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Biomedical subjects

K Murakami

Publications and source records attributed to K Murakami.

At least 469 records · Page 26Linked to original sources
PubMed1996

[Skull base metastasis from renal cell carcinoma presenting as abducens nerve paresis: report of two cases].

We report two cases of skull base metastasis from renal cell carcinoma. Case 1: A 55-year-old female presented with a skull base tumor located on the clivus. Partial removal of the tumor was performed via the transsphenoidal approach. Case 2: A 44-year-old male presented with a skull base tumor occupying the orbital, nasal, and paranasal cavities. The first operation, partial removal of the tumor, was performed via the transsphenoidal approach. Thereafter, the tumor regrowth and the patient's symptoms were progressive, so a second operation was performed via Le-Forte I craniotomy to prevent cranial nerve dysfunction and air way obstruction. The initial symptom of these two cases was abducens nerve paresis, which is caused by the tumor extending from the clivus to the cavernous sinus. The neuroradiological features were the destruction of skull base bone and angiographic tumor stain. Histopathological examination of the surgically resected specimens revealed clear cell carcinoma, and thereafter they were diagnosed as skull base metastasis from renal cell carcinoma. We emphasize the necessity of a thorough medical workup to enable speedy diagnosis of renal cell carcinoma in such cases.

Abducens Nerve↗
PubMed1996

Mutagenicity of chemicals produced from sodium dodecylbenzenesulfonate by treatment with ozone and ultraviolet irradiation.

The interaction of formaldehyde and glyoxal produced from linear dodecylbenzenesulfonate (DBS) in aqueous solution after simultaneous treatment with ozone and ultraviolet (UV) irradiation and the effect of DBS on the mutagenic activity of formaldehyde and glyoxal were investigated. The decomposition of DBS in aqueous solution resulted in the formation of the mutagens formaldehyde and glyoxal as intermediate products after the simultaneous treatment for 4 hr. Therefore, the aqueous solution containing decomposed DBS after the treatment for 4 hr was mutagenic for Salmonella typhimurium strains TA100 and TA104 in the presence and absence of S9 mix. However, the mutagenic activity was greater than the sum of the mutagenic activity of formaldehyde and glyoxal formed from DBS. The aqueous solution mixed with formaldehyde and glyoxal did not increase the mutagenicity above the sum of the mutagenic activity in the presence or absence of DBS. Furthermore, DBS at concentrations of 2.0 micrograms/plate or less did not affect the mutagenicity of the mixtures containing formaldehyde and glyoxal. In addition, there was little bacteriocidal effect of the mixed solution on the mutagenicity test strains. These results suggest that unidentified mutagenic intermediate products were produced from DBS after simultaneous treatment with ozone and UV irradiation for 4 hr.

Animals↗
PubMed1996

Hypertensive and hypotensive mice produced by the introduction and disruption of genes on the renin-angiotensin system.

We constructed in mice the chimeric renin-angiotensin cascade comprising human renin, human angiotensinogen, and the endogenous angiotensin-converting enzyme and angiotensin II (A II) receptors by crossmating separate lines of transgenic mice carrying either gene. Although hypertension did not develop in the single-gene carriers despite the observed tissue-specific expression of the transgenes, dual-gene strains exhibited a chronically sustained increase in blood pressure (BP). The systolic BP was 130 +/- 7 mmHg, which is about 30 mmHg higher than that of control mice. Administration of a selective antagonist directed at the A II receptor decreased the basal BP in both single-gene and dual-gene mice. In addition, we generated two lines of knockout mice by homologous recombination in mouse embryonic stem cells. One line consisted of angiotensionogen-deficient mice, which failed to produce angiotensinogen in the liver, resulting in the complete loss of plasma angiotensin 1. The systolic BP of the mice was 66.9 +/- 4.1 mmHg, significantly lower than that of the controls (100.4 +/- 4.4 mmHg). The second line consisted of A II-receptor type la-deficient mice, which also exhibited hypotension (24 mmHg lower than that of controls). These results demonstrated that the renin-angiotensin system plays an indispensable role in maintaining normal BP in vivo, and cannot be replaced by other hormonal and neuronal systems.

