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Biomedical subjects

F Hirata

Publications and source records attributed to F Hirata.

At least 19 recordsLinked to original sources
PubMed2001

Theoretical study for volume changes associated with the helix-coil transition of peptides.

We calculate the partial molar volumes and their changes associated with the coil(extended)-to-helix transition of two types of peptide, glycine-oligomer and glutamic acid-oligomer, in aqueous solutions by using the Kirkwood-Buff solution theory coupled with the three-dimensional reference interaction site model (3D-RISM) theory. The volume changes associated with the transition are small and positive. The volume is analyzed by decomposing it into five contributions following the procedure proposed by Chalikian and Breslauer: the ideal volume, the van der Waals volume, the void volume, the thermal volume, and the interaction volume. The ideal volumes and the van der Waals volumes do not change appreciably upon the transition. In the both cases of glycine-peptide and glutamic acid-peptide, the changes in the void volumes are positive, while those in the thermal volumes are negative, and tend to balance those in the void volumes. The change in the interaction volume of glycine-peptide does not significantly contribute, while that of glutamic acid-peptide makes a negative contribution.

Biopolymers↗
PubMed2000

A case of cytophagic histiocytic panniculitis associated with exertional rhabdomyolysis.

An 18-year-old man who suffered from panniculitis involving the entire left lower limb after exertional rhabdomyolysis is reported. A high fever (>39 degrees C) and leukocytosis (>20,000/microL) persisted for 1 week, and his general status deteriorated rapidly into pre-disseminated intravascular coagulation, complicated by pleural effusion and prolonged clotting time. His condition was dramatically improved by steroid pulse therapy and he has remained in good health for the 20 months since discharge. Histologic examination of subcutaneous tissue from the swollen left lower limb revealed pleomorphic small, medium or large lymphocytes, macrophages and neutrophils infiltrating the edematous subcutaneous adipose tissue in a lobular panniculitis-like pattern. The majority of inflammatory cells were T lymphocytes, with equal proportions of CD4+ and CD8+ cells. As polymerase chain reaction did not show bands suggesting T cell receptor gamma gene rearrangement, the proliferation of T lymphocytes was considered to be polyclonal. The T lymphocytes also expressed Fas ligand, suggesting the involvement of Fas-mediated cytotoxicity. This case may represent a new category of cytophagic histiocytic panniculitis induced by exertional rhabdomyolysis.

Adolescent↗
PubMed1999

Lipocortin (Annexin) I heterotetramer binds to purine RNA and pyrimidine DNA.

Lipocortin I-like protein with a molecular weight of 94,000 Da as judged by Western analysis was found to bind to ssDNA rather than to dsDNA in a Ca(2+)-dependent manner. This protein was also bound to [(32)P]poly(rA) and [(32)P]poly(rG) as measured by EMSA. Poly(rG), poly(rA), poly(dC), and poly(dT) were competitive against binding of either [(32)P]poly(rA) or [(32)P]poly(rG), while poly(rC), poly(rU), and poly(dA) were less effective binding competitors. The binding of this protein to poly(rA) or poly(rG) was inhibited by immunoprecipitable anti-lipocortin I (calpactin II) and anti-S100 protein antibodies, but not by an anti-Ig antibody. Phospholipids such as phosphatidylserine and phosphatidylinositol enhanced the binding of lipocortin I to poly(rA). Taken together, our present observations suggest that the lipocortin I-S100 protein heterotetramer binds to either purine RNAs or pyrimidine ssDNAs in a Ca(2+)- and phospholipid-dependent manner.

Animals↗
PubMed1998

Magnetic resonance imaging of the paranasal sinuses in divers.

BACKGROUND: CT and magnetic resonance imaging (MRI) frequently reveal asymptomatic paranasal sinus mucosal hypertrophy in the general population. HYPOTHESIS: Divers can suffer asymptomatic paranasal sinus mucosal injury secondary to barotrauma. METHODS: We examined 20 professional divers by MRI and compared them to 20 normal controls. Paranasal sinus mucosal hypertrophy was defined as mucosal thickening of 3 mm or greater. RESULTS: Nine divers had paranasal sinus mucosal hypertrophy vs. four controls (p = 0.09). There was no significant relationship between paranasal sinus hypertrophy and age, diving history, alcohol consumption, or smoking. CONCLUSION: Divers had a tendency toward paranasal sinus mucosal hypertrophy.

