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Biomedical subjects

H Kato

Publications and source records attributed to H Kato.

At least 613 records · Page 34Linked to original sources

The pathogenesis of Kawasaki disease and superantigens.

Kawasaki disease (KD) is an acute febrile illness in infants and children with systemic clinical symptoms, including coronary artery aneurysms. Findings seen in KD patients such as infiltration of T cells into vascular lesions, elevation of soluble interleukin 2 receptors in serum, an imbalance of T cell subsets, and transient depletion of T cells with CD11/CD18 suggest that the activation of T cells is involved in the pathogenesis of KD. In 1992, an interesting mechanism was proposed in which T cell activation by a certain superantigen is involved in the pathogenesis of KD. Examinations have been undertaken extensively to confirm the proposed hypothesis. We, however, still do not have reliable evidence supporting the above hypothesis. In the present paper we review the research papers which support or rule out the view described above. In addition, we discuss the relation between KD and systemic Yersinia pseudotuberculosis infection that manifests clinical symptoms quite similar to those in KD.

Bacterial Toxins↗

[A case of spontaneous intracranial hypotension with a remarkable leakage and collection of CSF].

We reported a case of spontaneous intracranial hypotension (SIH) who exhibited a remarkable leakage and collection of CSF in the spinal vertebral column. A 28-year old woman suddenly developed a severe occipital headache and vomiting. She had no headache while lying, but the headache was severe while sitting and standing. She had no recent history of trauma, but she fell down and hit her neck while skiing 6 months before the onset of headache. Neurological examination, urine and blood tests failed to reveal abnormal findings. Lumbar puncture showed a very low CSF pressure of 10 mmHg. Brain MRI demonstrated diffuse thickening and contrast enhancement of the meninges and spinal MRI displayed a CSF collection in the epidural spaces. RI cisternography showed a CSF leakage and an early accumulation of isotope in the kidneys and urinary bladder. Myelography revealed a CSF leakage at the C2 level from the spinal sac out to the extravertebral tissue and a CSF collection in the epidural spaces in the cervical to lumbar spinal canal. The root sleeves were also visualized by the CSF leakage. Thus, we demonstrated in this patient with SIH the location of CSF leakage at C2 dural sac and an extensive collection of leaked CSF in the epidural spaces, which apparently played a role in the occurrence of SIH.

Adult↗

[Role of pharmacists in the medical team--attempting palliative care].

The Pharmacy Department at our hospital is attempting to develop methods for palliative care, for example of cancer pain or smelly tumors. The participation of pharmacists on the medical team for home care is necessary, because the supply of proper drugs for patients' individual conditions is indispensable in palliative care. Communication between not only patients, but also between their families and us, as well as the maintenance of close contact with the medical team, are important in home care.

Cooperative Behavior↗

Identification of Lactobacillus species of human origin by a commercial kit, API50CHL.

The efficacy of a biochemical kit, API50CHL kit, for identification of intestinal and vaginal lactobacilli from humans was evaluated by comparing with the results of DNA-DNA hybridization assay. The results showed that in total only 52 of the 172 strains (30.2%) tested were identified correctly by the kit at species level. Especially all strains of some species, such as Lactobacillus gasseri and Lactobacillus crispatus, were misidentified as Lactobacillus acidophilus by the kit. However, the kit was found to be reliable for identification of Lactobacillus paracasei, Lactobacillus plantarum, Lactobacillus rhamnosus, and Lactobacillus salivarius. This suggests that the exact identification of Lactobacillus isolates from human stool and vaginal specimens by API50CHL kit is difficult without the support of modern genotypic technique.

Evaluation Studies as Topic↗

The effects of lesions in the nucleus basalis of Meynert and physostigmine on rat frontal cortex acetylcholine level.

