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Biomedical subjects

H Machida

Publications and source records attributed to H Machida.

At least 91 records · Page 5Linked to original sources
PubMed1990

[Transcatheter arterial embolization for massive abdominal bleeding in post-pancreatoduodenectomy--first report].

Transcatheter arteria embolization (TAE) was carried out for 10 cases (14 times) with massive intra-abdominal bleeding after pancreatoduodenectomy (PD). The results obtained were as follows: 1. The ten patients (carcinoma of the pancreas head 4, carcinoma of the papilla Vater: 3, carcinoma of the bile duct: 2. leiomyosarcoma of the duodenum: 1) included eight men and two women aged 45 to 75, with an average age of 63.7. The time span before TAE was instituted averaged 20.8 days. 2. Infection due to leakage noted in all cases. 3. A good course was noted when manifestation of symptoms related to poor sutures or the onset of intra-abdominal bleeding after PD was delayed and the time from the onset of intra-abdominal bleeding to TAE was short. 4. Bleeding sites could be determined in all cases. Pseudoaneurysm accounted for five and extravasation accounted for nine of the total of 14 bleeding sites. The prognosis was apparently good in cases of pseudoaneurysm as compared with that in cases of extravasation. 5. Bleeding was controlled in all cases. 6. No complication due to TAE occurred. These results indicate the TAE is a safe and effective procedure for the control of massive intra-abdominal bleeding after PD.

Abdomen↗
PubMed1989

Mechanism of selective inhibition of varicella zoster virus replication by 1-beta-D-arabinofuranosyl-E-5-(2-bromovinyl)uracil.

To investigate the mechanism of action of 1-beta-D-arabinofuranosyl-(E)-5-(2-bromovinyl)uracil (BV-araU) on varicella zoster virus (VZV) replication, we examined the metabolism of the drug in VZV-infected cells using 14C-labeled BV-araU. [14C]BV-araU was taken up by the cells infected with thymidine kinase-positive (TK+)VZV, but not so much by TK- VZV-infected or mock infected cells. Most of the radioactivity in TK+ VZV-infected cells that were incubated with [14C]BV-araU was recovered from their acid-soluble fraction, and little from their acid-insoluble fraction. By high performance liquid chromatographic assay of the acid-soluble fraction, it was proved that BV-araU was metabolized to its 5'-monophosphate, diphosphate, and triphosphate only in TK+ VZV-infected cells. The radioactivity was not detected in VZV nucleocapsids or in VZV DNA and cellular DNA isolated from TK+ VZV-infected cells, even if BV-araU was added at a 1000 times higher concentration than the 50% inhibitory dose for VZV replication in vitro. Furthermore, it was enzymatically proved that [14C]BV-araU was selectively and effectively phosphorylated to BV-araU monophosphate by VZV TK and that affinity of BV-araU triphosphate for VZV DNA polymerase was the quite strong. From these results, it can be concluded that marked inhibition of VZV replication by BV-araU is due to selective phosphorylation of BV-araU in the TK+ VZV-infected cells and strong inhibition of VZV DNA synthesis by BV-araU triphosphate, without detectable incorporation into VZV DNA.

Antiviral Agents↗
PubMed1989

[The rabbit thermo-regulatory system. Effects of high dose of sodium fluoride].

