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Biomedical subjects

K Asahi

Publications and source records attributed to K Asahi.

At least 19 recordsLinked to original sources
PubMed2005

Initial functional status predicts infections during steroid therapy for renal diseases.

BACKGROUND AND AIM: Corticosteroid therapy is an effective way of treatment for many renal diseases, however, it is sometimes associated with infections. Our aim is to identify useful predictive markers of infection during steroid therapy. METHODS: We examined 121 patients (M/F = 71/50, mean age 43.8, range 15 - 82 years) who were treated with corticosteroids (IgA nephropathy in 51, minimal-change disease in 17, membranous nephropathy in 16 rapidly progressive glomerulonephritis (RPGN) in 13, lupus nephritis in 12 and other disorders in 12). Karnofsky's performance score (KPS) was employed to assess the physical functional status at the time of diagnosis. Infections were defined as conditions that required more than 1-week care, and those that caused the patient's death. RESULTS: Nineteen patients (15.7%) had infections during treatment. A logistic multivariate analysis showed significant correlations between infection and the use of immunosuppressive agents (relative risk RR = 7.7, p = 0.0265), ages of 52.9 years or more (RR = 13.5, p = 0.0026), initial number of lymphocytes (Lym) less than 1.250/microl (RR = 14.2, p = 0.0011), and KPS less than 77.4 (RR = 12.1, p = 0.0020). All correlations with infection were independent of all the other variables listed above. CONCLUSION: KPS, along with age, Lym and the use of immunosuppressive agents, are useful for the prediction of infectious complications during steroid therapy.

Activities of Daily Living↗
PubMed2004

Close relationship of plasminogen activator inhibitor-1 4G/5G polymorphism and progression of IgA nephropathy.

BACKGROUND: The plasminogen activator inhibitor-1 (PAI-1) 4G/4G genotype influences the development of diabetic nephropathy and lupus nephritis. However, the association of the PAI-1 4G/4G genotype and IgA nephropathy (IgAN) has not been investigated. SUBJECTS AND METHODS: The PAI-1 and ACE polymorphisms were examined in 270 healthy volunteers and 202 biopsy-proven IgAN patients, including 117 untreated IgAN patients who had an annual health check, allowing an estimation of the time of onset of overt proteinuria and/or hematuria. The relationship between the gene polymorphisms and the pathogenesis of IgAN were examined in 202 IgAN patients and the relationship between the gene polymorphisms clinical and pathohistological findings were examined in 117 untreated IgAN patients cross-sectionally at the time of renal biopsy. RESULTS: 202 IgAN patients and 117 untreated IgAN patients did not have different frequencies in PAI-1 4G/5G (4G/4G : 4G/5 : 5G/5G = 82 : 90: 30, 45 : 55 : 17) and ACE I/D (DD : ID : II = 41 : 82 : 79, 21 : 54 : 42) gene polymorphisms compared with 270 healthy volunteers (4G/4G : 4G/5 : 5G/5G = 99 : 124 : 47, DD : ID : II = 53 : 106 : 111). However, IgAN with 4G/4G had significantly more advanced histological changes than IgAN with 4G/5G or 5G/5G both in glomerular and tubulointerstitial findings (p < 0.0005). The disease duration in IgAN with 4G/4G was shorter than in IgAN with 4G/5G + 5G/5G (6.22 +/- 6.38 and 8.80 +/- 9.79 years, respectively, p < 0.05). Creatinine clearance (Ccr) in IgAN with 4G/4G was significantly lower than IgAN with 4G/5G or 5G/5G (72.3 +/- 26.5 and 82.4 +/- 22.8 ml/min, respectively, p < 0.05). The mean urinary protein excretion in IgAN with 4G/4G was significantly more than in IgAN with 4G/5G or 5G/5G (1.10 +/- 1.48 and 0.70 +/- 1.01 g/day, respectively, p < 0.05). There was no difference between IgAN with the DD ACE genotype and IgAN with ID + II genotypes in either the clinical or histopathological findings. CONCLUSION: PAI-1 polymorphism is not associated with genesis of IgA nephropathy, but may be a risk factor for the progression of IgA nephropathy in Japanese.

