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Biomedical subjects

H Katoh

Publications and source records attributed to H Katoh.

At least 235 records · Page 13Linked to original sources
PubMed1996

Comparison of carbohydrate structures of serum alpha-fetoprotein by sequential glycosidase digestion and lectin affinity electrophoresis.

Serum alpha-fetoprotein (AFP) is a glycoprotein of which the sugar chain is considered to show structural changes with malignancies. Microheterogeneity of the serum AFP carbohydrate structure was studied in samples from 35 patients with benign and malignant diseases. Sera were digested directly, extensively, and sequentially with sialidase. beta-galactosidase and beta-N-acetylhexosaminidase. Before and after digestion, sera were examined by means of lectin affinity electrophoresis using eight lectins. Relationships between AFP carbohydrate structures and liver diseases were elucidated by the lectin-reactive profiles and the effect of glycosidase digestion. More than 94% of the AFP carbohydrate structures found in patients with benign and malignant liver diseases were biantennary complex-type oligosaccharides. Changes in the AFP carbohydrate structures at the early stage of hepatocellular carcinoma revealed the addition of alpha 1-->6 fucose to the reducing terminal N-acetylglucosamine and monosialylated AFPs. In both advanced hepatocellular carcinoma and AFP producing extrahepatic malignancies, AFP carbohydrate structures were characterized as the further addition of beta 1-->4 N-acetylglucosamine and heterogeneity in the galactose and N-acetylglucosamine residues. Sequential glycosidase digestion and lectin affinity electrophoresis is useful for analysing the carbohydrate structures of serum glycoprotein.

Carbohydrate Conformation↗
PubMed1996

Generation of novel killer hybridomas derived from proliferation-suppressed somatic cell hybrids between YACUT T cell lymphoma and normal lymphocytes activated in secondary mixed lymphocyte cultures.

Somatic cell hybridization between the YACUT T cell lymphoma cell line with normal lymphocytes activated in secondary mixed lymphocyte cultures (MLCs) consistently yielded IL-2-dependent CD4- CD8 alpha+ beta- Fc gamma RIII+ hybrids with cytotoxic function. The hybrids expressed T cell receptors other than that of YACUT origin, and fusion of the YACUT with a CD8 alpha+ beta+ Fc gamma RIII- T cell line also yielded hybrids with an unexpected CD8 alpha+ beta- Fc gamma RIII+ phenotype, which two observations strongly suggested that CD8+ T cells became the parental cell of the hybrids. Prolonged growth of the hybrids with IL-2 resulted in the generation of autonomously growing hybrids (hybridomas) without abrogating the cytotoxic function. The hybridomas exhibited MHC-unrestricted cytotoxicity in a Ca(2+)-dependent manner without prior stimulation and also mediated antibody-dependent cellular cytotoxicity. These results indicate that novel killer hybridomas can be produced following cell transformation of proliferation-suppressed cytotoxic YACUT x MLC cell hybrids. The killer hybridomas may be of value for analyzing recognition mechanisms and molecules involved in MHC-unrestricted cell-mediated cytotoxicity.

Animals↗
PubMed1996

Novel biochemical diagnostic method for aortic dissection. Results of a prospective study using an immunoassay of smooth muscle myosin heavy chain.

BACKGROUND: Aortic dissection is one of the most common aortic catastrophes. Although newer diagnostic methods as exemplified by image diagnostic techniques have greatly improved the diagnosis of aortic dissection, the diagnosis is still frequently missed today because the signs and symptoms of the disease are at times obscure. A reliable biochemical diagnostic method for aortic dissection would be beneficial. METHODS AND RESULTS: A novel biochemical diagnostic method for diagnosis of aortic dissection was developed that uses an immunoassay of monoclonal antibodies to smooth muscle myosin heavy chain. A prospective study was conducted to ascertain the usefulness of the method in the diagnosis of aortic dissection. Twenty-seven patients with aortic dissection admitted within the first 24 hours after onset were enrolled. Serial assay of serum smooth muscle myosin heavy chain showed significant elevations within the first 24 hours after onset of aortic dissection, with levels exceeding 10 ng/mL, with subsequent rapid reductions. The sensitivity of the assay within the first 12 hours was 90% with a specificity of 97%. Analysis of 65 patients with acute myocardial infarction showed that the method could accurately differentiate myocardial infarction from aortic dissection. CONCLUSIONS: The immunoassay of serum smooth muscle myosin heavy chain is a rapid and reliable biochemical method in the diagnosis of aortic dissection. The potential use of the method in clinical medicine is promising.

