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Biomedical subjects

Y Honma

Publications and source records attributed to Y Honma.

At least 163 records · Page 9Linked to original sources
PubMed1995

Morphological changes in human cerebral arteries after percutaneous transluminal angioplasty for vasospasm caused by subarachnoid hemorrhage.

Light and electron microscopy were used to study morphological changes in cerebral arteries after percutaneous transluminal angioplasty (PTA) for vasospasm in two patients with aneurysmal subarachnoid hemorrhage. One patient died of gastric bleeding 5 days after PTA. Postmortem examination of the inflated middle cerebral arteries revealed heterogeneously extended walls and dilated lumina. Throughout the vessel walls, the extracellular matrix, which was composed of nonmuscle components such as increased collagen, was stretched in conjunction with the medial muscle component. Also, torn and thinned areas of the wall and intramural hemorrhages were caused by overinflation. The second patient died of massive cerebral infarction caused by diffuse vasospasm 5 days after PTA. Prominent stretching of the walls at the atheromatous plaque margin in the dilated vessel was found in addition to the morphological changes observed in the first patient. These observations suggest that characteristic pathological alterations might be present in the vessel wall at the site of angioplasty. The major mechanism of the long-lasting effects of PTA seems to be the stretching and disruption of both the degenerative muscle and the proliferative nonmuscle components, mainly in the media of the vasospastic vessels.

Adult↗
PubMed1995

Growth, hemorrhage, and regression of multiple intracerebral vasoformative tumors: report of an unusual case.

A rare case of multiple hemorrhagic vascular tumors of the cerebrum and cerebellum is reported. Computed tomographic scans in a 16-year-old girl revealed multifocal brain lesions with "jewel ring"-like areas of contrast enhancement. An old hematoma cavity was found inside the surgical specimen. Histologically, it was a vascular tumor composed of anastomosing vascular channels with proliferating endothelial cells and hemorrhages at different stages. Upon further histopathological study, this lesion could not be classified as any known vascular tumor entity, although it resembled some vascular tumors, such as cavernous hemangioma and hemangioendothelioma. The patient received steroid and alpha interferon treatment. The lesions initially increased in number once, then resolved 10 months after onset. The neuroradiological and histopathological features in the present case were characteristic, and the clinical course was unusual.

Adolescent↗
PubMed1995

[Evaluation of advanced bladder tumor].

Ninety-two cases of advanced bladder tumor treated at the University of Tokyo and branch hospital from January 1977 to December 1992 were analyzed. The advanced bladder tumor was defined as that of higher than pT2 (according to the General Rule for Clinical and Pathological Studies on Bladder Cancer) or that with distant metastases. The following variants were evaluated, the therapeutic methods, the histological type, grade, stage, type of infiltration. The evidence of lymphatic infiltration, vessel infiltration, and lymph node metastases were also reviewed. The survival rate was calculated using Kaplan-Meier's method. In the cases with lymph node metastases, the survival rate was significantly lower than in the cases without metastases (p < 0.01), while no other factors affected the survival rate.

Combined Modality Therapy↗
PubMed1995

[A Japanese family with congenital abnormal plasminogen].

A Japanese family with congenital abnormal plasminogen is reported. The patient was a 44-year-old male with no past history of thrombosis. Since only the plasminogen (PLG) activity was reduced on laboratory tests before surgery for lumbar disc herniation, coagulation and fibrinolysis studies were performed in the patient and his family. The patient underwent resection of the nucleus pulposus and posteriorlateral fixation of the lumbar spine. The PLG activity was 8% in the patient and his sister, 55% in his father, and 53% and 48% in his nephew brothers. The PLG antigen level was normal in all members of his family examined. IEF of PLG antigen showed abnormal patterns in which all bands were shifted slightly to the cathode side in the patient and his sister, but his father and nephew brothers exhibited duplicated bands showing combinations of normal and abnormal patterns. From these results, the proband and his sister were considered to be homozygotes, and his father and nephew brothers to be heterozygotes for congenital abnormal plasminogen. Acute reactant substances (fibrinogen, CRP, CPK, C1IN, alpha 1AT, etc.) and PIC (plasmin, alpha 2-plasmin inhibitor complex) increased after the operation due to the surgical insult, but the surgery did not trigger thrombosis. This patient is considered not to have developed thrombosis although he was a homozygote for congenital abnormal plasminogen, because the anticoagulation process until thrombogenesis was normal.