The mechanism of sodium fluoride (NaF) induced hypothermia was investigated on relations between the monoamine synthesis and metabolism in the rabbit brain. Five male rabbits per a group, weighing about 2.5kg and having rectal temperatures of 38.4 to 39.3 degrees C, were used in this experiment. The rectal temperature measurements were made by means of an electric thermometer for 5 hours at intervals of 15 or 30 minutes. Through this experiment, animals were housed in a room kept at 22 to 23 degrees C. The following drugs were used in this experiment: NaF (40 mg/kg i.v.), barbital sodium (0.1 g/kg s.c.), hexamethonium bromide (C6, 10 mg/kg i.v.), ergotamine tartrate (30 mg/kg s.c.), phenoxybenzamine hydrochloride (15 mg/kg i.v.), propranolol hydrochloride (5 mg/kg s.c.), pindolol (0.3 mg/kg s.c.), atropine sulfate (30 mg/kg s.c.), 2, 4-dinitrophenol (DNP, 20 mg/kg i.v.), l-DOPA (20 mg/kg i.v.), 5-HTP (20 mg/kg i.v.) Results 1. Intravenous injection of 30 mg/kg of NaF induced a drop of 0.66 degrees C in rectal temperature. 2. Pretreatment with 0.1 mg/kg of barbital sodium or 10 mg/kg of C6 prominently inhibited the NaF-induced hypothermia. 3. The alpha-blockade caused by ergotamine tartrate and phenoxybenzamine or the beta blockade by propranolol hydrochloride and pindolol resulted in an approximate 50% inhibition of maximum drop in body temperature induced by NaF administration. Both alpha- and beta-blockades caused by ergotamine tartrate and propranolol or by phenoxybenzamine and pindolol, however, made a remarkable inhibition of the NaF effect. Cholinergic blockade brought on by atropine sulfate, on the other hand, had no effect against NaF-induced hypothermia. 4. Bilateral splanchnicotomy completely inhibited drops in rectal temperature. 5. Intravenous injection of NaF 40 mg/kg failed to counteract the rise of rectal temperature caused by DNP 20 mg/kg. 6. Pretreatment with l-DOPA made a prominent inhibition of NaF-induced hypothermia. The inhibiting effects of 5-HTP, however, were slight. 7. Administration of NaF made a significant decrease in norepinephrine levels in the rabbit hypothalamus, but had no effect on 5-HT levels.

Animals↗
PubMed1988

Effect of stilbenedisulfonate binding on the state of association of the membrane-spanning domain of band 3 from bovine erythrocyte membrane.

The membrane-spanning domain of bovine band 3, the anion transport protein of erythrocyte membrane, was purified in the presence of nonaethyleneglycol lauryl ether (C12E9) and the effect of a covalent attachment of 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS), a potent transport inhibitor, on the state of association of the domain isolated (the 58 kDa fragment) was studied via gel filtration, gel electrophoresis and sedimentation velocity experiments. It was indicated that the DIDS-unlabeled fragment in C12E9 solution forms heterogeneous aggregates which are larger in size than the dimer. This contrasted with the behavior that bovine band 3 is present as dimers or tetramers in the same medium (Nakashima and Makino (1980) J. Biochem. 88, 933-947). When DIDS was covalently attached, the fragment was present as a single molecular species which was indicated to be a dimer by molecular weight determination. The secondary structure of the fragment was not affected by DIDS. The change in the state of association caused by the DIDS-binding was also found in the presence of sucrose monolaurate (SE12), which was a more potent detergent for extraction of the 58 kDa fragment from membranes than C12E9. However, the complex with SE12 was extremely unstable.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1988

Effects of various nucleosides on antiviral activity and metabolism of 1-beta-D-arabinofuranosyl-E-5-(2-bromovinyl)uracil against herpes simplex virus types 1 and 2.

Uptake of 1-beta-D-arabinofuranosyl-E-5-(2-bromovinyl)uracil (BV-araU) into herpes simplex virus type 1 (HSV-1)- and 2 (HSV-2)-infected cells was elevated about 190 to 40 times, compared with that into mock-infected human embryo lung fibroblast cells. Uptake was not enhanced by infection with thymidine kinase-negative HSV-1 and HSV-2 mutants, however. In HSV-1-infected cells, 9.7% of BV-araU was phosphorylated to BV-araU triphosphate, but only 1.1% was phosphorylated in HSV-2-infected cells. The antiviral effect, uptake, and turnover of BV-araU were inhibited significantly by thymidine (dThd), moderately by deoxyuridine, and not at all by deoxycytidine. On the other hand, the antiviral activity of acyclovir (ACV) was inhibited only by dThd. The effect of BV-araU was influenced by dThd and dThd phosphates (mono-, di-, and triphosphates), and the effect of ACV was influenced only by dThd, which competitively inhibited the phosphorylation of ACV to ACV monophosphate. The combination of 5-fluorodeoxyuridine (FUdR)-BV-araU or FUdR-ACV had a synergistic effect on HSV-1 and HSV-2 replication. The effect of FUdR on the turnover of BV-araU in HSV-1- and HSV-2-infected cells was analyzed by high-performance liquid chromatography. In HSV-1-infected cells, 86% of the BV-araU was phosphorylated to BV-araU triphosphate, but no effect was observed in HSV-2-infected cells, in which 98% of the BV-araU remained as BV-araU monophosphate.