Aged↗
PubMed1996

Macrophage inflammatory protein-1 alpha expression in non-neoplastic and neoplastic lung tissue.

The chemokines are members of a bipartite superfamily of soluble proteins that have been implicated in a wide range of acute and chronic inflammatory processes, as well as other immunoregulatory functions. Macrophage inflammatory protein-1 alpha (MIP-1alpha) belongs to the C-C subfamily of these chemokines and is primarily a potent chemoattractant and activator of monocytes. MIP-1alpha is also thought to play a role in host defence. We examined the expression of MIP-1-alpha in normal lung, inflammatory lung tissue and lung cancer cells by the immunoperoxidase method using a MIP-1alpha monoclonal antibody. MIP-1alpha protein was found to be expressed not only by alveolar macrophages, but also by bronchial ciliated cells, hyperplastic alveolar type II cells and activated fibroblasts surrounding malignant tissue. Of 33 cases of lung cancer, 23 (70%) expressed MIP-1alpha. These observations suggest that lung cancer cells, non-neoplastic alveolar type II cells and fibroblasts can participate in inflammatory cell recruitment via the production of MIP-1alpha. Tumour derived MIP-alpha may also affect the interaction between lung cancer and host inflammatory cells.

Aged↗
PubMed1996

Early massive accumulation of In-111 pentetreotide in a metastatic liver tumor of islet cell carcinoma.

A 62-year-old woman was examined with In-111 pentetreotide and Ga-67 citrate. She had undergone an operation to resect a neuroendocrine tumor of the pancreas and still had masses in the liver. One of her hepatic lesions had been biopsied and acinar cell carcinoma was suspected. Fluid in the cyst of the tumor, however, contained a high concentration of gastrin and the tumor was strongly suspected of being a metastasis from the neuroendocrine tumor of the pancreas. The hepatic tumors quickly accumulated In-111 pentetreotide immediately after the injection, but there was no Ga-67 citrate uptake in the tumor. Five months after pentetreotide scintigraphy, her hepatic tumors were resected and histologically proven to be metastasis of islet cell carcinoma. In-111 pentetreotide provides information of the somatostatin-receptor status on the tumor and supports the diagnosis made by hormonal survey.

Biopsy↗
PubMed1996

Mitral valve repair for mitral regurgitation with ventricular septal defect in children.

BACKGROUND: We examined the results of intermediate and long-term follow-up of 25 patients aged 3 months to 11 years (mean, 2.6 +/- 2.3 years) who initially underwent conservative mitral valve repair for mitral regurgitation associated with ventricular septal defect between April 1973 and March 1991. METHODS: The preoperative degree of mitral regurgitation was 2+ in 3, 3+ in 17, and 4+ in 5 patients, and the major causes of mitral regurgitation were annular dilatation and prolapse of the anterior leaflet. Annuloplasty was performed in all except 2 patients, suturing of the cleft was done in 3 patients, and posterior mitral leaflet advancement was done in 2 patients. In addition, the papillary muscle was incised and adhesive chordae were removed in 1 patient, and adhesive fused chordae were detached from a leaflet in 1 other patient. RESULTS: There were no early deaths. Two patients with residual mitral regurgitation with or without mitral stenosis underwent reoperation for mitral valve replacement 2 months and 6 years after the mitral repair, respectively. Late death occurred in 2 patients, and the actuarial survival rate was 92.0% at 15 years after operation. The freedom from reoperation was 91.3% at both 10 and 15 years after the initial operation. Postoperative color Doppler flow imaging was performed in 22 of the 23 survivors, and results showed no mitral regurgitation in 4, mild regurgitation in 14, and moderate regurgitation in 4 patients. Four patients presently have mitral stenosis, with a mean transmitral pressure gradient greater than 10 mm Hg. The residual lesion of moderate mitral regurgitation with or without mitral stenosis developed in 6 of 11 patients in whom bilateral mitral annuloplasty was applied after the initial operation. Nineteen of the 22 survivors without reoperation were in New York Heart Association class I, and 3 were in class II. CONCLUSIONS: Clinical improvement was observed after conservative mitral repair in most pediatric patients with ventricular septal defect. However, careful follow-up for growth potential still appears to be needed to detect changes in mitral regurgitation and the development of mitral stenosis after valve repair, especially after bilateral annuloplasty.

