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Biomedical subjects

T Horio

Publications and source records attributed to T Horio.

At least 55 records · Page 3Linked to original sources
PubMed2000

The clinical and photobiological characteristics of solar urticaria in 40 patients.

Forty patients with solar urticaria, 16 male and 24 female, were examined personally during the past 25 years. The median age at onset of symptoms was 32 years, ranging from 13 to 76 years. Most commonly (45%) solar urticaria first appeared during the third decade. The mean duration of the disease was 3.6 years at presentation. The action spectrum was found in the visible light range in 24 patients (60%), in the ultraviolet (UV) A range in four, in the UVB in four, from the UVA to UVB in three, from the UVA to visible light in one and in a broad range from UVB to visible light in four patients. An inhibition spectrum was detected in 13 of 19 patients (68%), occurring at longer wavelengths than the action spectrum in 12 of these cases. The augmentation spectrum was found in only four of 14 patients (29%) examined. Twenty-four of 31 patients (77%) developed an urticarial reaction to autologous serum, which had been previously irradiated in vitro at the action spectrum for that patient. In a single patient, solar urticaria was caused by a drug, namely chlorpromazine. In two patients, polymorphic light eruption occurred in association with solar urticaria. No single modality of treatment was satisfactory, but combined use of antihistamines, sunbathing, psoralen UVA photochemotherapy and/or sunscreening agents partially suppressed the symptoms.

Adolescent↗
PubMed2000

Protective role of copper, zinc superoxide dismutase against UVB-induced injury of the human keratinocyte cell line HaCaT.

On the basis of our recent observation that copper, zinc-superoxide dismutase and manganese-superoxide dismutase change differently following a single exposure to ultraviolet-B irradiation in the human keratinocyte cell line HaCaT, we have examined the possible role of endogenous copper,zinc-superoxide dismutase or manganese-superoxide dismutase against ultraviolet-B-induced reactive-oxygen- species-mediated keratinocyte injury in vitro. To evaluate the individual defensive roles of copper, zinc-superoxide dismutase and manganese-super-oxide dismutase, we treated HaCaT cells with diethyldithiocarbamate, a chelating agent of ionic copper that inactivates copper,zinc-superoxide dismutase activities, tumor necrosis factor alpha, which enhances manganese-superoxide dismutase levels, or transforming growth factor beta1, which inhibits manganese-superoxide dismutase levels. After the treatment with each reagent, HaCaT cells in the three different conditions were exposed to a single dose of ultraviolet-B irradiation. We assessed ultraviolet-B-induced cytotoxicity by measuring both lactate dehydrogenase leakage and cell viability using trypan blue dye exclusion assay. The lactate dehydrogenase leakage in the supernatant from damaged HaCaT cells whose copper,zinc-superoxide dismutase levels were inactivated by diethyldithiocarbamate was significantly increased and the cell viability was significantly decreased in comparison with untreated groups at 8 and 24 h after ultraviolet-B irradiation. On the other hand, the lactate dehydrogenase release and cell viability for HaCaT cells whose manganese-superoxide dismutase levels were enhanced by tumor necrosis factor alpha or inhibited by transforming growth factor beta1 showed no significant difference from untreated groups. Furthermore, increased production of intracellular peroxides in HaCaT cells treated with diethyldithiocarbamate was observed by flow cytometric analysis at 8 h after ultraviolet-B irradiation. These results suggest that copper,zinc-superoxide dismutase may play a primary protective role against ultraviolet-B-induced injury of the human keratinocyte cell line HaCaT.

Animals↗
PubMed2000

Possible involvement of enhanced prostaglandin E2 production in the photosensitivity in xeroderma pigmentosum group A model mice.

Xeroderma pigmentosum group A (XPA) gene-deficient mice cannot repair UV-induced DNA damage and easily develop skin cancers by UV irradiation. Therefore, XPA-deficient mice are a useful model of human XP and represent a promising tool for photobiologic studies of the disorder. Exposure to ultraviolet (UV) B (280-320 nm) radiation greatly enhanced inflammation and immunosuppression in these mice. To investigate the molecular mechanisms of enhanced UV inflammation and immunosuppression, we determined the amount of prostaglandin (PG) E2, an inflammatory mediator and immunomodulator, and analysed the expression of cyclooxygenase (COX) mRNA in the ear skin of XPA-deficient mice after UV irradiation. In XPA-deficient mice, the amount of PGE2 significantly increased at 48 and 72 h after UVB irradiation to the level that was 8- and 16-fold higher than those in wild-type mice, respectively. The expression level of COX-2 mRNA increased in a time-dependent manner, although COX-1 mRNA was constantly expressed. Treatment with indomethacin, a potent inhibitor of PG biosynthesis, inhibited UV-induced ear swelling, abrogated local immunosuppression, and decreased the amount of PGE2 in the ear skin of XPA-deficient mice. These results indicate that the excess DNA photoproducts remaining in XPA-deficient cells after UV radiation may induce COX-2 expression. The induced production of PGE2 may be involved in the enhanced inflammation and immunosuppression caused by UV radiation in XPA-deficient mice and XP patients.