To clarify the relationship between acetylcholine (ACh) level in the frontal cortex and the area of lesion in the nucleus basalis of Meynert (nbM), we used ibotenic acid to bilaterally lesion the substantia innominata (SI), including the nbM, in rats and measured extracellular ACh by microdialysis. Baseline level of ACh (ACh-baseline) averaged 0.14 +/- 0.07 ng/40 microl/20 min (n=13) in the steady state. We also measured the size of the lesioned areas in the SI (nbM-lesion) by using a computed image analysis system. Both ACh level and nbM-lesion varied widely among animals. The bilateral nbM-lesion averaged 28 +/- 30% (n=13). The correlation coefficient between ACh-baseline and bilateral nbM-lesion was -0.871 (p<0.01). After intraperitoneal injection of physostigmine, maximum ACh levels increased to 0.18 +/- 0.06 ng/40 microl/20 min, and deltaACh (ACh-max/ACh-baseline) averaged 132 +/- 19% (n=8). There was no apparent correlation between deltaACh and bilateral nbM-lesion. These results show that the size of lesioned area in the bilateral SI was strongly correlated with the baseline ACh level in the frontal cortex, and indicate that the nbM is the major functional source of ACh in the frontal cortex. Our results also suggests that physostigmine possibly affects not only spared nbM-originated cholinergic fibers but also non-nbM-originated cholinergic fibers in the rat with the bilateral nbM lesion.

Acetylcholine↗

[SCC antigen].

Explore the source record for details and available documents.

Antigens, Neoplasm↗

Enhanced continent mechanism of tapered ileum by extramural support from pouch-abdominal wall: an experimental study in dogs.

PURPOSE: To construct a reliable continent tube, which is easy to catheterize, we created and evaluated a new continent cutaneous diversion using a tapered ileum combined with extramural support from the pouch-abdominal wall. MATERIALS AND METHODS: Six dogs underwent a procedure in which two ileal segments were tapered and anastomosed to the ileal pouch. One of the segments (continent) was placed between the back surface of the rectus muscle and the wall of the ileal pouch creating a continent tube. The other segment (control) was brought out into the abdominal skin directly without any support from the pouch-abdominal wall. Urodynamic and radiological studies were carried out postoperatively in all dogs. RESULTS: In the continent tubes, the maximum closure pressure with a full pouch was significantly higher than those with an empty pouch (p<0.01). The maximum closure pressures of the continent tubes were significantly higher than those of the control tubes when the pouch was empty (p<0.01). The leak point pressures of the continent tubes were significantly higher than those of the control tubes (p<0.001). In all dogs, the retrograde radiogram of the continent tubes showed perfect canalization without stenosis. CONCLUSION: This study suggests that the continent mechanism of tapered ileum can be greatly enhanced by fixing it between the abdominal and pouch walls, also allowing easy catheterization in contrast to the submucosal tunnel technique.

Abdominal Muscles↗

Molecular cloning and functional expression of feline thrombopoietin.

Feline thrombopoietin (TPO) was molecularly cloned to establish a basis for cytokine therapy of thrombocytopenia in cats. cDNA clones covering the whole coding sequence of feline TPO were isolated from feline liver. The feline TPO cDNA obtained in this study contained an open reading frame encoding 349 amino acid residues. The predicted amino acid sequence of feline TPO shared 78.7, 69.9, 72.9 and 83.0% similarity with sequences of human, murine, rat and canine TPO, respectively. Four cysteine residues and two of four N-glycosylation sites that are conserved among species were also found at the corresponding positions in feline TPO. The feline TPO cDNA fragment encoding the whole amino acid coding region was recloned into an expression vector, and the resulting vector was transfected into 293T cells using the calcium phosphate method. The supernatant of the transfected 293T cells stimulated the proliferation of a human megakaryoblastic leukemia cell line (UT-7/TPO) cells in a dose dependent manner, indicating that the feline TPO cDNA obtained in this study encodes biologically active feline TPO.

Amino Acid Sequence↗

Genetic analysis of protein C deficiency in nineteen Japanese families: five recurrent defects can explain half of the deficiencies.

We have been studying the molecular basis of protein C deficiency. In this study, we determined the molecular defects of protein C deficiency in 19 Japanese families by using a strategy combining polymerase chain reaction (PCR) and single-strand conformational polymorphism (SSCP) analysis. We identified 10 missense mutations, 1 in-frame deletion, 1 frameshift deletion, 1 frameshift addition, and 1 splice site mutation, 5 of which were novel. From the results of genetic analysis of 67 Japanese families with protein C deficiency reported in this and previous studies, the recurrent defects including Phe139Val and Met365Ile substitutions and a Lys150 d letion, a G8857 deletion, and a splice site mutation of G3079A were only found in Japanese subjects and seemed to be a founder effect. In contrast, Arg169Trp, Arg286His, Val297Met, and Asp359Asn substitutions, all occurring at CG dinucleotides, were commonly observed in not only Japanese but also Western populations, indicating that these are hot spots for mutation in the protein C gene. These 9 recurrent molecular defects were found in 43 families in total, accounting 64% of Japanese families with protein C deficiency. In particular, the recurrent defects of Phe139Val, Arg169Trp, Va1297Met, and Met36-4Ile substitutions and a G8857 deletion were found in 33 families in total, accounting for 49% of Japanese families with protein C deficiency. For the identification of the genetic defect in Japanese patients with protein C deficiency, screening of these recurrent defects by using restriction enzyme cleavage is a rational method.