Child↗
PubMed1996

Prevention of reoxygenation-induced arrhythmias in guinea pig papillary muscles.

Effects of various agents on reoxygenation-induced arrhythmias, action potentials, and tension of guinea pig papillary muscles were recorded to investigate the site of action. Triggered activities due to delayed afterdepolarizations (DADs) and aftercontractions were elicited on reoxygenation after 60-min substrate-free hypoxia. Low extracellular Ca2+ (0.1 mM) abolished arrhythmias, and high Ca2+ (4.9 mM) increased the amplitudes of DADs and aftercontractions. D-600 at the high concentration (20 microM) decreased the incidence of arrhythmias (p < 0.05 vs. no drug) and decreased the recovery of developed tension after reoxygenation (p < 0.001). Ryanodine (1 microM) abolished aftercontractions and arrhythmias but did not affect the recovery of developed tension. Tetrodotoxin (TTX 3 microM) and nicorandil (100 microM) decreased the incidence of arrhythmias (p < 0.05), but did not affect the recovery of developed tension or the amplitudes of aftercontractions. TTX caused only a slight decrease in Ca2+ transients in a fluo-3-loaded guinea pig ventricular myocyte. The Ca2+ entry through the Ca2+ channels apparently synchronized Ca2+ release from the sarcoplasmic reticulum, and D-600 at the high concentration apparently decreased the incidence of arrhythmias. TTX and nicorandil decreased arrhythmias, probably by decreasing the Na+ current or by increasing the ATP-sensitive K+ current, respectively.

Action Potentials↗
PubMed1996

Urticarial vasculitis with papular lesions in a patient with type C hepatitis and cryoglobulinemia.

We describe a case of urticarial vasculitis accompanied by erythematous wheals, palpable pupura, and subsequent necrotic ulcerated papular lesions in a patient with type C chronic hepatitis and type II cryoglobulinemia (IgM-kappa and polyclonal IgG). A 56-year-old man developed recurrent urticarial lesions on his lower extremities and trunk. The histology revealed leukocytoclastic vasculitis with perivascular immunoglobulin deposits. Subsequently, multiple reddish papular lesions with necrotic ulcerations appeared on the extensor aspect of his extremities and buttocks. Histology of these lesions showed cryoglobulinemic vasculitis with prominent fibrinoid necrosis of the vascular walls and cryoprecipitate within the vasculature as well as increased hyalinized collagen bundles. These papular lesions have not previously been described as cutaneous necrotizing venulitis to the best of our knowledge. It is suggested that the immune response to hepatitis C virus infection and cryoglobulins may be responsible for severe necrotizing venulitis, resulting in unusual cutaneous lesions.

Chronic Disease↗
PubMed1996

Absence of light-induced proton extrusion in a cotA-less mutant of Synechocystis sp. strain PCC6803.

cotA of Synechocystis sp. strain PCC6803 was isolated as a gene that complemented a mutant defective in CO2 transport and is homologous to cemA that encodes a chloroplast envelope membrane protein (A. Katoh, K.S. Lee, H. Fukuzawa, K. Ohyama, and T. Ogawa, Proc. Natl. Acad. Sci. USA 93:4006-4010, 1996). A mutant (M29) constructed by replacing cotA in the wild-type (WT) Synechocystis strain with the omega fragment was unable to grow in BG11 medium (approximately 17 mM Na+) at pH 6.4 or at any pH in a low-sodium medium (100 microM Na+) under aeration with 3% (vol/vol) CO2 in air. The WT cells grew well in the pH range between 6.4 and 8.5 in BG11 medium but only at alkaline pH in the low-sodium medium. Illumination of the WT cells resulted in an extrusion followed by an uptake of protons. In contrast, only proton uptake was observed for the M29 mutant in the light without proton extrusion. There was no difference in sodium uptake activity between the WT and mutant. The mutant still possessed 51% of the WT CO2 transport activity in the presence of 15 mM NaCl. On the basis of these results we concluded that cotA has a role in light-induced proton extrusion and that the inhibition of CO2 transport in the M29 mutant is a secondary effect of the inhibition of proton extrusion.