Adult↗
PubMed1994

Characterization of YM022: its CCKB/gastrin receptor binding profile and antagonism to CCK-8-induced Ca2+ mobilization.

We investigated the antagonistic activity of (R)-1-[2,3-dihydro-1-(2'- methylphenacyl)-2-oxo-5-phenyl-1H-1,4-benzodiazepin-3-yl]-3- (3-methylphenyl) urea (YM022), a benzodiazepine derivative, at CCKB/gastrin receptors. This compound potently inhibited [125I]CCK-8 binding to rat brain CCKB/gastrin receptors with a Ki value of 0.26 nM, but it showed weak affinity for rat pancreas CCKA receptors (Ki = 270 nM). Selectivity for CCKB/gastrin receptors was 1000-fold greater than that for CCKA receptors. Changes in intracellular free Ca2+ concentration ([Ca2+]i) in response to CCK-8 were measured in a rat anterior pituitary cell line GH3 by fura-2 fluorometry. CCK-8 (1-100 nM) dose-dependently increased [Ca2+]i in these cells, whereas YM022 had no effect on baseline [Ca2+]i even at the highest concentration of 100 nM. YM022 inhibited the mobilization of [Ca2+]i elicited by 10 nM CCK-8 in a concentration-dependent manner with an IC50 value of 4 nM. In conclusion, YM022 is an extremely potent and highly selective antagonist of CCKB/gastrin receptors. This compound is therefore useful for studying the physiological and pharmacological roles of CCKB/gastrin receptors.

Animals↗
PubMed1994

Ontogenetic development of gonadotropin-releasing hormone-like immunoreactive neurons in the brain of the chum salmon, Oncorhynchus keta.

In the chum salmon, gonadotropin-releasing hormone-immunoreactive (GnRH-ir) cells were first detected in the olfactory placode of embryos at 16 days after fertilization, and then appeared sequentially in the olfactory nerve and the distal part of the forebrain by hatching. Four months after hatching, the terminal nerve was differentiated along the olfactory nerve, and GnRH-ir fibers extended to the hypothalamus and hypophysis. GnRH-ir cells occurred later in the preoptic area in about 1-year-old juveniles. These data suggest that GnRH neurons originate in the olfactory placode and then migrate into the brain along the olfactory nerve.

Aging↗
PubMed1994

A novel mutation in Cu/Zn superoxide dismutase gene in Japanese familial amyotrophic lateral sclerosis.

Recently, several missense mutations in the Cu/Zn superoxide dismutase gene (SOD1) have been reported as a putative cause of chromosome-21q-linked familial amyotrophic lateral sclerosis (FALS). We have discovered a novel missense mutation (substitution of Thr for Ala4) in exon 1 (GCC to ACC) in two FALS patients from one Japanese FALS family. No mutations were found in 17 cases of sporadic ALS. The enzyme activity of recombinant fusion protein containing the Cu/Zn superoxide dismutase (SOD) with the Ala4-to-Thr mutation was significantly reduced in E. coli. On the other hand, in the expression system in insect cells using Baculovirus, the mutant SOD expressed an enzyme activity as high as wild-type SOD. These results suggest that the stability of SOD with the Ala4-to-Thr mutation is disrupted especially in the fusion protein. Autopsy was carried out on one of the two patients, and the pathological findings were typical of FALS with posterior column involvement. These results raise the possibility that mutation of the SOD1 is responsible for FALS with broader pathological involvement.

Amino Acid Sequence↗
PubMed1994

Purification and characterization of vibrio cholerae O139 fimbriae.

A Vibrio cholerae O139 (strain Al-1841) isolated from a patient with a cholera-like disease in Bangladesh predominantly produced new curved, wavy fimbriae (Al-1841 fimbriae) and small numbers of previously reported V. cholerae non-O1 S7-like pili. The former was purified and characterized. The molecular mass of the Al-1841 fimbrial subunit was less than 2.5 kDa, and it was immunologically different from that of V. cholerae non-O1 S7 pili. This novel fimbrial antigen was detected in all 182 Gram-negative strains from five genera tested but was absent from the Gram-positive bacteria tested. The purified Al-1841 fimbriae did not agglutinate human or rabbit erythrocytes.

Antibodies, Bacterial↗
PubMed1994

Inhibition by interleukin 4 of leukemia inhibitory factor-, interleukin 6-, and dexamethasone-induced differentiation of mouse myeloid leukemia cells: role of c-myc and junB proto-oncogenes.