Exons↗

Crystallization and preliminary crystallographic study of tropinone reductase II from Datura stramonium.

Tropinone reductase II is an NADPH-dependent oxidoreductase involved in a plant alkaloid metabolism. The enzyme from Datura stramonium has been crystallized using 2-methyl-2,4-pentanediol as a precipitant and a macro-seeding technique. The crystal belongs to space group P42212, with cell dimensions a = b = 62.8 and c = 128.4 A. A data set to 2.6 A resolution has been collected at a cryogenic temperature.

Alcohol Oxidoreductases↗

Suppression of Erk activation and in vivo growth in esophageal cancer cells by the dominant negative Ras mutant, N116Y.

Our previous studies demonstrated that introduction of a dominant negative H-ras mutant, N116Y, inhibits the growth of various types of cancer cells in vitro. In this study, we tested the efficacy of N116Y in blocking the growth of esophageal cancer cells using an adenoviral vector. Infection with N116Y adenovirus, (AdCMV-N116Y), in which N116Y expression is driven by the cytomegalovirus promoter, significantly reduced the in vitro growth of all esophageal cancer cell lines studied. Esophageal cancer cells that contained wild-type K-ras and H-ras (TE8, SGF3, SGF7) were more sensitive to AdCMV-N116Y than HEC46 cells that expressed mutant K-ras protein. Most importantly, direct injection of AdCMV-N116Y into TE8- or SGF3-induced tumors in nude mice suppressed their growth significantly. To examine the suppressive mechanism of N116Y, cell cycle profile and the activation of extracellular signal-regulated kinase 2 (Erk2) were examined by flow cytometry and Western blot analysis, respectively. In TE8 cells, progression into S phase was clearly blocked after infection with AdCMV-N116Y. Infection with AdCMV-N116Y did not strongly suppress the activation of Erk2 after EGF stimulation in serum-starved HEC46 cells, whereas it completely suppressed activation in TE8, SGF3 and SGF7 cells. Our observations suggest that N116Y reduces growth of human esophageal cancer cells and suppresses the activation of Erk2; they also indicate that N116Y is a potential candidate gene for human esophageal cancer gene therapy.

Adenoviridae↗

New genotypes of TT virus (TTV) and a genotyping assay based on restriction fragment length polymorphism.

A phylogenetic analysis, using the open reading frame I sequence of 93 TT viruses (TTV) obtained from various geographical areas, indicated that the virus could be classified into six different genotypes including three hitherto unreported genotypes. The high reliability of the six clusters was confirmed by bootstrap analysis. On the basis of these sequence data, a new simple genotyping assay based on a restriction fragment length polymorphism of TTV was developed. Using the enzymes NdeI and PstI, followed by cleavage with NlaIII or MseI, it was possible to distinguish between the six TTV genotypes. This system will provide the framework for future detailed epidemiological and clinical investigations.

Base Sequence↗

Sequential changes of dopaminergic receptors in the rat brain after 6-hydroxydopamine lesions of the medial forebrain bundle.

