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Biomedical subjects

T Arai

Publications and source records attributed to T Arai.

At least 163 records · Page 9Linked to original sources
PubMed2000

Insertion/deletion polymorphism in the angiotensin-converting enzyme gene affects heart weight.

BACKGROUND: Angiotensin (Ang) II, a major regulatory factor for left ventricular mass, is generated from Ang I by ACE. ACE levels are associated with an insertion/deletion (I/D) polymorphism in the ACE gene. The ACE polymorphism should result in varied Ang II concentrations and hence affect left ventricular mass. We therefore investigated whether ACE genotype is a predictor of heart weight. METHODS AND RESULTS: From 693 consecutive patients autopsied between 1994 and 1998 in our hospital, patients with valvular disease, myocardial infarction, or cardiomyopathy were excluded. The remaining 443 autopsy patients were the subjects of our study. The heart weight at autopsy was corrected for body surface area. Genomic DNA was purified from the kidney, and ACE genotype was determined by polymerase chain reaction. Heart weight in the DD genotype (249. 9+/-49.9 g/m(2)) was significantly higher than that in the ID (230. 0+/-51.2 g/m(2); P<0.05) and II (226.8+/-49.8 g/m(2); P<0.01) genotypes. Heart weight was also positively related to age (r=0.145, P<0.0001) and coronary stenosis index (r=0.147, P=0.0019). Multiple regression analysis showed that a history of hypertension (P<0.0001), age (P=0.0001), and DD genotype (P=0.0154) were independent predictors of heart weight. CONCLUSIONS: ACE genotype predicts cardiac mass; however, it was less effective than epigenetic factors such as hypertension or age.

Aged↗
PubMed2000

Nd:YAG laser irradiation of the human dental pulp: implications as a predictor of pulp hemodynamics.

BACKGROUND AND OBJECTIVE: The aim of study this was to evaluate in vivo the pulpal blood flow rate, pulpal responsiveness, systemic blood pressure, and pulse rate during Nd:YAG laser irradiation of an isolated tooth. STUDY DESIGN/MATERIALS AND METHODS: Thirteen volunteers from the Tsurumi Dental University faculty participated in this study after giving their consent to the Nd:YAG laser irradiation test protocol. Gingivobuccal areas adjacent to mandibular canines were used for clinical evaluation. Each area was coated with India ink and treated with a Nd:YAG laser for 30 sec at 120-mJ pulses at 10 pulses/sec. Pulpal blood flow was measured by a laser Doppler flowmeter during Nd:YAG laser irradiation of the tooth. All pulp responses were measured by an electric pulp tester before and after Nd:YAG laser irradiation. In addition, the systemic blood pressure and pulse rate were monitored throughout the laser irradiation procedure. RESULTS: For all subjects involved in this study, the pulpal blood flow rate increased during laser irradiation. Threshold values of the electric pulp tests increased in six cases and decreased in six cases. One case showed no change. After 1 month, the threshold values for each subject had returned to previously recorded values. Neither systemic blood pressure nor pulse rate was affected during Nd:YAG laser irradiation. Pulpal blood flow was strongly influenced immediately after Nd:YAG laser irradiation, seen as an increase in the flow rate. CONCLUSION: The results of this study suggest that effects of the Nd:YAG laser irradiation are similar to those of low power laser for the improvement of local blood flow.

Adult↗
PubMed2000

Receptors and lipid transfer proteins in HDL metabolism.