Adolescent↗
PubMed2003

Insulin resistance highly associates with hypertension in IgA nephropathy.

BACKGROUND: Insulin resistance has been reported to induce hypertension. Previous studies described that there was no relationship between insulin resistance and hypertension in patients with chronic renal diseases with mild to moderate renal dysfunction. The aim of the present study is to clarify the relationship between insulin resistance and blood pressure, renal function, histopathological changes and other characteristics in IgA nephropathy (IgAN). METHODS: Eighty-eight IgAN patients were included in this cross-sectional study. Hypertension was diagnosed according to the WHO/ISH criteria. Insulin resistance was evaluated by homeostasis model assessment (HOMA-IR). RESULTS: Male gender, age, body mass index, serum creatinine, urinary protein excretion, triglycerides and HOMA-IR were positively correlated with hypertension. C(Cr), serum albumin and HDL cholesterol were negatively correlated with blood pressure by Spearman's simple correlation test. By logistic multivariate analysis, C(Cr), insulin resistance, age and male gender were significantly correlated with hypertension, independently of all other variables. CONCLUSIONS: Insulin resistance is not directly related to renal dysfunction, but is also independently associated with hypertension in IgAN. Since hypertension is considered as a risk factor for renal disease progression, insulin resistance may be an indirect deteriorating factor for IgAN. To identify and improve insulin resistance may be another therapeutic target in the clinical management of IgAN.

Adult↗
PubMed2002

Sudden deafness: long-term follow-up and recurrence.

We examined the long-term outcome for patients with idiopathic sudden sensorineural hearing loss (sudden deafness), including the incidence of recurrence of sudden deafness. The subjects were 1,798 individuals who came to Nagoya University hospital within 2 weeks of the onset of unilateral sudden deafness. Only 14 of the patients had a history of being diagnosed with sudden deafness. After their visit to our hospital, one patient had a recurrence in the ipsilateral ear and four patients experienced sudden deafness in the contralateral ear. We performed hearing examinations on 88 patients who revisited our hospital more than 10 years after unilateral sudden deafness. Of these patients, there was one with a recurrence in the ipsilateral ear and one with sudden deafness in the contralateral ear. Thus, in this series the recurrence of sudden deafness was rare.

Adult↗
PubMed2001

[Analysis of 200 university hospital hearing aid clinic patients].

We statistically studied patients who visited our hearing aid clinic to determine what segment of the population may benefit from hearing aids. Subjects were 200 patients from 5 to 89 years of age who had visited the Hearing Aid Clinic of Otorhinolaryngology, Nagoya University Hospital, between January 1998 and March 2000. This clinic lent out hearing aids. Subjects were divided into 2 groups those having their own hearing aids either new or earlier (HA group) and those giving up hearing aids after a trial (non-HA group). Mean better hearing levels in pure tone average were 50.6 dB in the HA group and 44.5 dB in the non-HA group. Mean better maximum speech recognition scores were 81.5% in the HA group and 85.3% in the non-HA group. The distribution of better hearing has shown that patients with mild hearing loss (better pure tone average < 40 dB) account for more than a quarter of all hearing aid clinic patients. Among patients with mild hearing loss, 60% had their own hearing aids. The need for rehabilitation in the mild hearing loss population thus appears large. Their intent to wear hearing aids influenced whether patients agreed or declined hearing aids after a trial. The period from use until patients made a decision was 2 weeks in 65% of those declining use and 35% of those agreeing to use. Over 15% of those agreeing called for a trial period longer than 8 weeks. Hearing aid trials provide useful information for both patients and surgeons before choosing surgery for a difficult ear condition. In this research, 18 patients needed counseling about both amplification and surgery. Bridging between ear surgery and hearing aid wearing is a vital role of hearing aid clinics at university hospitals.

Adolescent↗
PubMed2000

Skin-specific caspase-1-transgenic mice show cutaneous apoptosis and pre-endotoxin shock condition with a high serum level of IL-18.