We investigated the sequential patterns of changes in dopamine uptake sites, D1 and D2 receptors in the brain of animals lesioned with 6-hydroxydopamine using quantitative receptor autoradiography. The rats were unilaterally lesioned in the medial forebrain bundle and the brains were analyzed at 1, 2, 4 and 8 weeks postlesion. Degeneration of the nigrostriatal pathway caused a significant loss of dopamine uptake sites in the ipsilateral striatum, substantia nigra (SN) and ventral tegmental area (VTA) in the lesioned animals. Dopamine D1 receptors were significantly increased in the ventromedial part of striatum of the ipsilateral side from 2 to 4 weeks postlesion. In the ipsilateral SN, a transient increase in dopamine D1 receptors was observed only 1 week after lesioning. However, the frontal cortex, parietal cortex and dorsolateral part of the striatum showed no significant change in dopamine D1 receptors throughout the experiments. On the other hand, dopamine D2 receptors were decreased increased in the ipsilateral SN and VTA from 1 week to 8 weeks postlesion. In the ipsilateral striatum, dopamine D2 receptors were increased in the dorsolateral part from 2 weeks to 8 weeks and in the ventromedial part from 2 weeks to 4 weeks. However, the frontal cortex and parietal cortex showed no significant change in dopamine D2 receptors during postlesion. In the contralateral side, most of regions examined showed no significant change in dopamine uptake sites, dopamine D1 receptors and dopamine D2 receptors during postlesion except for a transient change in a few regions. These results demonstrate that 6-hydroxydopamine can cause a severe functional damage in dopamine uptake sites in the striatum, SN and VTA. Our findings also suggest that the up-regulation in dopamine D2 receptors is more pronounced than that in dopamine D1 receptors in the brain after 6-hydroxydopamine treatment. Furthermore, our results support the existence of dopamine D2 receptors on the neurons of SN and VTA. Thus, our findings provide insights into the pathogenesis of Parkinson's disease.

Adrenergic Agents↗

Expression of proto-oncogenes and gene mutation of sarcomeric proteins in patients with hypertrophic cardiomyopathy.

Several mutations of cardiac beta-myosin heavy chain (beta-MHC) gene were reported in patients with hypertrophic cardiomyopathy (HCM). Involvement of proto-oncogenes has been shown in the mechanism of experimental cardiac hypertrophy. This study sought to examine the effects of c-H-ras and c-myc expression in the steady-state myocardium on hypertrophic changes and to evaluate the possible interaction between beta-MHC mutation and proto-oncogene expression in HCM. Endomyocardial biopsy was performed in 17 HCM patients (5 beta-MHC mutations and 1 troponin T mutation) and 7 control subjects (no mutation). Reverse transcription-polymerase chain reaction analysis revealed c-H-ras expression in all members of both groups. Cardiomyocyte size was correlated with the expression level of c-H-ras (P<0.001), and c-H-ras expression was upregulated in HCM patients (P<0.01). HCM patients with a beta-MHC mutation had the higher c-H-ras expression than did control subjects or patients without a mutation (P<0.01). c-myc mRNA was expressed in 7 of 17 HCM patients but not in control subjects. Myocyte size was greater in c-myc-positive HCM patients than in control subjects and c-myc-negative HCM patients (P<0.001 and P<0.05, respectively). The proto-oncogene expression did not affect clinical findings, myocardial fibrosis, or disarray. In conclusion, c-H-ras and c-myc expression in the steady-state myocardium may play a role in the hypertrophic mechanism in HCM. It is possible that ss-MHC gene mutation has some effect on the regulation of proto-oncogene expression in HCM.

Adolescent↗

Alterations in [3H]L-N(G)-nitroarginine binding in brain after transient global or transient focal ischemia in gerbils and rats.

We investigated the post-ischemic change in [3H]L-N(G)-nitroarginine binding as a marker of nitric oxide (NO) synthase in the animal brain after transient global ischemia or transient focal ischemia. Transient global ischemia in gerbils was induced for 10 min followed by 1 h to 7 days of recirculation. Transient focal ischemia in rats was induced for 45 min followed by 3 days of recirculation. Following transient global ischemia, [3H]L-N(G)-nitroarginine binding showed a significant increase in the striatum (17-18%) and hippocampal CA1 sector (24%) at 48 and 24 h after recirculation, respectively. The hippocampal CA3 sector also showed a significant elevation (32-40%) in [3H]L-N(G)-nitroarginine binding at 24 and 48 h after global ischemia. Furthermore, the dentate gyrus showed a significant increase (30-32%) in [3H]L-N(G)-nitroarginine binding at 5, 24 and 48 h after global ischemia. Thereafter, a significant reduction in [3H]L-N(G)-nitroarginine binding was observed only in the dentate gyrus 7 days after recirculation. In contrast, [3H]L-N(G)-nitroarginine binding was unchanged in the thalamus throughout the recirculation periods. Histological analysis revealed that transient global ischemia caused severe damage or cellular damage in the striatum and the hippocampal CA1 sector. The hippocampal CA3 sector and thalamus were mildly damaged, whereas the dentate gyrus was morphologically intact. Following transient focal ischemia, a marked elevation (50-52%) in [3H]L-N(G)-nitroarginine binding was found in the regions of the ipsilateral striatum in which severe infarction occurred. Our findings suggest that [3H]L-N(G)-nitroarginine binding increases in the striatum and hippocampus after transient global ischemia or transient focal ischemia. This increase in [3H]L-N(G)-nitroarginine binding may play a pivotal role not only in the pathogenesis of ischemic brain damage, but also in the restoration of injury areas after cerebral ischemia.

