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T Honda

Publications and source records attributed to T Honda.

At least 217 records · Page 12Linked to original sources

Markers indicating deterioration of pulmonary Mycobacterium avium-intracellulare infection.

To predict the natural history of pulmonary Mycobacterium avium-intracellulare (MAI) infection with nodular bronchiectasis, we retrospectively evaluated clinical manifestations, laboratory data, and bronchoalveolar lavage fluid (BALF) findings in 57 patients. The patients received follow-up chest computed tomographic scans and testing for sputum bacteriology between intervals of at least 12 mo. They were divided into two groups after observation for 28 +/- 13 mo: deteriorated (n = 34) and not-deteriorated (n = 23). There were no patients with spontaneous improvement. At the start of observation, the mean age was greater in the deteriorated group (69 +/- 9 yr) than in the not-deteriorated group (57 +/- 9 yr). The mean body-mass index was lower in the deteriorated group (19.2 +/- 3.1 kg/m(2)) than in the not-deteriorated group (21.5 +/- 1.5 kg/m(2)). C-reactive protein, erythrocyte sedimentation rate, and carbohydrate antigen 19-9 were significantly elevated in the deteriorated group. The BALF findings of the deteriorated group showed that the neutrophil cell counts were significantly increased. Thirty-four of 57 patients with pulmonary MAI infection with nodular bronchiectasis had progressive clinical and/or radiographic disease. The older and thinner patients tended to become worse. Neutrophil-related inflammation associated with a decrease in CD4+ lymphocyte might reflect the progression of pulmonary MAI infection with nodular bronchiectasis.

Aged↗

Complete nucleotide sequence of the prophage VT2-Sakai carrying the verotoxin 2 genes of the enterohemorrhagic Escherichia coli O157:H7 derived from the Sakai outbreak.

The enterohemorrhagic Escherichia coli (EHEC) O157:H7 strain RIMD 0509952, derived from an outbreak in Sakai city, Japan, in 1996, produces two kinds of verotoxins, VT1 and VT2, encoded by the stx1 and stx2 genes. In the EHEC strains, as well as in other VT-producing E. coli strains, the toxins are encoded by lysogenic bacteriophages. The EHEC O157:H7 strain RIMD 0509952 did not produce plaque-forming phage particles upon inducing treatments. We have determined the complete nucleotide sequence of a prophage, VT2-Sakai, carrying the stx2A and stx2B genes on the chromosome, and presumed the putative functions of the encoded proteins and the cis-acting DNA elements based on sequence homology data. To our surprise, the sequences in the regions of VT2-Sakai corresponding to the early gene regulators and replication proteins, and the DNA sequences recognized by the regulators share very limited homology to those of the VT2-encoding 933W phage carried by the EHEC O157:H7 strain EDL933 reported by Plunkett et al. (J. Bacteriol., p1767-1778, 181, 1999), although the sequences corresponding to the structural components are almost identical. These data suggest that these two phages were derived from a common ancestral phage and that either or both of them underwent multiple genetic rearrangements. An IS629 insertion was found downstream of the stx2B gene and upstream of the lysis gene S, and this might be responsible for the absence of plaque-forming activity in the lysate obtained after inducing treatments.

Bacterial Toxins↗

Proliferation of type II pneumocytes and alteration in their apical surface membrane antigenicity in pulmonary sarcoidosis.

STUDY OBJECTIVE: To evaluate both the proliferation of type II pneumocytes in the alveolitis associated with pulmonary sarcoidosis and any alteration in their surface membrane antigenicity. MATERIALS AND METHODS: We investigated 20 transbronchial lung biopsy (TBLB) specimens from 20 patients with pulmonary sarcoidosis, 7 TBLB specimens from 7 sarcoidosis patients without pulmonary involvement, and 19 normal lung specimens, using colloidal iron stain and immunostaining with anti-Thomsen-Friedenreich (TF) antigen and anti-surfactant protein-A monoclonal antibodies. RESULTS: The density of type II pneumocytes was significantly higher in the pulmonary sarcoidosis specimens ([mean +/- SD] 11.1+/-3.7 per 1 mm alveolar septal length) than in the nonpulmonary sarcoidosis (7.8+/-1.3) or normal lung specimens (7.2+/-0.8). TF antigen was directly expressed on the apical surface of some type II pneumocytes in the pulmonary sarcoidosis specimens, but it was completely masked by sialic acids in the nonpulmonary sarcoidosis specimens and in the normal lung tissues. CONCLUSIONS: In pulmonary sarcoidosis, type II pneumocytes proliferated and the antigenicity of the surface membrane was altered. It is suggested that these type II pneumocytes may be vulnerable to injury by natural anti-TF antibodies that are cytotoxic when present with complement. This damage may decrease alveolar surfactant and cause focal alveolar collapse proceeding to pulmonary fibrosis in some cases of pulmonary sarcoidosis.

