Biomedical subjects

T Katayama

Publications and source records attributed to T Katayama.

At least 91 records · Page 5Linked to original sources

PubMed1999

[Primary myelofibrosis with fatal mesenteric arterial thromboembolism caused by antiphospholipid syndrome].

A 60-year-old woman was admitted to our hospital in February 1993 due to dizziness, dyspnea, abdominal pain, and high susceptibility to bleeding. Physical examination revealed livedo reticularis of the foot, but did not detect hepatosplenomegaly. Examination of the peripheral blood detected pancytopenia, leukoerythroblastosis, and tear-drop erythrocytes. Primary myelofibrosis (PMF) was diagnosed on the basis of bone marrow biopsy findings. Antiphospholipid syndrome (APS) was confirmed by positive response to anti-cardiolipin antibody and recurrent splenic infarction. Because of factor XIII deficiency, the patient experienced severe gingival bleeding after tooth extraction. Her condition was complicated by mesenteric arterial thromboembolism and she died of sepsis 5 years after onset. Although the incidence of immunopathy in PMF patients is high, few studies to date have focused on APS patients presenting with a variety of severe embolic symptoms. Our patient required careful monitoring due to bleeding tendency and thromboemboli.

Antiphospholipid Syndrome↗

PubMed1999

[Ultrasonogram of carotid artery in endoarterectomy patients].

Ultrasonograms of the carotid artery were compared with the intraoperative finding of atheroma plaque in terms of stenosis, fragility, ulceration and calcification. Soft type, intermediate type and these mixed type plaques were fragile plaques in almost all cases. All hard type plaques were tough plaques. The detection of stenosis and calcification was satisfactory, however that of ulceration was not sufficient. The stenotic lesions frequently existed in bilateral carotid arteries and the intima was easy to become thick even after the endoarterectomy. The ultrasonogram was thought to be the essential study for the carotid artery lesions.

Aged↗

PubMed1999

[Rickettsiae].

Explore the source record for details and available documents.

Enzyme-Linked Immunosorbent Assay↗

PubMed1998

Site-directed mutational analysis for the ATP binding of DnaA protein. Functions of two conserved amino acids (Lys-178 and Asp-235) located in the ATP-binding domain of DnaA protein in vitro and in vivo.

DnaA protein, the initiator of chromosomal DNA replication in Escherichia coli, is activated by binding to ATP in vitro. We introduced site-directed mutations into two amino acids of the protein conserved among various ATP-binding proteins and examined functions of the mutated DnaA proteins, in vitro and in vivo. Both mutated DnaA proteins (Lys-178 --> Ile or Asp-235 --> Asn) lost the affinity for both ATP and ADP but did maintain binding activity for oriC. Specific activities in an oriC DNA replication system in vitro were less than one-tenth those of the wild-type protein. Assay of the generation of oriC sites sensitive to P1 nuclease, using the mutated DnaA proteins, revealed a defect in induction of the duplex opening at oriC. On the other hand, expression of each mutated DnaA protein in the temperature-sensitive dnaA46 mutant did not complement the temperature sensitivity. We suggest that Lys-178 and Asp-235 of DnaA protein are essential for the activity needed to initiate oriC DNA replication in vitro and in vivo and that ATP binding to DnaA protein is required for DNA replication-related functions.

Adenosine Triphosphate↗

PubMed1998

Modulation of apoptotic cell death by extracellular matrix proteins and a fibronectin-derived antiadhesive peptide.