Animals↗
PubMed2000

Promotive effects of a silk film on epidermal recovery from full-thickness skin wounds.

We examined the effects of the transparent fibroin film (silk film) on full-thickness skin wounds. Full-thickness dermatotomies (15 mm x 9 mm) were prepared on the dorsal wall of CRJ:CD-1 nu/nu (ICR nu/nu) mice. The area of the wounds dressed with silk film was reduced to 10% of that made by the dermatotomy 14 days after the dermatotomy and were covered with regenerated epidermis 21 days after the dermatotomy. In contrast, less recovery and epidermal regeneration were found 14 days after dermatotomy in the wounds dressed with a conventional hydrocolloid dressing (Duro Active). Furthermore, only partial incomplete epidemal growth was obtained 21 days after dermatotomy. Most importantly, the healing time of wounds dressed with silk film was 7 days shorter than those dressed with DuoActive dressing. The silk film showed an almost similar or slightly better promotive effect as the lyophilized porcine dermis (Alloask D), which is used as a dressing for burns, ulcers, and decubitis. Histologic findings revealed that there was greater collagen regeneration and less inflammation and neutrophil-lymphocyte infiltration of the wounds dressed with silk film than with DuoActive dressing. It is clear that regeneration of the epidermis and dermis of the wound beds covered with silk film was faster than with DuoActive dressing. Finally, silk film is easily obtainable, sterilizable, and transparent, and it allows easy observation of tissue recovery. Therefore, silk film offers advantages over other dressings and may be clinically useful for wound treatment.

Animals↗
PubMed2000

Effects of various taste stimuli on heart rate in humans.

Relationships between taste stimuli and heart rate were evaluated in 29 healthy university students. The test solutions were sucrose, NaCl, citric acid, quinine-HCl and monosodium glutamate (MSG). Heart rate increased by 7.1-13.6% for all the taste stimuli after use as compared with pre-stimuli values. The maximum increases in heart rate came approximately 25 s after the taste stimuli. After the increases, heart rate returned to pre-stimuli levels after between 80 and 100 s. Heart rate reached its maximum with citric acid. Recovery from the heart-rate increase was more delayed for quinine-HCl and MSG than for the other stimuli. Except for sucrose, increases in heart rate and the hedonic scale values of the taste solutions showed significant negative correlation. These findings show that the taste stimuli solutions increased the heart rate and that the increase differed with the concentration and taste solution used.

Heart Rate↗
PubMed2000

Ventricular adrenomedullin concentration is a sensitive biochemical marker for volume and pressure overload in rats.

This study was designed to investigate the pathophysiological significance of adrenomedullin (AM) concentration in volume- and pressure-overloaded cardiac hypertrophy. We measured ventricular AM concentrations and compared them with changes of alpha-actin and myosin heavy chain (MHC) mRNA isoforms after the creation of an aortocaval (AC) shunt as a volume-overload model or the injection of monocrotaline (MCT) as a pressure-overload model, respectively. The left ventricular AM levels after the creation of AC shunt and the right ventricular AM levels after the injection of MCT were significantly increased and correlated with changes of the alpha-actin and MHC mRNA isoforms. However, the ventricular AM mRNA expressions were increased and correlated with ventricular AM concentrations only in the AC shunt model. These results suggest that the ventricular AM levels are upregulated in both the volume- and pressure-overloaded cardiac hypertrophy by differential transcriptional regulation and that the ventricular AM may be a biochemical marker for the volume and pressure overload to the ventricle.

Adrenomedullin↗
PubMed2000

Urocortin, a member of the corticotropin-releasing factor family, in normal and diseased heart.

