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Biomedical subjects

T Matsui

Publications and source records attributed to T Matsui.

At least 37 records · Page 2Linked to original sources
PubMed2005

A novel apparatus for non-contact measurement of heart rate variability: a system to prevent secondary exposure of medical personnel to toxic materials under biochemical hazard conditions, in monitoring sepsis or in predicting multiple organ dysfunction syndrome.

BACKGROUND: The impaired balance of the low-frequency/high-frequency ratio obtained from spectral components of RR intervals can be a diagnostic test for sepsis. In addition, it is known that a reduction of heart rate variability (HRV) is useful in identifying septic patients at risk of the development of multiple organ dysfunction syndrome (MODS). We have reported a non-contact method using a microwave radar to monitor the heart and respiratory rates of a healthy person placed inside an isolator or of experimental animals exposed to toxic materials. APPARATUS DESIGN AND TESTING: With the purpose of preventing secondary exposure of medical personnel to toxic materials under biochemical hazard conditions, we designed a novel apparatus for non-contact measurement of HRV using a 1215 MHz microwave radar, a high-pass filter, and a personal computer. The microwave radar monitors only the small reflected waves from the subject's chest wall, which are modulated by the cardiac and respiratory motion. The high-pass filter enhances the cardiac signal and attenuates the respiratory signal. In a human trial, RR intervals derived from the non-contact apparatus significantly correlated with those derived from ECG (r=0.98, P<0.0001). The non-contact apparatus showed a similar power spectrum of RR intervals to that of ECG. CONCLUSIONS: Our non-contact HRV measurement apparatus appears promising for future pre-hospital monitoring of septic patients or for predicting MODS patients, inside isolators or in the field for mass casualties under biochemical hazard circumstances.

Adult↗
PubMed2005

Dapsone suppresses human neutrophil superoxide production and elastase release in a calcium-dependent manner.

BACKGROUND: Dapsone (4,4'-diaminodiphenyl sulphone) is a powerful therapeutic tool in many skin diseases including neutrophilic dermatoses. The drug has an outstanding therapeutic efficacy against many skin diseases characterized by neutrophil-rich infiltrates; however, mechanisms of its action are poorly understood. OBJECTIVES: We investigated the effects of dapsone on respiratory and secretory functions of human neutrophils triggered by the chemotactic peptide N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP), the physiological agonist C5a, and phorbol myristate acetate (PMA). METHODS: Human neutrophils were isolated from venous blood obtained from healthy donors. We detected extracellular production of superoxide (O(2) (-)) by cytochrome C reduction assay, and intracellular production of O(2) (-) by flow cytometry. Neutrophil elastase release was measured by the cleavage of the specific elastase substrate N-methoxysuccinyl-Ala-Ala-Pro-Val-p-nitroanilide. Measurement of cytosolic free calcium concentration was performed using the calcium-reactive fluorescence probe, Fluo-3. RESULTS: Dapsone suppressed intra- and extracellular production of O(2) (-) and elastase release triggered by fMLP and C5a, but not by PMA. Both fMLP and C5a signalled the above pathways by inducing calcium influx, but PMA functions bypassed calcium influx. Dapsone was capable of antagonizing the induction of calcium influx. CONCLUSIONS: These findings suggest that one mechanism of the anti-inflammatory action of dapsone is inhibition of calcium-dependent functions of neutrophils including release of tissue-damaging oxidants and proteases in the affected skin.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2005

Acarbose, an alpha-glucosidase inhibitor, improves insulin resistance in fructose-fed rats.

