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Biomedical subjects

T Kamada

Publications and source records attributed to T Kamada.

At least 109 records · Page 6Linked to original sources
PubMed1997

An approach to the detection of autonomic neuropathy by use of signal-averaged electrocardiography.

The beat-to-beat variation of PR interval, which is thought to be a reflection of autonomic nervous system, is difficult to measure with accuracy because the variation is too subtle. However, R wave amplitude in the P wave triggered SAECG is easily attenuated in comparison to that in the R wave triggered SAECG, which might be due to PR interval fluctuation. To determine whether autonomic neuropathy could be detected by use of SAECG, two types of SAECGs triggered by P and R waves were recorded in 23 diabetics with autonomic neuropathy and 41 age matched controls. The peak voltage of filtered QRS complex was measured in the R wave and P wave triggered SAECGs. Percent attenuation of the filtered QRS voltage was calculated by dividing the difference between the voltages in the R wave and P wave triggered SAECGs by the voltage in R wave triggered SAECG. The percent attenuation of filtered QRS voltage was significantly smaller in diabetics with autonomic neuropathy than controls (4.6% +/- 4.9% vs 16.3% +/- 15.0%; P < 0.001). These results suggest that the degree of attenuation of filtered QRS voltage in the P wave triggered SAECG would be useful for the detection of autonomic neuropathy.

Atropine↗
PubMed1997

Hepatitis C virus replicative levels and efficiency of genotyping by specific PCR and antibody assay.

We studied factors which influence the detection of hepatitis C virus genotypes by the group-specific PCR of the sequence within the core region gene and by the newly developed genotype-specific NS4 antibody assay. Genotyping was performed on 75 hepatitis C virus carriers in Japan, where patients with hepatitis C viremia are exclusively infected with genotype 1b, 2a, and 2b. PCR failed to identify genotypes in 8 (11%) patients, whereas 12 (16%) patients, including the 8 patients mentioned above, could not be genotyped by the serological assay. Serological genotypes showed almost complete agreement with those found by the PCR except that double infection was revealed in only two of the eight patients serologically judged to be coinfected with genotypes 1 and 2. In each assay, disease activity and levels of viremia assessed by a competitive reverse transcription PCR assay were significantly lower in patients infected with untypeable isolates than in those infected with typeable ones (P < 0.01). The PCR could identify the genotypes of isolates from all 64 patients with levels of viremia of > or = 10(6) copies/ml, and the genotype-specific antibody responses were found in 60 (94%) patients. In contrast, isolates from only 3 (27%) of 11 patients with low levels of viremia (< 10(6) copies/ml) could be genotyped by the PCR (P < 0.00001), and these patients showed the genotype-specific antibody responses (P < 0.00001). These findings suggest that low levels of hepatitis C virus replication may reduce the efficiency of genotyping by serological assay as well as by PCR.

Adult↗
PubMed1997

Prethrombotic state due to hypercoagulability in patients with permanent transvenous pacemakers.

Venous thrombosis is a relatively usual but serious complication of permanent transvenous pacing. However, the pathogenesis has not been defined. To clarify underlying abnormalities in the coagulation-fibrinolysis system in patients with permanent transvenous pacemakers, we measured serum levels of fibrinopeptide A (FPA), thrombin-antithrombin III complexes (TATs), plasmin-alpha 2 plasmin inhibitor complexes (PICs), D-dimer (D-D), beta-thromboglobulin (beta-TG), and platelet factor 4 (PF4) in 53 patients with permanent transvenous pacemakers and 10 control subjects. The patients were divided into two groups, as follows, according to the presence of mural thrombus documented along the pacing lead(s) by digital subtraction angiography and transesophageal echocardiography: Group Th (-), patients without venous route thrombus; and Group Th (+), patients with venous route thrombus. FPA and TAT levels increased significantly even in Group Th (-), and further increased in Group Th (+) compared with control subjects (FPA: 7.5 +/- 4.9, 15.3 +/- 8.8 vs 3.0 +/- 1.4 ng/mL, respectively, P < 0.05; TAT: 2.9 +/- 1.3, 4.8 +/- 2.3 vs 1.7 +/- 0.6 ng/mL, respectively, P < 0.05). There were no differences in levels of D-D, PIG, beta-TG, and PF4 among control subjects, Group Th (-), and Group Th (+). These findings suggest that the hypercoagulable state appears in patients with permanent transvenous pacemakers, even without apparent venous thrombosis. The patients with permanent transvenous pacemakers are thought to be in the prethrombotic state even if they have no venous route thrombosis.

