Biomedical subjects

T Honda

Publications and source records attributed to T Honda.

At least 433 records · Page 24Linked to original sources

PubMed1995

[A case of chronic eosinophilic pneumonia involving IL-5 and GM-CSF].

A 57-year-old woman was admitted because of dry cough and middle-grade fever. Chest rentogenogram showed a diffuse infiltrative shadow in the right middle and lower lung fields. The symptoms disappeared after treatment with minocycline, but a new dense shadow appeared in the right upper and middle lung fields. Eosinophilic pneumonia was diagnosed from the results of bronchoalveolar lavage and transbronchial lung biopsy. The symptoms were alleviated and the infiltrative shadow was effaced after treatment with predonisolone (40 mg/day). The results of a biopsy with human eosinophils suggested that the serum and bronchoalveolar lavage fluid contained IL-5 and GM-CSF.

Bronchoalveolar Lavage Fluid↗

PubMed1995

[A case of chronic pancreatitis with eosinophilic pleural effusion].

A 48-year-old man was admitted for the evaluation of a massive left pleural effusion. Thoracenthesis yielded a bloody excudate with a high percentage of eosinophils (27%) and high values of pancreatic enzymes (amylase 16,000 Somogyi, Elastase 35,000 ng/dl, Lipase 12,800 U/l, Trypsin 77,000 ng/ml). The amylase isozyme of the exudate was 100% pancreatic-type fraction. The blood showed no eosinophilia (4%). A computed tomographic scan and magnetic resonance image of the abdomen revealed a pancreatic pseudocyst in contact with the diaphragm, and thrombi in the inferior vena cava and the splenic vein. After pancreatic cystectomy and splenectomy, the pleural effusion resolved rapidly. Eosinophilic pleural effusion has been reported as a complication of several disorders: pneumonia, lung carcinoma, pulmonary tuberculosis, and pulmonary infarction. However, we know of no previous report of eosinophilic pleural effusion with pancreatitis. In this case, it is interesting that the massive eosinophilic pleural effusion associated with chronic pancreatitis resolved immediately after the operation, and the patient was discharged.

Chronic Disease↗

PubMed1995

[A case of multifocal choroiditis associated with progressive subretinal fibrosis].

Multifocal choroiditis associated with progressive subretinal fibrosis, which was reported by Cantrill and Folk in 1986, is characterized by acute multifocal choroiditis resulting in progressive subretinal fibrosis. All cases were young, healthy females. Our case was a 17-year-old female who complained of visual disturbance in her left eye. Ophalmoscopy showed multiple, small, yellowish-white hypopigmented, choroidial lesions in the posterior fundus of her left eye. These lesions showed hyperfluorescence in fluorescein angiography and hypofluorescence in indocyanine green (ICG) angiography. One month later the yellowish-white hypopigmented, choroidal lesions increased in number and subretinal fibrosis appeared in the macular area. Two months later subretinal fibrosis was also found in the area except for the macula. In her right eye, ophthalmoscopy and fluorescein angiography showed no abnormal findings, but ICG angiography revealed choroidal hypofluorescence areas. Two years later the subretinal fibrosis was increased and the yellowish-white lesions showed pigmentation.

Acute Disease↗

PubMed1995

[Septic lung caused by methicillin-resistant Staphylococcus epidermidis].

A 55-year-old man was admitted to our department one month after resection of rectal carcinoma, with complaints of fever and general malaise. Shock developed rapidly after admission. The chest X-ray film and computed tomography showed diffuse small nodular shadows and bilateral pleural effusion. Septic lung caused by Methicillin-resistant Staphylococcus epidermidis (MRSE) was diagnosed from the results of a bacteriological study. This bacteria is a Coagulase Negative Staphylococcus (CNS). Chemotherapy with Minocycline and Cefotiam was effective. Characteristic radiologic features of this case may be related to the early stage of adult respiratory distress syndrome (ARDS) and septic pulmonary microembolism.

Anti-Bacterial Agents↗

PubMed1995

[Comparison between the arthroscopic and open synovectomies for rheumatoid knee--a retrospective and random study on the results of the two methods].

