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Biomedical subjects

T Kawamura

Publications and source records attributed to T Kawamura.

At least 325 records · Page 18Linked to original sources
PubMed1997

[The clinical course and laboratory data of hemorrhagic colitis caused by Escherichia coli O157:H7].

An outbreak of E. coli O157 infection occurred in July 1996 in Sakai City, apparently associated with school lunches. About 5000 children were infected and more than 600 were hospitalized. In our hospital, we treated 13 patients of hemorrhagic colitis(HC) including 4 hemolytic uremic syndrome(HUS) patients then. First, a typical patient developed HUS was presented. A case was 8 years' old girl. She was developed HUS on the 6th day after the onset of HC. We treated her with plasma exchange. She was recovered on the 14th day from HUS without any sequela. In this report, I discussed about pathophysiology of HUS according to her clinical course. Secondly, I reported that analysis of the clinical courses and laboratory data of 818 patients hospitalized from the questionnaires sent by Osaka Prefecture Medical Association. One One hundred twenty two patients developed HUS. Patients with HUS produced bloody stools longer than the others, on the average(6.7 vs. 3.4 day). Mean serum C-reactive protein levels was 4.8mg/dl in patients with HUS but 1.5mg/dl in the other patients; the WBC count also was higher in HUS(17,780 vs. 9,700mm3). The mean serum Na level was lower in patients of HUS. Almost all patients were given antibiotics. The incidence of HUS among patients treated with new quinolones was lower than that of all patients. On the contrary, the higher incidence among patients with cephalosporins was observed.

Adolescent↗
PubMed1997

Massive uncomplicated vascular immune complex deposits in the kidney of a patient with systemic lupus erythematosus.

The case of a patient with systemic lupus erythematosus (SLE) is reported which was accompanied by renal dysfunction and massive vascular immune deposits in the kidney without active glomerular lesions. The renal biopsy showed arterioles and small arteries with circumferential periodic acid-Schiff (PAS) and Masson trichrome-positive homogenous material in the subendothelial area in the absence of thrombotic, necrotizing or inflammatory lesions. Immunofluorescence and electron microscopy examination demonstrated immune deposits in the vascular walls. Glomeruli showed only minor abnormalities with a trend to collapse. There was no improvement in renal dysfunction over a 4-year period until the patient's death, despite steroid therapy producing a decrease in disease activity. The autopsy showed similar vascular changes to those seen in the biopsy, however; glomeruli were either sclerotic or showed a trend to collapse. Massive uncomplicated vascular immune complex deposition without active glomerular lesions is rare. The present case indicates that this type of lupus vasculopathy may be a prognostic factor for the loss of renal function in SLE mediated by hemodynamic glomerular injury.

Aged↗
PubMed1997

[Clinical evaluation of nitrite test for the detection of bacteriuria].

A nitrite test for bacteriuria was compared with routine microscopic examination in 1,318 clinical urine specimens and with bacterial culture in 132. Sensitivity, specificity, positive predictive value and accuracy rate are as follows; for diagnosis of bacteriuria more than 10(4) CFU/ml, 53.4%, 88.6%, 90.4 and 65.2%, respectively; for more than 10(5) CFU/ml, 55.4%, 87.8%, 88.4% and 67.2%, respectively. The positive rate for the nitrite test was 21.4% for bacteriuria of > or = 10(4) CFU/ml in gram positive cocci and 56.9% in gram negative rods. False negative results were obtained from gram positive cocci without nitrate reductive activity or from patients with acute uncomplicated cystitis because of insufficient incubation time in urinary tract. However, this simple test is valuable in the detection of bacteriuria in clinical practice with high specificity.

Bacteria↗
PubMed1997

[A clinical study of 5 cases of acute eosinophilic pneumonia--the relationship between beginning to smoke and acute eosinophilic pneumonia].

We encountered 5 cases of acute eosinophilic pneumonia. All cases were young men who had recently begun smoking, and they showed an acute onset hypoxemia, diffuse shadows on chest X-ray, an elevation of eosinophils in the peripheral blood and broncho-alveolar lavage fluid, and rapid recovery. One of the 5 cases showed a re-elevation of eosinophils in the peripheral blood and broncho-alveolar lavage fluid after a smoking challenge test. It appears that one of the causes of acute eosinophilic pneumonia is beginning to smoke.