Cell adhesion to the extracellular matrix (ECM) has been implicated in apoptosis in anchorage-dependent cell types. We recently found that a peptide derived from fibronectin (termed III14-2) inhibits the integrin-mediated cell adhesion to ECM. Using this antiadhesive peptide and a variety of ECM proteins, we show here a critical role of the integrin-ECM protein interaction in apoptotic regulation of human umbilical vein endothelial cells (HUVEC). HUVEC in suspension underwent apoptosis under the serum-free conditions, as judged by nuclear and DNA fragmentations. This apoptosis was suppressed to varying degrees when alpha 5 beta 1, alpha v beta 3, and alpha 2 beta 1 integrins were occupied with either soluble or immobilized ECM proteins such as fibronectin, vitronectin, and type I collagen, respectively. Peptide III14-2, which had no effect by itself on the HUVEC apoptosis, disrupted the ligation of alpha 5 beta 1 and alpha v beta 3 but no alpha 2 beta 1 and ultimately led the cells to apoptosis, indicating that this antiadhesive peptide indirectly induces apoptosis by blocking cell survival signal delivered from alpha 5 beta 1 and alpha v beta 3 integrins. Genistein, a protein tyrosine kinase inhibitor, slightly reduced the rescuing effect of fibronectin, whereas sodium orthovanadate and bombesin, which increase in the level of protein tyrosine phosphorylation, made HUVEC less susceptible to apoptosis and blocked the effect of peptide III14-2. HUVEC adhesion to fibronectin substrate raised the tyrosine phosphorylation level of focal adhesion kinase and the expression of cytoprotective Bcl-2 protein, both of which were reversed by the antiadhesive effect of peptide III14-2. Thus, the opposing effects of ECM proteins, including fibronectin and vitronectin, and peptide III14-2 on HUVEC apoptosis appear to be due to the opposing effects of these factors on the signaling pathway which includes tyrosine phosphorylation of FAK and Bcl-2 expression.

Amino Acid Sequence↗

PubMed1998

The initiator function of DnaA protein is negatively regulated by the sliding clamp of the E. coli chromosomal replicase.

The beta subunit of DNA polymerase III is essential for negative regulation of the initiator protein, DnaA. DnaA inactivation occurs through accelerated hydrolysis of ATP bound to DnaA; the resulting ADP-DnaA fails to initiate replication. The ability of beta subunit to promote DnaA inactivation depends on its assembly as a sliding clamp on DNA and must be accompanied by a partially purified factor, IdaB protein. DnaA inactivation in the presence of IdaB and DNA polymerase III is further stimulated by DNA synthesis, indicating close linkage between initiator inactivation and replication. In vivo, DnaA predominantly takes on the ADP form in a beta subunit-dependent manner. Thus, the initiator is negatively regulated by action of the replicase, a mechanism that may be key to effective control of the replication cycle.

Adenosine Triphosphate↗

PubMed1998

Alzheimer-associated presenilin-1 gene is induced in gerbil hippocampus after transient ischemia.

To investigate the biological roles of the presenilin-1 (PS-1) gene after neuronal injury, the changes of PS-1 mRNA expression in the gerbil hippocampus after transient ischemia were examined. From 1 day to 3 day-reperfusion after 5 min-ischemia, PS-1 mRNA was induced in the hippocampus compared with the sham-operated control. The cells which induced the PS-1 genes were neurons of CA3 and dentate gyrus, the region relatively resistant to ischemic stress. These findings suggest that the induction of PS-1 genes may be associated with some responses of neurons damaged by transient ischemia.

Alzheimer Disease↗

PubMed1998

A stimulation factor for hydrolysis of ATP bound to DnaA protein, the initiator of chromosomal DNA replication in Escherichia coli.

Hydrolysis of ATP bound to DnaA protein by its intrinsic ATPase activity negatively controls chromosomal DNA replication in Escherichia coli. We developed a new in vitro assay system for ATP hydrolysis, which makes feasible a search for factors affecting the ATPase activity of DnaA protein. A crude cell extract enhanced the hydrolysis of ATP bound to DnaA protein, in a dose-dependent manner. Gel-filtration analyses revealed a single entity of the stimulation factor for the ATP hydrolysis and an apparent molecular mass of 170 kDa. The stimulation activity for ATP hydrolysis coeluted with the inactivation activity for DnaA protein initiating an oriC DNA replication, as determined by anion-exchange and gel-filtration column chromatographies. Activity of the stimulation factor required DNA and ATP. These observations suggested that IdaA protein, a previously described negative factor for DnaA protein, inactivated DnaA protein through stimulation of the hydrolysis of ATP bound to DnaA protein.

Adenosine Diphosphate↗

PubMed1998

High titers of antibodies inhibiting the binding of envelope to human cells correlate with natural resolution of chronic hepatitis C.