Insulin resistance is one of the determinants of postprandial hyperglycemia. Acarbose is an alpha-glucosidase inhibitor that delays the absorption of carbohydrates from the small intestine, thereby suppressing postprandial hyperglycemia. Recently, acarbose has been found to reduce the incidence of cardiovascular disease (CVD) in patients with diabetes. These observations suggest that intervention of postprandial hyperglycemia with acarbose is a promising strategy for the prevention of CVD in diabetic patients. However, the effects of acarbose on insulin sensitivity are not fully understood. In this study, we examined whether oral administration of acarbose could improve insulin sensitivity in fructose-fed rats, a widely used insulin-resistant animal model. Although plasma glucose levels remained unchanged during the experiments, serum insulin levels were significantly increased in fructose-fed rats, which were suppressed by 4 weeks of treatment with acarbose. Acarbose treatment also increased high-density lipoprotein levels in fructose-fed rats. Furthermore, treatment of acarbose inhibited the elevation of systolic blood pressure levels in fructose-fed rats. These results indicate that oral administration of acarbose improves insulin sensitivity in fructose-fed rats. Our present study suggests that the cardioprotecive effects of acarbose could be ascribed, at least in part, to its insulin-sensitizing property.

Acarbose↗
PubMed2005

Azelnidipine, a dihydropyridine-based calcium antagonist, inhibits angiotensin II-induced oxidative stress generation and downregulation of pigment epithelium-derived factor mRNA levels in microvascular endothelial cells.

We have previously shown that azelnidipine, a long-acting dihydropyridine-based calcium antagonist (DHP), inhibited tumor necrosis factor-alpha-induced endothelial cell (EC) activation through its antioxidative properties. However whether azelnidipine could also block the angiotensin II (Ang II)-signaling in ECs remains to be elucidated. Since Ang II-type 1 receptor interaction could contribute to exacerbation of diabetic retinopathy by downregulating pigment epithelium-derived factor (PEDF) gene expression in ECs, we examined here whether azelnidipine inhibited the Ang II-induced reactive oxygen species (ROS) generation and subsequent PEDF gene suppression in microvascular ECs. Azelnidipine, but not nitrendipine, the other popular DHFP completely inhibited the Ang II-induced ROS generation in ECs. Furthermore, azelnidipine, but not nitrendipine, was found to partially restore decreased PEDF mRNA levels in Ang II-exposed ECs. The present study suggests that azelnidipine could inhibit the Ang II-induced decrease in PEDF mRNA levels in ECs through its antioxidative properties. Upregulation of PEDF by azelnidipine may become a therapeutic target for the treatment of diabetic retinopathy associated with hypertension.

Angiotensin II↗
PubMed2005

Inhibition by advanced glycation end products (AGEs) of pigment epithelium-derived factor (PEDF) gene expression in microvascular endothelial cells.

Pigment epithelium-derived factor (PEDF) is a natural extracellular component of the retina with neuronal differentiating activity. Recently, decreased levels of PEDF in the mammalian eye have been shown to participate in the pathogenesis of diabetic retinopathy In addition, advanced glycation end products (AGEs), senescent macroprotein derivatives that form at an accelerated rate under diabetes, have also been implicated in the development and progression of diabetic retinopathy. However the role of AGEs in decreased levels of PEDF in the eye remains to be elucidated. In this study, we examined the effects of AGEs on PEDF gene expression in microvascular endothelial cells (ECs). Various types of immunochemically distinct AGEs, which were prepared in vitro by incubating bovine serum albumin with glucose, glyceraldehyde or glycolaldehyde, significantly decreased endothelial mRNA levels of PEDF Furthermore, H2O2 dose-dependently suppressed PEDF gene expression in ECs. Our present results suggest that AGEs could down-regulate mRNA levels of PEDF in ECs, probably via oxidative stress generation. The deleterious effects of AGEs on diabetic retinopathy could be due, at least in part, to their PEDF-inhibitory properties.

Cells, Cultured↗
PubMed2005

Minodronate, a nitrogen-containing bisphosphonate, inhibits advanced glycation end product-induced vascular cell adhesion molecule-1 expression in endothelial cells by suppressing reactive oxygen species generation.

