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S Jinno

Publications and source records attributed to S Jinno.

At least 37 records · Page 2Linked to original sources
PubMed1998

Quantitative analysis of GABAergic neurons in the mouse hippocampus, with optical disector using confocal laser scanning microscope.

The numerical densities (NDs) of glutamic acid decarboxylase (GAD) 67 immunoreactive (IR) neurons in the mouse hippocampus were estimated according to the optical disector method using a confocal laser scanning microscope (CLSM), and the cell sizes of disector-counted neurons were measured. Particularly, we focused on the dorsoventral differences of the NDs and cell sizes in individual subdivisions and layers. The NDs of GAD67-IR neurons were larger at the ventral level than at the dorsal level in most subdivisions and layers, except in the stratum pyramidale (SP) of the CA1 region and stratum radiatum (SR) of the CA3 region. In the whole hippocampus, the ND of GAD67-IR neurons was 5.7+/-0.2x103/mm3 at the dorsal level, and 7.3+/-0.3x103/mm3 at the ventral level. The laminar differences showed that the NDs of GAD67-IR neurons in the principal cell layers were generally larger than those in the dendritic layers in each subdivision. The ND of GAD67-IR neurons was largest in the SP of the CA1 region at the dorsal level (13.5+/-0.9x103/mm3), and smallest in the molecular layer (ML) of the dentate gyrus (DG) at the dorsal level (1.7+/-0.2x103/mm3). The mean cell sizes of GAD67-IR neurons also showed prominent dorsoventral and laminar differences. In the CA3 region, the mean cell size of GAD67-IR neurons was smaller at the dorsal level than at the ventral level, while in the DG, it was larger at the dorsal level than at the ventral level. On the other hand, the mean cell size of GAD67-IR neurons in the CA1 region showed no significant dorsoventral difference. In the whole hippocampus, the mean cell size of GAD67-IR neurons was slightly smaller at the dorsal level (somatic profile area 149.2+/-2.5 microm2) than at the ventral level (154.2+/-2.9 microm2). The laminar differences showed that the mean cell sizes of GAD67-IR neurons in the principal cell layers were generally larger than those in the dendritic layers in each subdivision. The mean cell size of GAD67-IR neurons was largest in the SP of the CA3 region at the ventral level (180.7+/-8.7 microm2), and smallest in the stratum lacunosum-moleculare (SLM) of the CA3 region at the dorsal level (115.9+/-7.9 microm2). The cell size distributions in individual layers revealed that GAD67-IR neurons were roughly classified into two subgroups. The composition of these subgroups suggested the heterogeneity of GAD67-IR neurons in the mouse hippocampus in view of cell size

Animals↗
PubMed1998

Development of novel chitosan derivatives as micellar carriers of taxol.

PURPOSE: To develop an intravenous injectable carrier composed of chitosan derivatives for taxol. METHODS: A chitosan with lauryl groups attached to amino groups to provide the hydrophobic moieties and, carboxymethyl groups attached to hydroxy groups to provide the hydrophilic moieties (N-lauryl-carboxymethyl-chitosan = LCC), was newly synthesized. The solubility of taxol in LCC micelles in aqueous solution was examined. The hemolysis test of LCC and the growth inhibition experiment of taxol-loading micelle using KB cells were also performed as in vitro assay. RESULTS: It was found that LCC solubilized taxol by forming micelles with particle sizes less than 100nm. This particle size was considered effective for passive targeting for tumors. The concentration of taxol in the micellar solution was very high, with a maximum of 2.37mg/mL. This maximum was 1000 times above that in a saturated solution of taxol at pH 7.4. Hemolysis testing as an in vitro assay indicated that LCC was safer than Polysorbate 80 (TO-10M) as intravenous surfactant in terms of induction of membrane damage. As judged by cytostatic activity against KB cells, taxol retained activity even when included in LCC micelles. LCC-entrapped taxol was more effective in cytostatic activity than free taxol in low concentrations. CONCLUSIONS: The results of solubilization capacity examination, hemolysis testing, and cytostatic activity suggest that LCC may be useful as a carrier of taxol.

Animals↗
PubMed1998

The analysis of mRNA expression of cytokines from skin lesions in Churg-Strauss syndrome.