In the present study we investigated the form of expression, action, second messenger, and the cellular location of urocortin, a member of the corticotropin-releasing factor (CRF) family, in the heart. Urocortin mRNA, as shown by quantitative RT-PCR analysis, is expressed in the cultured rat cardiac nonmyocytes (NMC) as well as myocytes (MC) in the heart, whereas CRF receptor type 2beta (CRF-R2beta), presumed urocortin receptor mRNA, is predominantly expressed in MC compared with NMC. Urocortin mRNA expression is higher in left ventricular (LV) hypertrophy than in normal LV, whereas CRF-R2beta mRNA expression is markedly depressed in LV hypertrophy compared with normal LV. Urocortin more potently increased the cAMP levels in both MC and NMC than did CRF, and its effect was more potent in MC than in NMC. Urocortin significantly increased protein synthesis by [(14)C]Phe incorporations and atrial natriuretic peptide secretion in MC and collagen and increased DNA synthesis by [(3)H]prolin and [(3)H]Thy incorporations in NMC. An immunohistochemical study revealed that urocortin immunoreactivity was observed in MC in the normal human heart and that it was more intense in the MC of the human failing heart than in MC of the normal heart. These results, together with the recent evidence of urocortin for positive inotropic action, suggest that increased urocortin in the diseased heart may modulate the pathophysiology of cardiac hypertrophy or failing heart, at least in part, via cAMP signaling pathway.

Animals↗
PubMed2000

Cardiac adrenomedullin gene expression and peptide accumulation after acute myocardial infarction in rats.

Plasma adrenomedullin (AM) has been shown to increase in the early phase of acute myocardial infarction (MI). However, little information is available regarding cardiac AM synthesis after MI. Accordingly, we examined the time course of ventricular AM production and potential stimulation of AM in the infarcted and noninfarcted regions in MI rats produced by coronary artery ligation. Compared with sham-operated rats, the ventricular AM peptide level 6 h after MI increased 1.5-fold in the infarcted region and 1.7-fold in the noninfarcted region in association with increased left ventricular end-diastolic pressure (EDP). Northern blot analysis also showed marked induction of AM gene expression in the infarcted region (11-fold) and the noninfarcted region (6-fold) 6 h after MI. The AM peptide level in the infarcted region reached its peak (2. 6-fold) 1 wk postinfarction and thereafter decreased to normal. In the noninfarcted region, however, the AM level remained elevated for at least 4 wk. Immunohistochemical studies demonstrated that intense immunostaining for AM was limited to myocytes in both the infarcted and noninfarcted regions. Interestingly, the AM level in the noninfarcted region correlated positively with infarct size (r = 0. 40, P < 0.01) and EDP (r = 0.52, P < 0.001). An oral angiotensin-converting enzyme inhibitor suppressed the overproduction of AM 1 wk postinfarction in association with decreases in EDP and mean arterial pressure. In summary, cardiac AM synthesis was rapidly induced in both the infarcted and noninfarcted regions after MI. The subsequent ventricular AM in the two regions demonstrated different time-concentration curves during 4 wk after MI. AM may be synthesized predominantly by cardiac myocytes, but not by fibroblasts, at least in part, in association with increased ventricular load after MI.

Adrenomedullin↗
PubMed2000

Inhibitory regulation of hypertrophy by endogenous atrial natriuretic peptide in cultured cardiac myocytes.

Atrial natriuretic peptide (ANP) may function as an endogenous regulator of cardiac hypertrophy, because the natriuretic peptide receptor has been found in the heart and because mice lacking its receptor have been shown to have a markedly elevated ventricular mass. We examined the role of endogenous ANP in cardiac hypertrophy in vitro. The effects of the blockade of endogenous ANP by its receptor antagonist, HS-142-1, on cell hypertrophy were investigated with the use of cultured neonatal rat ventricular myocytes. HS-142-1 increased the basal and phenylephrine (PE, 10(-5) mol/L)-stimulated protein syntheses in a concentration-dependent manner (1 to 300 microg/mL). A significant increase in the cell size of myocytes was also induced by this antagonist. In addition, the expression levels of skeletal alpha-actin, beta-myosin heavy chain, and ANP genes, markers of hypertrophy, were partially elevated by treatment with HS-142-1 (100 microg/mL) under nonstimulated or PE-stimulated conditions. A cGMP-specific phosphodiesterase inhibitor, zaprinast (5x10(-4) mol/L), and a cGMP analogue (10(-4) mol/L) suppressed the basal and PE-stimulated protein syntheses. Our observations suggest that endogenous ANP inhibits cardiac myocyte hypertrophy under basal and PE-stimulated conditions, probably through a cGMP-dependent process. ANP may play a role as an autocrine factor in the regulation of cardiac myocyte growth.

