Prolonged hyperbilirubinemia after living-related liver transplantation: a pediatric case report.
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Biopsy↗
Biomedical subjects
M Yoshioka
Publications and source records attributed to M Yoshioka.
Regulation of haptoglobin secretion by recombinant bovine cytokines in primary cultured bovine hepatocytes.
We examined the regulation of haptoglobin (Hp) secretion in primary cultured bovine hepatocytes using recombinant bovine (rb) proinflammatory cytokines. The concentrations of Hp in the supernatant of cultured hepatocytes after incubation with rb interleukin (IL)-6, rb tumor necrosis factor (TNF)-alpha, rbIL-1 beta or rbIFN-gamma alone or with combinations of two of these cytokines were measured by ELISA. The rbIL-6, rbTNF-alpha and rbIL-1 beta increased Hp synthesis, but rbIFN-gamma did not, and rbIL-6 was the most effective Hp inducer among these cytokines. The Hp secretion was accelerated synergistically by combined treatment with rbIL-6 and rbTNF-alpha, whereas it remained unchanged with a combination of rbIL-6 and rbIL-1 beta. In contrast, the combination of rbIL-6 and rbIFN-gamma downregulated Hp secretion. In conclusion, IL-6 is the principal cytokine in Hp secretion in bovine hepatocytes in vitro, and its activity may be regulated by other cytokines.
Albumins↗
Antigenic properties of the GroEL-like protein of Campylobacter rectus.
The purpose of this study was to clarify the antigenic properties of the GroEL-like protein of Campylobacter rectus using a specific polyclonal antibody directed to the purified 64-kDa GroEL-like protein (pAb-CrGroEL), a polyclonal antibody directed to the Actinobacillus actinomycetemcomitans GroEL-like protein (pAb-AaGroEL) and a monoclonal antibody against the recombinant human HSP60 (mAb-HuHSP60). In SDS-PAGE/Western immunoblotting analysis, mAb-HuHSP60, pAb-CrGroEL and pAb-AaGroEL were found to react with the GroEL-like protein (64-kDa) present in all C. rectus strains. A 150-kDa protein in C. rectus ATCC 33238 also reacted strongly with pAb-CrGroEL. This 150-kDa protein was found to be present on the surface-associated material of bacterial cells, as determined by transmission electron microscopy and immunogold labelling of cells with pAb-CrGroEL. Analysis of the first 20 N-terminal amino acids of the sequence of the 150-kDa protein revealed a strong homology (80%) with the C. rectus surface layer (S-layer) protein. Investigation of the biochemical nature of antigenic determinants using periodic acid and proteolytic enzymes showed that the C. rectus GroEL-like protein possessed immunodominant epitopes in both peptide and carbohydrate chains, and that the immunoreactive determinants of the 150-kDa protein belonged to carbohydrate. These results suggest that the GroEL-like protein and the S-layer protein of C. rectus may share the same carbohydrate epitopes.
Aggregatibacter actinomycetemcomitans↗
Behavioural and pharmacological relevance of stroke-prone spontaneously hypertensive rats as an animal model of a developmental disorder.
The present study evaluates juvenile stroke-prone spontaneously hypertensive rats (SHRSP) as an animal model of a developmental disorder, which is diagnosed according to hyperactivity-impulsivity and/or inattention. To characterize behavioural alterations, we studied motor activity, as well as emotional and cognitive behaviours in juvenile SHRSP, with and without methylphenidate, a psychostimulant. Ambulatory and rearing activities in the open-field environment were significantly higher in SHRSP than in Wistar-Kyoto rats (WKY). In the elevated plus maze task, the entries into open arms, as an index of impulsivity, were significantly increased in SHRSP. In the Y-maze task, spontaneous alternation behaviour, as an index of attention, was significantly lowered in the male SHRSP, but not in the female SHRSP, indicating that spontaneous alternation deficit is gender specific. Methylphenidate (0.01-1 mg/kg, i.p.) significantly attenuated locomotor hyperactivity at low doses and dose-dependently improved the spontaneous alternation deficit in SHRSP. Our findings reveal that juvenile SHRSP manifest problematic behaviours resembling a developmental disorder, attention-deficit/hyperactivity disorder (ADHD), namely hyperactivity-impulsivity and/or inattention. Methylphenidate alleviated the behavioural symptoms of hyperactivity and inattention. We propose that juvenile SHRSP are an appropriate animal model of a developmental disorder resembling ADHD, from behavioural and pharmacological perspectives.