Animals↗
PubMed1996

Nephrogenesis and renovascular development in angiotensinogen-deficient mice.

Angiotensinogen-deficient mice provide a model to examine the roles of angiotensin II as a renal growth factor in vivo. We monitored nephrogenesis and renovascular development in angiotensinogen-deficient mice from Embryonic Day 13 (E13) to 4 weeks after birth. Northern analysis of homozygote (Atg-/-) mice confirmed the absence of angiotensinogen mRNA in the liver and the kidneys. Embryonic kidneys in Atg-/- mice from E13 to E18 exhibited active nephrogenesis, as also observed in Atg+/- mice and Atg+/+ mice. Furthermore, metanephroi harvested at E12 from Atg-/- embryos showed branching morphogenesis of ureteric bud and tubulogenesis similar to metanephrol from Atg-/- embryos grown with exogenous angiotensin II in serum-free culture. In newborn Atg-/- mice, we observed uniform dilation of the pelvis accompanied by a coarse medulla, which was not noted in Atg+/- or Atg+/+ mice. Hydronephrosis in Atg-/- mice continued, and renal papillae underwent atrophy for the 4 weeks after birth. Another characteristic aspect of the morphology of Atg-/- mice was the thickening of vascular walls as little as 2 weeks after birth. Immunohistochemistry revealed recruitment of renin in hyperplastic vascular smooth muscle cells (VSMC) in Atg-/- mice after 2 weeks. Electron microscopy confirmed that the majority of hyperplastic VSMC contained various sized renin granules with abundant endoplasmic reticulum. In situ hybridization demonstrated that expression of renin mRNA became prominent in parallel with hyperplasia of VSMC, as well as recruitment of renin protein. Furthermore, at 4 weeks, Atg-/- mice expressed alpha-smooth muscle actin in the mesangium, whereas none was ever found in that of Atg+/- mice and Atg+/+ mice. In conclusion, the renin-angiotensin system seems not be essential for nephrogenesis in vivo. Furthermore, hyperplasia of VSMC and expression of the smooth-muscle phenotype in the mesangium are inducible even in the absence of angiotensin II, with hypotension, in vivo.

Angiotensinogen↗
PubMed1996

Expression of vacuolating cytotoxin in clinical isolates of Helicobacter pylori.

Our objective was to determine whether the prevalence of vacuolating cytotoxin production differed among Helicobacter pylori isolates obtained from patients with chronic gastritis, gastric ulcer, or duodenal ulcer. We examined the vacuolating cytotoxin production of 114 clinical H. pylori isolates in rabbit gastic epithelial cells (RGECs). We also tested two positive control strains (NCTC 11637 and NCTC 11916). Seventy-four of the 114 H. pylori clinical isolates (64.9%) produced intracellular vacuolation in RGEC cells, but there was no significant difference in the prevalence of intracellular vacuolation among the isolates of patients with chronic gastritis, gastric ulcers, and duodenal ulcers. We found no strong correlation between vacuolating cytotoxin production and peptic ulceration.

Animals↗
PubMed1996

Sofalcone for treatment of Helicobacter pylori infection.

It is difficult to regard sofalcone as a single drug for the treatment of Helicobacter pylori infection. However, sofalcone exerts multiple effects against H. pylori: it has antibacterial activity, induces morphological changes, inhibits adhesion to gastric mucin and inhibits lipolytic activity. The safety profile of sofalcone even on long-term administration is well established. Therefore, it may be possible to establish a new triple therapy for H. pylori infection using sofalcone combined with antibacterial drugs and proton pump inhibitors.

Anti-Bacterial Agents↗
PubMed1996

Atopic dermatitis successfully treated by eradication of Helicobacter pylori.