Antigens, Surface↗

[Plague].

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Anti-Infective Agents↗

[Brucellosis].

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Anti-Bacterial Agents↗

Ultrastructural studies on the formation and distribution of lipid droplets in the lung capillary endothelial cells in patients with sarcoidosis.

BACKGROUND AND AIM OF THE WORK: We previously reported the presence of definite morphological alterations in the capillary endothelium of sarcoid lung. The aim of this study was to examine ultrastructural changes and distribution of lipid droplets in the endothelium of lung capillaries of patients with sarcoidosis. METHODS: Tissue specimens were obtained by transbronchial lung biopsy or open lung biopsy from 16 patients with sarcoidosis and 13 controls. Biopsies were evaluated by electron microscopy following lead citrate and uranyl acetate staining. RESULTS: Typical lipid droplets were observed in pulmonary capillaries of 11 out of 16 sarcoid patients (69%); the droplet frequency was higher in sarcoid patients than in control specimens. Lipid droplets were characterized by biphasic density: most droplets contained eccentrically located vacuoles (saturated fatty acids) others were characterized by low density areas (unsaturated fatty acids). Biphasic droplets were covered by large lysosomal granules and were mainly distributed in the endothelium and pericytes. Interestingly, in the latter, vacuoles increased in size while small amounts of lysosomal granules were detectable. CONCLUSION: Our findings suggest that biphasic droplets increase in number in pulmonary capillaries of patients with sarcoidosis with a characteristic distribution pattern from the endothelium to pericytes.

Adult↗

Regulation of macrophage migration inhibitory factor (MIF) expression by glucose and insulin in adipocytes in vitro.

BACKGROUND: It has been reported that macrophage migration inhibitory factor (MIF) stimulated insulin secretion from pancreatic islet beta-cells in an autocrine manner, which suggests its pivotal role in the glucose metabolism. According to this finding, we evaluated MIF expression in cultured adipocytes and epididymal fat pads of obese and diabetic rats to investigate its role in adipose tissue. MATERIALS AND METHODS: The murine adipocyte cell line 3T3-L1 was used to examine MIF mRNA expression and production of MIF protein in response to various concentrations of glucose and insulin. Epididymal fat pads of Otsuka Long-Evans Tokushima fatty (OLETF) and Wistar fatty rats, animal models of obesity and diabetes, were subjected to Northern blot analysis to determine MIF mRNA levels. RESULTS: MIF mRNA of 3T3-L1 adipocytes was up-regulated by costimulation with glucose and insulin. Intracellular MIF content was significantly increased by stimulation, whereas its content in the culture medium was decreased. When the cells were treated with cytochalasin B, MIF secretion in the medium was increased. Pioglitazone significantly increased MIF content in the culture medium of 3T3-L1 cells. However, MIF mRNA expression of both epididymal fat pads of OLETF and Wistar fatty rats was down-regulated despite a high plasma glucose level. The plasma MIF level of Wistar fatty rats was significantly increased by treatment with pioglitazone. CONCLUSION: We show here that the intracellular glucose level is critical to determining the MIF mRNA level as well as its protein content in adipose tissue. MIF is known to play an important role in glucose metabolism as a positive regulator of insulin secretion. In this context, it is conceivable that MIF may affect the pathophysiology of obesity and diabetes.

3T3 Cells↗

[Usefulness and safety of the early rehabilitation program for patients with acute aortic dissection].

The usefulness and safety of the early rehabilitation program (2- and 3-week courses) were validated for patients with acute aortic dissection. This program undergone by 42 consecutive patients between 1996 and 1997 was compared to the conventional program undergone by 66 patients between 1993 and 1995, using the prognosis and complications for elderly patients. Mortality rate and morbidity rate were not significantly different between the early and conventional programs. The incidence of intensive care unit (ICU) syndrome in elderly patients was 16% (3 of 19 cases) vs 50% (15 of 30 cases), respectively (p < 0.05). The duration of hospital stays was 26 +/- 7 vs 37 +/- 13 days, respectively (p < 0.05). The early rehabilitation program for patients with acute aortic dissection was safe and useful to prevent complications in elderly patients, and was cost effective.

Acute Disease↗

[Chronic pulmonary thromboembolism diagnosed on the basis of characteristic mosaic patterns on lung computed tomograms].