Advanced glycation end products (AGEs), the senescent macroprotein derivatives that form in increased amounts in diabetes, have been implicated in the pathogenesis of diabetic vascular complications. Indeed, AGEs elicit oxidative stress generation in vascular wall cells through an interaction with their receptor (RAGE), thus playing an important role in vascular inflammation and altered gene expression of growth factors and cytokines. We have previously shown that minodronate, a nitrogen-containing bisphosphonate, blocked the angiogenic signaling of vascular endothelial growth factor in ECs through its antioxidative properties. However, the effects of minodronate on AGE-exposed ECs remain to be elucidated. In this study, we investigated whether and how minodronate could inhibit AGE-induced reactive oxygen species (ROS) generation and subsequent vascular cell adhesion molecule-1 (VCAM-1) gene expression in human umbilical vein endothelial cells (HUVEC). Minodronate or an NADPH oxidase inhibitor, diphenylene iodonium, completely inhibited the AGE-induced ROS generation in HUVEC. Geranylgeranyl pyrophosphate reversed the antioxidative properties of minodronate in AGE-exposed ECs. Furthermore, minodronate was found to prevent AGE-induced nuclear factor--KB activation and subsequently suppress VCAM-1 gene expression in HUVEC. These results demonstrate that minodronate could inhibit VCAM- 1 expression in AGE-exposed ECs by suppressing NADPH oxidase-derived ROS generation, probably via inhibition of geranylgeranylation of Rac, a component of endothelial NADPH oxidase. Our present study suggests that minodronate may have a therapeutic potential in the treatment of patients with diabetic vascular complications.

Antioxidants↗
PubMed2005

Pigment epithelium-derived factor is a pericyte mitogen secreted by microvascular endothelial cells: possible participation of angiotensin II-elicited PEDF downregulation in diabetic retinopathy.

Pigment epithelium-derived factor (PEDF) is a natural extracellular component of the retina with neuronal differentiating activity. Decreased levels of PEDF in the mammalian eye have been shown to participate in proliferative diabetic retinopathy. In addition, we have recently found in in vitro experiments that PEDF protected against pericyte apoptosis, the earliest histopathological hallmark of diabetic retinopathy. These observations suggest that the loss of PEDF in the mammalian eye plays an important role in the development and progression of diabetic retinopathy. However, the functional role of endothelial cell (EC)-derived PEDF in pericyte survival and the regulation of PEDF gene expression remain to be elucidated. In this study, we examined the effects of anti-PEDF antibody (Ab) on the viable cell number of cocultured pericytes with microvascular ECs. We further studied the effects of angiotensin II (Ang II) on PEDF gene expression in ECs. Anti-PEDF Ab significantly inhibited the growth-stimulating effects of cocultured ECs on pericytes. Furthermore, Ang II significantly decreased PEDF mRNA levels in ECs, which was completely reversed by an Ang II type 1 receptor blocker, telmisartan. Our present results suggest that PEDF is an EC-derived mitogen or survival factor for retinal pericytes. Suppression by Ang II of the EC-derived PEDF may be involved in exacerbation of diabetic retinopathy in patients with hypertension.

Adult↗
PubMed2004

Whole-head SQUID system in a superconducting magnetic shield.

We have constructed a mobile whole-head SQUID system in a superconducting magnetic shield - a cylinder of high Tc superconductor BSCCO of 65 cm in diameter and 160 cm in length. We compared the noise spectra of several SQUID sensors of SNS Josephson junctions in the superconducting magnetic shield with those of the same SQUID sensors in a magnetically shielded room of Permalloy. The SQUID sensors in the superconducting magnetic shield are more than 100 times more sensitive than those in a magnetically shielded room of Permalloy below 1 Hz. We tested the whole-head SQUID system in the superconducting magnetic shield observing somatosensory signals evoked by stimulating the median nerve in the right wrist of patients by current pulses. We present data of 64 and 128 traces versus the common time axis for comparison. Most sensory responses of human brains phase out near 250 ms. However monotonic rhythms still remain even at longer latencies than 250 ms. The nodes of these rhythm are very narrow even at these longer latencies just indicating low noise characteristics of the SQUID system at low-frequencies. The current dipoles at the secondary somatosensory area SII are evoked at longer latencies than 250 ms contributing to a higher-level brain function. The SQUID system in a superconducting magnetic shield will also have advantages when it is used as a DC MEG to study very slow activities and function of the brain.