Adult↗
PubMed1997

Preliminary study of improved perception of words with the same sound but different intonation in tinnitus patients following electrical stimulation of the ear.

The present study aimed to explain how tinnitus relief following electrical promontory stimulation affects detection of changes in pitch frequency. To determine the effects of tinnitus relief on the auditory system. Japanese words with the same sound but different intonation were used to verify the effects of tinnitus relief on pitch detection in tinnitus patients Eight out of 11 patients experienced relief of tinnitus following treatment. The averaged number of the ratio in 8 patients with relief of tinnitus, 0.58, was significantly higher (p < 0.02) than that in 3 patients without relief, 0.15. In comparison with averaged hearing level, there was no significant difference in averaged hearing level between 8 patients with relief of tinnitus (52.4 dBSL; SD: 11.4) and 3 without relief of tinnitus (58.0 dBSL; SD: 14.7) (p > 0.68). No significant difference in age between patients with and without relief of tinnitus was observed.

Aged↗
PubMed1997

High levels of serum interleukin-10 are associated with a poor response to interferon treatment in patients with chronic hepatitis C.

BACKGROUND: It still remains unclear whether some immunologic factors affect the response to interferon treatment. We therefore examined whether the pretreatment levels of serum interleukin-10 and soluble intercellular adhesion molecule-1 can be associated with the response to interferon treatment in patients with chronic hepatitis C. METHODS: One hundred and two patients with chronic hepatitis C treated with interferon alpha-2b were divided into three groups on the basis of patterns of biochemical interferon response. Pretreatment levels of serum interleukin-10 and soluble intercellular adhesion molecule-1 were determined using enzyme-linked immunosorbent assay. Hepatitis C virus (HCV) typing was performed with a serologic enzyme-linked immunosorbent assay. RESULTS: For patients with serotype I (n = 76) the numbers of sustained, transient, and non-responders were 12 (16%), 43 (56%), and 21 (28%), respectively. In serotype-I patients the pretreatment levels of serum interleukin-10 in non-responders were significantly higher than those in sustained or transient responders, although no significant differences were observed in HCV RNA quantity between them. There were no significant differences in the pretreatment levels of serum soluble intercellular adhesion molecule-1 among the three groups. CONCLUSION: These findings suggest that high serum interleukin-10 levels may be related to a poor response to interferon treatment in serotype-I patients with chronic hepatitis C.

Adult↗
PubMed1997

Myocardial iodine-123-metaiodobenzylguanidine images and autonomic nerve activity in normal subjects.

UNLABELLED: We studied the relationship between myocardial [123I]metaiodobenzylguanidine (MIBG) uptake and autonomic nerve activity in normal subjects. METHODS: MIBG scintigraphy and power spectral analysis (PSA) of heart rate variability were performed simultaneously in 15 normal subjects. Anterior planar images and SPECT images were taken at five and two points after the injection of [123I]MIBG, respectively. In 10 of 15 subjects, 201TI myocardial SPECT was performed immediately after MIBG scintigraphy. RESULTS: The heart/upper mediastinum MIBG uptake ratio in the planar image obtained at 240 min (r = 0.64, p < 0.01) and the washout rate of MIBG in the heart between 15 min and 240 min (r = 0.51, p < 0.05) showed significant correlation with the percentage of low frequency component of PSA (percent LF), an index of sympathetic nerve activity. Regional MIBG uptake in the inferior wall normalized by individual maximal uptake among all pixels was significantly correlated with the high frequency component of PSA, an index of parasympathetic nerve activity (r = -0.58, p < 0.05) and with mean R-R interval in a resting ECG (r = -0.82, p < 0.001) but did not correlate with percent LF, percent uptake of 201TI in the inferior wall or the liver/heart uptake ratio. CONCLUSION: These results indicate that myocardial MIBG uptake correlates with sympathetic nerve activity in normal subjects. Our data indicate that heterogeneous MIBG distribution in the left ventricle is a physiologic rather than artifactual phenomenon and may be related to vagal tone rather than sympathetic nerve activity.

3-Iodobenzylguanidine↗
PubMed1997

Ischemic damage and subsequent proliferation of oligodendrocytes in focal cerebral ischemia.

