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Biomedical subjects

H Tsukamoto

Publications and source records attributed to H Tsukamoto.

At least 145 records · Page 8Linked to original sources
PubMed1993

Pathophysiological characteristics of cutaneous microcirculation in patients with liver cirrhosis: relationships to cardiovascular hemodynamics and plasma neurohormonal factors.

To elucidate pathophysiological characteristics of the peripheral circulation in liver cirrhosis, cutaneous microcirculation was analyzed at the finger, palm, toe, and arch of the foot using laser Doppler spectroscopy in 19 patients with liver cirrhosis, and the results were correlated with cardiovascular hemodynamics (n = 10) and plasma neurohormonal factors (n = 8). Cutaneous blood flow at each area was all significantly reduced (P < 0.001, < 0.05, < 0.01, < 0.001, respectively) in patients with liver cirrhosis compared to those in normals (n = 20). Cutaneous blood mass was also significantly reduced (P < 0.05, < 0.01, < 0.001, respectively) except at the arch of foot in patients with liver cirrhosis. There were significant correlations between finger cutaneous blood flow and systemic vascular resistance (r = -0.73, P < 0.05), plasma norepinephrine level (r = -0.84, P < 0.01), plasma renin activity (r = -0.77, P < 0.01), plasma concentrations of aldosterone (r = -0.76, P < 0.05) and angiotensin II (r = -0.76, P < 0.05), between palm blood flow and plasma vasoactive intestinal polypeptide concentration (r = 0.83, P < 0.05). From these results and our previous data demonstrating increased forearm muscular blood flow in patients with liver cirrhosis, increases in arteriovenous anastomotic flow and the contribution of neurohormonal factors will represent pathophysiological mechanisms for these changes.

Adult↗
PubMed1993

Abnormal cutaneous vasomotion and reduced cutaneous blood mass remain in congestive heart failure even with normalized cardiovascular hemodynamics.

To elucidate the pathophysiologic role of cutaneous microcirculation in congestive heart failure, finger cutaneous microcirculation was analyzed in 17 patients with acute heart failure (AHF) and 12 patients with hemodynamically compensated heart failure (c-HF) by using laser Doppler spectroscopy; the results were correlated with simultaneously obtained cardiovascular hemodynamics. Mean finger cutaneous blood flow in AHF was significantly lower compared with c-HF (p < 0.01) and control (n = 20, p < 0.001). Mean finger cutaneous blood mass was significantly reduced in both AHF (p < 0.01) and c-HF (p < 0.01) compared with control. Frequency of characteristic giant concave waves indicating sudden occurrence of flow reduction (B wave) was significantly higher in AHF (p < 0.01) and c-HF (p < 0.05) than that in control. Frequency of B waves correlated significantly with pulmonary capillary wedge pressure (PCWP) (r = 0.73, p < 0.01) and pulmonary artery systolic pressure (r = 0.54, p < 0.05). When changes after medical treatments were compared there were significant correlations between changes in B-wave frequency and changes in PCWP (r = 0.89, p < 0.01) and changes in finger cutaneous blood flow and changes in total systemic peripheral resistance (r = -0.75, p < 0.05). Cutaneous microcirculation in AHF was characterized by decreased finger cutaneous blood flow and finger cutaneous blood mass and prominent B waves, which reflected abnormal vasomotion activity. B-wave prominence and reduced finger cutaneous blood mass remained in c-HF even with normalized cardiovascular hemodynamics.

Adult↗
PubMed1993

Peduncular hallucinosis following microvascular decompression for trigeminal neuralgia: case report.

A patient with peduncular hallucinosis following microvascular decompression is reported. A 63-year-old woman with trigeminal neuralgia had microvascular decompression through a lateral suboccipital approach. When a venous hemorrhage occurred on the surface of the pons during surgery, the two main tributaries of the superior petrosal vein were sacrificed to obtain a wider operative field. On the 1st postoperative day, the patient had no problems and the pain completely disappeared, but on the 2nd day, both visual and auditory hallucinations developed, which continued until the 5th postoperative day. The nature of the hallucinations was consistent with peduncular hallucinosis. The pathogenesis of this variety of hallucination is discussed.