Interleukin 4 (IL-4) inhibited the differentiation of mouse myeloid leukemia M1 cells induced by leukemia inhibitory factor (LIF), interleukin 6, or dexamethasone and conversely enhanced the induction of M1 cell differentiation by 1 alpha,25-dihydroxyvitamin D3. IL-4 blocked LIF-induced differentiation of M1 cells when it was added to the culture medium within 10 h after LIF, but IL-4 did not block differentiation when it was added 12 h after LIF. These results indicate that IL-4 inhibited a critical intermediate step in myeloid leukemia cell differentiation. LIF markedly stimulated the expression of junB mRNA within 2 h but suppressed the expression of c-myb and c-myc after 2- and 12-h treatment, respectively. IL-4 did not significantly affect LIF-induced junB expression or suppression of c-myb expression. However, it interfered significantly with the LIF-induced suppression of c-myc gene expression. Similar results were obtained when interleukin 6 was used to induce differentiation of M1 cells. Dexamethasone and 1 alpha,25-dihydroxyvitamin D3 did not induce junB gene expression but suppressed the expression of c-myb and c-myc. IL-4 also interfered with dexamethasone-induced suppression of c-myc gene expression. On the other hand, IL-4 enhanced 1 alpha,25-dihydroxyvitamin D3-induced down-regulation of c-myc gene expression, consistent with its enhancement of differentiation. These results indicate that the change in c-myc expression induced by IL-4 in M1 cells is closely associated with the effect of IL-4 on the induction of differentiation of M1 cells.

Animals↗
PubMed1994

Treatment of vasogenic brain edema with arginine vasopressin receptor antagonist--an experimental study.

We determined the effect of a centrally administered V1 receptor antagonist of arginine vasopressin on the brain water content in an animal model of vasogenic brain edema. Using adult rats, a cold injury was induced in the left hemisphere of the brain by applying a frozen copper rod. 50 ng of V1 receptor antagonist was administered into the left lateral ventricle 10 minutes prior to and/or 1 hour after injury. Twenty four hours after the cold injury, the brain water and sodium contents and plasma osmolality were measured. The V1 receptor antagonist significantly suppressed the increase of the brain water and sodium contents in the cortical structure adjacent to the lesion without any changes in plasma osmolality. Our results demonstrate the effectiveness of a V1 receptor antagonist of vasopressin on vasogenic brain edema.

Animals↗
PubMed1994

Familial amyotrophic lateral sclerosis with a mutation in the Cu/Zn superoxide dismutase gene.

Several missense mutations within exons 1, 2, 4 and 5 of the gene for Cu/Zn-binding superoxide dismutase (SOD1) have been discovered to be involved in the development of chromosome 21q-linked familial amyotrophic lateral sclerosis (FALS). We describe here an autopsied patient with FALS, in whom we have recently identified a novel missense mutation in exon 1 of the SOD1 gene. The neuropathological findings were compatible with those described previously in patients with FALS with posterior column involvement. This suggests that mutations of the SOD1 gene may be responsible for this form of FALS.

Adult↗
PubMed1994

Effects of herbimycin A and its derivatives on growth and differentiation of Ph1-positive acute lymphoid leukemia cell lines.

The molecular basis of the Philadelphia chromosome (Ph1) is a structurally altered c-abl (bcr/abl) gene which encodes an abnormally large protein with protein tyrosine kinase activity. Herbimycin A, an inhibitor of tyrosine kinase, preferentially inhibited the growth of Ph1-positive acute lymphoid leukemia (ALL) cell lines, as well as Ph1-positive chronic myeloid leukemia (CML) cell lines. Although noncytotoxic concentrations of herbimycin A induced erythroid differentiation of two CML-derived cell lines, K562 and KU812, in a previous study, the differentiation-inducing effect of herbimycin A on Ph1-positive ALL cell lines was less strong. Herbimycin A enhanced some differentiation-associated properties of one Ph1-positive ALL cell line, L2, but the effect of herbimycin A on the other Ph1-positive ALL cell lines was cytotoxic rather than cytostatic (differentiation-inducing). Several derivatives of herbimycin A were synthesized and their effects on the cell proliferation of Ph1-positive CML and ALL cell lines were examined. The sensitivities of the Ph1-positive cell lines to herbimycin A derivatives were different from the data on the rat kidney cell line infected with Rous sarcoma virus (v-src) derived from a previous study, suggesting bcr/abl kinase may differ in sensitivity from other tyrosine kinases. Moreover, the sensitivities of the ALL cell lines were not the same as those of the CML cell lines. These results suggest that a specific inhibitor of bcr/abl kinase could be an effective antileukemic agent against Ph1-positive CML or ALL.