In order to achieve a better understanding of the pathophysiology of ischemic white matter lesions, oligodendrocytic degeneration and subsequent proliferation were examined in the mouse model of middle cerebral artery occlusion. In situ hybridization histochemistry for proteolipid protein messenger RNA was employed as a sensitive and specific marker of oligodendrocytes, and immunohistochemistry for myelin basic protein was used as a compact myelin marker. Immunohistochemistry for microtubule-associated protein 2 and albumin was employed to monitor neuronal degeneration and the breakdown of the blood brain barrier, respectively. In the ischemic core of the caudoputamen, the immunoreactivity for microtubule-associated protein 2 disappeared and massive albumin extravasation occurred several hours after vessel occlusion, while proteolipid protein messenger RNA signals remained relatively strong at this time. The messenger RNA signals began to attenuate 12 h after ischemia and were hardly detectable 24 h after ischemia in the whole ischemic lesion. In situ end-labeling of fragmented DNA showed some cells with proteolipid protein messenger RNAs to have DNA fragmentation at this period. In contrast to proteolipid protein messenger RNA signals, the immunoreactivity for myelin basic protein was detected as long as five days after ischemia. An apparent increase in the cells possessing strong proteolipid protein messenger RNA signals was found five days after ischemia, mainly in the corpus callosum and the cortex bordering the infarcted areas. A double simultaneous procedure with in situ hybridization for proteolipid protein messenger RNA and immunohistochemistry for glial fibrillary acid protein or lectin histochemistry for macrophages/microglia showed proliferating oligodendrocytes to be co-localized with reactive astrocytes and macrophages/microglia. These findings show that oligodendrocytic damage occurred following ischemic neuronal damage and the breakdown of the blood brain barrier, but preceded the breakdown of myelin proteins in the ischemic lesion, that an apoptosis-like process was involved in ischemic oligodendrocytic death, and that surviving oligodendrocytes responded and proliferated in the outer border of the infarcted area.

Animals↗
PubMed1997

Endothelin-1 in the gastric mucosa in stress ulcers of critically ill patients.

OBJECTIVE: Gastric microcirculatory disturbances are involved in the pathogenesis of stress ulcers; however, vasomodulators causing this process are not fully understood. This study was conducted to investigate the role of endothelin 1 (ET-1), a potent vasoconstrictive peptide, in stress ulcers in critically ill patients. METHODS: Using sandwich enzyme immunoassay, we measured ET-1 content in plasma and the gastric mucosa of 16 critically ill patients with traumatic head injury on admission and of 11 healthy subjects. Gastric mucosal samples were obtained endoscopically. When gastric drainage contained occult blood, endoscopic examination was performed again, and ET-1 concentrations in injured and adjacent normal mucosa were compared. RESULTS: Plasma and mucosal ET-1 concentrations were significantly higher in critically ill patients on admission (6.1 +/- 0.6 pg/ml and 13.8 +/- 1.6 ng/g, respectively) compared with values in control subjects (2.7 +/- 0.4 pg/ml and 8.2 +/- 0.5 ng/g, respectively) (p < 0.01). The mucosal ET-1 concentration tended to be elevated in patients who had experienced hypoxia compared with those who had not (p = 0.07). In five patients who were again examined endoscopically, the ET-1 concentration in the injured mucosa was significantly higher than that in adjacent mucosa (19.2 +/- 3.2 and 10.1 +/- 1.6 ng/g, respectively; p < 0.05). CONCLUSIONS: These results suggest that endogenous ET-1 plays an important role in the local pathogenesis of stress ulcers, especially those caused by hypoxia.

Adult↗
PubMed1996

Helicobacter pylori extract stimulates inflammatory nitric oxide production.

This study examined whether an extract of Helicobacter pylori had the ability to stimulate an inflammatory synthesis of nitric oxide, a mutagen and precursor of nitrosocompounds. Macrophages and neutrophils were prepared from rat and incubated with the Helicobacter pylori extract. L-Arginine-dependent nitric oxide production in these cells was significantly stimulated by the co-incubation with the Helicobacter pylori extract. This ability of the extract was strongly attenuated by protease digestion or heating. These results indicate that Helicobacter pylori induces production of nitric oxide and participates in development of gastritis and gastric carcinogenesis.

Animals↗
PubMed1996

High expression of heparin-binding EGF-like growth factor in rat hepatocarcinogenesis.

Heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF) is a member of the EGF family and is highly expressed in hepatoma tissues but not in normal liver. However, it is unknown when HB-EGF is induced during hepatocarcinogenesis and what are the mechanisms underlying its high expression in hepatoma. To address this issue, the expression of HB-EGF was investigated during hepatocarcinogenesis in LEC (Long-Evans with a cinnamon-like coat color) rats, which spontaneously develop hepatitis and hepatoma. LEA (Long-Evans with an agouti coat color) rats were used as controls. Furthermore, the induction of HB-EGF mRNA by various agents was investigated in a rat hepatoma cell line and hepatocytes in primary culture. Expression of HB-EGF mRNA in the liver was very low at the stage of acute and chronic hepatitis and markedly increased at the stage of hepatoma in LEC rats. Non-involved tissues adjacent to hepatoma showed low expression of HB-EGF mRNA. Immunochemical studies revealed positive staining in hepatoma tissues. Induction of HB-EGF mRNA by several growth factors was observed in a hepatoma cell line but not in normal hepatocytes. Our results suggest that HB-EGF is associated with the early progression steps of hepatoma.

Animals↗
PubMed1996

Glycation and inactivation of sorbitol dehydrogenase in normal and diabetic rats.

Sorbitol dehydrogenase (SDH) is involved in the polyol pathway, which plays an important role in the pathogenesis of diabetic complications. We have measured the tissue distributions of SDH mRNA, both the immunoreactive enzyme levels and the enzyme activity. SDH mRNA was especially abundant in liver, kidney and testis. Both the activity and enzyme content are high in liver and kidney but not in testis. The discrepancy between mRNA and immunoreactive enzyme levels and the activity of SDH observed in testis was also seen in livers of streptozotocin-induced diabetic rats. SDH was found to exist in both glycated and non-glycated forms, with larger amounts of the glycated protein in the diabetic liver. Moreover, after incubation of purified enzyme with glucose or fructose, its activity was markedly decreased. These results indicate that glycation causes a decrease in SDH activity in liver under diabetic conditions. The same post-transcriptional event might occur to decrease the activity of SDH in testis in normal animals.

Animals↗
PubMed1996

Expression of vascular permeability factor/vascular endothelial growth factor in human hepatocellular carcinoma.

Vascular permeability factor (VPF)/vascular endothelial growth factor (VEGF) is unique in its ability to promote vascular permeability and endothelial cell growth, and its role in tumor development has received considerable attention. In this report, we describe the elevation of VPF/VEGF transcript expression in human hepatocellular carcinoma. Surgical samples of 23 patients with hepatocellular carcinoma were studied using reverse transcription-PCR analysis. The oligonucleotide primers were designed to amplify all four known splicing variants that could be expressed in the samples studied. Sixteen cases showed VPF/VEGF transcript expression in the tumor (16/23, 69.6%), whereas only 9 of the 23 patients showed it in the corresponding nontumoral part. There was no difference between the pattern of expression of VPF/VEGF isoforms in tumoral and nontumoral tissues. VPF/VEGF mRNA expression in the liver tumors was associated with fibrous capsule formation and septal formation (P < 0.05 respectively, Fisher's exact P test). In situ hybridization confirmed the presence of VPF/VEGF mRNA expression in tumor cells and less intensely in hepatocytes of nontumoral liver. We also found that VPF/VEGF expression in the tumor cell was increased in the area adjacent to necrotic regions (presumably hypoxic regions). As a regulator of vascular permeability and endothelial cell growth factor, VPF/VEGF may play an important role in the development of hepatocellular carcinoma.

Adult↗
PubMed1996

Ischemic tolerance in moderately symptomatic gerbils after unilateral carotid occlusion.

Ischemic tolerance following transient global cerebral ischemia has drawn considerable attention because of the putative cell defense mechanism which may be inducible by ischemic stress. The purpose of this study is to investigate the inducibility of ischemic tolerance in moderately symptomatic gerbils after unilateral carotid occlusion. Adult Mongolian gerbils were used. Under ether inhalation, the right common carotid artery was occluded for up to 30 min with an aneurysmal clip. Immediately after occlusion, neurological signs and motor function were evaluated and gerbils with moderate signs were selected for investigation of ischemic tolerance. Ischemia for 30 min to gerbils with moderate signs constantly caused neuronal death in the caudoputamen, but it was prevented by pretreatment with 10 min ischemia which was reversible but strong enough to produce heat shock protein 70. The results show that ischemic tolerance can be induced after hemispheric cerebral ischemia as in the case of global cerebral ischemia and suggest that ischemic tolerance may be relevant in human stroke.

Animals↗