We report on a 59-year-old woman who presented with characteristic findings on lung computed tomographic (CT) scans and was therefore suspected to have chronic pulmonary thromboembolism. She visited our hospital because of worsening exertional dyspnea over the preceding year, and because she was dissatisfied with an earlier diagnosis made by another institution. Chest roentgenograms disclosed nonhomogeneous hyperlucency in both lungs associated with linear and bundle shadows, dullness of the right costophrenic angle, and dilatation of the descending branch of the right pulmonary artery. The patient experienced moderate hypoxemia even at rest. Pulmonary function tests demonstrated a restrictive ventilatory pattern associated with reduced diffusion capacity. The lung CT scans disclosed a mosaic pattern of attenuation in the lung parenchyma, which probably reflected scattered areas of low perfusion. The unique characteristics of such CT findings drew our attention to chronic pulmonary thromboembolism as a possible diagnosis. We eventually confirmed the diagnosis on the basis of enhanced CT scans, pulmonary perfusion and ventilation scintigrams, and digital subtraction angiography. In our view, chronic pulmonary thromboembolism should be kept in mind as a possible differential diagnosis of the mosaic patterns of attenuation on lung CT scans.

Chronic Disease↗

Effect of subinhibitory concentrations of antimicrobial agents (quinolones and macrolide) on the production of verotoxin by enterohemorrhagic Escherichia coli O157:H7.

In Japan, antimicrobial agent therapy for patients with diarrhea due to enterovirulent organisms including enterohemorrhagic Escherichia coli (EHEC) is common, and norfloxacin (NFLX), fosfomycin, and kanamycin are recommended for EHEC treatment by the Japanese Ministry of Health and Welfare. The aim of this study was to analyze the effects of antimicrobial agents which have been used or recommended for the treatment of EHEC on the production of verotoxin (VT) in vitro. Subinhibitory concentrations of quinolones, NFLX, sparofloxacin (SPFX), and grepafloxacin (GPFX) markedly stimulated the productions of VT1 and VT2. The macrolide azithromycin (AZM), erythromycin (EM), and clarithromycin (CAM) did not stimulate the production of VT at a wide range of concentrations. These in vitro results indicate that when quinolones are prescribed for a patient infected with EHEC, the concentration of antimicrobial agents used in vivo and the susceptibility of the EHEC strains against quinolones should be taken into consideration.

Animals↗

[Clinical effectiveness of degradable starch microspheres (DSM) in patients with liver cancer].

Recently, degradable starch microspheres (DSM) have become available for use in patients with liver cancer in Japan. When DSM combined with a cytotoxic drug are infused through the hepatic artery, the steep drug concentration gradient to the tumor tissue results in a higher tissue drug concentration, which may elicit an increased antitumor response by blocking regional blood flow. Furthermore, the reduced systemic exposure of a coinjected drug can be translated into an increased regional extraction ratio due to blood flow reduction. DSM is infused via a catheter connecting to a subcutaneously implanted reservoir in outpatients. Pain is experienced by all patients. Other frequently observed adverse reactions are nausea and vomiting. However, these symptoms improve within a few hours. These observations indicate that intra-arterial chemotherapy combined with DSM may provide a more potent anticancer effect than a cytotoxic drug alone.

Antineoplastic Combined Chemotherapy Protocols↗

[Clinical evaluation of PCR method for detection of cytomegalovirus DNA].

Polymerase chain reaction (PCR) to detect Cytomegalovirus (CMV)-DNA from the clinical specimens is useful to diagnose CMV infection. Eighty-one specimens of 31 patients including peripheral blood, bronchioalveolar lavage fluid, biopsy tissues, feces, urine, sputum and etc. and normal peripheral blood from 59 volunteers were used in this study. After DNA extraction each samples was amplified by the seminested PCR using primers recognizing sequences in the Immediate-early gene of CMV. This PCR method specifically detected more than 10 virus copies even in the presence of the genomic DNA. CMV-DNA was detected in only one of 59 normal peripheral bloods (1.7%). Six of 31 patients were clinically diagnosed as CMV infection by anti-CMV therapy. These 6 patients were positive in the peripheral blood by PCR for CMV, and 5 of them were positive in other samples. However, 3, 5 and 1 of 25 patients, who were clinically diagnosed as not having CMV infection, were also positive in peripheral blood, in the other samples and in both, respectively. The PCR method was able to examine any clinical samples. To examine both the peripheral blood and the samples from infected organs is helpful for the diagnosis of CMV infection.

Adolescent↗

Regulation of reactive oxygen species-induced apoptosis and necrosis by caspase 3-like proteases.

