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Biomedical subjects

Y Endo

Publications and source records attributed to Y Endo.

At least 271 records · Page 15Linked to original sources
PubMed1997

Induction by interleukin-1 (IL-1) of the mRNA of histidine decarboxylase, the histamine-forming enzyme, in the lung of mice in vivo and the effect of actinomycin D.

It is known that the activity of histidine decarboxylase (HDC), the histamine-forming enzyme, is induced in response to various stimuli. However, it has repeatedly been reported that actinomycin D (Act D), a typical inhibitor of RNA synthesis, is either ineffective, or actually potentiates induction of this enzyme. Thus, it has been suggested that the induction of HDC may not require the formation of mRNA, i.e. that pre-formed, long-lived mRNA molecules may be responsible for the induction. In the present study, we examined the effects of interleukin-1alpha (IL-1alpha) on the amount of HDC mRNA present during the induction of HDC activity. In mice injected with IL-1alpha, HDC mRNA increased in the lung, spleen and stomach, but was hardly detectable in these tissues in control (saline-injected) mice. In the lung, the time course of the rise and fall in HDC mRNA was shorter than that of the rise and fall in HDC activity. In the present study, actinomycin D (Act D) did not inhibit the increase in HDC mRNA induced by IL-1alpha; in fact, it potentiated the elevation of both HDC mRNA and HDC activity. These results suggest that IL-1alpha induces HDC activity or its enzyme protein through the formation of short-lived HDC mRNA molecules. This is the first demonstration that Act D can enhance an increase in HDC mRNA: this potentiating, rather than inhibiting, effect is discussed.

Animals↗
PubMed1997

NGF and BDNF increase the immunoreactivity of vesicular acetylcholine transporter in cultured neurons from the embryonic rat septum.

The expression of vesicular acetylcholine transporter (VAChT), which transports ACh into synaptic vesicles, is coregulated with choline acetyltransferase (ChAT). Therefore, the effects of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) on the levels of VAChT in cultured neurons from the septum of embryonic rats were investigated by immunocytochemistry. NGF and BDNF increased the number of VAChT-immunoreactive neurons by approximately 1.5-fold and enhanced the immunoreactivity in each positive cell. These results suggest that the neurotrophins enhance not only synthesis but also storage of ACh in septal neurons.

Acetylcholine↗
PubMed1997

Exon/intron organization, chromosome localization, alternative splicing, and transcription units of the human apolipoprotein E receptor 2 gene.

Apolipoprotein E receptor 2 is a recently identified receptor that resembles low and very low density lipoprotein receptors. Isolation and characterization of genomic clones encoding human apolipoprotein E receptor 2 revealed that the gene spans approximately 60 kilobases and contains 19 exons. The positions of the exon/intron boundaries of the gene are almost identical to those of low and very low density lipoprotein receptors. Fluorescent in situ hybridization of human chromosomes revealed that the gene is located on chromosome 1p34. Isolation of a cDNA encoding a variant receptor and reverse transcription-polymerase chain reaction indicate the presence of multiple variants with different numbers of cysteine-rich repeats in the binding domain of the receptor. We also found a variant receptor lacking a 59-amino acid insertion in the cytoplasmic domain. The transcription start site was mapped to the position 236 base pairs upstream of the AUG translation initiator codon by primer extension analysis. Sequence inspection of the 5'-flanking region revealed potential DNA elements: AP-2, GC factor, PEA3, and Sp1. The minimal promoter region and a region required for nerve growth factor inducibility in PC12 cells were also determined.

Alternative Splicing↗
PubMed1997

Identification of NAP-22 and GAP-43 (neuromodulin) as major protein components in a Triton insoluble low density fraction of rat brain.

NAP-22 is a membrane-localized brain enriched acidic protein having a Ca(2+)-dependent calmodulin binding activity. Further fractionation of the NAP-22 containing membrane showed the localization of NAP-22 in a Triton insoluble fraction of low density. Besides NAP-22, this fraction was found to contain GAP-43 (neuromodulin), trimeric G proteins, and some GPI-anchored proteins such as Thy-1 and N-CAM-120. Presence of some protein tyrosine kinases, such as src and fyn, was also shown.