We report our recent clinical experience with a patient suffering from Churg-Strauss syndrome and the results of our investigation into the mRNA expression of cytokines in the patient's lesions as well as in the frozen sections from a previous patient. In both cases, blood IgG was at a high level. Cytokine mRNA expression differed according to the degree of cellular infiltration. In the presence of marked infiltration, counteracting Th1 and Th2 cytokines were simultaneously detected; the former included IL-12 and IFN-gamma, and the latter, IL-6 and IL-10. The concurrence of both types of cytokine could be attributed to several factors. For example, IL-6 is involved through some mechanism in the formation of immune complexes by IgG, and IL-12 and IFN-gamma appeared to participate in the development of granuloma. These suppositions support the suggested immunological etiology of the disease. It is also inferred that the dominance of one of the two types of cytokines depends on the clinical phase of the disease.

Biomarkers↗
PubMed1998

3-(5-Dimethylamino-1-naphthalenesulphonyl)-2-(3-pyridyl)thiazolidine (YHI-1) selectively inhibits human immunodeficiency virus type 1.

3-(5-Dimethylamino-1-naphthalenesulphonyl)-2-(3-pyridyl)thiazolidi ne (YHI-1), a synthetic analogue of D-cysteinolic acid isolated from sardines (Sardinops melanostictus), was found to be a specific inhibitor of human immunodeficiency virus type 1 (HIV-1) replication in various cell cultures. YHI-1 inhibited HIV-1IIIB replication with a 50% effective concentration (EC50) of 3.35, 10.23 and 4.61 microM in MT-4 cells, peripheral blood mononuclear cells and MAGI-CCR5 cells, respectively. However, no antiviral activity was observed with non-nucleoside reverse transcriptase inhibitor (NNRTI)-resistant HIV-1 strains, such as nevirapine-resistant HIV-1HE/NEV and MKC-442-resistant HIV-1IIIB-R, or with HIV-2ROD or SIVMAC. YHI-1 failed to inhibit reverse transcriptase (RT) activity in vitro with different template-primer systems. Time-of-addition experiments, the failure to inhibit NNRTI-resistant strains and the failure to show in vitro activity against RT suggest that a metabolite of YHI-1 inside the cell acts like an NNRTI. Thus, YHI-1 seems to belong to a new class of HIV-1 inhibitor and is a good candidate for further development.

Animals↗
PubMed1997

[Two cases of papillary adenocarcinoma of the thyroid gland associated with chylothorax].

Case 1. An 85-year-old woman had a papillary adenocarcinoma of the thyroid gland and a pleural effusion. The pleural effusion appeared to be a chylous exudate and it did not re-accumulate after thoracenthesis. Thoracic imaging indicated that the chylothorax was caused by direct invasion of the thoracic duct by the thyroid carcinoma. Case 2. A 53-year-old woman had a 20-year history of recurrent chylothorax. She died due to sepsis one year after the third admission for dyspnea and chylothorax. The autopsy findings included papillary adenocarcinoma of the thyroid gland with metastasis to the left supraclavicular lymph nodes. The thoracic duct was inflamed, fibrotic, and completely obstructed. Invasion by the carcinoma may have compressed and destroyed the thoracic duct, and caused chylothorax. Recurrent inflammatory granulation caused total obstruction of the thoracic duct. Reports of chylothorax associated with carcinoma of the thyroid gland are rare.

Adenocarcinoma, Papillary↗
PubMed1995

Induction of DNA polymerase beta and gamma in the lungs of age-related oxygen tolerant rats.

To clarify a mechanism for oxygen tolerance in young rats, 3 and 8 week-old rats were exposed to 100% oxygen. All 8 week-old (8W) rats died between 48 and 72h, whereas most 3 week-old (3W) rats survived for more than 72 h under hyperoxia. It was assumed that this difference is attributable to oxygen tolerance in 3W rats compared with 8W rats. To clarify this difference, we measured the change in the activity of DNA polymerase, which is related to the final step of DNA repair. DNA polymerase activity in crude lung extracts from 3W rats increased up to 72 h after oxygen exposure. On the other hand, the activity in 8W rats was decreased at 24 h and 48 h. The activity of DNA polymerase beta, which is related to nuclear DNA (nDNA) repair, was approximately seven times higher in 3W rats than in 8W rats. DNA polymerase beta activities in 3W rats decreased up to 48 h with oxygen exposure, but recovered to pre-exposure levels by 72 h. Moreover, an induction of DNA polymerase gamma, which is related to mitochondrial DNA (mtDNA) replication and/or repair, was observed only in 3W rat lungs after 24 h of oxygen exposure. From these results, we conclude that the induction of DNA polymerase beta and DNA polymerase gamma in lung tissue plays a key role in oxygen tolerance in very young rats.