Female↗
PubMed1993

Specific targeting of in vitro-activated human antitumour effector cells using anti-CD3 x anti-c-erbB-2 bispecific antibody.

Bispecific antibody (BSAb) consisting of anti-CD3 plus anti-c-erbB-2 Fab fragments for the application to adoptive tumour immunotherapy was prepared. This bifunctional hetero-F(ab')2 antibody reacted with both human CD3+ T cells and c-erbB-2 positive human tumour cells. Human CD8+ T cells activated with immobilized anti-CD3 plus interleukin 2 showed marginal cytotoxicity against tumour cells. However, addition of the prepared BSAb into the culture resulted in a marked augmentation of the cytotoxicity by the activated CD8+ T cells in a dose-dependent manner. The enhanced cytotoxicity of CD8+ T cells in the presence of BSAb was specific for c-erbB-2 positive tumour cells. Moreover, it was demonstrated that anti-CD3 x anti-c-erbB-2 BSAb was also effective for the specific targeting of various kinds of in vitro-activated antitumour effector cells such as lymphokine-activated killer cells, CD4+ helper/killer cells, gamma delta T cells and activated tumour-infiltrating CD8+ T cells. These results indicated that BSAb consisted of anti-CD3 and anti-c-erbB-2 will become a useful tool for the adoptive tumour immunotherapy of human cancer expressing c-erbB-2 oncogene products.

Animals↗
PubMed1993

Different clinical features in monozygotic twins: a case of 7q--syndrome.

We present male monozygotic twins who showed quite different clinical features. Blood chromosome analysis revealed 46,XY/46,XY,del(7) (q32-->qter) mosaicism in both twins. However, cultured skin fibroblasts from the twins showed different karyotypes. Twin 1, with a normal phenotype, had normal chromosomes and was 46,XY. Twin 2, on the other hand, had the characteristic manifestations of 7q- syndrome and chromosomes of 46,XY,del(7) (q32-->qter). DNA fingerprint analysis of their peripheral blood samples revealed the same pattern. However, DNA fingerprint patterns of cultured skin fibroblasts and buccal mucosal cells were different when a 7q terminal marker, probe g3, was used. These identical twins with discordant phenotypes can be explained by the occurrence of twinning and simultaneous erroneous mitosis. In addition, there might be a vascular communication which probably resulted in blood exchange and chromosomal mosaicism of the lymphocytes of the monozygotic twins.

Abnormalities, Multiple↗
PubMed1993

Arachidonate 12-lipoxygenase is localized in neurons, glial cells, and endothelial cells of the canine brain.

12-Lipoxygenase oxygenates the 12 position of arachidonic acid, producing its 12S-hydroperoxy derivative. We have been interested in the distribution of 12-lipoxygenase in the central nervous system. Previously, by the use of a monoclonal anti-12-lipoxygenase antibody, we proved that one of the arachidonate 12-lipoxygenases existed in canine brain. The present study was therefore designed to elucidate the exact immunohistochemical localization of arachidonate 12-lipoxygenase in canine brain, using a polyclonal anti-12-lipoxygenase antibody. Canine brains were irrigated thoroughly with ice-cold heparinized saline and phosphate-buffered saline to remove blood cells, and then were fixed in 4% periodate-lysine-paraformaldehyde at 4 degrees C for 3 hr. Immunostaining by the indirect method with the peroxidase-labeled antibody was performed for light microscopic observation. The immunohistochemical study demonstrated that many neurons and glial cells in the cerebrum, basal ganglia, and hippocampus were positively stained. Biochemical results as described previously and those of immunohistochemistry indicate that 12-lipoxygenase is definitely localized in various brain parenchymal cells.

Animals↗
PubMed1993

[Carrier and prenatal diagnosis of Duchenne and Becker muscular dystrophy by PCR methods].

The PCR methods for carrier and prenatal diagnosis of Duchenne and Becker muscular dystrophy are described. When a deletion of the dystrophin gene is detected in the proband, the deletion analysis is informative for prenatal diagnosis, and the quantitative PCR analysis of the concerned exons is necessary for carrier diagnosis. When a deletion is not detected, RFLPs analysis should be considered. We analyzed seven polymorphic makers (pERT87-15 combined with digestions with BamHI or XmnI, pERT87-8 combined with digestion with TaqI, and four CA repeat markers at the 5' end and the 3' untranslated regions of the dystrophin gene) by PCR methods. Every woman examined showed a heterozygous finding for at least one of these markers, making it possible to make carrier and prenatal diagnosis. However, it is important to keep in mind that a third of the patients are due to new mutations and that about 10% recombination rate, between the 5' and 3' ends of the dystrophin gene, can exist.