Electric Conductivity↗
PubMed2004

Brain-derived neurotrophic factor gene polymorphisms and Alzheimer's disease.

Several lines of evidence have made brain-derived neurotrophic factor (BDNF) an important candidate gene conferring risk for Alzheimer's disease (AD). Recently, three studies reported an association between two single-nucleotide polymorphisms (SNP)--i.e., C270T and G196A--in the BDNF gene and AD. This attempt to confirm these associations in a larger AD sample included examination of the linkage disequilibrium of these two SNPs. Comparison of 487 Japanese AD subjects with 471 cognitively normal elderly controls showed higher frequencies of the G allele (60.5 vs. 55.5%, p = 0.028) and of both the GG and GA genotypes (85.8 vs. 79.8%, p = 0.025) of the G196A polymorphism in AD subjects than in controls and higher frequency of the T allele of the C270T polymorphism in AD subjects who were negative for apolipotrotein E4 (2.0 vs. 4.4%, p = 0.035) or positive for AD family history (2.8 vs. 7.1%, p = 0.046). These findings suggest that BDNF gene polymorphisms play some role in the development of AD.

Aged↗
PubMed2004

Vertical transmission of Neospora caninum in BALB/c mice in both acute and chronic infection.

To examine the frequency of congenital infection by Neospora caninum, BALB/c mice were inoculated intraperitoneally with tachyzoites of N. caninum either during pregnancy (Group 1) or 4 weeks or more before pregnancy (Group 2). Further, the mice inoculated during pregnancy were bred at 4 weeks or more after delivery to form Group 3. Congenital transmission was observed in 76% of the neonates of the mice in Group 1 and in 50% of the neonates of the mice in Group 2. Interestingly, congenital transmission was observed in 86% of the neonates from Group 3. These results suggest that chronically-infected BALB/c mice efficiently transmit N. caninum infection to their offspring.

Animals↗
PubMed2004

Non-contact determination of vital sign alterations in hypovolaemic states induced by massive haemorrhage: an experimental attempt to monitor the condition of injured persons behind barriers or under disaster rubble.

To assess a non-contact method to determine the physical alteration of human subjects confined behind a barrier or under disaster rubble, an experimental, non-contact monitoring system was tested on rabbits in a hypovolaemic state. New Zealand male rabbits behind a barrier were subjected to hypovolaemic shock induced by the withdrawal of arterial blood (2ml per 100g body weight). The hypovolaemic state was determined by linear discriminant analysis using non-contact-derived variables: heart rate X1 and respiratory rate X2. Sixteen rabbits were equally divided between the hypovolaemic and control groups. To obtain the heart and respiratory rates simultaneously, the fast Fourier transform (FFT) was performed on the 1215MHz microwave radar analogue output. The linear discriminant function calculated by non-contact-derived variables was negative in the eight hypovolaemic rabbits and positive in the eight controls, so that the linear discriminant function could distinguish the hypovolaemic group from the control group. The Mahalanobis D-square (an index for classification accuracy) was 5908; the classification error rate corresponding to this value was small and negligible. The hypovolaemic rabbits developed metabolic acidosis (HCO3- 18.6+/-11.1 mmol l(-1) and pH 7.15+/-0.18 in arterial blood). The systolic blood pressure of the hypovolaemic group and the control was 56+/-4 and 83+/-6 mmHg, respectively (p < 0.01). The proposed method appears promising for applications to monitor the condition of human subjects behind barriers or under disaster rubble.

Acidosis↗
PubMed2004

Fluorescence detection of a new photosensitizer, PAD-S31, in tumour tissues and its use as a photodynamic treatment for skin tumours in dogs and a cat: a preliminary report.