A relationship between allergic diseases and Helicobacter pylori infection has recently been noted. We report a case of atopic dermatitis and H. pylori infection in a 14-year-old girl. She had had widespread diffuse skin erythema with erosions and pigmentation since the age of 3 years. Endoscopically, there was chronic antral gastritis with H. pylori infection and histological eosinophilic infiltration. A high titer of H. pylori-specific IgG was present in serum. She was treated with a proton pump inhibitor (lansoprazole 60 mg), an antibiotic (clarithromycin 800 mg), and plaunotol (a mucosal protective agent, 480 mg) for 2 weeks to eliminate the infection. After 10 days of treatment, erythema and itching were more widespread and vesicle formation was seen on the foot. Generalized skin lesions abated a few days later. After eradication of the bacterium by the treatment, eosinophils decreased from 38.8% to 19.0%, and the clinical signs of atopic dermatitis almost disappeared. Serum gastrin level and the pepsinogen I/II ratio were normalized and histological findings of gastric mucosa showed improvement. H. pylori-specific IgE antibody, analyzed by the Western blot method, gradually decreased with the eradication treatment.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1996

[Variations of the constrictor pharyngeal muscles in humans].

Fifteen halves of ten nonrandomized human cadavers were dissected under a stereoscopic microscope in order to examine the existence of variations in the constrictor pharyngeal muscles. Obvious variations of the constrictor muscles were found in three cases. The results are summarized as follows: 1. In the first case of variations, the superior constrictors arose from the pterygomandibular raphe and merged into the outer surfaces of the middle and inferior constrictors. This muscle was supplied by the upper part of the pharyngeal branches of the vagus. 2. In the second case, the muscle bundle of inferior constrictors originated from the thyroid cartilage and passed upward, joining the muscular fibers of the outer surface of the superior constrictors arising from the pterygomandibular raphe. Some of these muscular fibers extended to the surface of the posterior part of the pharyngobasilar fascia. This muscle was innervated by the lower part of the pharyngeal branches of the vagus. 3. In the third case, the lower part of the superior constrictors passed laterally between the stylopharyngeus and the glossopharyngeal nerve, running between the external and internal carotids in the retrostyloid space and reaching the cervical fascia around the submandibular triangle. This anomalous muscular bundle of superior constrictors was innervated by the carotid branch of the glossopharyngeal nerve and the middle part of the pharyngeal branches of the vagus.

Glossopharyngeal Nerve↗
PubMed1995

Localization of furin to the trans-Golgi network and recycling from the cell surface involves Ser and Tyr residues within the cytoplasmic domain.

Furin is a membrane-associated endoprotease that catalyzes cleavage of precursor proteins at Arg-X-Lys/Arg-Arg sites. Although, at steady state, furin is predominantly found in the trans-Golgi network (TGN), it also cycles between the TGN and the cell surface. Recently, the cytoplasmic tail of furin has been shown to be sufficient for its localization to the TGN. Within the cytoplasmic domain, there are Ser residues, which we now show are sites for phosphorylation by casein kinase II in vitro, and a Tyr-containing sequence, both of which have been shown to be important for other TGN proteins to localize to this compartment. In the present study, we show by site-directed mutagenesis that these residues are important for TGN localization and recycling of furin. Mutation of the Ser residues abrogated the TGN localization. By contrast, mutation of the Tyr residue did not affect the TGN localization but impaired the internalization from the plasma membrane. These observations suggest that distinct cytoplasmic determinants are responsible for retention in the TGN and retrieval from the cell surface of furin.

Amino Acid Sequence↗
PubMed1995

A second mutant allele of furin in the processing-incompetent cell line, LoVo. Evidence for involvement of the homo B domain in autocatalytic activation.

