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Biomedical subjects

Akira Tamura

Publications and source records attributed to Akira Tamura.

53 records · Page 3Linked to original sources
PubMed2003

Distribution of two types of lymphocytes (intraepithelial and lamina-propria-associated) in the murine small intestine.

The intestine, which is exposed to nutrition and to food-derived antigens and microbes including viruses and bacteria, might be an important site for the immune response. Crucial structural and functional differences exist between the small and large intestine, regional differences even having been demonstrated within the small intestine. Accordingly, intraepithelial lymphocytes (IELs) and lamina propria lymphocytes (LPLs) might be heterogeneous among the different intestinal regions. The aim of this study has been to describe, as accurately as possible, the numbers and T-cell receptor (TCR) phenotypes of IELs and LPLs present in distinct regions of the murine small intestine under physiological conditions. Using an immunohistological technique to differentiate IELs from LPLs, the differential enumeration of IELs and LPLs in distinct regions of the murine small intestine, based upon their definition originally determined by their location, has been performed for the first time and has demonstrated that (1) there are more IELs than LPLs in the duodenum and jejunum, but more LPLs than IELs in the ileum, (2) in the duodenum and jejunum, TCRgammadelta IELs account for 70%-75% of the total CD3(+) IELs, a much greater percentage than previously reported, (3) the ratio of TCRgammadelta to TCRalphabeta IELs is inverted in the ileum, with more than 75% IELs being TCRalphabeta-positive, (4) the lamina propria forms one functional unit throughout the small intestine in terms of the TCR subset components (TCRalphabeta:TCRgammadelta=3:1), and (5) the ileum is entirely different from other regions of the small intestine. To deepen our understanding of the functional significance of the small intestine as an immunologically competent organ, the precise distributions of IELs and LPLs, the ratio of their various subsets, and the strict distinction of IELs and LPLs, as described in this study, is indispensable.

Animals↗
PubMed2003

Phylogenetic characterization of Orientia tsutsugamushi isolated in Taiwan according to the sequence homologies of 56-kDa type-specific antigen genes.

Fourteen strains of Orientia tsutsugamushi isolated in Taiwan were characterized by sequencing 56-kDa type-specific antigen genes and patterns of restriction fragment length polymorphism (RFLP) predicted by a computer program. The strains showed high varieties in sequence homologies and were classified to 10 types by predicted patterns of RFLP. Furthermore, all Taiwan strains were not identical in typing with strains analyzed previously. These results suggest that there are various types of O. tsutsugamushi in Taiwan that are different from those distributed in other countries.

Antigens, Bacterial↗
PubMed2003

Effect of mild hypothermia on focal cerebral ischemia. Review of experimental studies.

The purposes of this review are to clarify the effect of hypothermia therapy on focal cerebral ischemia in rats, and to consider the relevancy of its application to human focal cerebral ischemia. Since 1990, 26 reports confirming the brain-protecting effect of hypothermia in rat focal cerebral ischemia models have been published. Seventy-four experimental groups in these 26 reports were classified as having transient middle cerebral arterial occlusion (MCAO) with mild hypothermia (group A; 43 groups), permanent MCAO with mild hypothermia (group B; 14 groups), permanent MCAO with deep hypothermia (group C; 8 groups) and transient or permanent MCAO with mild hyperthermia (group D; 9 groups). The results were evaluated as the % infarct volume change caused by hypothermia or hyperthermia compared with the infarct volume in normothermic animals. The effectiveness was confirmed in 36 (83%) of the 43 groups in group A, 10 (71%) of the 14 in group B, and six (75%) of the eight in group C. The infarct volume of eight of the nine groups in group D was markedly aggravated. The percent infarct volume change was 55.3% +/- 27.1% in group A, 57.6% +/- 24.7% in group B, 60.8% +/- 45.5% in group C, and 189.7% +/- 89.4% in group D. For effective reduction of the infarct volume, hypothermia should be started during ischemia or within 1 h, at latest, after the beginning of reperfusion in the rat transient MCAO model. However, it is not clear whether this neuroprotective effect of hypothermia can also be observed in the chronic stage, such as several months later. Keeping the body temperature normothermic in order to avoid mild hyperthermia seems to be rather important for not aggravating cerebral infarction. Clinical randomized studies on the efficacy of mild hypothermia for focal cerebral ischemia and sophisticated mild hypothermia therapy techniques are mandatory.