Knee joints affected by rheumatoid arthritis (RA) were randomized to either arthroscopic or open synovectomy, and the postoperative results were compared retrospectively. The materials consisted of 58 patients with 75 surgically treated knees. Arthroscopic synovectomy was performed on 37 knees of 30 patients, who were followed for five years and four months on average. Open synovectomy was performed on 38 knees of 28 patients, who were followed for five years and five months on average. The results were evaluated for ; recurrence of synovitis ; duration of the symptom-free period ; progressive bone changes on radiography ; range of motion (ROM) ; duration of hospital stay ; duration of surgery. Due to the less invasive surgical procedure, arthroscopic synovectomy resulted in less post operative pain, and there was no restriction of ROM after surgery, no need for postoperative rehabilitation, shorter hospital stay, lower incidence of osteoarthritic changes, and earlier return to the daily life. However, as synovial membrane removal was unavoidably insufficient, the effect of surgery lasted for only 18 months on average and recurrence of synovitis was observed in 73 % of patients. Open synovectomy meant relatively greater invasion and postoperative pain. Due to the restricted ROM in some cases, postoperative treatment was required and the hospital stay tended to be prolonged. Nevertheless, the recurrence rate was only 37 % during follow-up and the effect of surgery persisted for an average of 75 months, much better than that of arthroscopic synovectomy. In the treatment of RA knees, the indications for arthroscopic and open synovectomies should be carefully studied in the light of the merits and for demerits of each procedure.

Adult↗

PubMed1995

[Acute lung injury and chemical mediators].

The essential abnormality in acute lung injury is an increase in pulmonary permeability. The mechanisms involved are complex, and may include direct effects on endothelial cells; the actions of neutrophils, macrophages, and lymphocytes; and chemical mediators generated by these cells. Neutrophils are known to be important in acute lung injury, and the mediators they produce, especially protease and oxidants, may be responsible for endothelial cell injury. We studied the roles of neutrophil elastase and oxygen radicals in acute lung injury by Escherichia coli endotoxin in sheep with lung lymph fistulae. The results of these and other studies indicate that these substances are related to the increase in pulmonary permeability during the late phase of injury.

Acute Disease↗

PubMed1995

[Analysis of 4 cases of intralobar pulmonary sequestration].

Four cases with pulmonary sequestration treated in Tottori university hospital between January 1993 and December 1994 were reported. Case 1 was a 63-year-old male who had lung tumor without inflammatory findings. Differential diagnosis from lung cancer was needed, and aortography showed a aberrant artery from descending aorta. Pulmonary partial resection and division of aberrant artery were performed. Case 2 was a 71-year-old female who diagnosed pulmonary sequestration in other hospital 10 years ago. Tumor shadow did not progress compared with the old X-ray film. Because tumor size was remarkably diminished by aspiration of cystic tumor, conservative follow up was continued. Both case 3 and 4 were a 20-year-old man and 16-year-old female who had typical findings of pulmonary sequestration with inflammation and easily detection of aberrant artery by CT or aortography. Resection of sequestrated lung and division of aberrant arteries were performed in both cases. Pulmonary sequestration was the disease which should be always kept in our mind in differential diagnosis from various lung disease.

Adolescent↗

PubMed1994

Prior mechanical injury inhibits rise in intracellular Ca2+ concentration by oxygen-glucose deprivation in mouse hippocampal slices.

Prior mechanical brain microinjury has been found to have a preventive effect on brain ischemia. To investigate the mechanism responsible for this, the effect of mechanical brain injury on changes in intracellular free Ca2+ concentration ([Ca2+]i) in response to ischemic insult was studied in mouse hippocampal slices. The mechanical injury was made by inserting a 25G hypodermic needle into the CA1 region of the hippocampus in mice anesthetized with pentobarbital. Sagittal slices of the hippocampus were prepared two hours, and 1, 3, 7, and 14 days after the brain injury. Changes in [Ca2+]i in the slices by oxygen-glucose deprivation were analyzed from fluorescence images, using fura-2. Increases in [Ca2+]i induced by oxygen-glucose deprivation were inhibited in the vicinity of the injury 1 and 3 days after injury. [Ca2+]i levels were lower in the posterior side from the injury than in the anterior side 1 and 3 days after injury. No significant regional differences in [Ca2+]i responses were found 2 h or 7 and 14 days after the injury. Membrane potential and membrane resistance of CA1 neurons in the vicinity of the injury measured 1 day after the injury were not significantly altered in comparison with non-injured slices. These results indicate that mechanical brain injury inhibits ischemic [Ca2+]i increase. This inhibition may be induced not only by damage of the presynaptic fibers projecting to the CA1 neurons but also by the other certain factor(s) that prevent [Ca2+]i increase, and it appears to be related to the protective effect of prior mechanical injury against ischemic neuronal damage.

Animals↗

PubMed1994

Calcium-activated neutral proteinase (calpain) system in aging and Alzheimer's disease.