Furin is a Golgi membrane-associated endoprotease that is involved in cleavage of various precursor proteins predominantly at Arg-X-Lys/Arg-Arg sites. Furin itself is synthesized as an inactive precursor, which is activated through intramolecular autocatalytic cleavage at an Arg-X-Lys-Arg site. We previously found that human colon carcinoma LoVo cells have a frameshift mutation within the homo B domain of furin and thereby lack processing activity toward Arg-X-Lys/Arg-Arg sites. In this study, however, we identified a second furin mutation in this cell line. The mutation, a replacement of a conserved Trp residue within the homo B domain with Arg, results in lack of processing activity of the mutant furin. The combination of both mutations can account for the recessive nature of the processing incompetence of LoVo cells. Immunofluorescence analysis with three distinct anti-furin monoclonal antibodies revealed that neither furin mutant underwent the autocatalytic activation or left the endoplasmic reticulum for the Golgi. These data indicate that the homo B domain as well as the catalytic domain is required for autocatalytic activation of furin.

Amino Acid Sequence↗
PubMed1995

Effects of antithrombin III (AT III) and Trp49-modified AT III on plasma level of 6-keto-PGF1 alpha in rats.

We evaluated the effect of antithrombin III (AT III) on the plasma level of 6-keto-PGF1 alpha in rats to determine whether AT III may promote the release of prostacyclin (PGl2) from endothelial cells in vivo. The intravenous administration of AT III (250 U/kg) significantly increased the plasma levels of 6-keto-PGF1 alpha, with a peak seen 90 min post-administration. Neither Trp49-modified AT III, which lacks affinity for heparin but retains an inhibitory capacity for thrombin, nor heparin plus AT III, increased the plasma level of 6-keto-PGF1 alpha 90 min after administration. Indomethacin pretreatment inhibited the increase in plasma levels of 6-keto-PGF1 alpha produced by AT III. Observations suggest that AT III may promote the release of PGl2 from endothelial cells by interacting with heparin-like glycosaminoglycans in vivo, consistent with previous observations in cultured endothelial cells.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Thrombin induces GRO alpha/MGSA production in human umbilical vein endothelial cells.

Thrombin, besides being a potent coagulation factor, exerts influence on endothelial and leukocyte functions and may thus be involved in the regulation of inflammatory reactions. The present study investigated whether thrombin stimulates the production of growth-related cytokine/melanoma growth-stimulatory activity (GRO alpha/MGSA) in endothelial cells. Human umbilical vein endothelial cells (HUVEC) stimulated with thrombin were found to product GRO alpha/MGSA in a dose- and time-dependent manner. This action of thrombin was completely suppressed by preincubation with either hirudin or antithrombin-III (AT-III)-heparin. Interestingly, the thrombin receptor-activating peptide SFLLRN mimicked the action of thrombin. In addition, staurosporine, a protein kinase C (PKC) inhibitor, attenuated the production of GRO alpha/MGSA by thrombin, SFLLRN and phorbol 12-myristate 13-acetate (PMA), but left the action of interleukin-1 beta (IL-1 beta) unchanged. These results suggest that catalytic activation of thrombin receptor by thrombin results in GRO alpha/MGSA production, at least in part, via a pathway involving PKC in HUVEC.

Alkaloids↗
PubMed1995

Alterations of angiotensin II receptor contents in hypertrophied hearts.

Tsukuba hypertensive mice, which carry the human genes for renin and angiotensinogen, show cardiac hypertrophy as well as hypertension due to activation of the renin-angiotensin system (RAS). Here, we compared the cardiac angiotensin II (Ang II) receptor contents in these and normotensive control mice by means of ligand binding studies and competitive reverse transcription-polymerase chain reaction analyses. The content of the Ang II receptor type 1 (AT1) was significantly higher at both the protein (2.5-fold; p < 0.01) and mRNA (1.4-fold; p < 0.05) levels in the hypertensive mice than that in control mice. Almost identical levels of the Ang II receptor type 2 (AT2) expression were identified at the mRNA levels in the two types of mice, although the levels were less than 20% of those of AT1 mRNA in control mice. These results suggest that AT1 in the heart is upregulated in response to Ang II-induced hypertrophic change and that, in particular, the upregulation of AT1 in particular contributes to the development and/or maintenance of cardiac hypertrophy in conjunction with the increase in Ang II production, because AT1 is responsible for cardiac hypertrophy related to the RAS.