To study the pathophysiological roles of overexpressed caspase-1 (CASP1), originally designated as IL-1 beta-converting enzyme, we generated transgenic mice in which human CASP1 is overexpressed in their keratinocytes. The transgenic mice spontaneously developed recalcitrant dermatitis and skin ulcers, characterized by the presence of massive keratinocyte apoptosis. The skin of the mice contained the active form of human CASP1 and expressed mRNA for caspase-activated DNase, an effector endonuclease responsible for DNA fragmentation. Their skin and sera showed elevated levels of mature IL-18 and IL-1 beta, but not of IFN-gamma. The plasma from these animals induced IFN-gamma production by IL-18-responsive NK cells. Administration of heat-killed Propionibacterium acnes, a potent in vivo type 1 cell inducer, caused IFN-gamma-mediated lethal liver injury in the transgenic mice, which was completely inhibited by treatment with neutralizing anti-IL-18 Ab. These results indicated that in vivo overexpression of CASP1 caused spontaneous apoptotic tissue injury and rendered mice highly susceptible to exogenous type 1 cell-inducing condition in collaboration with endogenously accumulated proinflammatory cytokines.

Animals↗
PubMed2000

Abnormal information processing in dementia of Alzheimer type. A study using the event-related potential's field.

Electrical field changes of event-related potentials (ERPs) were investigated in 26 patients with dementia of Alzheimer's type (DAT) and 12 age-matched normal subjects. The patients were assessed with the Clinical Dementia Rating and Mini-Mental State. Each patient selected had only mild to moderate mental disability. Auditory oddball stimulation was presented at 1.5 s intervals and 1,000 Hz for the nontarget and 2,000 Hz for the target tones, both at 85 dB. The target tones were 20% of all the tones. The reference-independent data (latency, global field power: GFP, dissimilarity index: DISS and location of centroids) were obtained and analyzed for each ERP component. The momentary electric strength or 'hilliness' of the ERPs landscape was indicated by GFP. The patients showed prolonged latencies and decreased P300 GFP amplitudes and of N100 GFP. These findings suggest that the abnormal electrical field of ERP may reflect abnormal information processing following the attentional process for target stimuli in DAT patients.

Aged↗
PubMed2000

Evidence for apoptosis after intercerebral hemorrhage in rat striatum.

The overall hypothesis that cell death after intracerebral hemorrhage is mediated in part by apoptotic mechanisms was tested. Intracerebral hemorrhage was induced in rats using stereotactic infusions of 0.5 U of collagenase (1-microL volume) into the striatum. After 24 hours, large numbers of TUNEL-positive stained cells with morphologies suggestive of apoptosis were present in the center and periphery of the hemorrhage. Double staining with Nissl and immunocytochemical labeling with antibodies against neuronal nuclei and glial fibrillary acidic protein suggested that these TUNEL-positive cells were mostly neurons and astrocytes. Electrophoresis of hemorrhagic brain extracts showed evidence of DNA laddering into approximately 200-bp fragments. Western blots showed cleavage of the cytosolic caspase substrate gelsolin. The density of TUNEL-positive cells at 24 and 48 hours after hemorrhage was significantly reduced by treatment with the broad-spectrum caspase inhibitor zVADfmk. It was unlikely that apoptotic changes were due to neurotoxicity of injected collagenase because TUNEL-positive cells and DNA laddering were also obtained in an alternative model of hemorrhage where autologous blood was infused into the striatum. Furthermore, equivalent doses of collagenase did not induce cell death in primary neuronal cultures. These results provide initial evidence that apoptotic mechanisms may mediate some of the injury in brain after intracerebral hemorrhage.

Amino Acid Chloromethyl Ketones↗
PubMed2000

Reduction of tissue plasminogen activator-induced hemorrhage and brain injury by free radical spin trapping after embolic focal cerebral ischemia in rats.