It is believed that HDL exerts its anti-atherogenic effects through the process of delivering cholesterol from peripheral tissues back to the liver for removal from the body (i.e., reverse cholesterol transport). The metabolic life cycle of HDL lipid and apolipoproteins during reverse cholesterol transport involves both its modification in plasma by lipid transfer proteins and the clearance from plasma of HDL lipid and protein mediated by hepatic cell surface proteins. We review recent work from our laboratory that focuses on specific metabolic steps in reverse cholesterol transport and the results of altering these steps on plasma HDL levels and atherosclerosis. Recently, SR-BI was shown to be an authentic HDL receptor mediating the selective uptake of HDL lipids into cells without degradation of HDL proteins. We discuss the evidence for additional receptor activity mediating HDL protein catabolism in the liver from studies in obese (ob/ob) mice, which have markedly increased HDL due to a defect in hepatic catabolism of apoA-I and apoA-II. In addition, we review recent findings that phospholipid transfer protein deficiency in mice results in markedly reduced HDL levels. Lastly, we highlight our findings that overexpression of SR-BI in LDL receptor-deficient mice results in decreased atherosclerosis.

Animals↗
PubMed2000

Prostaglandin E1 improves hepatic encephalopathy produced by ischaemia-reperfusion liver injury in rats.

OBJECTIVE: To investigate the action of prostaglandin E1 on hepatic encephalopathy. DESIGN: Prospective, randomised, controlled animal study. SETTING: University animal laboratory. SUBJECTS: Male Wistar rats. INTERVENTIONS: After passive avoidance learning, acute liver failure was induced by occlusion of the left portal vein and the hepatic artery for 90 min. Then memory retention was evaluated 48 h later. The effects of prostaglandin E1 on memory retention were examined in animals treated with the agent systemically (intravenous injections with prostaglandin E1 twice before and after surgery, 20 microg/kg each time) and animals treated with the agent topically (intracerebroventricular injection with prostaglandin E1, 0.1 microg/h for 48 h beginning at liver ischaemia). MEASUREMENTS AND RESULTS: Marked damage was found on plasma analysis in animals subjected to liver ischaemia, and the memory retention was also impaired. Intravenous administration of prostaglandin E1 improved both the liver injury and memory retention. However, intracerebroventricular administration of prostaglandin E1 alleviated neither. CONCLUSION: These findings show that prostaglandin E1 contributes to the amelioration of hepatic encephalopathy by improving liver function.

Alprostadil↗
PubMed2000

Autologous blood transfusion in patients with hepatocellular carcinoma undergoing hepatectomy.

BACKGROUND: Homologous blood transfusion (HBT) has the risk of an immunosuppressive effect and may adversely affect the prognosis of patients with carcinomas. Autologous blood transfusion (ABT) has not yet become a standard procedure in gastroenteric cancer surgery. We investigated the usefulness and problems of ABT combined with the use of recombinant human erythropoietin (rh-EPO). METHODS: An evaluation of autologous blood transfusion (ABT) combined with recombinant human erythropoietin (rh-EPO) treatment was conducted in 46 patients with hepatocellular carcinoma undergoing hepatectomy. Preoperative autologous blood donation (ABD) was accomplished for 25 of the 46 patients. The preoperative changes in hemoglobin and hematocrit in relation to route of administration of erythropoietin were studied. In addition, intraoperative blood requirements and the postoperative complications for patients who predonated were compared with those of patients who underwent surgery without autologous predonation. RESULTS: The proportion of patients not requiring additional homologous blood transfusions (HBT) during operation was significantly higher in the ABD group than in the non-ABD group (88% versus 38%). The incidence of postoperative complications was significantly higher in patients receiving HBT than in nontransfused patients and in those receiving ABT. CONCLUSIONS: Preoperative autologous blood donation in combination with rh-EPO therapy markedly reduced the requirement for homologous blood transfusion during surgery in patients with hepatocellular carcinoma having hepatectomy.

Blood Transfusion, Autologous↗
PubMed2000

Particle size analysis of high density lipoproteins in patients with genetic cholesteryl ester transfer protein deficiency.