Most cases of hepatitis C virus (HCV) infection result in chronic disease; however, a very small fraction of patients naturally clear the virus and resolve chronic hepatitis. In an attempt to correlate immune response with chronic disease resolution, we compared the antibody response in patients with different outcomes of the infection. Antibody responses to HCV structural proteins were assessed in 34 patients originally diagnosed with acute hepatitis. Five cases resolved acute infection, 22 developed chronic hepatitis, and 7 naturally resolved chronic hepatitis C. To estimate HCV neutralizing antibodies we used the neutralization of binding (NOB) assay, which evaluates inhibition of the envelope-2 protein binding to human cells. Enzyme-linked immunosorbent assay was used for the quantitative assessment of serum antibodies. The presence of HCV RNA was ascertained by reverse transcription-polymerase chain reaction. In 6 of 7 patients naturally recovered from chronic hepatitis C, the emergence and the persistence (for more than 3 months) of high serum titers (>1/600) of NOB antibodies coincided with virus clearance and clinical resolution of hepatitis. NOB antibody activity was observed in only 2 of 5 patients recovered from acute hepatitis C. Chronic patients who did not show any resolution during the course of the study developed low or no NOB antibodies. Because of the correlation between prolonged high NOB titers and natural resolution of chronic hepatitis C, vaccination or passive immunization aimed at high titers of NOB antibodies may be valuable new therapeutic approaches for chronic hepatitis C.

Adult↗

PubMed1998

Surgery for cholecystocholedocholithiasis in a patient with asymptomatic essential thrombocythemia: report of a case.

Essential thrombocythemia (ET) is a myeloproliferative disorder characterized by a remarkable increase in the platelet count and various clinical symptoms. The perioperative management of patients with ET has yet to be determined, especially when there are no clinical symptoms. We report herein the case of a woman with gallstones whose preoperative hematological data showed remarkable thrombocythemia, but her coagulation studies were normal. The Philadelphia chromosome was negative and bone marrow cytology showed a marked increase in megakaryocytes. Surgery was performed under a diagnosis of cholelithiasis with ET. Considering her severe thrombocythemia and obesity, sufficient heparin was administered to prevent deep vein thrombosis; however, this precipitated postoperative bleeding, necessitating a reoperation. A functional abnormality of the patient's platelets was suspected, and the aggregation by adenosine diphosphate was subsequently found to be significantly inhibited. As patients having ET with no symptoms might have depressed platelet aggregability despite remarkable thrombocythemia, when abdominal surgery is performed, prophylactic therapy for deep vein thrombosis should be avoided. Hence, the preoperative aggregation study of platelets might offer useful information about whether postoperative antithrombotic therapy is indicated.

Anticoagulants↗

PubMed1998

Health economics of care for patients with cancer and intractable disease in Japan.

Concern about the economic aspect of cancer care is increasing. However, economic evaluations for cancer care are deficient in a number of areas, despite recent important contributions. To generate better evidence for economic evaluation of care for patients with cancer and intractable disease, the recent trends and problems with economic evaluations in these areas in Japan are examined. Several examples of economic evaluations, such as those concerned with bone marrow transplantation for leukemias, breast-conserving treatment for early breast cancer, and antiemetic treatment for patients receiving cancer chemotherapy, showed substantial possibilities for evaluating value for money in health care with a view to establishing an effective and efficient health care system.

Cost-Benefit Analysis↗

PubMed1998

Malignant fibrous histiocytoma of the stomach: report of two cases.