Antiviral Agents↗
PubMed1988

Efficacies of antiherpesvirus nucleosides against two strains of herpes simplex virus type 1 in Vero and human embryo lung fibroblast cells.

Antiviral activities of five nucleoside analogs against the VR-3 and WT-34 strains of herpes simplex virus type 1 (HSV-1) were investigated in Vero and human embryo lung fibroblast (HEL) cells. In HEL cells, the compounds showed antiviral activities against both strains of HSV-1, but in Vero cells, the antiviral activities of the compounds were reduced in proportion to their antiviral indexes (the 50% inhibitory dose [ID50] for cell growth divided by the 50% plaque reduction dose for virus). The ratio of the ID50 in Vero cells to the ID50 in HEL cells was larger in VR-3-infected cells than in WT-34-infected cells. The following results were obtained. (i) Thymidine kinase (TK; EC 2.7.1.21) activity in the VR-3- or WT-34-infected Vero cells was about half that in VR-3- or WT-34-infected HEL cells. Induction of viral TK was especially low in the VR-3-infected Vero cells. (ii) The ID50 of the plaque reduction assay in hypoxanthine, aminopterin, and thymidine medium revealed that the activity of cellular thymidylate synthetase (EC 2.1.1.45) was important in viral replication in VR-3-infected Vero cells. (iii) The VR-3-infected cells required larger thymidine and thymidine phosphate pools for viral replication than the WT-34-infected cells did, although uptake of 1-beta-D-arabinofuranosyl-E-5-(2-bromovinyl) uracil into infected cells was equal for both strains. (iv) In the VR-3-infected Vero cells, the quantity of 1-beta-D-arabinofuranosyl-E-5-(2-bromovinyl)uracil triphosphate was smaller than that in VR-3-infected HEL cells and WT-34-infected Vero and HEL cells.

Acyclovir↗
PubMed1988

Comparison of two bromovinyl nucleoside analogs, 1-beta-D-arabinofuranosyl-E-5-(2-bromovinyl)uracil and E-5-(2-bromovinyl)-2'-deoxyuridine, with acyclovir in inhibition of Epstein-Barr virus replication.

The effect of 1-beta-D-arabinofuranosyl-E-5-(2-bromovinyl)uracil (BV-araU), a new antiviral drug, on Epstein-Barr virus (EBV) was studied and compared with those of E-5-(2-bromovinyl)-2'-deoxyuridine (BVdU) and acyclovir (ACV). BV-araU effectively inhibited EBV replication both in superinfected Raji cells and in virus producer P3HR-1(LS) cells, as determined by density gradient centrifugation, in situ cytohybridization with an EBV DNA probe, and cRNA-DNA hybridization. The 50% effective doses for viral DNA replication were 0.26, 0.06, and 0.3 microM for BV-araU, BVdU, and ACV, respectively. The relative efficacy on the basis of the in vitro therapeutic index was BVdU (6,500) greater than BV-araU (1,500) greater than ACV (850). Synthesis of EBV-induced polypeptides with molecular weights of 145,000 and 140,000 was inhibited by these drugs. Kinetic analysis of reversibility of inhibition of EBV DNA replication after removal of the drugs indicated that BV-araU, like BVdU, has a more prolonged inhibitory effect than ACV. These results indicate that the 2' OH group in the arabinosyl configuration of BV-araU results in marked reduction in anti-EBV activity while slightly diminishing cytotoxicity.