Animals↗
PubMed2003

Relationship between heart rate variability and left ventricular remodeling after reperfused first anterior wall acute myocardial infarction.

The aim of the present study was to test the hypothesis that inadequate improvement in heart rate variability (HRV) in the healing stage of acute myocardial infarction (AMI) is associated with left ventricular (LV) remodeling. The study group comprised 20 patients (14 men, 6 women; mean age, 61+/-12 years) with a reperfused first anterior AMI (</=24 h). The standard deviation of normal RR intervals (SDNN) was calculated from the 24-h ambulatory electrocardiogram recorded on day 3 of admission and at predischarge from the hospital. Left ventriculography was performed immediately after primary angioplasty and at predischarge. The change in SDNN (deltaSDNN) was compared with the change in the LV end-systolic volume index (deltaLVESVI), a parameter of LV remodeling. SDNN increased from 73+/-19 ms on day 3 to 109+/-35 ms at predischarge (p=0.0003). SDNN at predicharge and deltaSDNN correlated negatively with deltaLVESVI (r=-0.52, p=0.02, and r=-0.61, p=0.004, respectively), whereas SDNN on day 3 did not correlate with deltaLVESVI. Multiple regression analysis selected deltaLVESVI (p=0.02) as an independent factor of deltaSDNN. This study indicates that deltaSDNN and SDNN at predicharge are associated with deltaLVESVI in patients with a reperfused first anterior wall AMI, indicating that persistently reduced HRV is associated with postinfarction LV remodeling.

Aged↗
PubMed2003

Osteopontin is released from the heart into the coronary circulation in patients with a previous anterior wall myocardial infarction.

The present study was designed to clarify whether osteopontin, an extracellular matrix protein, is released from the heart into the coronary circulation in patients with a previous (>3 months) anterior wall myocardial infarction (MI). Using a commercially available enzyme immunoassay kit, plasma concentrations of osteopontin were measured in 30 patients (26 men, 4 women; mean age, 61+/-12 years). Blood samples were obtained from the aortic root and coronary sinus. The difference in the plasma concentrations of osteopontin in the aortic root and coronary sinus, which reflects the cardiac production of osteopontin released into the coronary circulation, was compared with the left ventricular ejection fraction (LVEF) and volumes obtained from contrast left ventriculography. Plasma osteopontin concentrations were significantly higher in the coronary sinus than in the aortic root (672+/-446 vs 610+/-398 ng/ml, p=0.02). The transcardiac gradient of plasma osteopontin concentration correlated negatively with LVEF (r=-0.55, p=0.0005) and positively with left ventricular (LV) end-diastolic (r=0.63, p=0.0001) and end-systolic volume indexes (r=0.79, p<0.0001). This is the first study to show that in patients with a previous anterior wall MI osteopontin is released from the heart into the coronary circulation in proportion to the LV systolic function and volumes, suggesting that this extramatrix protein is associated with post-MI LV remodeling.

Aged↗
PubMed2003

Effects of atorvastatin and pravastatin on malondialdehyde-modified LDL in hypercholesterolemic patients.

The aim of the present study was to compare the effects of atorvastatin and pravastatin on lipid parameters and the concentration of malondialdehyde-modified low-density lipoprotein (MDA-LDL) in hypercholesterolemic patients. A total of 17 patients (10 men, 7 women; mean age, 68+/-9 years) who were indicated for drug therapy based on the National Cholesterol Education Program II underwent an 8-week regimen of atorvastatin (10 mg/day) or pravastatin (10 mg/day) with a 4-week washout period between drugs. After an overnight fast, lipid parameters and MDA-LDL concentration were measured before and after the 8-week treatment with each drug. Both atorvastatin and pravastatin produced significant reductions in low-density lipoprotein (LDL) cholesterol and MDA-LDL concentrations, with a significant increase in high-density lipoprotein cholesterol concentration. The percent reductions in LDL cholesterol and MDA-LDL concentration were significantly greater with atorvastatin than pravastatin (46 +/-6% vs 24+/-10%, p<0.0001, and 44+/-10% vs 14+/-13%, p<0.0001, respectively). The ratios of percent reductions in MDA-LDL concentrations and percent reductions in LDL cholesterol concentrations were significantly greater for atorvastatin than pravastatin (0.96+/-0.19 vs 0.59+/-0.55, p<0.0001). In conclusion, atorvastatin reduced serum concentrations of LDL cholesterol and MDA-LDL to a greater degree than pravastatin, indicating that atorvastatin not only has stronger lipid-lowering effects, but also stronger antioxidative effects than pravastatin.