Amino Acid Sequence↗
PubMed1997

Fourier-Transform Microwave Spectroscopy of the Argon-Diacetylene van der Waals Complex

The rotational spectrum of the argon-diacetylene van der Waals complex, produced in a supersonic molecular beam at 1 K, has been observed with a Fourier-transform microwave spectrometer. We observed 22 a-type rotational transitions with Ka up to 3. Three rotational constants, five centrifugal distortion constants, and one higher-order centrifugal distortion constant were determined precisely by least-squares analysis. The complex is shown to have a planer T-shaped structure with C2v symmetry. The structural analysis provides that the Ar atom is located 3.68 A from the center of mass of diacetylene. Force constants for the van der Waals vibrations were determined from the centrifugal distortion constants. It has been found that this complex has a much steeper and more harmonic intermolecular potential than the argon-acetylene complex. Copyright 1997 Academic Press. Copyright 1997Academic Press

Journal Article↗
PubMed1997

Gynandroblastoma of the ovary: a case report with an immunohistochemical and ultrastructural study.

An ovarian gynandroblastoma in a 60-year-old woman is described. The cut-surface of the right ovary showed multiple macrofollicles separated by white fibrous tissues and multiple ill-defined yellowish nodules. The tumour consisted of substantial amount of a granulosa cell element and a Sertoli cell element with intermingled Leydig cells. Immunohistochemically, the tumour cells in both the granulosa cell and Sertoli cell elements were positive for cytokeratin CAM5.2. The granulosa cell element showed strong membrane staining of Ewing's sarcoma antigen 013 and the Sertoli cell element was locally positive. Vimentin was observed in both the Sertoli cell element and the granulosa cells. Both elements and the Leydig cells were uniformly negative for epithelial membrane antigen, muscle specific actin, CD31 and CD34. The tumour was aneuploid by flow cytometry. The patient was well with no evidence of tumour five months after surgery.

Female↗
PubMed1997

Small cell neuroendocrine carcinoma of the ovary.

A 64-year-old woman (gravida 0, para 0) had a unilateral ovarian mass measuring 14 cm in its greatest diameter, which was mostly solid. Microscopically, the tumour was characterized by two predominant proliferating patterns: a carcinoid-like pattern with trabecular, tubular, glandular, or insular arrangements and a closely packed nesting pattern with central coagulation necrosis and occasional glandular arrangements. These two patterns were intermingled, and numerous mitotic figures were present. Electron microscopy showed neurosecretory granules in the cells, which were argyrophilic and positive for neuroendocrine markers (chromogranin, leu 7, neuron-specific enolase, and synaptophysin). The tumour was aneuploid by flow cytometry. The patient received chemotherapy postoperatively, developed brain and multiple bone metastases and died of disease 10 months after surgery. This tumour must be distinguished from other small cell neoplasms, especially ovarian small cell carcinoma of the hypercalcaemic type.

Biomarkers↗
PubMed1997

Bacterial translocation as a cause of septic shock in humans: a report of two cases.

While bacterial translocation has been reported to occur under numerous conditions in animal models, there has been no paper to date focusing on bacterial translocation as a direct cause of septic shock in humans. We present herein the cases of two patients who developed septic shock believed to have been directly caused by bacterial translocation. Neither of the patients had a focus of infection, the intestinal walls were intact in gross appearance, and the peritoneal cavity had not been contaminated by surgery. Moreover, in both patients, the same organisms were detected in the blood, ascites fluid, and mesenteric lymph nodes, and bacilli were found in the intestinal wall.

Aged↗
PubMed1997

Effects of acute hyperthermia on the carotid baroreflex control of heart rate in humans.