Adult↗
PubMed1998

MR imaging of the central nervous system in divers.

BACKGROUND: Magnetic resonanse imaging (MRI) frequently reveals asymptomatic cerebral infarctions in the general population. HYPOTHESIS: The central nervous system (CNS) of divers is affected by a hyperbaric environment even if they are asymptomatic. METHODS: We examined 25 uniformed service divers by MRI and compared them with normal controls. RESULTS: Of 25 divers, 9 had CNS lesions vs. 2 of 25 controls (p = 0.02). There was a significant relationship between the CNS lesions, age, and smoking. CONCLUSION: The divers had a risk of accumulating CNS lesions. These results suggested that divers should undergo periodic medical evaluations and MRI brain scanning.

Adult↗
PubMed1997

Neutrophil extracted lipocortin inhibits corticotropin secretion in the AtT-20 D16:16 clonal mouse pituitary cell line. Lipocortin inhibition of ACTH release in vitro.

The mechanism of short-term glucocorticoid (GC) inhibition of the hypothalamic-pituitary-adrenal axis is not well understood. The direct anti-inflammatory activities of lipocortins (LCs) have suggested a role for them as extra- and intracellular mediators of the biological effects of GCs. It has been reported that recombinant human (rh) LC1 inhibits corticotropin (ACTH) release from pituitary tissue in vitro but not from AtT-20 D16:16 corticotrophs. Using the same cell line we have tested whether other exogenous rhLCs or native LC extracted from polymorphonucleate neutrophils (neLC), likely LC1, have an effect on ACTH secretion. It is shown that: (1) basal release was not affected by a short-term incubation with neLC; (2) secretion induced by corticotropin-releasing factor (CRF) and other secretagogues (phorbol ester, potassium ion or calcium ionophore) was inhibited by neLC; (3) GC inhibition of CRF-stimulated release was reverted by a monoclonal anti-neLC antibody; (4) rhLC2, rhLC5 and the fragment 212-234 of rhLC5 were without effect. Thus, only neLC is effective on AtT-20 D16:16 cells, suggesting for this annexin a role in the early phase GC inhibition of ACTH secretion.

Adrenocorticotropic Hormone↗
PubMed1997

Rat alveolar macrophage cytokine production and regulation of neutrophil recruitment following acute ozone exposure.

The alveolar macrophage generation of interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) cytokines has been implicated in the recruitment of neutrophils into acutely injured lungs. To examine the role of these cytokines in neutrophil chemotaxis, cytokine mRNA transcripts and content were examined in macrophages lavaged from rats immediately following 6 hr exposure to air or 1 ppm ozone. Ozone exposure enhanced the number of lavaged macrophages demonstrating mRNA transcripts and immunocytochemical staining for IL-1 beta and TNF-alpha. These changes occurred prior to ozone-induced increases in permeability and lavageable neutrophils. The supernatant from in vitro macrophage cultures demonstrated ozone-associated enhancements in neutrophil chemotactic activity and in IL-1 beta and TNF-alpha levels. However, treatment of the macrophage-conditioned media with anti-IL-1 beta and anti-TNF-alpha antibodies separately and in combination demonstrated that these cytokines were not directly responsible for the observed neutrophil chemoattraction. However, coculturing the macrophages with anti-IL-1 beta and anti-TNF-alpha together, but not separately, resulted in a 44% inhibition of media chemotactic activity, suggesting that maximal macrophage generation of chemoattractants was dependent on either IL-1 beta or TNF-alpha. The mRNA transcripts for the neutrophil chemoattractants macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant (CINC) were found to be enhanced in cultured macrophages from ozone-exposed rats, but reduced on incubation with anti-IL-1 beta and anti-TNF-alpha together. These results demonstrated that ozone-induced enhancements in IL-1 beta and TNF-alpha productions appear not to be associated directly with neutrophil chemoattraction, but are more likely involved in stimulating the generation of the neutrophil chemoattractants MIP-2 and CINC.