Animals↗
[Veno-venous ECMO for the respiratory failure after coronary artery bypass grafting].
We encountered a 60-year-old man with severe respiratory failure after CABG. The patient received veno-venous extracorporeal membrane oxygenation (ECMO) in which blood was drained from the right atrium through a cannula and was returned via a cannula in the left femoral vein. During ECMO, the flow rate was 2.8-3.0 l/min (about 40 ml/kg/min) and the assist was needed for 5 years. Veno-venous ECMO is a simple and effective therapy for acute respiratory failure unresponsive to conventional treatment.
Acute Disease↗
Suppressive effect of zearalenone, an estrogenic mycotoxin, on bovine neutrophil chemiluminescence.
The effects of zearalenone (ZEA), an estrogenic mycotoxin produced by Fusarium fungi, on bovine neutrophils were investigated in vitro using chemiluninescence, a bactericidal parameter. ZEA suppressed luminol-dependent, phorbol 12-myristate 13-acetate (PMA)-elicited chemiluminescence in a dose-dependent manner at concentrations of 10(-4) M and 10(-5) M. No significant suppression was observed at concentrations lower than 10(-6) M. The possible mode ofaction of 10(-4) M ZEA on the cell activity was investigated with special reference to intracellular Ca2+ ([Ca2+]i) release and estrogen receptors. The 10(-4) M ZEA treatment significantly impaired [Ca2+]i release. When pretreated with a low dose (10(-6) M) of PMA, the cells resisted the ZEA-induced chemiluminescence suppression. However, pretreatment of the cells with the estrogen receptor blockers Tamoxifen and ICl 182,780 (both at 10(-6) M) did not annul the suppressive ZEA action. Considering that PMA is an activator of protein kinase C (PKC), a signal transducing enzyme, and in association with a rise in [Ca2+]i causes cytosolic PKC to shift to the plasma membrane where the activated PKC triggers a varied array of cellular responses, the pharmacological dose of ZEA might have suppressed chemiluminescence by hindering the release of [Ca2+]i and the PKC shift. The results of pretreatment with estrogen receptor blockers, however, did not support the suggestion that the ZEA treatment affected the cells via estrogen receptor pathways.
Animals↗
Involvement of interleukin-1beta/nitric oxide pathway in the postischemic impairment of long-term potentiation of the rat hippocampus.
To investigate whether postischemic cerebral dysfunction occurs via the interleukin-1 beta/nitric oxide (IL-1beta/NO) pathway, we examined the effects of an IL-1beta antagonist on long-term potentiation (LTP) impairment and excessive NO production in the rat hippocampus after 10-min global ischemia. Intracerebroventricilar administration of the IL-1beta antagonist attenuated NO production and rescued LTP impairment in the perforant path-dentate gyrus synapses, observed 1 day and 4 days after ischemic insult, respectively. There was an inverse relationship between LTP in the dentate gyrus synapses and hippocampal NO production. Centrally applied IL-1beta mimicked the consequences of transient ischemia in LTP formation and hippocampal NO production in non-ischemic rats. These findings indicate that the IL-1beta/NO pathway is involved in the hippocampal LTP impairment observed in the postischemic brain.
Animals↗
Effects of CP-99, 994, a tachykinin NK(1) receptor antagonist, on abdominal afferent vagal activity in ferrets: evidence for involvement of NK(1) and 5-HT(3) receptors.
The effect of CP-99, 994, a tachykinin NK(1) receptor antagonist, on abdominal vagal afferent nerve activity in the ferret was investigated. Substance P (1 microg/kg, i.v.) increased vagal afferent activity by 449.0+/-51.9% and this was reduced to 145.9+/-5.7% (p<0.01) by pre-treatment with CP-99, 994 (1 mg/kg, i.v.), and to 149.5+/-1.5% (p<0.001) by granisetron (1 mg/kg, i.v.), a 5-HT(3) receptor antagonist. In addition, the increase in vagal nerve activity induced by 5-HT (25 microg/kg, i.v., 552.0+/-57.0% increase from pre-injection level) was significantly reduced (401.3+/-10.6% increase from pre-injection level, p<0.05) by CP-99, 994 (100 microg/kg, i.v.). These results provide evidence for an involvement of peripheral NK(1) and 5-HT(3) receptors in substance P-induced vagal afferent activation. While the functional consequences (if any) of such peripheral effects were not investigated, they could contribute either directly (e.g. by blockade of receptors on vagal afferents) or indirectly (e.g. modulation of 5-HT release or reduction of local inflammatory response) to the antiemetic effects of CP-99, 994 against cisplatin and other emetic agents acting primarily via the vagus.