Acute Disease↗
PubMed1996

Mechanism of resistance to NO-induced neurotoxicity in cultured rat dopaminergic neurons.

We previously reported that mesencephalic dopaminergic neurons are resistant to cytotoxicity induced by nitric oxide (NO). This study investigated the intracellular mechanism that protects dopaminergic neurons against NO toxicity in rat mesencephalic cultures. Peroxynitrite anion, an active metabolite of NO, caused significant cytotoxic effects against dopaminergic and nondopaminergic neurons, but NO caused cytotoxic effects restricted to nondopaminergic neurons. In addition, we studied the effects of ascorbate, an anti-oxidant, on NO-induced neurotoxicity against dopaminergic neurons and found that coadministration of ascorbate failed to affect resistance against NO-induced neurotoxicity. These findings suggest that the protecting mechanism from NO neurotoxicity in dopaminergic neurons is based on inhibition of conversion of NO to peroxynitrite anion, is independent of the NO redox state, and is possibly due to suppression of superoxide anion production. Furthermore, we investigated NO-induced neurotoxicity with or without pretreatment with sublethal doses of methylphenylpyridium ion (MPP+). Following pretreatment with 1 microM MPP+, which did not show significant cytotoxic effects against dopaminergic neurons, NO demonstrated significant cytotoxicity. Therefore, MPP+ may inhibit the protecting systems from NO neurotoxicity in dopaminergic neurons.

1-Methyl-4-phenylpyridinium↗
PubMed1996

Activation by estrogen of the number and function of forbidden T-cell clones in intermediate T-cell receptor cells.

When estrogen (1 mg/mouse) was subcutaneously administered once into mice, the number of liver MNC increased but the number of thymocytes decreased profoundly from Day 3 to Day 20. Phenotypic characterization revealed that the proportion of intermediate (int) TCR cells with IL-2 receptor beta-chain (IL-2R beta) was elevated in both the liver and the thymus. Attention was then focused on how forbidden clones were distributed among various T-cell subsets, including IL-2R beta+ int TCR cells and IL-2R beta-high TCR cells. IL-2R beta+ int TCR cells are generated through the extrathymic pathway in the liver and an alternative intrathymic pathway, whereas IL-2R beta- high TCR cells are generated through the mainstream of T-cell differentiation in the thymus. It was demonstrated that forbidden clones, V beta 3+ and V beta 11+ cells, in BALB/C mice (Mls-1b2a) were confined to IL-2R beta+ int TCR cells, irrespective of the administration of estrogen. Interestingly, the proportion of forbidden clones among int TCR cells increased in the liver but decreased in the thymus after the administration of estrogen. Liver MNC that contained a high level of forbidden clones showed unexpected high levels of spontaneous proliferation and of the proliferative response to immobilized anti-V beta mAb (even in the combination of forbidden clone stimulations). The present results reveal that the levels of both int TCR cells and forbidden clones that induce hepatocyte damage preferentially increase in the liver, one of the prime target organs in autoimmune diseases, when estrogen is administered.

Animals↗
PubMed1996

Newly developed ST-T abnormalities on the electrocardiogram and chronologic changes in cardiovascular risk factors.

An ST-T abnormality on an electrocardiogram (ECG) is known to independently predict subsequent morbidity and mortality from cardiovascular diseases. But how ST-T abnormality develops in relation to chronologic changes in cardiovascular risk factors has not been fully discussed. Sixty-eight men whose ECG had been initially normal but who exhibited ST-T abnormality later (ST-T subjects) were identified among 21,579 apparently healthy adults who had undergone comprehensive health examinations for > 10 years. Echocardiography proved that 26 of 29 examinees among ST-T subjects had left ventricular hypertrophy. Antihypertensive drugs were given to 26 of the ST-T subjects. Their cardiovascular risk factors were chronologically reviewed from 10 years before the onset of definite ST-T abnormality, and were compared with those of 68 men whose ECG had remained consistently normal for 10 years (controls). Mean values of systolic and diastolic blood pressure gradually increased over 10 years (from 127/78 to 144/84 mm Hg) among ST-T subjects, but showed little change (from 122/76 to 124/77 mm Hg) during the same period in controls. The time course of blood pressure over 10 years was similar in ST-T subjects, irrespective of final blood pressure level. Mean serum cholesterol and glucose increased over 10 years in both ST-T and control subjects. Uric acid decreased over 10 years (from 6.1 to 5.6 mg/dl) only in ST-T subjects. Multivariate analysis revealed that blood pressure and uric acid before onset of ST-T abnormality were chronologically changed independent of other risk factors. The time course of risk factors may be of great importance in the development of cardiovascular disorders.