Animals↗

Two sib cases of Leber congenital amaurosis with cerebellar vermis hypoplasia and multiple systemic anomalies.

Leber's congenital amaurosis (LCA), a type of congenital blindness, is clinically and genetically heterogeneous and often associated with systemic anomalies. We report on two sisters who were born to a consanguineous couple and had retinitis pigmentosa-like pigmented retinal lesions, alternating exotropia, bilateral cataracts, and anomalous coarse facies characterized by deformed skull with narrow forehead, low anterior hairline, hypertelorism, short philtrum, thin upper lip, and prominent jaw; cerebellar vermis hypoplasia; dilatation of the fourth ventricle; severe mental retardation; tremor; brisk deep tendon reflexes and abnormal behavior; and skeletal abnormalities such as limited extension of elbow and/ or finger joints and talipes equinovalgus. Skin defect and renal anomalies were seen in only one patient. Our patients are the first familial LCA associated with cerebellar vermis hypoplasia, and the disease involving particular multiple systemic anomalies may represent a distinct clinical entity.

Abnormalities, Multiple↗

A second p53-related protein, p73L, with high homology to p73.

The p53 protein, which regulates the rate of cell division and death, is the most frequently mutated tumor suppressor to be identified so far in human cancers. Recently, a gene with significant homology to p53, termed p73, has been identified in a chromosomal region that is implicated in the molecular pathogenesis of neuroblastoma. We have cloned a second human p53-related gene, termed p73L, which shows strong amino-acid similarity to p73. The p73L gene is mapped to human chromosome 3q27-28 using in situ hybridization technique. p73L encodes a protein of 586 amino acids and its putative DNA binding domain (DBD) has high identities to those of p53 (60.6%) and to p73 (87.8%). Northern blot analysis, which demonstrated that the expression profiles of p73L and p73 mRNAs are distinct in some tissues, implies that p73 and p73L may have separate, distinct roles in different tissues.

Amino Acid Sequence↗

Plasmin can reduce the function of human beta2 glycoprotein I by cleaving domain V into a nicked form.

beta2-Glycoprotein I (beta2GPI) is a highly glycosylated plasma protein with the ability to bind negatively charged substances such as DNA, heparin, dextran sulfate, and negatively charged phospholipids. The most relevant physiological role of beta2GPI is supposed to be the regulation of the function of anionic phospholipids like cardiolipin (CL). beta2GPI consists of a single polypeptide chain (326 amino acid residues) with a molecular mass of about 50 kD and with five tandem repeated domains (I, II, III, IV, and V). In the previous study, we found that factor Xa can produce the nicked form by cleaving Lys 317-Thr 318, using recombinant human domain V (r-Domain V). However, the reaction was extremely slow. In the present paper, we found that plasmin can produce the nicked form of domain V, using recombinant domain V (r-Domain V) and beta2GPI from human plasma. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, r-Domain V was rapidly cleaved into a nicked form by plasmin, very slowly by factor Xa, but not by thrombin, tissue-type plasminogen activator, urokinase, and tissue factor/factor VIIa. The cleavage site of r-Domain V and beta2GPI by plasmin was proved to be Lys 317-Thr 318 by amino acid sequence analysis of the digest and of the C-terminal peptide isolated by high-performance liquid chromatography. The cleavage was completely inhibited by plasmin inhibitor (alpha2PI). The nicked form was demonstrated to show reduced affinity for CL with a dissociation constant of one order of magnitude larger than that of the intact beta2GPI. To determine whether the specific cleavage of beta2GPI by plasmin can occur also in plasma, human plasma was first acid-treated to inactivate alpha2PI and then incubated with urokinase. About 12% of beta2GPI in plasma was nicked when alpha2PI activity decreased to 80%. The nicked form was not generated in plasminogen-depleted plasma. These results suggest that plasmin can produce the nicked form of beta2GPI with the reduced ability to bind phospholipids in vivo.

Amino Acid Sequence↗