We investigated the detailed distribution of high-density lipoproteins (HDL) particle size in patients with cholesteryl ester transfer protein (CETP) deficiency. Serum samples pre-stained with Sudan black B were electrophoresed using 4-30% polyacrylamide gradient gels, and the Stokes diameter of HDL particles was determined in 23 patients with genetic CETP deficiency, nine patients with hyperalphalipoproteinemia and seven subjects with normal HDL cholesterol concentrations. The mean Stokes diameter of HDL particles in CETP deficient patients (11.2+/-0.6 nm) was significantly greater than hyperalphalipoproteinemia (10.7+/-0.3 nm, P<0.05) and normal subjects (9.5+/-0.4 nm, P<0.01). A significant relationship was found between mean HDL size and serum CETP mass concentrations (P<0.05). When the particle size of all detected HDL bands was investigated, extra-large HDL particles larger than 12 nm were found in 14 of the 23 patients with CETP deficiency, which were not found in any of the hyperalphalipoproteinemia patients or normal subjects. Serum low-density lipoproteins (LDL) cholesterol and total cholesterol concentrations were lower in CETP deficiencies with extra-large HDL particles than those in non-carriers (P<0.01). These results indicate that extra-large HDL may be an index to clarify the relationship between genetic CETP deficiency and atherosclerosis.

Adult↗
PubMed2000

Identification, characterization and cDNA cloning of two novel proteins secreted into the external space of the regenerating leg of Periplaneta americana.

We have isolated two proteins (Rap 60 and Rap 40) that were expressed specifically in regenerating legs of the American cockroach (Periplaneta americana). These proteins appear to be derived from a precursor protein with 443 amino acid residues termed regeneration-associated protein (RAP). Rap 60 and Rap 40 corresponded to Glu 223 to Ser 443 and Glu 223 to Glu 366 of RAP, respectively. Hence, Rap 40 is the N-terminal part of Rap 60. These proteins contained 13 repeats of a novel motif, [Glu/Asp-Glu/Asp-Val/Ala-Lys]. The gene encoding RAP was shown to be expressed during embryogenesis and by newly-formed epidermal cells of regenerating legs. Rap 60 and Rap 40 were secreted into the external space of regenerating leg saccules, where they accumulated, suggesting that they are components of extracellular matrix of regenerating leg saccules.

Amino Acid Sequence↗
PubMed2000

Changes in pulmonary histology and exfoliated bronchoalveolar cells induced by in vivo introduction of the tumor necrosis factor-alpha gene.

An inflammatory cytokine, tumor necrosis factor (TNF)-alpha, has been implicated in the pathogenesis of inflammatory lung diseases such as interstitial pneumonia (IP). To clarify the role of the inflammatory cytokine in the pathogenesis of lung inflammation, we introduced a murine TNF-alpha gene into murine lungs by the hemagglutinating virus of Japan (HVJ)-liposome method. Seven days after the TNF-alpha gene introduction resulted in marked cellular infiltration of alveoli, and mild histological change was observed 28 days after the gene introduction. Electron microscopic analysis revealed minimal deposition of collagen fibrils. Analysis of the BAL revealed that the total cell number was markedly increased 3 and 7 days after the gene introduction, and more than 90% of the cells were macrophages. The increase in the cell number was returned to below the normal level 28 days after the gene introduction. During the development of IP, TNF-alpha may regulate pathologic change of the pulmonary interstitium and alveolar cells.

Animals↗
PubMed2000

Fulminant hepatic failure in the elderly: a clinicopathological study of autopsy cases aged over 65 years.

The pathology of fulminant hepatic failure (FHF) in the elderly is little known because of its very low frequency. Thirteen autopsy cases, all above 65 years of age (mean +/- SD, 72 +/- 6 years), and 10 younger control cases, all below 40 years of age (30 +/- 7 years), were analyzed. The elderly group comprised 10 cases with subacute FHF and three cases with acute FHF, while the younger group comprised seven cases with subacute FHF and three cases with acute FHF. The most predominant pathological type in the elderly group was submassive hepatic necrosis (10 cases), followed by acute hepatitis with bridging hepatic necrosis (AH-BHN; two cases) and massive hepatic necrosis (one case). In two cases of submassive hepatic necrosis, hepatic regeneration seemed to be insufficient for the suggested history. The underlying diseases and terminal complications were significantly more frequent in the elderly group than in the younger group. In conclusion, the immune response in the elderly group is found to be strong enough to cause massive or submassive hepatic necrosis. However, impaired hepatic regeneration is occasionally observed in the elderly cases and AH-BHN is often lethal because of frequent underlying diseases and severe complications.