Blood Pressure↗
PubMed1996

Acceleration of proliferative activity of esophageal squamous cell carcinoma with invasion beyond the mucosa: immunohistochemical analysis of Ki-67 and p53 antigen in relation to histopathologic findings.

BACKGROUND: The authors observed patients with superficial esophageal squamous cell carcinoma (s-ESC). Those with cancer invasion beyond the muscularis mucosae (SM-carcinoma) had an extremely poor prognosis, compared with those with intramucosal carcinoma (M-carcinoma). Therefore, we surveyed cell proliferative activities in relation to pathologic findings of the s-ESC. METHODS: p53 protein expression and Ki-67 labeling index (LI) were surveyed with detailed pathologic examinations of 75 s-ESC lesions from 70 patients who underwent esophagectomy. The results were compared by statistical analysis using the chi-square test and unpaired Student's t-test. RESULTS: p53 protein expression was observed in 57.3% of the patients with s-ESC. The frequency and intensity of its accumulation correlated with the depth of cancer invasion and was markedly elevated in invasion beyond the muscularis mucosae. The LI of Ki-67 positive nuclei was also increased with cancer invasion. The values in the intraepithelial carcinoma and in carcinoma with invasion to the muscularis mucosae were 48.5 +/- 13.7% [mean +/- standard deviation (SD)] and 66.6 +/- 12.9%, respectively, and the difference is significant, P < 0.01. In the SM-carcinomas, the LIs of Ki-67, with or without lymph node metastasis, were 73.5 +/- 10.0% and 64.4 +/- 11.3%, respectively, and the former was higher than the latter with a significant difference, P < 0.05. CONCLUSIONS: Cancer cell proliferative activities were markedly accelerated in s-ESC cases with cancer invasion beyond the muscularis mucosae and lymph nodal involvement, which was associated with a poorer prognosis of the SM-carcinoma compared with the M-carcinoma, and must be one of the important indices to decide the indication of local resection for s-ESC.

Aged↗
PubMed1996

Different mechanisms of glutamate-induced neuronal death between dopaminergic and non-dopaminergic neurons in rat mesencephalic culture.

Parkinson's disease is characterized by dopaminergic neuronal degeneration, but its pathogenic mechanism is still unknown. In the dopaminergic neurons, oxygen radicals such as hydrogen peroxide are released through dopamine oxidation. Many factors are involved in radical formation, but glutamate and nitric oxide (NO) are the major effectors of the radical-induced neurotoxicity mediated primarily through calcium influx. In the cultured embryonic rat mesencephalon, we investigated the dopaminergic and non-dopaminergic neuronal death induced by glutamate and by NO-generating agents. Although glutamate had a neurotoxic effect on both dopaminergic and non-dopaminergic neurons, it showed slightly greater effect in the dopaminergic neurons. In contrast to glutamate, NO-generating agents (S-nitrosocysteine and sodium nitroprusside) showed neurotoxic effects restricted exclusively to non-dopaminergic neurons. Although N omega-nitro-L-arginine, and NO synthase inhibitor, had no significant effect on the glutamate-induced cytotoxicity in dopaminergic neurons, it had a significant antagonistic effect on that in non-dopaminergic neurons. These findings indicate the presence of two different mechanisms of glutamate-induced neuronal death, one being neurotoxicity not mediated by NO, found in dopaminergic neurons, and the other being that mediated via NO, found in non-dopaminergic neurons.

Analysis of Variance↗
PubMed1996

Methylphenylpyridium ion (MPP+) enhances glutamate-induced cytotoxicity against dopaminergic neurons in cultured rat mesencephalon.