Thrombolytic stroke therapy with tissue plasminogen activator (tPA) remains complicated by serious risks of cerebral hemorrhage and brain injury. In this study, a novel model of tPA-induced hemorrhage was used in spontaneously hypertensive rats to examine the correlates of hemorrhage, and test methods of reducing hemorrhage and brain injury. Homologous blood clot emboli were used to occlude the middle cerebral artery in spontaneously hypertensive rats, and delayed administration of tPA (6 hours postischemia) resulted in high rates of cerebral hemorrhage 24 hours later. Compared with untreated rats, tPA significantly increased hemorrhage volumes by almost 85%. Concomitantly, infarction and neurological deficits were worsened by tPA. A parallel experiment in normotensive Wistar-Kyoto rats showed markedly reduced rates of hemorrhage, and tPA did not significantly increase hemorrhage volumes. To examine whether tPA-induced hemorrhage was caused by the delayed onset of reperfusion per se, another group of spontaneously hypertensive rats was subjected to focal ischemia using a mechanical method of arterial occlusion. Delayed (6 hours) reperfusion via mechanical means did not induce hemorrhage. However, administration of tPA plus delayed mechanical reperfusion significantly increased hemorrhage volumes. Since reperfusion injury was implicated, a final experiment compared outcomes in spontaneously hypertensive rats treated with tPA plus the free radical spin trap alpha-phenyl tert butyl nitrone (alpha-PBN) versus tPA alone. tPA-induced hemorrhage volumes were reduced by 40% with alpha-PBN, and infarction and neurological deficits were also decreased. These results indicate that (1) blood pressure is an important correlate of tPA-induced hemorrhage, (2) tPA interacts negatively with reperfusion injury to promote hemorrhage, and (3) combination therapies with anti-free radical treatments may reduce the severity of tPA-induced hemorrhage and brain injury after cerebral ischemia.

Animals↗
PubMed2000

Role for matrix metalloproteinase 9 after focal cerebral ischemia: effects of gene knockout and enzyme inhibition with BB-94.

It has been shown recently that matrix metalloproteinases (MMPs) are elevated after cerebral ischemia. In the current study, we investigated the pathophysiologic role for MMP-9 (gelatinase B, EC.3.4.24.35) in a mouse model of permanent focal cerebral ischemia, using a combination of genetic and pharmacologic approaches. Zymography and Western blot analysis demonstrated that MMP-9 protein levels were rapidly up-regulated in brain after ischemic onset. Reverse transcription polymerase chain reaction showed increased transcription of MMP-9. There were no differences in systemic hemodynamic parameters and gross cerebrovascular anatomy between wild type mice and mutant mice with a targeted knockout of the MMP-9 gene. After induction of focal ischemia, similar reductions in cerebral blood flow were obtained. In the MMP-9 knockout mice, ischemic lesion volumes were significantly reduced compared with wild type littermates in male and female mice. In normal wild type mice, the broad spectrum MMP inhibitor BB-94 (batimastat) also significantly reduced ischemic lesion size. However, BB-94 had no detectable protective effect when administered to MMP-9 knockout mice subjected to focal cerebral ischemia. These data demonstrate that MMP-9 plays a deleterious role in the development of brain injury after focal ischemia.

Animals↗
PubMed2000

Cassiopeia flap: modification of Limberg flap for saving normal skin.

Local flaps have the advantages of texture matching and increased flap survival rate. The proper local flap planning for each lesion causes the dermatologist to be reluctant to employ them. We propose a modified local flap, the "Cassiopeia flap", with three simple marking points made on the ends of the diameter and on the equidistant point along the diameter; two points from equilateral triangles form a "W (Cassiopeia)". We applied this modification to ten lesions on the face, scalp, trunk and thigh with excellent results.

Dermatologic Surgical Procedures↗
PubMed2000

Nitric oxide inhibits the formation of advanced glycation end products.