Calpains (CANPs) are a family of calcium-dependent cysteine proteases under complex cellular regulation. By making selective limited proteolytic cleavages, they activate or alter the regulation of certain enzymes, including key protein kinases and phosphatases, and induce specific cytoskeletal rearrangements, accounting for their suspected involvement in intracellular signaling, vesicular trafficking, and structural stabilization. Calpain activity has been implicated in various aging phenomena, including cataract formation and erythrocyte senescence. Abnormal activation of the large stores of latent calpain in neurons induces cell injury and is believed to underlie neurodegeneration in excitotoxicity, Wallerian degeneration, and certain other neuropathologic states involving abnormal calcium influx. In Alzheimer's disease, we found the ratio of activated calpain I to its latent precursor isoform in neocortex to be threefold higher than that in normal individuals and those with Huntington's or Parkinson's disease. Immunoreactivity toward calpastatin, the endogenous inhibitor of calpain, was also markedly reduced in layers II-V of the neocortex in Alzheimer's disease. The excessive calpain system activation suggested by these findings represents a potential molecular basis for synaptic loss and neuronal cell death in the brain in Alzheimer's disease given the known destructive actions of calpain I and its preferential neuronal and synaptic localization. In surviving cells, persistent calpain activation may also contribute to neurofibrillary pathology and abnormal amyloid precursor protein trafficking/processing through its known actions on protein kinases and the membrane skeleton. The degree of abnormal calpain activation in the brain in Alzheimer's disease strongly correlated with the extent of decline in levels of secreted amyloid precursor protein in brain. Cytoskeletal proteins that are normally good calpain substrates become relatively calpain resistant when they are hyperphosphorylated, which may contribute to their accumulation in neurofibrillary tangles. As a major effector of calcium signals, calpain activity may mirror disturbances in calcium homeostasis and mediate important pathologic consequences of such disturbances.

Aging↗

PubMed1994

Evidence for multiple pathways to cellular senescence.

Normal cells in culture generally senesce whereas tumor-derived cells are often, but not without exception, immortal and grow indefinitely. For cells to escape the senescence program, normal genes must be lost or inactivated as shown by somatic cell genetic studies. For example, the introduction of specific chromosomes by microcell-mediated chromosome transfer has been shown to induce senescence of human and rodent tumor cell lines, and the mapping of over ten senescence genes has been achieved by this method. In this study, we observed that two different normal chromosomes induce senescence in the same human endometrial carcinoma cell line, which suggests that multiple pathways to senescence are inactivated in this cell line. This hypothesis has implications for the mechanisms of cellular senescence and its role in carcinogenesis. Furthermore, this hypothesis can explain why not all tumor-derived cells are immortal.

Animals↗

PubMed1994

Effects of cholecystokinin (CCK) and other secretagogues on isoforms of protein kinase C (PKC) in pancreatic acini.

We used rat pancreatic acini and measured the effects of various agents on digestive enzyme secretion, diacylglycerol (DAG) and the cellular distribution of protein kinase C (PKC) enzyme activity as well as isoforms of PKC determined by quantitative immunoblot analysis. TPA, but not CCK-8, caused translocation of PKC enzyme activity from the cytosol fraction to the membrane fraction. Immunoblot analysis detected PKC-alpha, PKC-delta, PKC-epsilon and PKC-zeta. PKC-beta, PKC-gamma and PKC-eta were not detected. TPA caused translocation of all isoforms from cytosol to membrane, whereas CCK-8 caused translocation of PKC-delta and PKC-epsilon, carbachol caused translocation of PKC-epsilon, and bombesin and secretin caused no detectable translocation of any isoform. Specific receptor antagonists could prevent, as well as reverse completely, the translocation of PKC isoforms caused by CCK-8 or carbachol. Agonists added in sequence with an interposed addition of a specific receptor antagonist caused cycling of PKC-epsilon between cytosol and membrane fractions. Each receptor-mediated agonist that caused translocation of PKC also increased DAG, and with CCK-8 and carbachol cycling of PKC-epsilon between cytosol and membrane was accompanied by corresponding cyclic changes in cellular DAG. CCK-JMV-180, bombesin and secretin increased DAG but did not cause translocation of any PKC isoform. Translocation of a PKC isoform could be accounted for by whether the increased DAG originated from PIP2 (accompanied by translocation) or from phosphatidylcholine (no accompanying translocation). Thus it appeared that DAG, in pancreatic acini, is functionally compartmentalized depending on the source of the lipid. Studies using CCK-8 and CCK-JMV-180 indicated that occupation of the low affinity state of the CCK receptor by either peptide increased DAG from phosphatidylcholine, whereas occupation of the very low affinity state by CCK-8 increased DAG from PIP2 and caused translocation of PKC-delta and PKC-epsilon. TPA stimulated amylase secretion, indicating that activation of PKC can stimulate enzyme secretion; however, with the various receptor-mediated secretagogues there was no consistent, unequivocal correlation between translocation of an isoform of PKC and accompanying changes in enzyme secretion.