Acyclovir↗
PubMed1987

Antiviral activity of various 1-beta-D-arabinofuranosyl-E-5-halogenovinyluracils and E-5-bromovinyl-2'-deoxyuridine against salmon herpes virus, Oncorhynchus masou virus (OMV).

1-beta-D-Arabinofuranosyl-E-5-bromovinyluracil (BVaraU), 1-beta-D-arabinofuranosyl-E-5-iodovinyluracil (IVaraU), 1-beta-D-arabinofuranosyl-E-5-chlorovinyluracil (CVaraU) and 1-beta-D-arabinofuranosyl-5-vinyluracil (VaraU) were examined for antiviral activity against salmon herpesvirus, Oncorhynchus masou virus (OMV) in vitro using Yamame (Oncorhynchus masou) kidney cells (YNK). BVaraU, IVaraU, CVaraU and VaraU were highly active against OMV; 50% inhibitory concentration (IC50): 0.01, 0.003, 0.003, 0.003 microgram/ml, respectively. The IC50 of 5-bromovinyl-2'-deoxyuridine (BVDU) was 0.3 microgram/ml. The lower activity may be due to cleavage of it N-glycosyl linkage by pyrimidine nucleoside phosphorylases (i.e. thymidine phosphorylase) during the incubation period. The arabinofuranosyl counterparts are resistant to this (these) enzyme(s). Both OMV-induced DNA polymerase and cellular DNA polymerase alpha were strongly inhibited by BVaraU 5'-triphosphate (BVaraUTP). In an in vivo study, daily immersion of OMV-infected chum salmon (Oncorhynchus keta) fry into aqueous solution of BVaraU (5 micrograms/ml, 30 min/day, 30 times) did not increase the life span of infected fish.

Animals↗
PubMed1987

Esophageal function following Livaditis repair of long gap esophageal atresia.

Proximal pouch esophagomyotomy (Livaditis) allows for repair of long gap esophageal atresia (EA). Postoperative esophageal functional studies in these patients are lacking. Six such infants were followed for up to 42 months. Esophageal function was assessed clinically and by barium swallow, manometry, 24 hr pH monitoring, esophagoscopy, and biopsy. Operative complications included two minor anastomotic leaks and two asymptomatic diverticula at the myotomy site. All patients had dysmotility on barium swallow. Gastroesophageal reflux (GER) was seen in four. Manometry showed a variable aperistaltic segment in each infant but lower esophageal sphincter pressures and relaxation were retained. Twenty-four hour pH monitoring showed an increase in frequency and duration of GER. All four patients biopsied had esophagitis. Five of the six patients showed normal growth velocity. Livaditis modified repair of EA was not associated with significant surgical complications. Esophageal motility showed abnormalities similar to those reported after the standard repair of EA. Myotomy did not adversely affect the esophageal function.

Biopsy↗
PubMed1987

Comparative metabolism of E-5-(2-bromovinyl)-2'-deoxyuridine and 1-beta-D-arabinofuranosyl-E-5-(2-bromovinyl)uracil in herpes simplex virus-infected cells.