Abdomen↗
Sodium-coupled glucose transporter as a functional glucose sensor of retinal microvascular circulation.
To clarify the function of the Na(+)-coupled glucose transporter in the regulation of cellular tone of cultured retinal pericytes, we investigated the effects of extracellular glucose concentration on cell size. The surface area and diameter of cultured bovine retinal pericytes under different glucose concentrations were measured by using a light microscope with a digital camera. We also examined the effects of extracellular Na(+) and Ca(2+), inhibitors of the Na(+)-coupled glucose transporter and Na(+)-Ca(2+) exchanger, a Ca(2+) channel blocker, and nonmetabolizable sugars on cell size. The surface area and diameter of the cells changed according to extracellular glucose concentrations. alpha-Methyl glucoside, which enters the cell through the Na(+)-coupled glucose transporter, induced cellular contraction. However, the cells did not contract in response to 2-deoxyglucose, which enters the cell through a facilitated glucose transporter. Glucose-induced cellular contraction was abolished in the absence of extracellular Na(+) and Ca(2+). Moreover, phlorizin, an inhibitor of the Na(+)-coupled glucose transporter, and 2',4'-dichlorobenzamil-HCl, an inhibitor of the Na(+)-Ca(2+) exchanger, also abolished glucose-induced cellular contraction, whereas nicardipine, a Ca(2+) channel blocker, did not. Our results indicate that high extracellular glucose concentrations induce contraction of bovine retinal pericytes via Na(+) entry through a Na(+)-coupled glucose transporter, suggesting that the Na(+)-coupled glucose transporter may act as a functional glucose sensor of retinal microvascular circulation.>
Amiloride↗
Gestational age and gender-specific in utero V(D)J recombinase-mediated deletions.
Recent studies have brought to the forefront the importance of somatic mutations during human fetal development and malignant transformation in children, specifically leukemia. Therefore, a better understanding of the frequency and mutational spectrum of spontaneous in utero mutations is essential for understanding the genetic mechanisms associated with pediatric malignancies. Previously we reported that the frequency of somatic mutations during the late stages of fetal development was dependent on both gestational age and gender. Here we present the hypoxanthine-guanine phosphoribosyltransferase (HPRT) reporter gene mutational spectra analysis for 60 T-cell mutant isolates from the umbilical cord blood of preterm newborns to gain insight into background mutational events during the late stages of fetal development. Logistic regression analyses showed a significant increase in HPRT deletions mediated by V(D)J recombinase in preterm newborns compared with full-term newborns (P = 0.009). A comparative analysis of deletion mutations also revealed that V(D)J recombinase-mediated HPRT deletions increased with decreasing gestational age (P = 0.012) and were significantly higher in females than males of the same developmental status (P = 0.031). Developmental and gender-specific differences in HPRT deletions mediated by V(D)J recombinase provide insight into the gender-specific differences seen in infant leukemia.
Base Sequence↗
Evaluation of the genotoxicity of the phytoestrogen, coumestrol, in AHH-1 TK(+/-) human lymphoblastoid cells.
Coumestrol, a phytoestrogen found in high levels in alfalfa and red clover, is of concern since endocrine disorders have been observed in farm animals exposed to high levels of phytoestrogens. Previous studies found that coumestrol was an effective inducer of DNA strand breaks, micronuclei, and mutations in the Hypoxanthine phosphoribosyl transferase (HPRT) gene of Chinese hamster ovary cells. In the experiments presented here, we extended the previous studies to examine the effect of coumestrol exposure on AHH-1 TK(+/-) human lymphoblastoid cells. Micronuclei were induced with the highest frequency occurring at day 2 after exposure. Flow cytometric analysis of annexin V-FITC-7-aminoactinomycin D stained cells indicated that the primary pathway of cell death was by apoptosis. Mutations were induced in the Thymidine Kinase (TK) gene and were due primarily to the induction of clones with the slow-growth phenotype. Subsequent molecular analysis revealed the loss of exon 4 in the coumestrol-induced clones, indicative of loss-of heterozygosity and consistent with a proposed inhibition of topoisomerase-II activity as a mechanism of action for coumestrol. Taken together, these results suggest that coumestrol exhibits both mutagenic and clastogenic properties in cultured human lymphoblastoid cells.