Amylases↗

PubMed1994

Correlation between cell-associated mannose-sensitive hemagglutination by Vibrio parahaemolyticus and adherence to a human colonic cell line Caco-2.

Cell-associated hemagglutination (cHA) activity with human erythrocytes was examined for 468 clinical and 71 environmental strains of Vibrio parahaemolyticus. Approximately 95% of the strains tested were cHA positive irrespective of source or Kanagawa phenomenon. 75% of clinical strains showed relatively strong mannose-sensitive hemagglutination (MSHA), whereas 88% of the environmental strains showed relatively weak mannose-resistant hemagglutination (MRHA). Adherence of V. parahaemolyticus to Caco-2 cells was also determined. A clear positive correlation between cell-associated MSHA and adherence to Caco-2 cells was observed.

Bacterial Adhesion↗

PubMed1994

Serotonergic synaptic input to cholinergic neurons in the rat mesopontine tegmentum.

Serotonergic synaptic inputs to cholinergic neurons in the laterodorsal and pedunculopontine tegmental nuclei were examined with pre-embedding dual-label immunoelectron microscopy. Numerous serotonin-immunoreactive axon terminals visualized with a silver-enhanced immunogold method were present in both of these tegmental nuclei. Serotonergic terminals occasionally made synaptic contacts with the soma and proximal dendrites of cholinergic tegmental neurons labelled with a choline acetyltransferase-immunoreactive peroxidase-anti-peroxidase diaminobenzidine reaction product. In the rostralmost region of the laterodorsal tegmental nucleus, a few serotonergic neurons of the dorsal raphe nucleus were interspersed among cholinergic neurons. Some dendrites of these serotonergic neurons appeared to contain synaptic vesicles. Both myelinated and unmyelinated serotonergic axons were present in the mesopontine tegmentum. The presence of serotonergic synapses onto tegmental cholinergic neurons is consistent with previous behavioral and electrophysiological findings suggesting an inhibitory role of serotonin in the induction of rapid eye movement sleep and its phenomenology through an action on cholinergic neurons in the mesopontine tegmentum.

Animals↗

PubMed1994

DCC gene alteration in human endometrial carcinomas.

The present study was undertaken to define the gene(s) of importance on the long arm of chromosome 18 (chromosome 18q) in endometrial carcinomas. We analyzed loss of heterozygosity (LOH) at 3 loci on chromosome 18q and DCC gene expression by the reverse-transcriptase/polymerase chain reaction (RT-PCR) method. Among 61 tumors that were informative, 16 (26%), estimated to be a minimum number, showed allelic losses at one or more chromosome 18q loci. Deletions in these tumors possibly involved the region within or near the chromosome 18q 21.3 band where the DCC gene was localized. Moreover, the incidence of altered DCC mRNA expression was high in these tumors. Appropriate transcription was lost in 5 of 7 (71%) carcinoma cell lines in addition to 14 of 28 (50%) surgically resected tumors. Histopathological differentiation and clinical stage of disease were not related to LOH frequency or to DCC mRNA expression. These results suggest that the target for allelic loss on chromosome 18q seen in endometrial carcinomas is the DCC gene, and that inactivation of this gene may be critical for the development of most endometrial carcinomas.

Alleles↗

PubMed1994

Distribution of 111In- and 125I-labeled monoclonal antibody 17-1A in mice bearing xenografts of human pancreatic carcinoma HuP-T4.