Acute Disease↗
PubMed2000

Anaesthetic management of children with congenital insensitivity to pain with anhidrosis.

Congenital insensitivity to pain with anhidrosis (CIPA) is a rare sensory neuropathy, which affects patients' pain sensation and thermoregulation. There are several issues to consider when planning anaesthesia for those with this congenital disorder. Over a 20-year period, six patients with CIPA underwent 20 surgical procedures under general anaesthesia in our institution. We analysed our experience with these patients retrospectively. We conclude that patients with CIPA are able to undergo surgical procedures under general anaesthesia without major problems.

Adolescent↗
PubMed2000

Bioartificial nerve graft for bridging extended nerve defects in rat sciatic nerve based on resorbable guiding filaments.

A long defect (15 mm) in rat sciatic nerve was repaired with a bioartificial nerve graft composed of a silicone tube and seven synthetic filaments of five types (polyamide, catgut, polydioxanone, and two types of polyglactin, normal and quickly-absorbed) inserted longitudinally into the tube. In all cases in which filaments were used a regenerating bridge was obtained in the tube after three months in contrast to empty silicone tubes, in which no structure was observed. There was a 6%-46% recovery of isometric muscle contractility of the anterior tibial and gastrocnemius muscles with positive pinch reflex test in most cases. Myelinated axons were seen in the regenerating tissue between the filaments but not directly in contact with them, and there were varying numbers of macrophages close to the filaments. Silicone tubes with filaments, regardless of type of filament, induced nerve tissue to regenerate and resulted in functional recovery through a 15 mm nerve gap not achieved with empty tubes. Nerve promoting factors may be applied to the filaments and the model is a valuable tool for further development of artificial nerve grafts.

Animals↗
PubMed2000

Construction of ELISA system to quantify human ST2 protein in sera of patients.

The human ST2 gene can be specifically induced by growth stimulation in fibroblastic cells, and can also be induced by antigen stimulation in Th2 cells. The gene encodes a soluble secreted protein, ST2, and a transmembrane protein, ST2L, which are closely related to the interleukin-1 receptor. To gain insight into the biological roles of the ST2 gene, three monoclonal antibodies (MAbs) against human ST2 gene products were obtained. To obtain these antibodies, immunization was carried out using two different immunogens: purified soluble human ST2 protein (hST2), and COS7 cells, which express the extracellular portion of human ST2L. 2A5 and FB9 MAbs were derived from the immunization with soluble hST2, and HB12 was derived from the COS7 cell immunization. All three antibodies were shown to detect native forms of the human ST2 gene products by immunoprecipitation, flow cytometry, and enzyme-linked immunosorbent assay (ELISA). In the competitive ELISA using biotinylated and nonlabelled MAbs, neither FB9 nor HB12 affected the binding of 2A5 to ST2 gene products. Based on this result, we constructed a sandwich ELISA system using 2A5 and FB9 to measure the concentration of soluble hST2 in sera. The ELISA, combined with the flow cytometry using these antibodies, will be a useful tool for elucidating the functions of human ST2 gene products in individuals.

Animals↗
PubMed2000

Telomere shortening with aging in human liver.