Parkinson's disease is characterized by chronic progression of dopaminergic neuronal death, the mechanism of which is still unknown. Although methyl-4-phenylpyridium ion (MPP+) or MPP(+)-like substance, that can reduce mitochondrial complex I activity, is supposed to be a causative agent for Parkinson's disease, it is difficult to explain the chronic neuronal degeneration for years. It is important to identify other putative agents capable of causing chronic cell death besides MPP+. We hypothesized that treatment with small doses of MPP+, not causing severe damage to dopaminergic neurons but merely reducing the activity of mitochondrial complex I, can be a model of Parkinson's disease, and that glutamate can be a putative agent causing chronic neuronal degeneration. Using primary culture of the rat mesencephalon, we investigated glutamate-induced cytotoxicity against dopaminergic and non-dopaminergic neurons with or without the pretreatment with MPP+. Brief exposure to glutamate showed similar cytotoxicity against both dopaminergic and non-dopaminergic neurons. An N-methyl-D-aspartate receptor antagonist completely blocked the glutamate-induced cytotoxicity against both dopaminergic and non-dopaminergic neurons. In the dopaminergic neurons, MPP+ caused cytotoxicity that was not blocked by co-administration of MK-801. After pretreatment with small doses of MPP+, sub-lethal doses of glutamate caused severe cell damage restricted to dopaminergic neurons, suggesting that MPP+ potentiates the glutamate-induced cytotoxicity only against dopaminergic neurons. As glutamate is putatively capable of causing cytotoxicity against dopaminergic neurons, the present findings might be important in considering the pathogenesis of dopaminergic neuronal degeneration and a possible therapeutic application of glutamate receptor antagonists in Parkinson's disease.

1-Methyl-4-phenylpyridinium↗
PubMed1996

Effects of long-term enalapril treatment on persistent microalbuminuria in normotensive type 2 diabetic patients: results of a 4-year, prospective, randomized study.

The beneficial effect of long-term treatment with an angiotensin-converting enzyme (ACE) inhibitor on urinary microalbumin excretion (UAE) and renal function was investigated in a 4 year, randomized prospective study in normotensive patients with non-insulin-dependent (Type 2) diabetes mellitus. Sixty-two normotensive patients with Type 2 diabetes mellitus and microalbuminuria but normal renal function were randomized to receive either enalapril 5 mg day-1 or no treatment. In the enalapril-treated patients, UAE was reduced from 115.4 +/- 80.1 to 95.6 +/- 61.7 mg 24 h-1 after 12 months (p < 0.05) and to 75.3 +/- 44.8 mg 24 h-1 after 48 months (p < 0.001). In the untreated group, UAE increased slowly from 93.9 +/- 69.9 to 150.0 +/- 144.5 mg 24 h-1 after 48 months. No changes in creatinine clearance, blood pressure or HbA1C were seen in either group during the 4-year period. In normotensive Type 2 diabetic patients with early stage of diabetic microalbuminuria. This effect is long-lasting and probably independent of the antihypertensive action of the drug.

Aged↗
PubMed1996

Restricted appearance of self-reactive clones into T cell receptor intermediate cells in neonatally thymectomized mice with autoimmune disease.

Neonatally thymectomized (NTx) mice fall victim to such autoimmune diseases as gastritis and pancreatitis with aging. Self-reactive T cell clones are known to be consistently generated through TCR intermediate (i.e. TCRint) cell differentiation in normal mice (i.e. via the extrathymic pathways and an alternative intrathymic pathway). It was investigated whether the generation of such clones in NTx mice follows this rule or whether they are generated by default via mainstream T cell differentiation in the thymus. The majority of T cells generated in NTx mice were TCRint cells in all organs tested. In contrast to athymic mice, which carry only TCRint cells with aging, a leaky appearance of high TCR (i.e. TCRhi) cells emerged in the lymph nodes and other organs of NTx mice. Self-reactive clones estimated by anti-Vbeta monoclonal antibodies in conjunction with the Mls system were confined to TCRint cells in all tested organs, including a target organ, the stomach, in NTx mice. A leaky population of TCRhi cells did not contain a significant number of self-reactive clones. Moreover, such self-reactive clones among TCRint cells in NTx mice with autoimmune disease were shown to be nonanergic in the proliferation assay. The present results suggest that the generation of self-reactive clones is totally due to TCRint cell differentiation, although it is still undetermined whether the expanding TCRint cell population is generated via the extrathymic pathway or an alternative intrathymic pathway. It is shown here not to be due to a failure of the TCRhi cell-differentiation pathway in NTx mice.