We describe here the detection by fluorescence of a new photosensitizer, PAD-S31, in tumours in dogs and cats and the effect of photodynamic therapy (PDT) by using PAD-S31 for skin tumours in two dogs and one cat. PAD-S31 is a hydrophilic photosensitizer that has two peaks at absorption wavelengths 406 and 665 nm in distilled water. In a preliminary experiment in mice transplanted with SCCVII and colon 26, PAD-S31 was retained in tumour tissues rather than in other organs. The tumours resected from dogs and cats after intravenous administration of PAD-S31 at a dose of 15 mg/kg emitted strong red fluorescence under light illumination of 402 nm wavelength. Animals given PAD-S31 showed no cutaneous photosensitivity under room light illumination. Irradiation at laser light 670 nm wavelength (fluence rate 150 mW/cm2 and total light dosage 150 J/cm2) on cutaneous mast cell tumours in dogs ( n=2 ) and a cutaneous basal cell tumour in a cat induced complete remission. These results suggest PAD-S31 could be a promising photosensitizer for use in a small animal veterinary practice.

Animals↗
PubMed2004

Salmonella Enteritidis outbreak associated with a school-lunch dessert: cross-contamination and a long incubation period, Japan, 2001.

A Salmonella Enteritidis (SE) outbreak in Japan was investigated with an observational study, analytical epidemiology and bacteriological examination (including phage typing). The outbreak occurred among 96 schoolchildren, and was caused by SE phage type 1. The outbreak source was dessert buns served at a school lunch (RR 42.55, 95 % CI 5.93-305.11, P < 0.001). The buns were probably cross-contaminated from eggs from a factory with a history of SE-contaminated products. The incubation period was longer than usual (3-16 days, median 8 days). A low contaminating dose may account for the long incubation period and low attack rate. Outbreak detection was hampered by the absence of routine Salmonella surveillance in Japan. The investigation was complicated by concurrent illnesses from other SE phage types. It was successful, in part, because adequate food samples were available for microbiological testing.

Child↗
PubMed2004

Mild hypothermia inhibits IL-10 production in peripheral blood mononuclear cells.

BACKGROUND: Hypothermia is often associated with compromised host defenses and infections. Deterioration of immune functions related to hypothermia have been investigated, but the involvement of cytokines in host defense mechanisms and in infection remains unclear. Therefore, we determined whether mild hypothermia affects the production of several types of cytokines in peripheral blood mononuclear cells (PBMCs), and the balance between pro-inflammatory and anti-inflammatory states. METHODS: PBMCs obtained from 12 healthy humans were cultured with phytohemagglutinin (PHA) in normothermic (37 degrees C: control) or hypothermic (33 degrees C) conditions for 24 h. The production levels of tumor necrosis factor (TNF)-alpha, the interleukins (ILs) IL-6, IL-8 and IL-10, and interferon (IFN)-gamma in the culture supernatants were measured by means of enzyme-linked immunosorbent assay (ELISA). RESULTS: Under hypothermic conditions (33 degrees C), PHA-induced production of IL-10 and IFN-gamma in PBMCs was significantly lower, by 34% and 84%, respectively, when compared with controls, while production of TNF-alpha, IL-6 and IL-8 did not change. The magnitude of reduction of IL-10 in hypothermic conditions resulted in IL-10/pro-inflammatory cytokine ratios decreasing to approximately 30-45% of those of controls. CONCLUSIONS: The present study clearly demonstrates that mild hypothermia (33 degrees C) inhibits IL-10 and IFN-gamma production in cultured PBMCs. The profound inhibition of IL-10 and the pro-inflammatory reaction-dominated state induced suggests that the host defense mechanism against secondary infection may be maintained rather than inhibited in hypothermia. Thus, the reduction of IL-10 could be an important characteristic of immune responses in mild hypothermia.

Adult↗
PubMed2004

Vital role of the itch-scratch response in development of spontaneous dermatitis in NC/Nga mice.