Age Factors↗
PubMed1995

Requirement for tyrosine phosphorylation of Cdk4 in G1 arrest induced by ultraviolet irradiation.

Exposure to ultraviolet light arrests the function of mammalian fibroblasts in the G1 phase of the cell cycle, as well as the S and G2 phases. Although p21, an inhibitor of cyclin-dependent kinase (Cdk) that is induced by DNA damage may partly account for the arrest in G1 (ref. 1), the mechanism is little understood. Here we show that tyrosine phosphorylation of Cdk4 is required for this arrest. In rat fibroblast, Cdk4 is tyrosine-phosphorylated during G1 progression, and its dephosphorylation is required for S phase. When cells are ultraviolet-irradiated, their arrest in G1 is accompanied by an increase in phosphorylation level. Conversely, cells expressing unphosphorylatable Cdk4F17 fail to arrest in G1, and suffer significantly elevated chromosomal aberrations and cell death.

Animals↗
PubMed1995

Pharmacology of calcitonin gene related peptide release from sensory terminals in the rat trachea.

In an intraluminally perfused rat trachea model, we have observed the following. (i) Capsaicin evoked a concentration-dependent calcitonin gene related peptide (CGRP) release from the trachea. Its effects were mimicked by the capsaicin analogue resiniferatoxin and blocked by capsazepine, a competitive antagonist of capsaicin. Capsazepine did not attenuate the peptide release evoked by bradykinin, nicotine, or prostaglandin E2. (ii) Elevation of extracellular H+ resulted in a proton concentration dependent increase in CGRP release, but this was not inhibited by capsazepine. (iii) Indomethacin treatment did not alter capsaicin- or proton-induced CGRP release; in contrast bradykinin- and nicotine-induced release were significantly reduced. (iv) Chemical destruction of sympathetic nerve fibers by systemic pretreatment with 6-hydroxydopamine reduced CGRP release evoked by nicotine, but the release produced by capsaicin or bradykinin remained unchanged. These results suggest that the effect of capsaicin on tracheal CGRP release occurs via activation of specific capsaicin receptors on primary sensory C-fibers, while protons act at a different site from that acted upon by capsaicin in the trachea. Cyclooxygenase products are likely involved in the effects of bradykinin and nicotine, but not those of capsaicin and protons. Sympathetic activation may mediate nicotine-, but not bradykinin- or capsaicin-induced CGRP release. These observations indicate that factors present in the extravascular--extracellular melieu of the trachea can evoke the release of CGRP from sensory C-fibers and that there are multiple mechanisms whereby these agents may interact with the afferent terminals.

Animals↗
PubMed1995

[A surviving case of disseminated tuberculosis complicated with severe respiratory failure, pancytopenia, DIC, drug induced fever and pneumothorax in an elderly patient].

We reported a survival case of a 78-year-old female with disseminated tuberculosis complicated with severe respiratory failure, pancytopenia, DIC, drug induced fever and pneumothorax. Atypical symptoms and presence of chronic illness make the early diagnosis of disseminated tuberculosis in the elderly difficult. In this report, we emphasized that both a high awareness of possible clinical diagnoses and the performance of some clinical procedures including bronchoalveolar lavage were useful. Disseminated tuberculosis in the elderly with multiple complications which is rare condition, was discussed.

Aged↗
PubMed1995

[Clinical significance of levels of lung surfactant protein A in serum, in various lung diseases].