Animals↗
PubMed1996

Prognostic relevance of urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitors PAI-1 and PAI-2 in gastric cancer.

Expression of urokinase-type plasminogen activator (uPA), plasminogen activator inhibitor-1 (PAI-1) and plasminogen activator inhibitor-2 (PAI-2) was evaluated in 125 surgically resected gastric cancers by immunohistochemical analysis. Tissue was stained immunohistochemically with a monoclonal antibody against human uPA and monoclonal antibodies against human PAI-1 and PAI-2. In addition, DNA ploidy patterns were determined by cytofluorometer after staining with propidium iodide. We found that 82 (66%) of the 125 gastric cancers expressed uPA as diffuse cytoplasmic staining, as intensely outlined luminal borders. PAI-1 expression was observed in 62 (50%) of 125 gastric cancer as a fine, diffuse and granular pattern in the cytoplasm. PAI-2 expression was observed in 65 (52%) of the 125 gastric cancers as a diffuse cytoplasmic staining. uPA-positive tumours showed a higher incidence of infiltration, lymph node metastasis and peritoneal dissemination that uPA-negative ones. Patients with uPA-positive tumours proved to have a significantly poorer prognosis than those with negative ones. PAI-1-negative tumours showed a higher incidence of liver metastasis and carried a poorer prognosis than PAI-1-positive ones. There was no significant correlation between uPA or PAI-1 expression and DNA ploidy patterns. Conversely, there was no significant relationship between PAI-2 expression and clinicopathological parameters and prognosis. According to the expression of uPA and PAI-1 status, groups of 19 uPA(-)/PAI-1(-), 44 uPA(+)/PAI-1(-), 23 uPA(-)/PAI-1(+) and 39 uPA(+)/PAI-1(+) were subdivided. Tumours with uPA(+)/PAI-1(-) had a significantly higher incidence of liver metastasis, lymph node metastasis and serosal invasion than the other groups of tumours. Patients with uPA(+)/PAI-1(-) tumours had a significantly poorer prognosis than those with uPA(-)/PAI-1(+) tumours. These results indicate that uPA expression is a useful biological prognostic indicator, and that uPA expression is a useful biological prognostic indicator, and that uPA and PAI-1 may play an important part in the tumour progression and metastasis in gastric cancer.

Adult↗
PubMed1996

Interference of free fatty acids from the hepatopancreas of mussels with the mouse bioassay for shellfish toxins.

Determination of free fatty acids (FFA) in hepatopancreas of mussel, Mytilus coruscus, contaminated by diarrhetic shellfish poisoning (DSP) toxins, was carried out by high-performance liquid chromatography-fluorometry as their 9-anthryldiazomethane derivatives. The FFA in the hepatopancreas of mussels during May 30-June 14 were 443-666 micrograms/g. A marked increase in FFA content was observed on June 20 (2197 micrograms/g hepatopancreas) and June 27 (6322 micrograms/g hepatopancreas). The proportion of polyunsaturated fatty acids (PUFA), including 20:4n-6, 20:5n-3, and 22:6n-3, in mussel FFA increased during the experimental period. Diatoms almost completely dominated the phytoplankton community at the experimental site, suggesting that diatoms were the origin of the PUFA accumulated in mussels. The toxicity of FFA in mussel hepatopancreas on June 27 was sufficiently high as to interfere with the mouse bioassay by injection of an extract of shellfish, the official method for DSP toxin analysis.

Animals↗
PubMed1996

Ulinastatin reduces elevation of cytokines and soluble adhesion molecules during cardiac surgery.