Malignant fibrous histiocytoma (MFH) in the stomach is very rare, and only four cases have been reported. As a result, there is still little understanding of its clinical and pathological features. We recently experienced two cases of gastric MFH. The first case was a 78-year-old man with epigastralgia and a loss of body weight. Endoscopy revealed an ulcerated submucosal tumor. A gastrectomy was performed and the diagnosis of MFH was made histopathologically. The second case was a 77-year-old man with pulmonary symptoms. An image diagnosis indicated a strong suspicion of lung cancer, and a right middle and lower lobectomy was thus performed. One month after the operation, a bleeding gastric tumor was found and therefore a gastrectomy was performed. Both tumors were diagnosed as MFH. From the analysis of six reported cases including ours, a preoperative correct diagnosis is found to be difficult although the lesion has grown to a considerable size at the time of operation. Since a metastatic lung lesion was first detected in two out of six cases, it is thus recommended that the stomach should be examined when lung MFH is found. Considering the high mortality and the short survival in the six cases, the prognosis for gastric MFH seems to be poorer than that in the extremities. However, lymph node metastasis is uncommon, and a curative resection is possible in some cases such as in our second case.

Adult↗

PubMed1998

The effects of estrogen deficiency on glycosylation of odontoblasts in rats.

To investigate the effects of estrogen deficiency on odontoblast metabolism, we induced osteoporosis in rats by ovariectomy and examined the glycosylation of the matrix component in odontoblasts. Peanut agglutinin (PNA) lectin histochemistry, which detects D-galactose and N-acetylgalactosamine sugars, was conducted in incisor odontoblasts of ovariectomized (OVX) and sham-operated (sham) rats. At 5 wk after the operation, bone mineral density and serum level of estrogen in OVX rats were lower than those in sham rats. PNA binding sites were found in the odontoblasts in incisors, and the binding sites in OVX rats were much stronger than those in sham rats. Furthermore, PNA binding sites were localized at the predentin matrix in OVX rats, but the reaction in sham rats was not detected. Because D-galactose and N-acetylgalactosamine sugars bound to PNA are important constituents of proteoglycans in dentin matrix and the PNA binding sites reflect the proteoglycan production of odontoblasts, these results indicated that galactosyl glycosylation of proteoglycans in odontoblasts is influenced by estrogen deficiency in rat incisors.

Acetylgalactosamine↗

PubMed1998

Expression of an ADP-ribosylation factor like gene, ARF4L, is induced after transient forebrain ischemia in the gerbil.

To elucidate the molecular mechanisms underlying post-ischemic phenomena including delayed neuronal death, we screened for genes which were induced in the hippocampus after transient global ischemia in the Mongolian gerbil by a differential display method, and cloned a gerbil homologue of human ADP-ribosylation factor 4L (ARF4L). Although the physiological roles of ARF4L are unknown, it is likely that ARF4L participates in vesicle transport between the endoplasmic reticulum (ER) and Golgi complex as it contains a GTP binding site, myristoylation site and coatmer binding motif (KKXX). In situ hybridization analysis indicated that the expression of ARF4L mRNA was elevated in neurons of the dentate gyrus (DG) and CA1 regions. In DG, the signals were detected 3 h after ischemia and peaked at 6 h with subsequent gradual reduction. On the other hand, in the CA1 region where cell death occurs in this model, ARF4L mRNA was slightly detected from 1 to 2 days after ischemia but was absent after 3 days. Other vesicle transport-related genes such as ARF1, ARL4 and beta-COP were also induced after 5-min ischemia, suggesting that vesicle transport was activated in hippocampal neurons after ischemic stress. To determine the cause of the induction of ARF4L gene expression after transient ischemia, we examined the changes in ARF4L mRNA expression in HEK 293 cells under hypoxic conditions compared with HSP70. The expression of ARF4L mRNA was elevated at 12 h after hypoxia exposure, similarly to HSP70. These results will help to elucidate the association of upregulation of vesicle transport systems including ARF4L and stress responses of neurons after transient ischemia.

ADP-Ribosylation Factor 1↗

PubMed1998

Mesangial cell apoptosis induced by a fibronectin fragment.