To assess the utility of measuring lung surfactant protein A (SP-A) in serum, a newly developed SP-A kit (Teijin TDR-30) was used at four facilities to measure serum SP-A levels in patients with various lung diseases. Serum SP-A levels in healthy volunteers were 24.6 +/- 9.6 ng/ml (mean +/- SD). serum SP-A levels did not differ significantly between different age groups (thirties through seventies). A cut-off level of 43.8 ng/ml was calculated, based on the values of the healthy volunteers. The serum SP-A levels in patients with idiopathic interstitial pneumonia (IIP: 67.9 +/- 42.5 ng/ml), pulmonary alveolar proteinosis (PAP: 7.0 +/- 45.7 ng/ml), and collagen disease with interstitial pneumonia (CDIP: 55.3 +/- 37.9 ng/ml) were significantly higher than those in healthy volunteers. When calculated with the cut-off value stated above, the positive rate of diagnosis for IIP was 71.4%. SP-A levels correlated closely with the clinical course; SP-A levels rose significantly during exacerbations of IIP. Measurement of SP-A in serum is useful for the diagnosis of IIP, PAP, and CDIP, and for monitoring exacerbations of IIP.

Adult↗
PubMed1994

Cdc25A is a novel phosphatase functioning early in the cell cycle.

The cdc25+ tyrosine phosphatase is a key mitotic inducer of the fission yeast Schizosaccharomyces pombe, controlling the timing of the initiation of mitosis. Mammals contain at least three cdc25+ homologues called cdc25A, cdc25B and cdc25C. In this study we investigate the biological function of cdc25A. Although very potent in rescuing the S.pombe cdc25 mutant, cdc25A is less structurally related to the S.pombe enzyme. Northern and Western blotting detection reveals that unlike cdc25B, cdc25C and cdc2, cdc25A is predominantly expressed in late G1. Moreover, immunodepletion of cdc25A in rat cells by microinjection of a specific antibody effectively blocks their cell cycle progression from G1 into the S phase, as determined by laser scanning single cell cytometry. These results indicate that cdc25A is not a mitotic regulator but a novel phosphatase that plays a crucial role in the start of the cell cycle. In view of its strong ability to activate cdc2 kinase and its specific expression in late G1, cdc2-related kinases functioning early in the cell cycle may be targets for this phosphatase.

Amino Acid Sequence↗
PubMed1994

Multiple mechanisms for the effects of capsaicin, bradykinin and nicotine on CGRP release from tracheal afferent nerves: role of prostaglandins, sympathetic nerves and mast cells.

Application of capsaicin (CAP), bradykinin (BK) or nicotine (NIC) to intraluminally perfused rat tracheas induced an increase in calcitonin gene-related peptide (CGRP) levels in the perfusates. Depletion of sensory afferent CGRP with systemic CAP pretreatment resulted in a significant reduction of CGRP release evoked by CAP, BK or NIC. Chemical destruction of sympathetic nerve fibres by systemic pretreatment with 6-hydroxydopamine reduced CGRP release evoked by NIC, but did not alter the release produced by CAP or BK. Elimination of the tracheal mast cell population by pretreatment with compound 48/80 did not alter the effects of CAP, BK or NIC. CGRP release evoked by BK and NIC, but not CAP, was diminished by indomethacin, suggesting that cyclooxygenase products mediate the actions of BK and NIC. Prostaglandins, PGE1, PGE2, PGF2 alpha and PGI2, displayed stimulatory effects on CGRP release in the trachea. There are evidently multiple mechanisms mediating CGRP release from sensory terminals in rat trachea. It appears that CAP exerts a direct action on sensory nerves, while the effects of BK and NIC are mediated by PG synthesis. Sympathetic activation may be involved in NIC, but not BK, induced PG-mediated CGRP release.

Animals↗
PubMed1994

Nicotine and acetylcholine induce release of calcitonin gene-related peptide from rat trachea.

In the present study, we observed that nicotine, the nicotinic analogue cytisine, and acetylcholine (ACh) evoked a concentration-dependent (5 x 10(-6)-5 x 10(-5) M) release of calcitonin gene-related peptide (CGRP) from the rat trachea. After a prolonged exposure to capsaicin, nicotine-induced CGRP release was absent, suggesting that the release of CGRP by nicotine is derived from capsaicin-sensitive afferent terminals. Nicotine- and cytisine-induced release displayed a significant degree of tachyphylaxis after sequential exposures. The release of CGRP evoked by capsaicin was also reduced after nicotine and cytisine desensitization. This indicates that similar mechanisms may mediate the tachyphylactic effect of capsaicin and nicotine. Hexamethonium and mecamylamine blocked the effect of nicotine but not that of ACh, whereas atropine significantly attenuated the release of CGRP outflow induced by ACh. Physostigmine and neostigmine did not alter resting release of CGRP from rat trachea, although exogenous (10(-5) M) ACh-induced CGRP release was enhanced in the presence of neostigmine, suggesting minimal tonic cholinergic activity in this model. We conclude that activation of nicotinic and muscarinic receptors in the rat trachea can induce local release of CGRP. These observations indicate that cholinergically induced airway responses may be mediated in part by activation of the peripheral terminals of primary afferent sensory neurons and subsequent release of local neuropeptides.