Aged↗
PubMed2003

Natural hypothermia immediately after transient global cerebral ischemia induced by spontaneous subarachnoid hemorrhage.

OBJECT: Spontaneous subarachnoid hemorrhage (SAH) has an aspect of graded transient global cerebral ischemia. The purpose of the present study was the documentation of sequential changes in body temperature immediately after SAH-induced transient global cerebral ischemia in humans. METHODS: Patients admitted within 12 hours after the initial onset of SAH were examined retrospectively (426 patients). Patients with unruptured cerebral aneurysms served as a control group (73 patients). Body temperature measured at the axilla on admission was analyzed. The grade of SAH was established according to the Glasgow Coma Scale (GCS): Grade I, GCS Score 15; Grade II, GCS Score 11 to 14; Grade III, GCS Score 8 to 10; Grade IV, GCS Score 4 to 7; and Grade V, GCS Score 3. The mean body temperature of patients in the control group was 36.49 +/- 0.45 degrees C (mean +/- standard deviation). The mean body temperature of patients in the SAH group who had been admitted within 4 hours of onset for Grades I to V were significantly different (p < 0.001, analysis of variance [ANOVA]): 36.26 +/- 0.7 degrees C, 59 patients; 35.98 +/-0.85 degrees C, 73 patients; 35.52 +/- 0.79 degrees C, 25 patients; 35.9 +/- 1.09 degrees C, 108 patients; and 35.56 +/- 1.14 degrees C, 73 patients, respectively. These values were significantly lower than those in control volunteers, except for patients with Grade I SAH. The reduction in body temperature was unrelated to the location of the cerebral aneurysm and was not the product of circadian rhythm. The temperatures of patients in the SAH group who were admitted beyond 4 hours after onset for each grade were significantly different (p < 0.01, ANOVA): 36.8 +/- 0.91 degrees C, 36 patients; 36.74 +/- 0.68 degrees C, 31 patients; 36.73 +/- 0.38 degrees C, three patients; 37.41 +/- 1.37 degrees C, 17 patients; and 38.9 degrees C, one patient, respectively. These values were significantly higher than those in patients admitted within 4 hours of SAH onset for all grades except Grade V, and significantly higher than control values in patients with Grades I and IV SAH. CONCLUSIONS: These results indicate that body temperature falls and then rises immediately after the SAH-induced transient global cerebral ischemia without cardiac arrest in humans. The reduction in temperature may be a natural cerebral protection mechanism that is activated shortly after ischemic insult.

Adult↗
PubMed2003

In vitro reactivation of human immunodeficiency virus-1 upon stimulation with scrub typhus rickettsial infection.

While a number of microbial infections induce a transient burst in viral load in individuals infected with human immunodeficiency virus-1 (HIV-1), a recent study has suggested that scrub typhus may suppress HIV-1 infection. We investigated the effects of Orientia tsutsugamushi on HIV-1 infection. In vitro HIV-1 infection experiments were conducted using peripheral blood mononuclear cells (PBMC) acutely infected with R5 and X4 HIV-1 or PBMC derived from patients receiving highly active antiretroviral therapy (HAART) whose plasma viral load was undetectable. Stimulation of PBMC with O. tsutsugamushi induced production of proinflammatory cytokines and beta-chemokines, and markedly down-regulated expression of CCR5. Although pretreatment with O. tsutsugamushi rendered PBMC resistant to R5 HIV-1, it otherwise enhanced HIV-1 replication. Stimulation by O. tsutsugamushi induced HIV-1 replication in PBMC from patients receiving HAART. These findings suggest that scrub typhus does not necessarily suppress HIV-1 infection and does have potential to enhance HIV-1 replication.