Antibiotics, Antineoplastic↗
PubMed1994

Acycloguanosine and herbimycin A co-operatively inhibit proliferation and induce erythrodifferentiation of human myeloid leukemia K562 cells.

Acycloguanosine (9-[(2-hydroxyethoxy)methyl]guanosine) induced human erythroleukemia K562 cells to differentiate into hemoglobin-producing cells, and cell growth was highly sensitive to this nucleoside analog. Herbimycin A also induced erythrodifferentiation of the cells, and selectively inhibited proliferation of the cells. Selective inhibition of the proliferation in K562 cells was greatly enhanced by combined treatment with acycloguanosine and herbimycin A, while the growth of another erythroleukemia cell line without bcr/abl gene (HEL) and normal mouse bone marrow cells was hardly affected by the treatment.

Acyclovir↗
PubMed1994

Characterization of muscarinic cholinoceptor in primary culture of smooth muscle cells from human prostate.

We obtained a primary culture of prostatic cells by an explant method from patients with benign prostatic hypertrophy (BPH). Ultrastructural morphology and growth characteristics of these cells conformed to those reported for smooth muscle cells isolated from vascular and visceral tissue sources. The cells retained their original character including the presence of androgen receptor, acid phosphatase and normal chromosomal number. [3H]-methyl-quinuclidinyl benzilate (QNB) saturation experiments showed the existence of a homogeneous population of binding sites with a high affinity and low capacity (KD = 0.17 +/- 0.05 nM., Bmax = 15,000 sites per cell). Inhibition of [3H]-methyl-QNB binding by nonlabelled compounds showed these [3H]-methyl-QNB binding sites to be M2 muscarinic cholinoceptors. cAMP formation induced by forskolin and isoproterenol was inhibited by carbamoyl choline and oxotremorine. These results suggest that prostatic smooth muscle cells contain M2 muscarinic cholinoceptors and that these cholinoceptors couple adenylate cyclase inhibition.

Cells, Cultured↗
PubMed1994

Evidence for conformational change of fatty acid-binding protein accompanying binding of hydrophobic ligands.

Conformational change of rat liver fatty acid-binding protein was investigated by making use of change of protease-susceptibility in the presence or absence of bound oleic acid and clofibrate. Delipidated fatty acid-binding protein was rapidly digested by Achromobacter lysyl endopeptidase, bovine alpha-chymotrypsin, and Staphylococcal V8 protease, while protein recombined with oleic acid was strongly refractory to proteolysis. This observation indicates that a striking change in the conformational state of the protein occurred upon lipid binding, and seems to support the recent hypothesis that the large segment homologous to fatty acid-binding proteins found in a fatty acid-regulated ion channel constitutes a regulatory domain of the channel [Petrou, S., Ordway, R.W., Singer, J.J., and Walsh, J.V., Jr. (1993) Trends Biochem. Sci. 18, 41-42]. Clofibrate, which is a potent peroxisome proliferator and structurally unrelated to oleic acid, also conferred similar protease resistance upon the protein. A possible physiological aspect of the present observation is that the cellular level of free fatty acids, which have metabolic importance and cytotoxicity as well, regulates the turnover rate of fatty acid-binding proteins by modulating the protease susceptibility of the protein.

Animals↗
PubMed1994

Surface marker analysis of the vascular and epithelia lesions in cattle with sheep-associated malignant catarrhal fever.

Surface marker analysis of the vascular and epithelial lesions in cattle with sheep associated malignant catarrhal fever (MCF) were done by immunohistochemistry using 7 monoclonal antibodies. MHC class I and II antigens were expressed in the degenerated portion of the vascular walls in addition to infiltrated leukocytes. The major population of mononuclear cells in these lesions were phenotypically macrophages. The other cells had BoCD4 or BoCD8, but rarely gamma delta T cell markers. These results suggest involvement of MHC restriction and macrophages, in addition to autoaggressive cytotoxic T lymphocytes, in the development of MCF vascular lesion.

Animals↗