We previously showed that in passive Heymann nephritis (PHN) rats, a large quantity of fibronectin (FN) fragments containing the central cell-binding (CCB) domain and adjacent domains are generated in the kidney and excreted into urine (Nishizawa et al., Biol Pharm Bull 1998; 21: 429-433). To ascertain whether the FN fragments could affect the progression of PHN, we investigated the effect of a 150 K FN fragment containing the CCB and carboxyl-terminal heparin-binding (Hep 2) domains on cultured rat mesangial cells. When rat mesangial cells cultured on FN-coated plates were exposed to the 150 K FN fragment, some mesangial cells detached from the FN substrate and then underwent apoptosis as judged by nuclear and DNA fragmentations. The 150 K FN fragment competitively inhibited the mesangial cell adhesion to the FN substrate in a dose-dependent manner. Furthermore, gelatinzymography of the conditioned medium of mesangial cells showed that the 150 K FN fragment induced and/or potentiated the extracellular matrix (ECM)-degrading proteinases including matrix metalloproteinases (MMPs) of mesangial cells. These results indicate that the 150 K FN fragment may elicit mesangial cell apoptosis by disrupting the mesangial cell adhesion through two distinct ways: the inhibition of mesangial cell adhesion and the ECM-degradation by the 150 K FN fragment-induced MMPs. Thus, FN fragments containing the CCB and adjacent domains generated in the kidneys of PHN rats may be involved in the evolution of the renal injury.

Journal Article↗

PubMed1998

Long-term administration of G-CSF for aplastic anaemia is closely related to the early evolution of monosomy 7 MDS in adults.

There is an increasing incidence of the evolution of myelodysplastic syndrome (MDS) from aplastic anaemia (AA) with immunosuppressive treatment. In paediatric patients G-CSF is also reported to increase MDS evolution, but this process is not precisely understood in children or in adults. Therefore risk factors of MDS evolution in adults are evaluated here. Of 72 patients, five developed MDS. In 47 patients without cyclosporine (CyA) or antithymocyte globulin (ATG) therapy, only one developed MDS with trisomy 8, 242 months after diagnosis. But of 25 patients treated with either CyA or ATG, four developed monosomy 7 MDS within 3 years. Of these 25 patients, 18 were treated with G-CSF and the four patients (22.2%) who developed MDS were found in this group. The cumulative dose and the duration of G-CSF administration were significantly elevated in patients who developed MDS when compared with those who did not, 822.3 +/- 185.0 v 205.4 +/- 25.5 microg/kg (P<0.05) and 187.5 +/- 52.5 v 72.0 +/- 24.6 d (P<0.002), respectively. However these two values for CyA did not differ significantly. Statistically, treatment with CyA, G-CSF and combined G-CSF and CyA were significantly related to MDS evolution. The administration of G-CSF for more than a year was the most important factor (P=0.00). These results suggested that a close relationship exists between G-CSF and subsequent monosomy 7 MDS from AA in adults who receive immunosuppressive therapy. Long-term administration of G-CSF should be prohibited in order to prevent MDS evolution.

Adolescent↗

PubMed1998

Detection of Coxiella burnetii specific DNA in blood samples from Japanese patients with chronic nonspecific symptoms by nested polymerase chain reaction.

The nested polymerase chain reaction (PCR) was used for direct species-specific detection of Coxiella burnetii in blood samples from 52 patients with chronic nonspecific symptoms, but no diagnostic or treatment history of Q fever. All patients had been in ill-health with general fatigue, muscle and joint pain, headache, etc., for one to more than 10 years. Seventeen (33%) showed evidence of C. burnetii infection, based on amplification of 438-bp fragments specific to C. burnetii by nested PCR, and 94% of positive patients reported close contact with animals. In contrast, five (9.6%) of 52 samples from healthy adult controls and two (2.8%) of 70 cord blood samples were positive by nested PCR. These data suggest a high prevalence of infection among adult patients with long term, nonspecific complaints who live in close contact with animals and the possible existence of a chronic post-acute Q fever syndrome in Japan.

Adolescent↗

PubMed1998

Genetic analysis enables definite and rapid diagnosis of cerebrotendinous xanthomatosis.

Mutations in the sterol 27-hydroxylase gene (CYP27) cause cerebrotendinous xanthomatosis (CTX). Early diagnosis of CTX is crucial because treatment with chenodeoxycholic acid can prevent or reverse some of the neurologic disability associated with the disease. We report the identification of three types of mutations (Arg441Trp, Arg372Gln, and Arg441Gln) in the CYP27 gene in five patients with suspected CTX from four unrelated families by restriction endonuclease analysis.

Adult↗