Dystrophin↗
PubMed1993

[A case of systemic lupus erythematosus who developed nodular shadows in the lung in parallel with the disease activity].

A 35-year old woman was admitted to our hospital in April 1991 due to the appearance two nodular shadows on chest X-ray. The patient's past medical history was as follows; In 1986, she developed polyarthralgia, facial eruptions and Raynaud's phenomenon which was treated with prednisolone. In 1988, investigations revealed proteinuria where by the diagnosis of SLE complicated with lupus nephritis was established. Subsequently, treatment with cyclophosphamide was carried out. However, in January 1991, there was further increase in urine proteins in accompaniment with systemic eruptions. In addition, laboratory findings showed an increasing titre of anti-DNA antibody and decreasing serum compliments. In April 1991, as indicated before, a chest X-ray revealed nodular shadows in the right upper and lower lung fields, therefore, a transbronchial lung biopsy was performed. The histology revealed inflammatory infiltrates in the bronchoalveolar tissue, fibrosis of the septa- and exudates in the alveolar space. These findings suggested fibrosing alveolitis. It was true considered that these lesions in the lung were associated with the exacerbation of SLE. In view of this, the dose of prednisolone was increased to 60 mg/day. Consequently, the nodular shadows regressed and the clinical course of SLE improved. It is well appreciated that some patients with SLE develop variable pulmonary involvement, however, this case is of great interest due to the fact that multiple nodular shadows on chest X-ray are very rare in SLE.

Adult↗
PubMed1992

Structure of serum transferrin in carbohydrate-deficient glycoprotein syndrome.

The structure of the defective transferrin in carbohydrate-deficient glycoprotein syndrome was characterized. Structurally abnormal sugar chains were not found in reversed phase chromatograms of pyridylaminated derivatives from the transferrin of two patients in different families. Electrospray ionization mass spectrometry of the whole transferrin molecules revealed an abnormal species that was smaller than normal tetrasialotransferrin by 2,200 daltons, just the size of the disialylated biantennary sugar chain. These data indicated that the disialotransferrin specifically found in this syndrome is missing either of two N-linked sugar chains, suggesting a metabolic error in the early steps of protein glycosylation.

Carbohydrate Metabolism, Inborn Errors↗
PubMed1992

[MR imaging of corpus callosal injuries].

The MR imaging and CT findings of corpus callosal injury were analyzed in 32 of 224 patients with acute head injuries. MR imaging was more sensitive than CT in the detection of callosal injuries. All 9 hemorrhagic lesions were visualized on both MR imaging and CT. Fifteen of 23 nonhemorrhagic lesions were not visualized on CT, although all nonhemorrhagic lesions were visualized on MR imaging. Twenty-four lesions of the corpus callosum were located in the splenium, but no lesion was located in the rostrum. Diffuse axonal shear injuries were visualized in 25 patients with callosal injury as associated traumatic lesions. Twenty-three patients with callosal injury had low initial Glasgow Coma Scale scores (less than 9), but 9 patients had high scores. Associated diffuse axonal shear injuries, especially in the brain stem could be a possible explanation for this difference. MR imaging is useful to detect traumatic lesions of the corpus callosum.

Accidents, Traffic↗
PubMed1992

Mitochondrial tRNA(Ile) mutation in fatal cardiomyopathy.

A patient with mitochondrial encephalomyopathy who died from progressive intractable cardiac failure at the age of 18 is reported. At the age of 4, he presented with short stature, but multiorgan disorders including deafness, focal glomerulosclerosis, epilepsy and dilated cardiomyopathy appeared later in his clinical course. Laboratory tests showed hyperlactatemia and hyperpyruvatemia. Histopathological findings demonstrated mitochondrial myopathy with ragged red fibers and focal cytochrome C oxidase-deficient fibers in skeletal and cardiac muscles. The activity of cytochrome C oxidase was 30% less than the control level in skeletal muscle. Sequencing of the entire mitochondrial tRNA genome revealed a novel point mutation in the tRNA(Ile) region (nt 4269). This A-to-G substitution was found in none of the 30 controls by screening using mispairing PCR and Ssp I digestion methods, suggesting that this new mutation was pathogenic in our case.