Base Sequence↗
Immunosuppressive and non-immunosuppressive immunophilin ligands improve H(2)O(2)-induced cell damage by increasing glutathione levels in NG108-15 cells.
We examined the effects of FK506 and its non-immunosuppressive derivative, GPI1046, on H(2)O(2)-induced oxidative cell damage in NG 108-15 cells. Our results suggest that the protective properties of GPI1046 are equipotent with those of FK506 and may be mediated by increased intracellular concentrations of glutathione (GSH). Thus, non-immunosuppressive immunophilin ligands such as GPI1046 might be potentially for neurodegenerative diseases, particularly since they do not have serious side effects such as immune deficiency.
Cell Line↗
Unusual presentation of measles giant cell pneumonia in a patient with acquired immunodeficiency syndrome.
The typical clinical presentation of measles in a normal immunocompetent host includes cough, coryza, conjunctivitis, Koplik's spots, and rash. However, in an immunocompromised host, measles may have an atypical clinical presentation and may be commonly associated with severe pneumonia or encephalitis. We report a fatal case of measles pneumonia without any clinical features that suggest measles in a patient with acquired immunodeficiency syndrome.
Acquired Immunodeficiency Syndrome↗
Loss of alveolar basement membrane type IV collagen alpha3, alpha4, and alpha5 chains in bronchioloalveolar carcinoma of the lung.
Type IV collagen, the major component of basement membrane (BM), is composed of six genetically distinct alpha(IV) chains. This study investigated for the first time the expression of these six alpha(IV) chains immunohistochemically, using alpha(IV) chain-specific monoclonal antibodies, in normal lung and in small (less than 2 cm in diameter) adenocarcinoma of the lung with a bronchioloalveolar growth pattern at the periphery. Small adenocarcinomas were histopathologically classified into three subtypes: bronchioloalveolar carcinoma (BAC) without collapse, BAC with collapse, and adenocarcinoma with bronchioloalveolar features. In normal lung, alveolar BM was composed of alpha1(IV)/alpha2(IV) chains and alpha3(IV)/alpha4(IV)/alpha5(IV) chains. In non-collapsed areas of BAC, alveolar BM was composed of linear alpha1(IV)/alpha2(IV) chains and discontinuous alpha3(IV)/alpha4(IV)/alpha5(IV) chains. In collapsed areas of BAC, alveolar BM was composed of linear and thick alpha1(IV)/alpha2(IV) chains only, because of the complete loss of alpha3(IV)/alpha4(IV)/alpha5(IV) chains. In invasive areas of adenocarcinoma with bronchioloalveolar features, alpha1(IV)/alpha2(IV) chains around the cancer cell nests were disrupted, in addition to the complete loss of alpha3(IV)/alpha4(IV)/alpha5(IV) chains. In conclusion, during the process of stromal invasion of lung adenocarcinoma, type IV collagen of alveolar BM is remodelled from the complete type, composed of alpha1(IV)/alpha2(IV)/alpha3(IV)/alpha4(IV)/alpha5(IV) chains, to the incomplete type, composed of only alpha1(IV)/alpha2(IV) chains, before the disruption of alpha1(IV)/alpha2(IV) chains. These findings may help to clarify the molecular mechanisms of cancer invasion.
Adenocarcinoma, Bronchiolo-Alveolar↗
Electron-microscopic and immunohistochemical studies of eyelid reopening in the mouse.
The development of the eyelids was studied in the mouse from birth to day 12. In transmission electron microscopy (TEM), the desmosome-mediated cell-to-cell adhesions were clearly observed from day 0 to 10 after birth in the junctional region where the upper and lower eyelids fuse. The keratinizing cells in the junctional region, especially in the middle area where the separation occurs by about day 12, gradually elongated toward both surfaces of the fused eyelid with development. In immunohistochemistry, the existing pattern of keratin-positive cells showed distinct developmental changes. Expression of keratin 1 started to extend from the epidermal surface to the junctional region by day 4, and reached the conjunctival part of the junctional region by about day 8. After day 10 keratin 1 began to disappear from the epidermal surface, and by about day 12 keratin 1 almost disappeared from the entire epithelium of the eyelids. Expression pattern of keratin 7 was very similar to that of keratin 1. These findings indicate that epithelial cell differentiation progresses from the skin through to the junctional region to conjunctiva, which may play a role in the eyelids, separation.