Cytokines↗
PubMed2002

Regeneration of hippocampal pyramidal neurons after ischemic brain injury by recruitment of endogenous neural progenitors.

The adult brain is extremely vulnerable to various insults. The recent discovery of neural progenitors in adult mammals, however, raises the possibility of repairing damaged tissue by recruiting their latent regenerative potential. Here we show that activation of endogenous progenitors leads to massive regeneration of hippocampal pyramidal neurons after ischemic brain injury. Endogenous progenitors proliferate in response to ischemia and subsequently migrate into the hippocampus to regenerate new neurons. Intraventricular infusion of growth factors markedly augments these responses, thereby increasing the number of newborn neurons. Our studies suggest that regenerated neurons are integrated into the existing brain circuitry and contribute to ameliorating neurological deficits. These results expand the possibility of novel neuronal cell regeneration therapies for stroke and other neurological diseases.

Animals↗
PubMed2002

Ultrastructural and MRI study of the substantia nigra evolving exofocal post-ischemic neuronal death in the rat.

To clarify the morphological characteristics of exofocal post-ischemic neuronal death (EPND) in the substantia nigra (SN), we investigated the course of light- and electron-microscopic changes of the SN of rats subjected to occlusion of the left middle cerebral artery (MCA) for 1, 2, 4, 7 and 12 days. To assess cellular edema, sequential magnetic resonance (MR) mapping of the apparent diffusion coefficient (ADC) and the T2 value test was performed. Histological and electron-microscopic examination on day 1 showed dotted chromatin clumps in the nuclei of some neurons and mild swelling of the perivascular endfeet of astrocytes in the ipsilateral SN. On day 2, a few cells of the ipsilateral SN pars reticulata (SNr) revealed key morphological signs of apoptosis--apoptotic body-like condensation and segregation of the chromatin and DNA fragmentation-like nuclear remnants. On day 4, 38% of neurons became swollen (pale neurons) with cytoplasmic microvacuoles, which appeared to originate from rough endoplasmic reticulum (rER), mitochondria and Golgi apparatus. Twenty percent of neurons showed massive proliferation of the cisternae of the rER, some of which were fragmented or had lost their normal parallel arrangement. In addition, MR mapping revealed a transient ADC decrease with a T2 increase (signifying a phase of cellular edema), which coordinated with the phase of ultrastructural cellular swelling. Further, the total number of neurons started to decrease gradually, the perivascular endfeet of astrocytes were markedly swollen, and the neuropil became loose on day 4. On day 7, reactive astrocytes and dark neurons occurred most frequently. These results suggest that the EPND in the SN after occlusion of the MCA in adult rats is due to both apoptosis and necrosis, although necrosis seems to be the dominant mechanism of the EPND. However, the morphologic resemblances of EPND to delayed neuronal death suggest these processes have a common pathomechanism.

Animals↗
PubMed2002

Differences in the extent of primary ischemic damage between middle cerebral artery coagulation and intraluminal occlusion models.

The authors studied the differences between heat-shock/stress protein 70 (hsp70) gene expression and protein synthesis in the unilateral middle cerebral artery (MCA) microsurgical direct occlusion (Tamura's) model and the unilateral intraluminal occlusion model. In Tamura's model, expression of hsp70 mRNA and HSP70 protein and decreased protein synthesis were detected in the ischemic areas, including the ipsilateral cortex and caudate. These phenomena, however, were not observed in the areas outside the MCA territory, including the ipsilateral thalamus, hippocampus, and substantia nigra. These results were consistent among the experimental rats. In the intraluminal occlusion model, however, induction of both hsp70 mRNA and HSP70 protein and impairment of protein synthesis were noted in the areas outside the MCA territory, including the ipsilateral thalamus, hypothalamus, hippocampus, and substantia nigra, as well as in the MCA territory, including the ipsilateral cortex and caudate. These results were not consistent among the experimental rats. These different results might be due to widespread damage resulting from internal carotid artery (ICA) occlusion in the intraluminal occlusion model. Accordingly, the authors suggest that this model be called an ICA occlusion model, rather than a pure MCA occlusion model.