Adolescent↗
PubMed1992

Human c-erbB-2 proto-oncogene product as a target for bispecific-antibody-directed adoptive tumor immunotherapy.

To develop an efficient strategy for the targeting of anti-tumor effector cells, we prepared bispecific antibody (BsAb) containing anti-CD3 and an anti-c-erbB-2 proto-oncogene product. The prepared BsAb specifically reacts with both c-erbB-2-positive tumor cells and CD3+ CTL. Human CD4+ helper/killer T cells, induced from peripheral-blood mononuclear cells by activation with immobilized anti-CD3 monoclonal antibody (MAb) plus IL-2, showed no significant cytotoxicity against tumor cells. However, treatment of human CD4+ helper/killer cells with the BsAb caused the induction of specific cytotoxicity against c-erbB-2-positive tumor cells. CD4+ helper/killer cells also produced significant amounts of IL-2 during co-culture with c-erbB-2-positive tumor cells in the presence of the BsAb. Moreover, by combination with the BsAb, CD4+ helper/killer cells showed a strong in vivo anti-tumor effect against c-erbB-2 transfectant or human colon-cancer cells implanted in nude mice. Our results strongly suggest that the c-erbB-2 proto-oncogene product on human tumor cells may be a good target for BsAb-directed adoptive tumor immunotherapy.

Antibodies, Monoclonal↗
PubMed1992

Increased 4-hydroxynonenal levels in experimental alcoholic liver disease: association of lipid peroxidation with liver fibrogenesis.

The precise role of lipid peroxidation in the pathogenesis of alcoholic liver disease is still being debated. To explore the issue, this study was undertaken to investigate the status of lipid peroxidation, antioxidants and prooxidants at two discrete stages of experimental alcoholic liver disease. Male Wistar rats were intragastrically fed a high-fat diet plus ethanol for 5 or 16 wk (the duration that resulted in initiation of centrilobular liver necrosis or liver fibrosis, respectively). Lipid peroxidation was assessed in isolated microsomes and mitochondria with three parameters: malondialdehyde equivalents as determined by thiobarbituric acid assay, conjugated diene formation and 4-hydroxynonenal as a 2,4-dinitrophenylhydrazone derivative. To assess antioxidant systems, hepatic concentrations of glutathione, methionine and alpha-tocopherol were determined. The concentration of nonheme iron, a known prooxidant, was also measured. At wk 5, centrilobular liver necrosis was already evident in the ethanol-fed animals, with two- or threefold increases in plasma AST and ALT levels. At this stage, neither malondialdehyde equivalents nor conjugated diene values were elevated, and the 4-hydroxynonemal level was below 0.2 nmol/mg protein. Hepatic concentrations of methionine and alpha-tocopherol in these animals were increased two- and threefold, respectively, whereas the reduced glutathione level remained unchanged. When alcoholic liver disease had progressed to perivenular or bridging fibrosis at wk 16, all three parameters of lipid peroxidation showed consistent increases that were accompanied by significant reductions in the hepatic glutathione and methionine levels. Interestingly, the control animals pair-fed with the high-fat diet also had significantly elevated 4-hydroxynonenal levels at wk 16 compared to the wk 5 level.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldehydes↗
PubMed1992

Role of cytochrome P-450 2E1 in ethanol-, carbon tetrachloride- and iron-dependent microsomal lipid peroxidation.