The purpose of this study was to examine the effect of hyperthermia on the carotid baroreceptor-cardiac reflexes in humans. Nine healthy males underwent acute hyperthermia (esophageal temperature -38.0 degrees C) produced by hot water-perfused suits. Beat-to-beat heart rate (HR) responses were determined during positive and negative R-were-triggered neck pressure steps from +40 to -65 mm Hg during normothermia and hyperthermia. The carotid baroreceptor-cardiac reflex sensitivity was evaluated from the maximum slope of the HR response to changes in carotid distending pressure. Buffering capacity of the HR response to carotid distending pressure was evaluated in % from a reference point calculated as (HR at 0 mm Hg neck pressure-minimum HR)/HR range x 100. An upward shift of the curve was evident in hyperthermia because HR increased from 57.7 +/- 2.4 beats/min in normothermia to 88.7 +/- 4.1 beats/min in hyperthermia (P < 0.05) without changes in mean arterial pressure. The maximum slope of the curve in hyperthermia was similar to that in normothermia. The reference point was increased (P < 0.05) during hyperthermia. These results suggest that the sensitivity of the carotid baroreflex of HR remains unchanged in hyperthermia. However, the capacity for tachycardia response to rapid onset of hypotension is reduced and the capacity for bradycardia response to sudden hypertension is increased during acute hyperthermia.

Acute Disease↗
PubMed1997

Molecular characteristics of malignant lymphomas in cats naturally infected with feline immunodeficiency virus.

Neoplastic disease, especially malignant lymphomas, are often observed in cats infected with feline immunodeficiency virus (FIV). In order to clarify the characteristics of lymphoma cells and to investigate the pathogenesis in FIV-infected cats, we examined the lymphoma tissues developed in five cats naturally infected with FIV by Southern blot analyses using feline immunoglobulin (Ig), T-cell receptors (TCR) and FIV probes. All of the five cases were serologically positive for anti-FIV antibody and negative for feline leukemia virus antigen. Of these five lymphoma samples, two displayed rearrangement of the Ig heavy chain gene and deletion of the Ig light (kappa) chain gene, indicating that the tumor cells were committed to B-cell development. One tumor sample was identified as a T-cell lymphoma because of the presence of a rearranged TCR beta-chain gene. The other two cases were considered to be non-T non-B cell lymphoma because they did not show any rearrangement of the Ig and TCR genes. Therefore, no consistent tumor type was found in lymphoma cases infected with FIV. Clonal integration of FIV provirus was not detected in any of the five lymphoma samples obtained from FIV-infected cats using Southern blot analysis, although FIV proviral genome was detected in the genomic DNA of all the lymphoma samples by using a polymerase chain reaction (PCR). These results indicated that FIV might not play a direct role in tumorigenesis of lymphoma in cats.

Animals↗
PubMed1997

Behavioral correlates of transneuronal degeneration of substantia nigra reticulata neurons are reversed by ablation of the subthalamic nucleus.

In rats, acute injury of neurons in the caudate nucleus (CN) and globus pallidus (GP) by local injection of ibotenic acid (IA) or by transient forebrain ischemia has caused transneuronal cell death of neurons in the substantia nigra reticulata (SNr) weeks after the initial injury. Recently transient expression of an immediate early gene c-fos was induced specifically in neurons of the subthalamic nucleus (STN) and SNr at 36-48 h after the IA-lesions, prior to the delayed degeneration of SNr neurons. These cellular and molecular events may alter the level of inhibitory output from the basal ganglia and lead to movement disorders. To test (i) whether movement disorders occur in the early period after unilateral lesions of the CN and GP by IA-injection, and (ii) whether ablation of the STN reverses the early movement disorders, we used a modified version of Porsolt forced swim test in which the lesion-induced asymmetry of motor function becomes apparent as rotation when the animals are forced to swim. Following unilateral IA-lesions of the right CN and GP in rats, rapid contraversive rotation appeared transiently 36-48 h after the lesions, and, in turn, slow ipsiversive rotation appeared at 3-5 days postlesion. Prior ablation of the ipsilateral STN reversed these early movement disorders produced by the unilateral IA-lesions of the CN and GP and instead created persistent contraversive rotation 7-10 days after the lesions. Each phase of the dominant rotation behavior was dependent on asymmetrical limb motor activity; decreased left limb activity caused contraversive rotation, and increased left limb activity caused ipsiversive rotation. Reversal of these early movement disorders suggests that ablation of the STN prevents the transneuronal degeneration of the SNr.