Animals↗
PubMed1995

Strain-specific presence of two TGN38 isoforms and absence of TGN41 in mouse.

TGN38 and TGN41 are isoforms of an integral membrane protein that is predominantly localized to the trans-Golgi network (TGN) in rat cells. They have been proposed to form a heterodimer and to be involved in the budding of exocytic transport vesicles from the TGN. By cDNA cloning and analysis using polymerase chain reaction, we found that there were two TGN38 isoforms in a strain of mouse (ICR), whereas other strains examined (BALB/c, DBA/2, and C57BL/6) had only one TGN38. The major difference between the two isoforms was in the number of characteristic octapeptide repeats. Apart from this, there were several nucleotide substitutions between them. The two isoforms appeared to be derived from two distinct genes but not from one gene via alternative splicing. Furthermore, we failed to show the presence of TGN41 in all the strains examined. This result suggests that TGN38 may function as a monomer or a homodimer in mouse cells.

Amino Acid Sequence↗
PubMed1995

Cloning of the rat angiotensin II type 2 receptor gene and identification of its functional promoter region.

We have cloned the rat angiotensin II receptor type 2 (AT2) gene, whose physiological function remains unclear. Sequence analysis indicated that exons 1 and 2 exist in the 5'-untranslated region and the initiation codon ATG is located in exon 3. The 1.6-kb genomic fragment at positions -1567 to +26 relative to the putative transcription start site was found to contain a functional promoter region using transient chloramphenicol acetyltransferase assay. This is the first report demonstrating the nucleotide sequence of the promoter region of this gene.

Animals↗
PubMed1995

Thalamocortical synapses between axons from the mediodorsal thalamic nucleus and pyramidal cells in the prelimbic cortex of the rat.

A combined anterograde axonal degeneration and Golgi electron microscopic (Golgi-EM) study was undertaken to identify thalamocortical synaptic connections between axon terminals from the mediodorsal thalamic nucleus (MD) and pyramidal cells in layers III and V of the agranular prelimbic cortex in the rat. The morphological characteristics of thalamocortical synapses from MD were also examined by labeling axon terminals with anterograde transport of wheat germ agglutinin-horseradish peroxidase (WGA-HRP). WGA-HRP labeled axon terminals from MD to the prelimbic cortex were small in size (0.5-1 microns in diameter), contained round synaptic vesicles, and formed axospinous synapses with asymmetrical membrane thickenings. With Golgi-EM methods, gold-toned apical dendrites in layer III were analyzed by reconstruction of serial ultrathin sections. Following lesions in the thalamus, degenerating thalamocortical axon terminals formed asymmetrical contacts exclusively on dendritic spines of the identified apical dendrites. More thalamocortical synapses were found on apical dendrites of layer V pyramidal cells than on apical dendrites of layer III pyramidal cells. In addition to thalamocortical synapses, a very few unlabeled symmetrical synapses were found on apical dendrites and somata of pyramidal cells, but they were not quantified and their sources are unknown.

Animals↗
PubMed1995

Molecular cloning and functional analysis of a new activin beta subunit: a dorsal mesoderm-inducing activity in Xenopus.

A cDNA that encodes a new member of the TGF-beta superfamily most similar to activin beta A, beta B, and recently reported beta C has been isolated from Xenopus laevis. Expression of the gene in early embryos suggested its biological importance in Xenopus embryogenesis. Microinjection of a synthetic mRNA transcribed from the cDNA into ventral blastomeres of early Xenopus embryo led to the formation of secondary body axis. Mesodermal marker genes were induced in isolated animal cap by a similar mRNA injection. These results demonstrate that the gene encodes a new member of activin subfamily whose function is closely related to mesoderm induction.

Activins↗