Age Factors↗
Complete cure of malignant lymphoma of the stomach with a huge adrenal lesion achieved by preoperative chemotherapy and surgery: report of a case.
We report herein the case of a 53-year-old woman with malignant lymphoma of the stomach who was successfully treated by preoperative chemotherapy and surgery. The patient consulted our hospital with the chief complaint of upper abdominal pain. Endoscopy demonstrated a protruding lesion at the antral posterior wall of the stomach, and a post-biopsy pathological diagnosis of diffuse large cell type B-cell lymphoma was established. Moreover, abdominal ultrasonography, computed tomography, and magnetic resonance imaging demonstrated a tumor measuring approximately 10cm in diameter in the left adrenal gland. A total of three courses of chemotherapy using the CHOP regimen were given preoperatively. The CHOP regimen consisted of 100mg of prednisolone administered for 8 days together with 1.9mg of vincristine, 1,000mg of cyclophosphamide, and 60mg of epirubicin administered intravenously on the first day. This resulted in tumor shrinkage, and a distal gastrectomy, lymph node dissection, and left adrenalectomy were subsequently performed. Since the pathological findings of the resected tissue specimen demonstrated complete elimination of the malignant lymphoma, this combination of procedures was defined as having resulted in a complete response. The postoperative course of this patient was uneventful. She is still alive without any sign of tumor recurrence 6 years after her operation, and is being followed up at the outpatient clinic.
Adrenal Gland Neoplasms↗
Reconstruction of the portal vein using a peritoneal patch-graft.
BACKGROUND: Reconstruction of the portal vein with autologous veins requires extra incisions. Prosthetic material is associated with an increased risk of infection. We therefore created an animal model of portal vein reconstruction using the peritoneum. METHODS: A 2.5 x 2.5 cm piece of the peritoneum was resected from Landrace pigs weighing 30 to 40 kg and was dipped in 100% alcohol for 10 minutes. The anterior wall of the portal vein measuring 1.2 x 0.6 cm was resected. The peritoneal patch-graft fitting the defect of the portal vein was used to repair it. RESULTS: All 7 pigs survived the surgery, and were killed at 2, 7, 7, 14, 21, 35 and 49 days, respectively, after surgery. There was no evidence of thrombosis or obstruction of the reconstructed portal vein or any other complications. Complete endothelialization of the patches were noted at day 14. CONCLUSIONS: Our patch-graft technique using the peritoneum is considered to be a good and safe alternative for reconstruction after partial resection of the portal vein in clinical surgery.
Animals↗
Aminoguanidine prevented the impairment of learning behavior and hippocampal long-term potentiation following transient cerebral ischemia.
The present study was performed to investigate whether increases in nitric oxide (NO) production via inducible nitric oxide synthase (iNOS) were involved in impairment of learning behavior and hippocampal long-term potentiation (LTP) following transient ischemia. Rats with four-vessel occlusion (4-VO) were used as an ischemic model. One week after permanent occlusion of the vertebral arteries, the common carotid arteries were clamped for 10 min under halothane anesthesia. Aminoguanidine (10 mg/kg i.p.), a relatively selective iNOS inhibitor, or saline was administered 30 min before common carotid arteries occlusion, and every 24-h for 4 days. We investigated whether hippocampal NO production was increased by ischemic insult using microdialysis on days 1, 4 and 7 after 4-VO. On days 1 and 4 after 4-VO, increases in NO production were observed, and this effect was inhibited by aminoguanidine. Four days after 4-VO, rats were subjected to the Y-maze test and contextual fear conditioning. Ischemic insults impaired learning behavior, and aminoguanidine ameliorated the impairment induced by 4-VO. Four days after 4-VO, the changes in the population spike amplitude were recorded as an index of LTP in Schaffer collateral-CA1 (carotid artery 1), the mossy fiber-CA3 and the perforant path-dentate gyrus synapses. LTP was significantly inhibited by 4-VO, except in mossy fiber-CA3 synapses. Pretreatment with aminoguanidine prevented the reduction of LTP in perforant path-dentate gyrus, but not in Schaffer collateral-CA1 synapses. These results suggest that post-ischemic increase in NO production via iNOS impaired the learning behavior. There is an association between behavioral performance and LTP formation in perforant path-dentate gyrus synapses, but neither in Schaffer collateral-CA1 nor in mossy fiber-CA3 synapses.
Animals↗