BACKGROUND: Advanced glycation end products (AGEs) are elevated in renal failure and have been implicated in the pathogenesis of several uremic complications. Their formation is closely associated with oxidative stress. The recent observation that nitric oxide (NO) has an antioxidant effect led us to examine the possible role of NO in the generation of AGEs. METHODS: We examined the effect of NO donors, 2, 2'-(hydroxynitrosohydrazono)bis-ethanamine (NOC18) and S-nitroso-N-acetyl-DL-penicillamine (SNAP), on the in vitro formation of pentosidine, which was used as a surrogate marker for AGEs. Bovine serum albumin was incubated under air at 37 degrees C in a medium containing either several AGE precursors or uremic plasma. To elucidate further the mechanism of the NO effect on AGE formation, we examined the generation of free radicals and carbonyls in pentose-driven pentosidine formation. RESULTS: NO donors significantly inhibit the formation of pentosidine in a dose-dependent manner. The effect is abolished by the addition of a NO scavenging agent, 2-(4-carboxyphenyl)-4,4,5, 5-tetramethylimidazoline-1-oxyl 3-oxide (carboxy-PTIO). The inhibitory effect results from NO but not from the NO donor molecule. It is best explained by the ability of NO to scavenge carbon-centered radicals, hydroxyl radical, and carbonyl compounds. CONCLUSIONS: NO inhibits pentosidine formation by scavenging free radicals and by inhibiting carbonyl compound formation. NO might be implicated in the atherogenic and inflammatory effects of AGEs: Reduced NO production and increased oxidative stress associated with atherosclerotic lesions may accelerate AGE formation and, thus, exacerbate endothelial dysfunction and accelerate the development of atherosclerosis in uremia.

Adult↗
PubMed2000

Air-bone gap and resonant frequency in large vestibular aqueduct syndrome.

BACKGROUND: Conductive hearing loss is occasionally recognized in large vestibular aqueduct (LVA) syndrome; however, the incidence rate and the cause are not known. OBJECTIVE: To compare air and bone conduction levels between patients with LVA syndrome and those with idiopathic sudden sensorineural hearing loss, and to investigate the cause of the air-bone gap. STUDY DESIGN: Retrospective study. SETTING: The patients were treated at a tertiary referral center. PATIENTS: Twenty-eight ears of 15 patients with LVA syndrome and 28 ears of patients with idiopathic sudden sensorineural hearing loss were examined. The latter patients were selected from a computerized database to match the former patients in air conduction levels. MAIN OUTCOME MEASURES: Pure-tone audiometry, multiple frequency tympanometry, acoustic reflex, otoacoustic emission, vestibular evoked myogenic response. RESULTS: The air-bone gap in patients with LVA syndrome was always larger than that in patients with idiopathic sudden sensorineural hearing loss with the same air conduction level. The resonant frequency in patients with LVA syndrome was rather low compared with that in normal control subjects, in contrast to the finding that resonant frequency was significantly high in patients with otosclerosis. CONCLUSIONS: An air-bone gap exists to some degree in almost all patients with LVA syndrome. The air-bone gap may not be associated with the movement restriction of the stapes as it is with otosclerosis.

Acoustic Impedance Tests↗
PubMed1999

2-Isopropylidenehydrazono-4-oxo-thiazolidin-5-ylacetanilide (OPB-9195) treatment inhibits the development of intimal thickening after balloon injury of rat carotid artery: role of glycoxidation and lipoxidation reactions in vascular tissue damage.

We have pursued the hypothesis that the carbonyl modification of proteins by glycoxidation and lipoxidation reactions plays a role in atherogenesis. Human atherosclerotic tissues with fatty streaks and uremic arteriosclerotic tissues were examined, with specific antibodies, to detect protein adducts formed with carbonyl compounds by glycoxidation or lipoxidation reactions, i.e. advanced glycation end products (AGEs) or glycoxidation products, such as carboxymethyllysine (CML) and pentosidine, and lipoxidation products, such as malondialdehyde (MDA)-lysine and 4-hydroxy-nonenal (HNE)-protein adduct. All the four adducts were identified in the proliferative intima and in macrophage-rich fatty streaks. If the carbonyl modification is not a mere result but is a contributor to atherogenesis, inhibition of glycoxidation and lipoxidation reactions might prevent vascular tissue damage. We tested this hypothesis in rats following balloon injury of their carotid arteries, a model exhibiting a remarkable intimal thickening, which are stained positive for all the four adducts. Oral administration of 2-isopropylidenehydrazono-4-oxo-thiazolidin-5-ylacetanili de (OPB-9195), an inhibitor of both glycoxidation and lipoxidation reactions, in rats following balloon injury effectively prevented the intimal thickening. These data suggest a role for the carbonyl modification of proteins by glycoxidation and lipoxidation reactions in most, if not all, types of vascular tissue damage ('carbonyl stress'), and the usefulness of inhibitors of carbonyl reactions for the treatment of vascular tissue damage.