Actins↗
PubMed2000

Identification of an alpha-tubulin mutant of fission yeast from gamma-tubulin-interacting protein screening: genetic evidence for alpha-/gamma-tubulin interaction.

gamma-Tubulin has been determined to be a central element of microtubule nucleation and, thus, indispensable for cellular organization of the microtubule. Utilizing the fact that human gamma-tubulin can function in the fission yeast Schizosaccharomyces pombe, we have generated a unique mutant screening procedure which can specifically select mutants of genes encoding gamma-tubulin-interacting proteins. One of the isolated mutants, cs76, turned out to carry a mutation in the alpha 1-tubulin gene (nda2(+)). This result suggests a direct interaction between the alpha- and gamma-tubulins. We located the mutation site in the nda2 gene and characterized the mutant phenotype. Our results demonstrate the importance of the alpha-/gamma-tubulin interaction in microtubule nucleation and should complement previous knowledge.

Alleles↗
PubMed2000

Development of non-bacterial thrombotic endocarditis after percutaneous transvenous mitral commissurotomy for severely calcified mitral stenosis.

We encountered a case of mitral stenosis, complicated with non-bacterial thrombotic endocarditis, that developed after percutaneous transvenous mitral commissurotomy (PTMC). A 71-year-old female Japanese patient had severe congestive heart failure and underwent PTMC for critical and severely calcified mitral stenosis. Four weeks later, the echocardiogram demonstrated a highly echoic protrusion in the postero-medial commissure of the mitral valve. There was little evidence of inflammation at that time. She had been anticoagulated adequately since she was admitted. The patient underwent replacement of the mitral valve. She did not show any evidence of systemic embolization. Microscopic evaluation showed only organized thrombus but no evidence of inflammation in the mitral valve. Silent development of non-bacterial thrombotic endocarditis after PTMC should be recognized as a rare but potentially lethal complication of PTMC.

Aged↗
PubMed2000

Recurrent follicular and lichenoid papules of sarcoidosis.

We describe a 62-year-old Japanese woman who exhibited recurrent follicular lichenoid lesions of sarcoidosis. The skin lesions appeared all over the surface of the body without any other organ involvement, and spontaneously regressed within 1 year. Two years later, the lesions recurred on the trunk, especially in the intertriginous areas such as the submammary areas and in fatty folds of the abdomen, and on the thighs and upper arms, with the appearance of uveitis of the right eye. Histological examinations showed that small epithelioid cell granulomas were localized in the perifollicular areas. The present case was characterized by a unique distribution of follicular lichenoid eruptions, which are rare manifestations of sarcoidosis and recurrence of the lesions.

Biopsy↗
PubMed1999

Effects of adrenomedullin on cultured rat cardiac myocytes and fibroblasts.

The direct effects of adrenomedullin, a novel vasorelaxant peptide, on protein synthesis and atrial natriuretic peptide release in myocytes and on DNA and collagen syntheses in fibroblasts were examined using cultured ventricular cardiocytes. The protein synthesis of cardiac myocytes was not affected by adrenomedullin under non-stimulated conditions. Endothelin-1-induced protein synthesis in myocytes was slightly but significantly elevated by adrenomedullin. Likewise, the secretion of atrial natriuretic peptide from myocytes stimulated by endothelin-1 was increased by adrenomedullin. In cardiac fibroblasts, adrenomedullin clearly inhibited DNA synthesis and collagen production in a dose-dependent manner under both basal and angiotensin II-stimulated conditions. DNA and collagen syntheses by cardiac fibroblasts were suppressed by both 8-bromo cAMP and forskolin. Furthermore, a cAMP-specific phosphodiesterase inhibitor decreased DNA and collagen syntheses in fibroblasts and enhanced the inhibitory effects of adrenomedullin on these syntheses. Our observations suggest that adrenomedullin has opposite effects on cultured cardiac myocytes and fibroblasts and that the effects of adrenomedullin at least on fibroblasts are probably mediated through a cAMP-dependent pathway. As adrenomedullin is produced and secreted from both types of cardiac cells, adrenomedullin may play a role as an autocrine/paracrine modulator in the process of cardiac remodeling, mainly by suppressing mitogenesis and collagen synthesis in fibroblasts.