Reactive oxygen species (ROS) and caspases have been implicated as potential mediators of cell death. However, their mechanistic relationship remains to be elucidated. Here we investigated the roles of caspases in apoptosis and necrosis induced by ROS, generated by the mixture of xanthine and xanthine oxidase (X/XO). A low concentration of XO (0.025 U/ml) induced DNA fragmentation with little cellular membrane damage 3 h after treatment, suggesting the induction of apoptosis. The same treatment induced membrane blebbing, a morphological change typical of apoptosis, 15 min after treatment. A high concentration of XO (0.1 U/ml) damaged cell membranes with little concomitance of DNA fragmention, suggesting the induction of necrosis. ROS also activated caspase 3-like proteases and caspase 3 itself together with the release of cytochrome c which might be the cause of caspase activation. Apoptosis induced by low concentrations of XO and necrosis induced by high concentrations of XO was inhibited by z-DEVD-CH2F, an irreversible inhibitor of caspase 3. However, rapid induction of membrane blebbing was not inhibited by z-DEVD-CH2F. These results suggest that both apoptosis and necrosis could be induced by ROS through the activation of caspase 3-like protease; however, caspase 3 activation is not needed for ROS-induced membrane blebbing.

Apoptosis↗

Design and synthesis of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid, a novel and highly active inhibitor of nitric oxide production in mouse macrophages.

New derivatives with electron-withdrawing substituents at the C-2 position of 3-oxoolean-1-en-28-oic acid were synthesized. Among them, 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO) was 400 times more potent than previous compounds we have made as an inhibitor of production of nitric oxide induced by interferon-gamma in mouse macrophages (IC50, 0.4 nM). The potency of CDDO was similar to that of dexamethasone, although CDDO does not act through the glucocorticoid receptor.

Animals↗

Direct association of presenilin-1 with beta-catenin.

Families bearing mutations in the presenilin-1 (PSI) gene develop Alzheimer's disease (AD). However, the mechanism through which PS1 causes AD is unclear. The co-immunoprecipitation with PS1 in transfected COS-7 cells indicates that PSI directly interacts with endogenous beta-catenin, and the interaction requires residues 322450 of PSI and 445-676 of beta-catenin. Both proteins are co-localized in the endoplasmic reticulum. Over-expression of PS1 reduces the level of cytoplasmic beta-catenin, and inhibits beta-catenin-T cell factor-regulated transcription. These results indicate that PSI plays a role as inhibitor of the beta-catenin signal, which may be connected with the AD dysfunction.

Alzheimer Disease↗

Presenilin 1 associates with glycogen synthase kinase-3beta and its substrate tau.

Families bearing mutations in the presenilin 1 (PS1) gene develop Alzheimer's disease. Previous studies have shown that the Alzheimer-associated mutations in PS1 increase production of amyloid beta protein (Abeta1-42). We now show that PS1 also regulates phosphorylation of the microtubule-associated protein tau. PS1 directly binds tau and a tau kinase, glycogen synthase kinase 3beta (GSK-3beta). Deletion studies show that both tau and GSK-3beta bind to the same region of PS1, residues 250-298, whereas the binding domain on tau is the microtubule-binding repeat region. The ability of PS1 to bring tau and GSK-3beta into close proximity suggests that PS1 may regulate the interaction of tau with GSK-3beta. Mutations in PS1 that cause Alzheimer's disease increase the ability of PS1 to bind GSK-3beta and, correspondingly, increase its tau-directed kinase activity. We propose that the increased association of GSK-3beta with mutant PS1 leads to increased phosphorylation of tau.

Adult↗

Direct innervation of sensory fibers from the dorsal root ganglion of the cervical dura mater of rats.

STUDY DESIGN: Sensory innervation in the cervical dura mater of rats was investigated immunohistochemically in whole tissues and transverse sections of the decalcified vertebral column. OBJECTIVE: To investigate the origin and distribution of sensory innervation in the cervical dura mater. SUMMARY OF BACKGROUND DATA: It has been generally accepted that irritation of the cervical structures is one of the major causes of pain in the neck and the upper extremities. Sensory fibers in the cervical dura mater are possible mediators of pain. However, there is little information about sensory innervation in the cervical dura mater, including the epiradicular sheath. METHODS: Ten Wistar rats were used for wholemount immunohistochemical observations of the cervical dura mater. The vertebral columns of five rats were processed for immunohistochemistry after decalcification. In all specimens, sensory fibers were demonstrated by the peptide immunohistochemistry, and sensory innervation was examined. RESULTS: The cervical dura mater was arbitrarily divided into three areas: ventral, dorsal, dorsal root ganglion. A large number of fibers were in the dorsal root ganglion area and were distributed in the corresponding segments. Some calcitonin gene-related peptide immunoreactive fibers in the dorsal root ganglion were directly innervated from dorsal root ganglion area neurons and did not form nerve bundles, similar to the sinuvertebral nerve. Several immunoreactive fibers were seen in the ventral area; fibers were rarely observed in the dorsal area. CONCLUSIONS: A large number of sensory fibers are segmentally distributed in the cervical dura mater, and some of them are directly traced from dorsal root ganglion neurons.

Animals↗