PURPOSE: To investigate whether ulinastatin pretreatment (6000 U.kg-1 before CPB and before declamping of aorta) influenced the production of cytokines and adhesion molecules in the peripheral circulation. METHODS: This prospective randomized study was performed in 22 patients undergoing cardiac surgery. They were divided into two groups. Patients in Group I were untreated and in Group II treated with ulinastatin. The soluble intercellular adhesion molecule-1 (S-ICAM-1), soluble endothelial leukocyte adhesion molecule-1 (S-ELAM-1), interleukin 8 and 6 (IL- 8, 6) were measured using ELISA kits. RESULTS: Serum S-ICAM-1 concentration in Group I increased from the preoperative value of 297 +/- 27 ng.kg-1 to 418 +/- 106 ng.kg-1 at 60 min after declamping of the aorta (P < 0.01) but did not change in Group II. Serum S-ELAM-1 concentration did not change in either group. Serum concentration of IL-8 and IL-6 in Group I (37 +/- 44 pg.kg-1, and 59 +/- 59 pg.kg-1, preoperatively) increased to 169 +/- 86 pg.kg-1 and 436 +/- 143 pg.kg-1 at 60 min after declamping of the aorta (P < 0.001, P < 0.001). The increases were greater than those from 25 +/- 6 pg.kg-1 and 30 +/- 26 pg.kg-1 to 56 +/- 36 pg.kg-1 and 132 +/- 78 pg.kg-1 in Group II (P < 0.001, P < 0.001). The levels of S-ICAM-1 correlated with those of IL-8 (r = 0.5, P < 0.001). CONCLUSION: These results suggest that ulinastatin may suppress the increase in IL-8 production and the expression of ICAM-1 during cardiac surgery.

Adult↗
PubMed1996

Angiotensin converting enzyme gene polymorphism and renal artery resistance in patients with insulin dependent diabetes mellitus.

The present study was carried out to elucidate whether renal hemodynamic changes are associated with angiotensin converting enzyme (ACE) gene polymorphism in patients with insulin dependent diabetes mellitus (IDDM). We studied 32 Japanese patients with IDDM (aged 15 +/- 3 years in mean +/- SD) without renal failure or retinopathy. Renal hemodynamics were examined by duplex Doppler sonography and arterial resistance index was calculated. ACE genotypes were determined by polymerase chain reaction amplification. Resistance index (RI) of arcuate arteries in IDDM patients with DD genotype was significantly elevated, being 0.64 +/- 0.04, 0.66 +/- 0.05, and 0.71 +/- 0.05 for II, ID and DD genotype groups, respectively (II vs. DD, p < 0.02). In patients with DD genotype with normoalbuminuria (n = 27), it was also significantly elevated in DD genotype patients (II vs. DD, p < 0.02). In addition, multiple regression analysis with a forward elimination procedure showed that only the ACE genotype was associated with RI of arcuate arteries (R2 = 0.24, p < 0.01) among the parameters of sex, age, IDDM duration, body mass index, HbA1c, plasma glucose levels, serum levels of total cholesterol and creatinine, urinary albumin excretion index, mean blood pressure and ACE genotype. The present study demonstrated that renal arterial resistance is elevated in IDDM patients with DD genotype. ACE gene polymorphism which could be linked to intrarenal circulatory disturbance may be associated with the initiation and progression of diabetic nephropathy.

Adolescent↗
PubMed1996

Neuromagnetic evidence of pre- and post-central cortical sources of somatosensory evoked responses.

Somatosensory evoked magnetic fields (SEFs), corresponding with electrical median nerve stimulation, were measured using an MRI-linked, whole-head MEG system. In total 184 hemispheres, SEFs were measured, involving 22 normal volunteers and 70 patients with intracranial lesions. The first SEF peak appeared 20.2 +/- 1.5 msec (mean +/- S.D.) after stimulation. The first peak was followed by a second and third peak, 7.7 +/- 3.2 msec and 14.6 +/- 5.4 msec respectively after the first. Corresponding isofield maps suggested a single current dipole oriented in the anterior direction for the first peak, posterior for the second and either anterior or posterior for the third. Using a spherical model and a single current dipole source, the localization of each peak was estimated and superimposed on individually determined MRI images. On a grand average basis, the first-peak dipole was localized on the posterior surface of the central sulcus, "area 3b." The second-peak dipole was localized 3.7 mm medial (P < 0.001) and 2.0 mm superior (P < 0.001) to the first-peak dipole, on the anterior wall of the central sulcus, "area 4." This study with a large number of subjects was able to statistically distinguish two adjacent cortical sources, located on opposite walls of the central sulcus, and within a few millimeters of each other.

Adult↗