Adrenomedullin↗
PubMed1999

Lethal level overexpression of gamma-tubulin in fission yeast causes mitotic arrest.

gamma-Tubulin is a member of the tubulin superfamily and plays essential roles in microtubule nucleation. While the level of other tubulins, alpha- and beta-tubulin, is strictly regulated in higher eukaryotes and overexpression of beta-tubulin is toxic in yeasts, gamma-tubulin can be overexpressed by fivefold in fission yeast without any obvious defect in growth. Extreme overexpression of gamma-tubulin in mammalian cells caused growth arrest; however, the exact level of gamma-tubulin and the critical level of gamma-tubulin necessary for growth defect were undetermined. We have constructed strains that over- or underexpress gamma-tubulin by placing the gamma-tubulin gene under the control of the inducible nmt1 promoter and its variants. Among these, the weakest promoter was able to produce enough gamma-tubulin to support normal growth when its expression was induced. A strain in which the gamma-tubulin gene was placed under the control of the strongest inducible promoter achieved 160-fold overexpression of gamma-tubulin and its growth was suppressed. Normal cytoplasmic microtubules were mostly lost in gamma-tubulin overexpressing cells and gamma-tubulin was accumulated around the periphery of nuclei. Many of the cells were arrested in mitosis. A small fraction of cells did proceed to undergo nuclear division; however, its process looked either significantly deterred or abnormal. Our results presented here suggest that excess gamma-tubulin disrupts the microtubule array and significantly deters the formation of the mitotic spindle, most likely because of random nucleation of microtubules from excess gamma-tubulin in the cytoplasm.

Blotting, Western↗
PubMed1999

Acknowledgment

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Journal Article↗
PubMed1999

Age-dependent abnormalities of hematopoietic stem cells in (NZW x BXSB)F1 mice.

The (NZW x BXSB)F1 (W/BF1) mouse is known as an autoimmune-prone strain which develops lupus nephritis, thrombocytopenia due to platelet-specific autoantibodies, leukocytosis, and myocardial infarction. In this experiment, we investigated the age-dependent abnormalities of the hematopoietic stem cells (HSCs) and hematopoiesis in this mouse. White blood cell counts (especially Mac-1- or Gr-1-positive cells) in the peripheral blood of 12-week-old W/BF1 mice increased in comparison with those of four-week-old W/BF1 or normal mice. To investigate whether the abnormal hematopoiesis can be attributed to the HSCs of W/BF1 mice, colony-forming unit in spleen (CFU-S) and colony-forming unit in culture (CFU-C) assays were performed. Day 12 CFU-S counts of 12-week-old W/BF1 mice significantly increased in comparison with those of four-week-old W/BF1 mice or normal mice. In the CFU-C assay, CFU-GEMM and CFU-GM counts in 12-week-old W/BF1 mice increased in comparison with those of four-week-old W/BF1 or control mice. The bone marrow cells (BMCs) from 12-week-old W/BF1 mice showed a high level of G-CSF and a low level of GM-CSF in mRNA expression. To examine the effect of HSCs from 12-week-old W/BF1 mice on the onset of autoimmune diseases and the abnormal hematopoiesis, T- and B-cell-depleted BMCs of four-week-old or 12-week-old W/BF1 mice were transplanted to C3H mice. Recipient C3H mice that had received the BMCs from 12-week-old W/BF1 mice showed an earlier onset of autoimmune diseases and a shorter survival rate than those that had received the BMCs from four-week-old W/BF1 mice. These data suggest that the HSCs from 12-week-old W/BF1 mice showing the symptoms of autoimmune diseases have the capacity to induce autoimmune diseases earlier than the HSCs from four-week-old W/BF1 mice.

Age of Onset↗
PubMed1999

Suppressive effect of ultraviolet (UVB and PUVA) radiation on superantigen production by Staphylococcus aureus.

It is well known that Staphylococcus aureus (S. aureus) proliferates on the moist skin lesion of atopic dermatitis. Reduction of bacteria colonization from skin lesions by antibiotics has been reported to be effective for the treatment of atopic dermatitis. S. aureus produces superantigens which can activate T cells and possibly enhance the inflammatory reaction. Photo(chemo)therapy has been successfully used for the treatment of severe cases of atopic dermatitis. We have previously reported that photo(chemo)therapy had bacteriostatic effect on S. aureus. Now we examined the effect of UVB and psoralen plus UVA (PUVA) on superantigen production from S. aureus. We isolated S. aureus from six atopic dermatitis patients. S. aureus was irradiated in vitro with UVB (0, 5, 10 mJ/cm2) or PUVA (0.001% psoralen plus 0, 5, 10 mJ/cm2 UVA) and incubated 4 h with 100 strokes per min. After incubation, the amounts of superantigens in the supernatant were measured using ELISA kit. The production of superantigens decreased in an ultraviolet dose-dependent manner. The suppressive effects of UV radiation on superantigen production may be involved in the therapeutic efficacy of photo(chemo)therapy for atopic dermatitis.

Dermatitis, Atopic↗