Progressive telomere shortening with aging was studied in the normal liver tissue of 94 human subjects aged between 0 and 101 years old to determine the rate of telomere loss in 1 year. Telomere length demonstrated accelerated shortening with reduction of 55 base pairs (bp) per year. The mean telomere length in five neonates was 12.9 +/- 2.6 kilobase pairs (kbp), and that in one centenarian was 8.3 kbp. Mean telomere lengths by age group were 13.2 +/- 2.0 kbp (< or = 8 years; 10 subjects), 7.8 +/- 1.9 kbp (40-79 years; 29 subjects), and 7.5 +/- 2.0 kbp (> or = 80 years; 53 subjects), with reduction thus appearing to show slowing on the attainment of middle age. The difference of mean telomere lengths for two groups with or without advanced malignancies of other than liver origin was not significant in the older two groups. Despite the slow turnover of liver tissue, the overall reduction rate of telomere length decrease in 1 year was almost the same as that of digestive tract mucosa, with its very rapid renewal.

Adolescent↗
PubMed2000

Aminoguanidine induces haematuria of non-glomerular origin in spontaneously hypertensive rats.

BACKGROUND: Administration of N(G)-nitro-L-arginine methyl ester (L-NAME), a non-selective inhibitor of nitric oxide synthase (NOS), induces glomerulosclerosis in spontaneously hypertensive rats (SHR). We investigated the effects of administering aminoguanidine (AG), a selective inhibitor of inducible NOS (iNOS), on glomerular histology, serum creatinine concentration, albuminuria and haematuria in SHR. METHODS: SHR and Wistar Kyoto rats (WKR) (age, 7 weeks) were given a daily water supply with or without 0.1% AG. Every 4 weeks, 24 h urine samples were collected and checked for haematuria by a dipstick method, and systolic blood pressure was measured. After 16 weeks, serum creatinine, albuminuria and glomerulosclerosis indices (GSI) were evaluated, and the size of urinary erythrocytes in AG-treated SHR was measured by flow cytometry. Glomeruli were observed by transmission and scanning electron microscopy. Some AG-treated SHR received a furosemide injection and then urinary erythrocyte size was determined. RESULTS: Systolic blood pressure, serum creatinine, albuminuria and GSI were similar between the untreated and AG-treated groups in both strains. However, AG treatment induced significant haematuria in SHR, but not in WKR. Electron microscopy did not provide any evidence for glomerular bleeding sites in AG-treated SHR. In urine with osmolalities exceeding 750 mOsm/kg, haematuria of AG-treated SHR consisted of erythrocytes smaller in size than venous erythrocytes. After furosemide injection leading to near isotonic urine, the size of urinary erythrocytes was similar to that of venous erythrocytes. CONCLUSIONS: The absence of morphological evidence for glomerular bleeding sites and similar intrinsic size between urinary and venous erythrocytes suggest that AG induces a non-glomerular type of haematuria in SHR.

Albuminuria↗
PubMed2000

Cell mediators of inflammation in the Alzheimer disease brain.

Lesions of Alzheimer disease are associated with low-grade but sustained inflammatory responses. Activated microglia agglomerate in the center of senile plaques. Reactive astrocytes marginate the amyloid beta-protein (A beta) deposits and extend their processes toward the center of plaques. Both microglia and astrocytes are known to secrete a wide variety of molecules involved in inflammation and are potential sources of proinflammatory elements in the brain. Dystrophic neurites occur in senile plaques with such glial reactions, suggesting the relevance of inflammatory responses to the neuronal degeneration in Alzheimer disease. Activated glial cells are, therefore, targets of anti-inflammatory therapy of Alzheimer disease. However, evidence also indicates that these cells eliminate A beta from the brain. A beta is produced continuously in both the normal and the AD brain. Under normal conditions, A beta is removed successfully before it accumulates as extracellular amyloid fibrils. Even in Alzheimer disease, a large portion of A beta may be cleared from the brain with a small portion being left and deposited as neurotoxic senile plaques. Both in vivo and in vitro studies showed the effective uptake of A beta by microglia. Before clinical application, it must be determined whether the treatment that suppresses glial activation and inflammatory responses inhibits A beta removal by glial cells.

Alzheimer Disease↗