Animals↗
PubMed1997

Long-term glucocorticoid treatments decrease local cerebral blood flow in the rat hippocampus, in association with histological damage.

The present study examined the influence of a long-term treatment with glucocorticoid on local cerebral blood flow of the hippocampus in rats, estimated with the hydrogen clearance method. Either a cholesterol (100 mg, as a control) or corticosterone (100 mg) bead was implanted subcutaneously in rats for a period of three months, beginning at 12 weeks of age. The effects of the treatments on the local circulation of the hippocampus were evaluated three to four months after the termination of the treatments. Hippocampal cerebral blood flow in corticosterone-treated rats was significantly lower (P<0.05) than that in control rats, and fluctuated over a day in lower amplitude than the controls. Severe histological damage was observed in the CA1 and CA3 cell fields of the hippocampus in corticosterone-treated rats. These neuropathological changes were characterized by soma shrinkage and condensation, or nuclear pyknosis, as reported previously. We concluded that a long-term glucocorticoid exposure resulted in an impairment of the hippocampal functions, accompanied by neuronal damage similar to that found in aged hippocampus. The present results support the hypothesis that glucocorticoids accelerate age-related changes in the brain.

Animals↗
PubMed1997

Vascular endothelial growth factor and lymph node metastasis in primary lung cancer.

The relationship between vascular endothelial growth factor (VEGF) and lymph node metastasis was studied in 90 cases of primary lung cancer without distant metastasis. As a result of quantitative reverse transcription polymerase chain reaction (RT-PCR) analysis, the VEGF121 mRNA expression levels in lung cancer tissues with nodal metastasis (n = 35) were higher than in those without nodal metastasis (n = 55). However, no significant difference could be found in VEGF121 mRNA expression levels as stratified by tumour size (T1N0M0 vs T2N0M0). Simultaneously, ten lymph nodes (four node positive and six node negative) together with the corresponding primary lung tumours and adjacent normal lung tissue, were studied for VEGF expression. The VEGF mRNA expression in metastatic lymph nodes was intense in three out of the four cases examined. Further, while VEGF expression levels in metastatic lymph nodes were conspicuously higher than those for the primary site, all its expression levels in non-metastatic nodes were inferior to those of the primary tumours. Except for macrophages, the VEGF antigen was identified mainly in the cytoplasm of metastatic cancer cells and the endothelial cells of blood or lymphatic vessels in lymph nodes. Although the detailed mechanisms and the significance of strong VEGF expressions in metastatic lymph nodes are still unknown, these data are consistent with a model whereby VEGF increases the opportunity for nodal metastasis through neoblood and lymphatic vessels.

Aged↗
PubMed1997

Inhibition of lymph node metastasis by an anti-angiogenic agent, TNP-470.

We assessed the inhibitory action of TNP-470 on lymph node metastasis in a metastatic model system using athymic nude mice. Mice were injected subcutaneously with 5 x 10(6) HT-1080 cells in the right groin. TNP-470 (10, 30 and 100 mg kg-1) was injected subcutaneously nine times in total every other day from the 7th day after tumour inoculation. Axillar and inguinal lymph nodes were dissected, and DNA was extracted 5 weeks after tumour inoculation. Specific detection of a human beta-globin-related sequence in metastasized human tumour cells in nude mice was done by the polymerase chain reaction (PCR) technique and analysed by Southern blotting. Anti-tumour effects on primary sites were seen only in the 100 mg kg-1 treatment group. Lymph node metastasis of transplanted HT-1080 cells was seen in all mice of the no treatment group (5/5). On the other hand, incidences of lymph node metastasis in treated mice were 2/4 mice (100 mg kg-1, 2/5 mice (30 mg kg-1) and 4/5 mice (10 mg kg-1). The inhibition ratios of lymph node metastasis were 82.3% at 10 mg kg-1, 97.2% at 30 mg kg-1 and 97.5% at 100 mg kg-1 respectively. This agent may be useful to inhibit lymph node metastasis.