Animals↗
PubMed2002

Relation of Helicobacter pylori infection to plasma vitamin B12, folic acid, and homocysteine levels in patients who underwent diagnostic coronary arteriography.

OBJECTIVE: The aim of this study was to test the hypothesis that chronic atrophic gastritis induced by Helicobacter pylori (H. pylori) causes malabsorption of vitamin B12 and folate in food, leading ultimately to an increase in circulating homocysteine levels. METHODS: We performed endoscopy with stomach biopsy and measured fasting plasma homocysteine, vitamin B12, and folate levels in 93 patients who underwent diagnostic coronary arteriography. The patients were divided into two groups according to the presence (n = 57) or absence (n = 36) of H. pylori infection. Positive H. pylori infection was defined as positive H. pylori histology of biopsy specimens from the stomach. The extent of atrophic gastritis was endoscopically graded from 0 to 6. RESULTS: There were no differences in age, sex, or traditional coronary risk factors between the two groups. Atrophy scores of the stomach were greater in patients with H. pylori infection than in patients without (3.9 +/- 1.4 vs 2.2 +/- 1.8, p < 0.0001). Patients with H. pylori infection had lower levels of vitamin B12 (630 +/- 222 vs 747 +/- 259 pg/ml, p = 0.02) and folate (6.2 +/- 2.1 vs 7.4 +/- 2.8, p = 0.046), as well as higher levels of homocysteine (11 +/- 4.9 vs 8.3 +/- 2.1 nmol/ml, p = 0.01), than did patients without H. pylori infection. Plasma homocysteine levels correlated inversely with plasma vitamin B12 and folate levels and positively with atrophic scores. CONCLUSIONS: This study suggests that H. pylori-induced chronic atrophic gastritis decreases plasma vitamin B12 and folic acid levels, thereby increasing homocysteine levels. However, this effect does not seem to be strong.

Aged↗
PubMed2002

Effect of preinfarction angina on heart rate variability in the early phase of the first anterior wall acute myocardial infarction.

The aim of this study was to clarify the effect of preinfarction angina on heart rate variability (HRV) in anterior wall acute myocardial infarction (AMI). A total of 36 patients experiencing their first anterior wall AMI were prospectively examined. The patients were divided into 2 groups according to the presence (group A, n=24) or absence (group B, n = 12) of preinfarction angina. HRV was assessed on 24-h Holter electrocardiograms recorded on day 3. Peak creatine kinase activity was significantly lower in group A than in group B (2,747+/-1,939 vs 4,891+/-2,639 IU/L, p<0.05). The SD of all RR intervals and ultra-low frequency, very low frequency, and low frequency powers was significantly less reduced in group A than in group B (86+/-24 vs 64+/-22 ms, p<0.05; 2,098+/-1,462 vs 867+/-502 ms2, p<0.01; 1,430+/-1,042 vs 546+/-344ms2, p<0.01; and 354+/-272 vs 186+/-136ms2, p<0.05; respectively). High frequency power, low frequency/high frequency, and pNN50 did not differ significantly between the 2 groups. In conclusion, preinfarction angina has a favorable influence on HRV in the early phase of anterior wall AMI.

Aged↗
PubMed2002

[Body temperature in the super-acute phase of the cerebrovascular disorders: mainly focused on the subarachnoid hemorrhage].