Animals↗
PubMed1996

Modulation of cell death pathways to apoptosis and necrosis of H2O2-treated rat thymocytes by lipocortin I.

Lipocortin I, also called annexin I, a calcium and phospholipid binding protein, protected rat thymocytes from H2O2-elicited necrosis and facilitated H2O2-induced apoptosis, while anti-lipocortin I antibody enhanced H202-elicited necrosis by blocking H202-induced apoptosis. Essentially similar results were obtained with phospholipase A2 inhibitors and activators such as 3,4-octyadecyl-benzylacrylic acid and melittin, respectively. Available evidence suggests that lipocortin I modulates signals for cell death pathways of H2O2-treated rat thymocytes to apoptosis and necrosis by regulating cellular phospholipase A2 activities but not by inhibiting membrane lipid peroxidation.

Animals↗
PubMed1996

Cyclic GMP inhibits phosphoinositide turnover in choroid plexus: evidence for interactions between second messengers concurrently triggered by 5-HT2C receptors.

The present study examined the effects of the nitric oxide generator sodium nitroprusside (SNP), a membrane-permeable cGMP analog (dibutyryl-cGMP) and low calcium buffer incubation on choroid plexus serotonin 5-HT2C receptor-mediated inositol monophosphate (IP) production. SNP (100 microM) substantially inhibited 10(-6)M serotonin-stimulated IP production (-46%, P < 0.02). Serotonin-stimulated IP production was increased in low calcium buffer (+280%, P < 0.01) in which serotonin-stimulated cGMP formation is attenuated. Addition of dibutyryl-cGMP (500 microM) inhibited IP formation in low calcium buffer. The present data are suggestive of an inhibitory effect of cGMP on IP formation in choroid plexus, and raise the intriguing possibility of interactions between second messenger systems concurrently activated by 5-HT2C receptors.

Animals↗
PubMed1996

Thermogenic responses to high-energy phosphate contents and/or hindlimb suspension in rats.

Effects of chronic depletion of high-energy phosphate compounds by feeding beta-guanidinopropionic acid (beta-GPA) with or without hindlimb suspension (HS) on body temperature were studied in rats. Lower rectal and skin temperatures were observed in rats after 10 d of HS. Suspension-related enlargement of the interscapular brown adipose tissue (BAT), associated with adrenal hypertrophy, was seen. Feeding beta-GPA also caused a hypothermia and BAT enlargement. It is suggested that the hypothermic response to HS may be due to decreased contractile activity and metabolic rate in skeletal muscles, associated with stress. It is also speculated that the changes in the thermogenesis in rats fed beta-GPA might be related to a stimulated ATP synthesis with sacrificed heat production, but not associated with stress.

Animals↗
PubMed1996

Involvement of endothelins in immediate and late asthmatic responses of guinea pigs.

To explore the pathophysiological roles of endothelin isopeptides and receptor subtypes in asthmatic responses, a guinea pig model for asthma was used to test the effects of antiendothelin (ET) serum and selective ET receptor antagonists for antigen-induced specific airway conductance changes as measured by whole-body plethysmography. In this model, all of the animals so far tested demonstrated both the immediate and late asthmatic responses. Although preimmune serum had no apparent effects, anti-ET antiserum suppressed the maximal reduction of specific airway conductance in both the immediate and late asthmatic responses, which suggested that ET(s) are involved in the pathophysiology of both the immediate and late asthmatic responses. The ETB selective antagonists, BQ788 and RES701-1, blocked the immediate asthmatic response but not the late asthmatic response, whereas the ETA antagonists, BQ123 and (Shionogi) 97-139, suppressed only the late asthmatic response without influencing the immediate asthmatic response. In vitro constrictive responses of isolated tracheas and bronchi to ET1 were inhibited mainly by BQ123 and BQ788, respectively, which suggested that distribution of ETA and ETB receptors for bronchoconstriction are topographically distinct along airways. Furthermore, thromboxane A2 and platelet activating factor (PAF) antagonists were effective in suppressing the late asthmatic response but not the immediate asthmatic response. Taken together, our present observations suggest that ET(s) influences pulmonary functions by constricting airway smooth muscle via ETB receptors during the immediate asthmatic response and by modulating pulmonary inflammation via ETA receptors during the late asthmatic response, respectively.