Animals↗
PubMed1997

HsMCM6: a new member of the human MCM/P1 family encodes a protein homologous to fission yeast Mis5.

BACKGROUND: The tight regulatory mechanism that prevents more than one round of chromosomal DNA replication per cell cycle is thought to require the function of Mcm/P1 proteins. We report here the structural and functional analyses of HsMcm6, a human homologue of the Mis5 of Schizosaccharomyces pombe. RESULTS: We demonstrate here that the transcription of the HsMCM6 gene was repressed in quiescent cells but was rapidly induced at the G1/S phase by growth factor stimulation. The 5' regulatory region of the HsMCM6 gene was found to harbour four putative E2F binding motifs, and these were responsible for the promoter activity. The HsMcm6 protein level oscillated during the cell cycle, with a peak at the G1/S phase. We also showed that the cell-cycle dependent change of subcellular localization of HsMcm6 resembles those of other Mcm/P1 proteins. HsMcm6 consists of two forms, a form extractable by Nonidet P-40 and the nucleus-bound form. A demonstration of the association of HsMcm6 with HsMcm2 and HsMcm7 in vivo supports the idea that they behave as a heteromeric complex. We mapped the HsMCM6 gene at 2q12-14. CONCLUSION: The results indicate that the behaviour of HsMcm6 is reminiscent of replication licensing factor like other Mcm/P1 family members.

Amino Acid Sequence↗
PubMed1997

Brain-derived neurotrophic factor increases the stimulation-evoked release of glutamate and the levels of exocytosis-associated proteins in cultured cortical neurons from embryonic rats.

Differentiation and survival of neurons induced by neurotrophins have been widely investigated, but little has been reported about the long-term effect of brain-derived neurotrophic factor (BDNF) on synaptic transmission. Among many steps of neurotransmission, one important step is regulated release of transmitters. Therefore, the release of glutamate and GABA from cortical neurons cultured for several days with or without BDNF was measured by an HPLC-fluorescence method. Although BDNF had little effect on the basal release of glutamate, high K(+)-evoked release was greatly increased by BDNF. BDNF also tended to increase evoked release of GABA. Recently, several proteins involved in the step of "regulated release" have been identified. Thus, the effect of BDNF on the levels of these proteins was then investigated. Neurons were cultivated with or without BDNF, collected, and electrophoresed for western blotting. BDNF increased levels of synaptotagmin, synaptobrevin, synaptophysin, and rab3A, which were known as vesicle protein. Levels of syntaxin, SNAP-25, and beta-SNAP were also increased by BDNF. In addition, the numbers of cored and clear vesicles in nerve terminals or varicosities were also increased by BDNF. These results raise the possibility that BDNF increases regulated release of neurotransmitters through the up-regulation of secretory mechanisms.

Animals↗
PubMed1997

Contrasting effects of lipopolysaccharides (endotoxins) from oral black-pigmented bacteria and Enterobacteriaceae on platelets, a major source of serotonin, and on histamine-forming enzyme in mice.

By measurement of serotonin levels, the translocation of platelets to various tissues was examined following intravenous injection of a lipopolysaccharide (LPS) into C3H/HeN mice. There was a rapid platelet accumulation (within 5 min and particularly in the lung), followed by a slower accumulation in the liver, which reached its plateau 3-5 h later. The severity of the anaphylactoid shock corresponded well with the magnitude of the rapid response. LPSs from the oral black-pigmented bacteria, Porphyromonas gingivalis and Prevotella intermedia, were much more potent in inducing the rapid platelet response than were those from the Enterobacteriaceae Escherichia coli and Salmonella typhimurium. However, LPSs from these Enterobacteriaceae were significantly more potent than those from black-pigmented bacteria in inducing the slow platelet response. There was also a contrast between their abilities to induce histidine decarboxylase, which forms histamine from histidine: LPSs from the Enterobacteriaceae were much more potent than those from black-pigmented bacteria.

Acetylmuramyl-Alanyl-Isoglutamine↗