BACKGROUNDS AND PURPOSE: Body temperature in the acute phase of cerebrovascular disorders(CVDs) may influence the outcome. However, the natural course of body temperature after CVDs has not yet been clarified. The purpose of this study was to elucidate the natural courses of body temperature after CVDs. PATIENTS AND METHODS: We retrospectively investigated 681 patients with CVDs(subarachnoid hemorrhage(SAH): 478, cerebral ischemia: 47, intracerebral hemorrhage(ICH): 156) who were admitted within 24 h after onset. The body temperature was measured with an electronic thermometer at the axilla on admission. The body temperatures of 73 patients with non-ruptured cerebral aneurysms on admission(admitted between 09:00 and 15:00) were used as normal control group. RESULTS: The body temperature in the control group was 36.49 +/- 0.45 degrees C. In comparison, the temperature in the SAH group was significantly lower(35.88 +/- 1.00 degrees C, n = 338, p < 0.001) when the patients were admitted within 4 h after onset, and significantly higher (36.80 +/- 0.85 degrees C, n = 140, p < 0.05) when they were admitted after 4 h and up to 24 h. There was a significant negative correlation between the severity of the SAH and body temperature within 4 h and a significant positive correlation beyond 4 h. Body temperature in the cerebral ishcemia group was significantly lower than in the control group(36.09 +/- 0.59 degrees C, n = 17, p < 0.05) when the patients were admitted within 2 h, but was close to that in the control group when they were admitted beyond 2 h and up to 24 h after onset (36.45 +/- 0.58 degrees C, n = 30). The falls of body temperature in the super-acute phase in the SAH and the cerebral ischemia groups were observed in patients admitted between 09:00 and 15:00. Although body temperature in the ICH group was slightly lower when the patients were admitted within 4 h and slightly higher when admitted beyond 4 h and up to 24 hours after onset, no significant differences were observed in comparison with the control group. In the super-acute phase of the cerebral ischemia and the ICH, body temperature tended to be lower in the patients with worse condition. CONCLUSION: This study clearly demonstrated that body temperatures in patients with CVDs changed rapidly within 24 h after onset. Body temperature in the SAH group within 4 h and that in the cerebral ischemia group within 2 h after onset was significantly lower than in the control group. These temperature falls were not the products of circadian rhythm. The temperature in the SAH group beyond 4 h and up to 24 h after onset rose significantly. Comparison with normal controls and consideration of the circadian rhythm are important when studying changes of body temperature in patients with CVDs.

Acute-Phase Reaction↗
PubMed2001

Akt protein kinase inhibits non-apoptotic programmed cell death induced by ceramide.

A growing body of evidence now suggests that programmed cell death (PCD) occurs via non-apoptotic mechanisms as well as by apoptosis. In contrast to apoptosis, however, the molecular mechanisms involved in the regulation of non-apoptotic PCD remain only poorly understood. Here we show that ceramide induces a non-apoptotic PCD with a necrotic-like morphology in human glioma cells. Characteristically, the cell death was not accompanied by loss of the mitochondrial transmembrane potential, cytosolic release of cytochrome c from mitochondria, or the activation of the caspase cascade. Consistent with these characteristics, this ceramide-induced cell death was inhibited neither by the overexpression of Bcl-xL nor by the pan-caspase inhibitor zVAD-fmk. However, strikingly, the ceramide-induced non-apoptotic cell death was inhibited by the activation of the Akt/protein kinase B pathway through the expression of a constitutively active version of Akt. The results for the first time indicate that the Akt kinase, known to play an essential role in survival factor-mediated inhibition of apoptotic cell death, is also involved in the regulation of non-apoptotic PCD.

Adenoviridae↗
PubMedDate not supplied

Factors associated with attitude and hypothetical behaviour regarding brain death and organ transplantation: comparison between medical and other university students.

The aim of this study was to investigate the factors, including knowledge, that determine an individual's attitudes and behaviours regarding brain death and organ transplantation using questionnaires among medical and other university students. A total of 522 students (388 medical and 134 other) answered a questionnaire. The survey included the individual's knowledge about brain death, attitudes towards brain death and organ transplantation, and hypothetical behaviours assuming their willingness to donate their own or their family's organs. Medical students were more likely to have knowledge about brain death and to accept brain death and organ transplantation compared with other students, while there was no difference in their willingness to donate their own or their family's organs. Logistic regression analysis was used to assess the effects of various factors on the attitudes and behaviours. In both medical and other students, confidence in brain-death diagnosis by doctors was independently associated with their willingness to donate their own organs after the adjustment for other factors, including knowledge (odds ratio [OR], 1.85; 95% confidence interval [CI], 1.15 to 2.97 and OR, 4.97; 95% CI, 1.01 to 24.39, respectively). An increase in knowledge may cause positive attitudes towards brain death and organ transplant. Meanwhile, reducing uncertainty about the brain-death diagnostic process might have a beneficial effect on the willingness to donate organs.

Adult↗