Acetylcholine↗
PubMed1994

Synthesis and evaluation of novel thiazolidine derivatives as thromboxane A2 receptor antagonists.

A series of 3-benzoyl or 3-phenylsulfonyl-2-substituted thiazolidine derivatives were synthesized, and evaluated for their thromboxane A2 (TXA2) receptor-antagonizing effect on (15S)-15-hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5(Z),13(E)-dienoic acid (U-46619)-induced aggregation of rabbit platelet-rich plasma (PRP). A simple 2-aryl-thiazolidine derivative, 3-benzoyl-2-(4-hydroxy-3-methoxyphenyl)thiazolidine (5a), showed mild TXA2 receptor antagonist activity. Modification of 5a led to 2-chloro-4-[3-(4-chlorophenylsulfonyl)thiazolidin-2-ylmet hyl]phenoxyacetic acid (29d), which showed 10 times more potent TXA2 receptor antagonist activity than 5a.

Animals↗
PubMed1994

[Epidemiology of emphysema: analysis by autopsy in a series of elderly patients].

Epidemiologic studies indicate that various factors are involved in causing emphysema, although it is uncertain exactly how these factors contribute. Thus the correlation between pathological changes and clinical manifestations was studied. Results of autopsies done on 1940 men and 1791 women from 1978 to 1992 were analyzed retrospectively. Emphysema was graded, from macroscopic findings as follows: none (E 0), slight (E 1), moderate (E 2), and severe (E 3). The severity of anthracocsis was graded as well. Information regarding clinical diagnosis, smoking habits, and available spirometric data were obtained by reviewing the medical records. Prevalence of each grade of emphysema was: in men, E 0-48.6%, E 1-31.6%, E 2-15.8%, and E 3-4.0%; in women, E 0-81.6%, E 1-13.7%, E 2-3.7%, and E 3-0.8%. Pneumonia, lung cancer, and gastric ulcer were significant complications of emphysema, and may have contributed to the cause of death. The effects of various risk factors on the severity of emphysema were evaluated by multiple linear regression analysis. Male sex, age, smoking habit, and grade of the anthracosis were independent factors affecting the development of emphysema. Among them, anthracosis grade and smoking habit were found to be strongly contributing factors. Emphysema grade and FEV1% were significantly correlated, but several patients with moderate or severe emphysema did not show airflow obstruction. Therefore, receiver operating characteristic (ROC) curves were constructed to evaluate the value of the FEV1% in the diagnosis of emphysema. The diagnostic value of the FEV1% alone was low, so a multiple linear regression equation with three factors (sex, smoking habit, and FEV1%) was constructed.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1993

Cyclin G: a new mammalian cyclin with homology to fission yeast Cig1.

A new gene encoding a cyclin-like protein has been isolated from a rat fibroblast cDNA library by cross-hybridization with a mixture of c-src family proto-oncogene kinase domains as a probe. This putative cyclin, called cyclin G, contains a typical cyclin box at the N-terminus but no apparent 'destruction box' or 'PEST' sequence. Interestingly, in its C-terminus region, it has a sequence homologous with a tyrosine phosphorylation site of the epidermal growth factor receptor. Although this cyclin is phylogenetically related to HCS26 of Saccharomyces cerevisiae, it most resembles Cig1, a B-type cyclin, of Schizosaccharomyces pombe, which has been suggested to act at the G1/S phase of the cell cycle. Cyclin G mRNA is induced within 3 h after growth stimulation and remains elevated with no apparent cell cycle dependency, indicating its close association with growth stimuli but not with the cell cycle.

Amino Acid Sequence↗