Analysis of Variance↗
PubMed1995

Down-regulation of bcl-xs gene expression in rat thymocytes by dexamethasone.

In order to test a hypothesis that the expression of bcl-x gene promotes apoptosis by antagonizing the function of bcl-2 gene product, time course of the expression of bcl-x was investigated using the dexamethasone-treated rat thymocytes which were undergoing apoptosis. Unexpectedly, dexamethasone suppressed the expression of bcl-x in a dose- and time-dependent manner. Such decrease was detected even in the presence of cycloheximide, suggesting that the suppression is due to the genomic (primary) effect of dexamethasone. Since the expression of bcl-xL, as measured by a specific nucleotide probe, was not detected at a quantifiable level, the decrease was apparently attributed to that in bcl-xS. Our present observations propose a new role of the bcl-xS gene product, in which the bcl-x gene product may be necessary for survival of immature thymocytes rather than for their apoptosis.

Animals↗
PubMed1995

Restriction fragment length polymorphism of the apolipoprotein B gene and response to dietary fat and cholesterol.

OBJECTIVE: The relationship between response to dietary fat and cholesterol, and the EcoRI restriction fragment length polymorphism (RFLP) of the apolipoprotein B(apoB) gene was examined. DESIGN: Forty-nine free-living subjects took part in a prospective double-blind crossover dietary intervention study. The apoB EcoRI cutting site was present in five women and 18 men (E+) and absent in 15 women and 11 men (E-). INTERVENTION: Subjects consumed a low fat (25% energy), low cholesterol (less than 200 mg/day) diet. After two weeks on this background diet (baseline) subjects were randomly assigned to consume a liquid supplement for three weeks which was either fat and cholesterol free or which contained fat (30 to 36 g) and cholesterol (650 to 780 mg). After the first three-week period subjects switched to the other supplement. Blood samples were collected for plasma lipid analysis after an overnight fast on two consecutive days at the end of baseline and on three consecutive days after each three-week supplement period. RESULTS: There was no significant difference in response to diet between the RFLP groups. Changes in plasma total, low density lipoprotein (LDL), high density lipoprotein(HDL), HDL2 and HDL3 cholesterol or plasma triglyceride were not different between the two RFLP groups. There was a significant difference between RFLP groups for baseline HDL2-cholesterol (0.31 +/- 0.04 and 0.16 +/- 0.02 mmol/L for E- and E+ subjects, respectively) which was independent of sex and apoE genotype (P = 0.032). CONCLUSIONS: These results indicate that the EcoRI RFLP of the apoB gene is not associated with response to dietary fat and cholesterol.

Apolipoproteins B↗
PubMed1994

IL-1 beta regulates the expression of the Gi2 alpha gene via lipid mediators in guinea pig tracheal muscle.

When isolated guinea pig muscle preparations were incubated with human recombinant IL-1 beta, mRNA level of Gi2 alpha but not of Gs alpha increased in a time and dose dependent manner. The increase was partially blocked by inhibitors of lipoxygenase (NDGA) and cyclooxygenase (indomethacin) and PAF antagonist (SC47014A), while U46619 (thromboxane A2 mimetic), LTD4, 15-HETE and PAF partially mimicked it. The IL-1 beta induced Gi2 alpha expression was almost completely inhibited by anti-phospholipase A2 antiserum, whereas preimmune serum had no apparent effects. From these observations, we suggest that IL-1 beta first induces the synthesis and release of Type II inflammatory phospholipase A2, which in turn stimulates the expression of Gi2 alpha gene via production of various lipid mediators.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