Bacterial Proteins↗
PubMed1996

Effects of Mg2+ on Ca2+ waves and Ca2+ transients of rat ventricular myocytes.

It has been shown that the occurrence of the transient inward current, which is responsible for triggered activity, was often associated with propagating regions of increased intracellular Ca2+ concentration ([Ca2+]i), i.e., the "Ca2+ wave." To investigate the mechanism of antiarrhythmic action of Mg2+, we have studied effects of high concentrations of Mg2+ on Ca2+ waves in isolated rat ventricular myocytes. [Ca2+]i was estimated using the Ca(2+)-indicating probe indo 1. Ca2+ waves in myocytes, stimulated at 0.2 Hz, were induced by perfusion of isoproterenol (10(-7) M). High Mg2+ concentration suppressed Ca2+ waves in a concentration-dependent manner (36% at 4 mM, 70% at 8 mM, and 82% at 12 mM). The Ca2+ channel blocker verapamil also suppressed Ca2+ waves in a similar way. In contrast with marked depression of Ca2+ transients by verapamil, Ca2+ transients were not affected by high Mg2+ concentration (8 mM). High Mg2+ concentration also reduced frequencies of Ca2+ waves in the absence of electrical stimulation, whereas verapamil failed to reduce frequencies of Ca2+ waves. Reduction in frequency of Ca2+ waves by high Mg2+ concentration was associated with slowing of propagation velocity of Ca2+ waves. To examine whether suppressive effects of high Mg2+ concentration on Ca2+ waves were related to an increase in intracellular Mg2+ concentration ([Mg2+]i), the effect of high-Mg2+ solution on [Mg2+]i was examined in myocytes loaded with mag-fura 2. An increase in extracellular Mg2+ concentration from 1 to 12 mM increased [Mg2+]i from 1.06 +/- 0.16 to 1.87 +/- 0.22 mM (P < 0.01) in 30 min. To examine the effect of high Mg2+ concentration on amount of releasable Ca2+ in the sarcoplasmic reticulum, the effect of high Mg2+ concentration on the Ca2+ transient induced by a rapid application of caffeine was examined. High-Mg2+ solution increased the peak of the caffeine-induced Ca2+ transient. These results suggest that the inhibitory effect of Mg2+ on Ca2+ waves was not due to inhibition of the sarcolemmal Ca2+ channel but could be due to a decreased propensity for the sarcoplasmic reticulum to divest itself of excess Ca2+.

Animals↗
PubMed1996

Genetic studies of a new mutant strain showing shivering in the mouse.

A new mutant with shivering, Hula dance Sendai (tentatively named hus gene), was found in the IVCE strain. A congenic strain, C57BL/6JJcl-hus, was established by the cross-intercross method using IVCE-hus as the donor strain and C57BL/6JJcl as the recipient. No significant differences were observed in the age of the onset of shivering and life span between B6-hus and IVCE-hus mice. Genetic analyses demonstrated that this mutation is governed by an autosomal recessive gene (Mbphus) and is an allele of the Mbpshi gene (Chr. 18).

Aging↗
PubMed1996

Macrophages and neutrophils infiltrating into the liver are responsible for tissue factor expression in a rabbit model of acute obstructive cholangitis.

Acute obstructive cholangitis (AOC) is one of the most fatal outcomes in sepsis, and frequently complicates disseminated intravascular coagulation (DIC). Recently we found that the plasma tissue factor (TF) level increased and changed in parallel with plasma markers of DIC in patients with AOC. To elucidate the role of TF in the pathogenesis of coagulopathy in AOC, we investigated the plasma levels of TF and its localization by immunohistochemical staining in rabbit models of AOC. Plasma TF activity significantly increased 3 h after the insult (0.63 +/- 0.1¿9 U/ml; p < 0.01) compared with that beforehand (0.05 +/- 0.02 U/ml), then reached a maximum level at 6 h (0.94 +/- 0.16 U/ml). The fluctuations in plasma TF activity correlated with those of the coagulation parameters including platelet count, fibrinogen, prothrombin time, and antithrombin III activity. Immunohistochemically, enhanced expression of TF was mainly detected in macrophages and neutrophils that had infiltrated into the liver sinusoids and around the bile duct, but not in the sinusoidal endothelial cells. A double immunofluorescence study revealed the concomitant presence of TF and fibrin at sites where macrophages and neutrophils had conglomerated. However, we could not detect an apparent change in TF expression in the lung or kidney. These data suggest that macrophages and neutrophils infiltrating into the liver sinusoids and around the bile duct play a pivotal role in TF expression, leading to coagulopathy in the acute phase of obstructive cholangitis in rabbits.