BACKGROUND: The prognosis of pancreatic adenocarcinoma still remains poor because of the lack of reliable diagnostic tests for early stages of the disease. Monoclonal antibody 17-1A (MoAb 17-1A) has been studied extensively, and the antigen recognized by MoAb 17-1A is expressed by adenocarcinomas of the pancreas and stomach, as well as other normal and malignant epithelial tissues. The potential of MoAb 17-1A was investigated for its ability to detect pancreatic carcinomas. The use of MoAb 17-1A in treatment also was studied. METHODS: Immunoreactivity of MoAb 17-1A with human pancreatic carcinoma cell line HuP-T4 was examined histochemically by the avidin-biotinylated enzyme complex method. MoAb 17-1A was labeled with 125I by the Iodogen method and 111In using either diethylenetriaminepentaacetic anhydride (cDTPA) or 1-(p-benzyldiazonium) diethylenetriaminepentaacetic acid (aDTPA). After injection in nude mice bearing HuP-T4 xenografts, the biodistribution of 111In- and 125I-labeled MoAb 17-1A was examined at various time points. RESULTS: Positive staining of MoAb 17-1A was noted for HuP-T4 cells. A statistically significant (P < 0.01) greater tumor uptake was observed at 3 days after intravenous injection of 125I-labeled MoAb 17-1A when compared with 125I-labeled nonspecific immunoglobulin G. 125I- and 111In-labeled MoAb 17-1A was concentrated in HuP-T4 carcinoma 1.9-4.8 times higher than in the spleen, heart, liver, and pancreas. CONCLUSIONS: MoAb 17-1A was found to bind selectively to human pancreatic carcinoma HuP-T4. Tumor exhibited higher uptake of radiolabeled MoAb 17-1A compared with adjacent normal tissues. These results suggest that MoAb 17-1A may be applicable to the radioimmunodetection and radioimmunotherapy of pancreatic adenocarcinomas.

Absorption↗

PubMed1994

Secretion of amyloid precursor protein and laminin by cultured astrocytes is influenced by culture conditions.

Although normally quiescent, astrocytes in the adult brain respond to various types of brain injury by rapidly dividing, swelling, extending cellular processes, and expressing increased amounts of glial fibrillary acidic protein (GFAP). These phenomena are collectively referred to as "astrogliosis." Similarly, astroglia in primary culture stop dividing when they attain confluency, yet, as seen in situ, they retain their proliferative capacity for extended periods and resume rapid division when subcultured. To examine the impact of glial division on secretion of neurite-promoting factors, conditioned medium (CM) was removed from subconfluent, newly confluent, and long-term confluent ("aged") neonatal rat astrocyte cultures, and from aged confluent cultures that had been repassaged, "lesioned" (scraping with a rubber policeman), or triturated 3 days before harvest. Secretion of neurite-promoting factor(s) by glial cells into these CM was then assayed by treating neuroblastoma cultures with these various CM and quantitating neurite elaboration. Extensive neurite sprouting was elicited by CM from cultures just reaching confluency and from repassaged, lesioned, or triturated cultures. CM from aged confluent cultures did not induce sprouting. These results indicate that secretion of neurite-promoting factor(s) is regulated by glial division, and suggest that gliosis in situ may contribute to neurite sprouting by similar mechanisms. Immunoblot analysis demonstrated the presence in CM of varying amounts of laminin and amyloid precursor protein (APP), including isoforms containing the Kunitz-type protease inhibitor domain. CM from subconfluent cultures contained trace amounts of these proteins, but CM from cultures just reaching confluency contained significant amounts. Although CM from aged cultures contained barely detectable levels of either protein, trituration or repassage of aged cultures dramatically increased secretion of these proteins. APP- and laminin-enriched CM fractions promoted neuritogenesis to a similar level as respective unfractionated CM; anti-APP and anti-laminin antisera blocked this effect. Purified human brain APP promoted neuritogenesis when added to non-conditioned medium and aged CM. Increased secretion of APP and laminin therefore mediates at least a portion of CM-induced neuronal sprouting; these proteins may perform analogous functions during astrogliosis in situ.

Amyloid beta-Protein Precursor↗

PubMed1994

The effect on enterotoxicity of protease purified from Vibrio cholerae O1.

The effect on enterotoxicity of protease purified from Vibrio cholerae O1 was investigated by the inoculation of live vibrio cells into protease-treated loops of the ileal loop model. Fluid accumulation ratios in the protease-treated loops were elevated in a dose-dependent manner by challenge with live vibrio cells but not by that with toxin. An enhancement effect of protease on enterotoxicity was observed in both serotypes of V. cholerae O1 and V. cholerae non-O1. It is suggested, therefore, that the enterotoxicity was enhanced by treatment with protease when live vibrio cells were inoculated into the ileal loops of rabbits.

Animals↗

PubMed1994

An acylated cyanidin glycoside from the red-purple flowers of Dendrobium.

A new acylated anthocyanin was isolated from the red-purple flowers of Dendrobium 'Pramot' (phalaenopsis type cv) as a major anthocyanin. The structure of this pigment was determined to be cyanidin-3-O-malonyl)-beta-D-glucopyranoside) 7,3'-di-O-(6-O-(4-O-(beta-D- glucopyranosyl)oxybenzoyl)-beta-D-glucopyranoside) mainly based on the spectroscopic evidence.

Acylation↗