Aged↗
PubMed1999

Phosphate depletion enhances tissue-nonspecific alkaline phosphatase gene expression in a cultured mouse marrow stromal cell line ST2.

Alkaline phosphatases (ALP) are highly ubiquitous enzymes present in the majority of animals from bacteria to higher vertebrate. Although their wide distribution in nature has suggested that these enzymes should perform important biological functions, their detailed roles or natural substrates remain unknown. In Escherichia coli, the extracellular phosphate (Pi) limitation induces the ALP gene, indicating the role of extracellular Pi in ALP gene regulation. However, little is known about the similar mechanisms in mammalian cells. This study was designed to examine the effect of low Pi medium on the ALP activity and its expression in the mouse stromal cell line ST2. The enzymatic property was classified into tissue-nonspecific ALP (TNSALP). After treatment by Pi starvation for 3 days, there was a 2-fold increase in the specific activity of TNSALP. RT-PCR analysis revealed that the mRNA of the TNSALP gene was highly stimulated. These results indicated that the effect of Pi depletion on ALP activity was regulated at the TNSALP transcriptional level, suggesting that the possible role of the Pi sensing system for biological functions of ALP might have been conserved in evolution. Our findings also made it possible to discuss the physiological roles of ALP in vivo.

Alkaline Phosphatase↗
PubMed1999

Intradermal transfer of caspase-1 (CASP1) DNA into mouse dissects: role of CASP1 in interleukin-1beta associated skin inflammation and apoptotic cell death.

Caspase-1 (CASP1) interleukin-1beta (IL-1beta) converting enzyme (ICE) has been cloned as a specific enzyme which activates the biologically inactive pro-form of IL-1beta into biological active IL-1beta. Based on the significant homology to Ced-3, Caenorhabditis elegans apoptotic gene and, proof of apoptotic activity of ICE in rat fibroblasts, ICE was renamed as CASP1. In contrast to in vitro functions, the in vivo significance of high expression of CASP1 in skin remains to be elucidated. We transferred plasmid DNA encoding murine CASP1 with beta-actin promoter into mouse skin. The CASP1 DNA-injected skin, but not skin injected with control plasmid without CASP1, developed localized erythema with subcutaneous nodules. The nodules were associated with marked inflammatory infiltrates. The apoptotic cells detected by the TUNEL method were distributed in and around the inflammatory foci. The plasma IL-1beta level of CASP1 DNA-injected mouse was elevated compared with that of the control DNA-injected mouse. These inflammatory reactions of CASP1 DNA-injected skin were suppressed by treatment with neutralizing anti-murine IL-1beta antibodies, but the TUNEL positive apoptotic cells were still detected. This study clearly demonstrate dual roles of CASP1 in causing IL-1beta associated granulomatous skin infiltration and inducing apoptotic cell death in vivo.

Animals↗
PubMed1999

Factors affecting hearing results after stapes surgery.

Factors affecting auditory improvement after stapes surgery were investigated retrospectively on a study group of 106 otosclerotic ears (86 subjects). While the closure of the air-bone (A-B) gap after surgery was good at 2 kHz and 4 kHz, it was poor at 8 kHz and at frequencies lower than 1 kHz. Under 1 kHz, the lower the frequency, the worse the A-B gap after surgery. Stapedotomy and partial stapedectomy showed better post-operative hearing gain at 4 kHz than total stapedectomy. Total stapedectomy scored significantly better at 250 Hz and 500 Hz than stapedotomy. There was a close relationship between the pre-operative and post-operative A-B gap at frequencies under 1 kHz. The smaller the pre-operative A-B gap, the better the closure of the post-operative A-B gap at these frequencies. It was speculated that otosclerotic ears with a larger pre-operative airbone gap might have another lesion in the middle ear other than the oval window.

Adult↗