Acute Disease↗
PubMed1996

[Suppression by methylprednisolone of the expression of LFA-1 by alveolar macrophages in irradiated rat lungs].

A common side effect of radiotherapy is the development of fibrosis in the irradiated tissue. To study the effects of methylprednisolone on acute radiation-induced lung injury, we counted neutrophils, lymphocytes, and macrophages, and measured the expression on alveolar macrophages of lymphocyte function associated molecule-1 (LFA-1) in bronchoalveolar lavage fluid recovered from irradiated rat lungs. Twenty 10-week-old male Wistar rats were divided into 4 groups of 5 rats each: (1) a radiation group (R), which received 20 Gy of radiation from 60Co to the left hemithorax in one fraction; (/) a methylprednisolone treatment group (RS), which received the same dose of radiation as the R group, along with 2.0 mg x kg-1 of methylprednisolone (6 alpha methylprednisolone 21-acetate) by intramuscular injection 6 hours before and every 48 hours after irradiation; (3) an untreated control group (C); and (4) a methylprednisolone control group (S), which received the same dosage of methylprednisolone as the RS group. Rats were kept under specific-pathogen-free conditions. Bronchoalveolar lavage of the left lung was done in all 4 groups 2 week after irradiation. The number of neutrophils in the recovered fluid was significantly higher in the R and RS groups than in the C and S groups. The expression of LFA-1 on alveolar macrophages was significantly higher in the R group than in the RS, C, and S groups. The number of neutrophils in bronchoalveolar lavage fluid and the expression of LFA-1 on alveolar macrophages were significantly higher in the R group than in the RS groups. These results suggest that the increase in the expression of LFA-1 on alveolar macrophages and the increase in the number of neutrophils in bronchoalveolar lavage fluid are related to acute radiation-induced lung injury. Methylprednisolone suppressed the expression of LFA-1 on alveolar macrophages and the increase in the number of neutrophils measured in bronchoalveolar lavage fluid 2 weeks after irradiation.

Animals↗
PubMed1996

[Tizanidine for preanesthetic medication].

The effect of tizanidine given as a premedication on perioperative hemodynamics (mean blood pressure, heart rate), sedation, hypnosis and midazolam requirements for induction were assessed in 68 patients scheduled for elective surgery under general anesthesia. Patients were assigned to three groups. Group 1 was premedicated 90 min prior to induction with tizanidine 4 mg po (n = 28); group 2 was premedicated with tizanidine 2 mg po (n = 12); group 3 received no premedication (n = 28). In group 1, increase of mean blood pressure on anesthesia induction was attenuated significantly and sedative and hypnotic effects were stronger significantly compared with other groups. We also found that the amounts of midazolam necessary for loss of consciousness were significantly less in patients who had received tizanidine 4 mg. In conclusion, tizanidine is a useful drug as preanesthetic medication for general anesthesia.

Adjuvants, Anesthesia↗
PubMed1996

The origin of SL family mice.

The origin of SL family mice was studied by analyzing 100 microsatellite loci, the major histocompatibility complex, the Mx gene, murine leukemia provirus, and mammary tumor provirus. From the genetic profile of family members and their history, we assumed the existence of a proto-SL mouse, an ancestor of all SL family members. Many alleles were contributed to the proto-SL by the ancestors related to strains A2G and CF#1, and/or some wild mice. Among four existing family members, SL/Am and SL/Ni mice were almost identical and presumably closest to the proto-SL. The SL/Kh mouse was derived from a cross of the proto-SL and AKR mice, because SL/Kh mice inherited a considerable number of genes from AKR mice, the most outstanding of which were those of the provirus Emv-11 and Thy-1.1. The SL/QDj mice seemed to be a recombinant inbred strain between SL/Am and SL/Kh mice, because their alleles at all 100 microsatellite loci were shared by SL/Am or SL/Kh strains or both. All four SL family members shared the major histocompatibility complex haplotype q.

Animals↗