phosphorylation of KDR/flk-1 at pTyr996 and pTyr1054/1059, but not pTyr951, was also detected, evidence that endothelial cell KDR/flk-1 was activated. These results suggest that both hepatocytes and endothelial cells are targets of riddelliine-induced injury. We speculate that damage to both populations of cells may lead to dysregulated VEGF synthesis by hepatocytes and activation of KDR/flk-1 by endothelium leading to the induction of sustained endothelial cell proliferation, culminating in the development of hepatic hemangiosarcoma.     

THE EXPERIMENTAL PRODUCTION OF NECROSIS OF THE LIVER IN THE GUINEA PIG

Through the intravenous injection of various substances differing very much in character, multiple necrosis can be produced in the liver of the guinea pig. In the mouse the effect of these substances is absent or much less marked. Different substances seem to differ, however, in their power to produce necrosis. In control animals necrosis in the liver is much more rare. It is found especially in animals subjected to various injurious influences. The necrotic areas are usually situated between the portal and central areas of the liver acini. Their development is not due to thromboses interfering with the circulation in certain areas of the liver. They are probably due to a weakening of the circulation in the liver or to interference with the metabolism of the cells as a result of the injection of foreign substances. Mechanical factors (pressure on the liver cells) may have an additional effect. This necrosis may be compared etiologically to the acute gastric ulcers which can be produced through a great variety of toxic substances in the guinea pig.     

Characterization of the Sendai virus V protein with an anti-peptide antiserum.

The Sendai virus V protein, which is a fusion of the P and V ORFs of the P gene, was characterized with antisera to a portion of the V ORF and compared to the P protein. The only property found in common with P is that V is also highly phosphorylated, and this is so even when these proteins are expressed independently of the other viral proteins. Otherwise, V was not found in virions, was not strongly associated with viral nucleocapsids like P, and anti-V had no effect on viral RNA synthesis in vitro under conditions where anti-P was highly inhibitory. The available evidence suggests that V may play a role in RNA synthesis, but it is not an essential one like that of the P protein.     

Autoimmune vasculitis in MRL/Mp-lpr/lpr mice: orthochromatic basophils participate in the development of delayed-type hypersensitivity angiitis.

The pathogenesis of autoimmune vasculitis is poorly understood. Understanding the immunologic mechanisms governing this disease requires precise identification of the cells which comprise the lesion. In this report, we have evaluated tissue sections from MRL/lpr mice from 16 to 45 weeks of age, representing all stages of clinical vasculitis. We demonstrate that basophil myelocytes participate in the evolution of the delayed-type hypersensitivity (DTH) response which initiates and perpetuates autoimmune vasculitis in these mice. These findings raise questions regarding the immunologic mechanisms by which basophils develop in this lesion and the interaction of basophils. VSMCs and lymphocytes in vasculitic angiodestruction.