The antiviral activities and metabolic fates of E-5-(2-bromovinyl)-2'-deoxyuridine (BrVdUrd) and 1-beta-D-arabinofuranosyl-E-5-(2-bromovinyl)uracil (BrVaraUra) were compared in a dThd kinase-deficient human fibroblast cell line, infected with parental strains of herpes simplex virus, and other strains expressing no viral dThd kinase activity. Metabolic experiments were performed at concentrations well above the ID50 for each compound because radiolabeled agents were not available. BrVaraUra and its nucleotides qualitatively displayed chromatographic and anabolic characteristics which closely paralleled those of BrVdUrd and its nucleotides. Monophosphorylation of both drugs was dependent upon the presence of viral dThd kinase activity except in the case of one dThd kinase-negative type 1 mutant (SC16R5C1) which retained BrVdUrd/BrVaraUra kinase activity. Intracellular uptake of either parent compound was absent during mock-infection and minimal in the cases of infection with mutants unable to phosphorylate the parent compound. Parental type 1 strains were able to induce diphosphorylation and triphosphorylation of both compounds to a similar, dose-dependent degree. Extracts of type 2-infected cells contained greater quantities of BrVdUrd and its monophosphate compared with BrVaraUra and its monophosphate, after identical drug exposure and infection conditions. As previously observed for BrVdUrd, diphosphorylated and triphosphorylated nucleotides of BrVaraUra were not detected after type 2 infection. BrVdUrd and BrVaraUra metabolic breakdown pathways differed, however, as evidenced by the formation of E-5-(2-bromovinyl)uracil (BrVUra). Unlike BrVdUrd, BrVaraUra formed no BrVUra in infected cells, suggesting that replacement of 2'-deoxyribose with arabinose makes the compound biologically more stable, presumably because of resistance to enzymatic breakdown by pyrimidine nucleoside phosphorylases. In this dThd kinase-negative cell line, BrVdUrd and BrVaraUra displayed qualitatively similar susceptibility profiles in that activities were type 1 selective and dThd kinase dependent. Antiviral activities against dThd kinase-positive type 1 strains were similar with both compounds. These data would suggest that BrVdUrd and BrVaraUra have identical type-specific dThd-dTMP kinase-dependent mechanisms of cellular uptake and phosphorylation, but that the latter is not subjected to phosphorolysis and resultant formation of an inactive metabolite. Furthermore, the absence of presence of phosphorolysis of the parent nucleoside does not apparently adversely affect in vitro antiviral activity.

Arabinofuranosyluracil↗
PubMed1987

Palatopharyngeal incompetence in association with esophageal dysmotility, acquired glucocorticoid deficiency, and deficient tear production.

An 8 1/2-year-old male is described with the rare triad of acquired adrenal insufficiency, esophageal dysfunction, and alacrima. In addition, he had velopharyngeal insufficiency, which is a previously unreported feature of this syndrome. Although the pathophysiology of this disorder remains to be demonstrated, a defect may be present, linking hormone-receptor cyclic AMP-mediated processes with abnormalities in parasympathetic and voluntary neuronal innervation or transmission.

Child↗
PubMed1986

Comparison of susceptibilities of varicella-zoster virus and herpes simplex viruses to nucleoside analogs.

The susceptibilities of varicella-zoster virus (VZV) and herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) to 17 nucleoside analogs were compared by a plaque reduction assay with human embryonic lung fibroblast cells. The susceptibility of VZV to certain nucleoside analogs was different from that of HSV-1. Against VZV the 5-halogenovinyl-arabinosyluracils were the most potent of the compounds tested.

Antiviral Agents↗
PubMed1986

Susceptibility of varicella-zoster virus to thymidine analogues.

Ten strains of varicella-zoster virus (VZV) were tested for susceptibility to 17 nucleoside analogues by a plaque reduction assay using human embryonic lung fibroblast cells. The compounds employed were 5-substituted arabinosyluracils and 2'-deoxyuridines, 2'-fluoro-arabinosylpyrimidines (F-araPyr) and acyclovir. In terms of the 50% plaque reduction dose (PD50), 4- to 40-fold difference were found between the 10 strains of VZV in susceptibilities to each compound. VZV was highly susceptible to 5-halogenovinyl-arabinosyluracils (XV-araUs); the PD50 values of these compounds were less than 0.001 micrograms/ml. VZV was much more susceptible than herpes simplex virus (HSV) type 1 to XV-araUs, but less susceptible than either HSV type 1 or type 2 to 5-ethyl-2'-deoxyuridine, 5-ethyl-arabinosyluracil and acyclovir.

Acyclovir↗