This study investigated the role of cytochrome P-450 2E1 in enhanced microsomal lipid peroxidation in experimental alcoholic liver disease. We also examined the contribution of this isoform to the increased microsomal injury in alcoholic liver disease caused by carbon tetrachloride-induced or iron-induced oxidant stress. Adult male Wistar rats were intragastrically infused with a high-fat diet and ethanol or glucose for 16 wk; this resulted in hepatic lipid peroxidation and fibrogenesis in the ethanol-fed animals. Microsomes were isolated by differential centrifugation in the presence of 100 mumol/L deferoxamine, washed twice in buffer without deferoxamine and incubated in the absence or presence of ethanol (50 mmol/L), carbon tetrachloride (150 mumol/L), ferric citrate (50 mumol/L) or ferric citrate plus ethanol at 37 degrees C for 30 min in an NADPH-generating system. The basal rate of lipid peroxidation in microsomes isolated from ethanol-fed rats was increased by 52% compared with that in microsomes from controls. Carbon tetrachloride-induced and ferric citrate-induced lipid peroxidation were also accentuated in microsomes from ethanol-fed rats, by 76% and 108%, respectively. Ethanol added in vitro significantly reduced basal (-58%) and ferric citrate-induced (-48%) lipid peroxidation in microsomes from ethanol-fed rats, whereas it had an insignificant effect on that in control microsomes. In fact, this protective effect of ethanol on microsomes from ethanol-fed rats resulted in attenuation of the difference in the level of microsomal lipid peroxidation between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Hepatic mitochondrial glutathione depletion and progression of experimental alcoholic liver disease in rats.

Long-term ethanol feeding has been shown to selectively reduce hepatic mitochondrial glutathione content by impairing mitochondrial uptake of this thiol. In this study, we assessed the role of this defect in evolution of alcoholic liver disease by examining the mitochondrial glutathione pool and lipid peroxidation during progression of experimental alcoholic liver disease to centrilobular liver necrosis and fibrosis. Male Wistar rats were intragastrically infused with a high-fat diet plus ethanol for 3, 6 or 16 wk (the duration that resulted in induction of liver steatosis, necrosis and fibrosis, respectively). During this feeding period, the cytosolic pool of glutathione remained unchanged in the ethanol-fed animals compared with that in pair-fed controls. In contrast, the mitochondrial pool of glutathione selectively and progressively decreased in rats infused with ethanol for 3, 6 or 16 wk, by 39%, 61% and 85%, respectively. Renal mitochondrial glutathione level remained unaffected throughout the experiment. Serum ALT levels increased significantly in the ethanol-fed rats at 6 wk and remained elevated at 16 wk. In the mitochondria with severely depleted glutathione levels at 16 wk, enhanced lipid peroxidation was evidenced by increased malondialdehyde levels. Thus a progressive and selective depletion of mitochondrial glutathione is demonstrated in the liver in this experimental model of alcoholic liver disease and associated with mitochondrial lipid peroxidation and progression of liver damage.

Alanine Transaminase↗
PubMed1992

Hypophyseal metastatic hypernephroma mimicking a pituitary adenoma. Case report.

A patient with a remote history of nephrectomy for hypernephroma presented a visual field defect with hypopituitarism. Neuro-imaging studies showed a highly vascularized sellar mass with suprasellar extension. Surgery, which was performed via the subfrontal approach, disclosed the pituitary tumor to be a hypernephroma. Although anterior pituitary involvement is rare, chiasmal compression is much rarer in metastatic pituitary carcinomas, a review of previously reported cases of metastatic pituitary hypernephroma and our own case indicated that pituitary metastasis from this carcinoma, in contrast to other metastatic pituitary tumors, often mimics pituitary adenoma.

Adenoma↗
PubMed1992

A case of pigmentary type of orthochromatic leukodystrophy with early onset and globoid cells.

We report herein a sporadic case of the pigmentary type of orthochromatic leukodystrophy with early onset and very rapid clinical course. The patient's development was normal until 2 years old, when he experienced visual disturbance. Rapid deterioration resulted in death 1.5 years after the onset. Metachromatic leukodystrophy, globoid cell leukodystrophy and adrenoleukodystrophy were excluded by biochemical assays. Autopsy findings were compatible with the diagnosis of the pigmentary type of orthochromatic leukodystrophy. However, there were unique findings of severe neuronal loss and the collection of globoid-like cells in the interface of the gray matter and the white matter. Immunohistochemical staining of myelin basic protein, proteolipid protein and galactocerebroside demonstrated that these myelin constituents were equally preserved in the posterior column, while absent in the lateral and anterior columns of the spinal cord.

Autopsy↗