BACKGROUND: The itch sensation and the resultant response, scratching, are important symptoms of atopic dermatitis (AD) and have a significant impact on the quality of life of affected patients. However, the influence of the itch-scratch response on the pathology of AD has not been precisely elucidated. OBJECTIVES: To investigate the role of scratching behaviour in the development of spontaneous dermatitis using conventionally raised NC/Nga mice (Conv-NC mice), which are known to be an animal model for human AD. METHODS: Capsaicin-sensitive sensory nerves of the mice were ablated by neonatal capsaicin treatment (Cap-NC mice), and the development of spontaneous dermatitis in the Cap-NC mice was compared chronologically with that in Conv-NC mice. RESULTS: Scratching behaviour was almost completely prevented in Cap-NC mice raised for 84 days under conventional conditions, and the development of dermatitis and elevation of the serum IgE level were significantly suppressed. Histological analysis revealed that the numbers of infiltrating eosinophils and mast cells in the lesional skin of Cap-NC mice were lower than those in Conv-NC mice. Immunological studies showed that the capability of spleen T cells to produce both T-helper (Th) 1 (interferon-gamma) and Th2 [interleukin (IL)-5 and IL-13] cytokines was diminished in Cap-NC mice. Furthermore, serum levels of IL-18 were approximately twice higher in Conv-NC mice than in Cap-NC mice. CONCLUSIONS: These observations suggest that scratching behaviour contributes to the development of dermatitis by enhancing various immunological responses in the murine AD model, implying that prevention of the itch sensation and/or itch-associated scratching behaviour is an effective treatment for AD.

Animals↗
PubMed2004

Non-specific multiple ulcers of the small intestine unrelated to non-steroidal anti-inflammatory drugs.

AIM: Non-steroidal anti-inflammatory drug (NSAID) enteropathy is a cause of chronic blood and protein loss from the intestine. The aim of this investigation was to compare NSAID enteropathy with enteropathy not related to chronic NSAID use. PATIENTS/METHODS: During the period 1967-97, 12 cases of non-specific small intestinal multiple ulcers were laparotomised because of chronic and persistent blood loss for a prolonged period. The clinical features before and after surgery, and the small intestinal lesions, were compared between NSAID users and non-users. RESULTS: Three patients were NSAID users and the other nine were not. Initial clinical manifestations, haemoglobin concentrations, serum protein values, and inflammatory reactions were similar in the two groups. In both groups there were multicentric stenoses in the small intestine. In those not using NSAIDs, the stenoses were accompanied by multiple, sharply demarcated small ulcers with minimal and non-specific chronic inflammatory infiltrates. The small intestinal ulcers in NSAID users showed linear and circumferential alignment. NSAID users were free from medication during the subsequent period of observation, whereas repeated laparotomy and medication were required in eight of the nine patients not using NSAIDs. CONCLUSION: There appears to be a chronic enteropathy, not related to the use of NSAIDs, in which non-specific multiple ulcers are found. This enteropathy may be a distinct entity that causes persistent blood and protein loss from the intestine.

Adult↗
PubMed2003

Vesicular transport route of horseradish C1a peroxidase is regulated by N- and C-terminal propeptides in tobacco cells.

Peroxidases (PRX, EC 1.11.1.7) are widely distributed across microorganisms, plants, and animals; and, in plants, they have been implicated in a variety of secondary metabolic reactions. In particular, horseradish (Armoracia rusticana) root represents the main source of commercial PRX production. The prxC1a gene, which encodes horseradish PRX (HRP) C, is expressed mainly in the roots and stems of the horseradish plant. HRP C1a protein is shown to be synthesized as a preprotein with both a N-terminal (NTPP) and a C-terminal propeptide (CTPP). These propeptides, which might be responsible for intracellular localization or secretion, are removed before or concomitant with production of the mature protein. We investigated the functional role of HRP C1a NTPP and CTPP in the determination of the vesicular transport route, using an analytical system of transgenically cultured tobacco cells (Nicotiana tabacum, BY2). Here, we report that NTPP and CTPP are necessary and sufficient for accurate localization of mature HRP C1a protein to vacuoles of the vesicular transport system. We also demonstrate that HRP C1a derived from a preprotein lacking CTPP is shunted into the secretory pathway.

Cells, Cultured↗