Brachial plexus injury in snowboarding.
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Adult↗
Biomedical subjects
Y Hara
Publications and source records attributed to Y Hara.
B cells play an important role in lipopolysaccharide-induced bone resorption.
The host immune system, especially activated T cells, plays a crucial role in inflammatory bone resorption and osteoclastogenesis. Previously, we showed that T cells are involved in inflammatory bone resorption in vivo. However, little is known about whether B cells are involved in inflammatory bone resorption and how B cells take part in osteoclastogenesis. Therefore, the aim of this study was to examine whether B c ells truly influence inflammatory bone resorption in vivo. Alveolar bone resorption in normal mice, in SCID mice that lack both B and T cells, and in B cell-reconstituted SCID mice was compared histopathologically after repeated injections of lipopolysaccharide (LPS) into the gingiva. Furthermore, we examined whether the B cells that are stimulated by LPS are involved in osteoclastogenesis in vitro. As a result, the B cell-reconstituted SCID mice showed stronger inflammatory bone resorption than the SCID mice. Also, in vitro, LPS-stimulated B cells enhanced osteoclastogenesis and anti-tumor necrosis factor (TNF)-alpha antibody completely blocked osteoclastogenesis induced by LPS-stimulated B cells. These results suggest that B cells promote inflammatory bone resorption through TNF-alpha.
Animals↗
Experience with laparoscopic splenectomy for ABO-incompatible living renal transplantation without plasmapheresis.
A 25-year-old male, blood type A, was admitted to our hospital for renal transplantation from his father of AB blood type. Before transplant, we performed laparoscopic splenectomy. The serum anti-B antibody titer fell from 1:8 to 1:2. Therefore, plasmapheresis was not performed. The total ischemic time was 80 minutes. Five immunosuppressive agents, including tacrolimus, mycophenolate mofetil, prednisolone, basiliximab, and deoxyspergualine, were administered in the initial period. On the 47th day, value of cytomegalovirus antibody, which was routinely measured, became positive. Hence, we administered ganciclovir, with a fall in antibody. Sixty-five days after transplant, he was discharged with a serum creatinine of 1.0 mg/dL. We concluded that it was possible to perform ABO-incompatible renal transplantation with no need for plasmapheresis or rituximab.
ABO Blood-Group System↗
Influence of the numbers of islets on the models of rat syngeneic-islet and allogeneic-islet transplantations.
One of the main barriers to widespread application of islet transplantation is the limited availability of human pancreatic islets. The reduction of graft islet mass for transplantation to a recipient is one of the strategies in islet transplantation. However, transplantation of only a small number of islets may result in primary nonfunction. To optimize the sites and numbers of islets for transplantation, we analyzed these factors using pancreatic islets from Lewis or F344 rats transplanted into rats rendered diabetic by streptozotocin (50 mg/kg IV) and confirmed as such prior to transplantation (>300 mg/dL blood glucose). Approximately 500 to 1500 islets were injected via the portal vein or under the renal capsule into the diabetic F344 rats. The blood glucose level of all animals bearing 1500 syngeneic or allogeneic islets transplanted to the liver or under the kidney capsule exhibited restored normoglycemia (<200 mg/dL) at 1 day after transplantation. Graft function deteriorated after only 3 days in three animals (5.8%). The loss of graft function after 3 days occurred in 10 of 28 rats transplanted with 1000 to 1200 syngeneic islets, 4 of 19 rats transplanted with 800 to 900 syngeneic islets, and 7 of 17 rats transplanted with 500 to 600 syngeneic islets. There was no significant difference in the loss of graft function between the sites of transplantation via portal vein or under the kidney capsule. In conclusion, higher frequencies of primary nonfunction occurred with less than 1500 islets transplanted. They were independent of the sites in the rat-islet transplantation model.
Animals↗
The reduction of hypoxia-induced and reoxygenation-induced apoptosis in rat islets by epigallocatechin gallate.
The survival of transplanted tissue is affected by the detrimental consequences of hypoxia followed by reoxygenation. The majority of transplanted cells undergo apoptosis due to hypoxia and reoxygenation (H/R) injury, but protection from H/R has been less examined. In this study, we examined whether epigallocatechin gallate (EGCG) protected rat islets from H/R injury. Rat islets, freshly prepared from F344 rat strain by collagenase digestion and density centrifugation, were seeded in triplicate at concentrations of 100 per well in 24-well plates for culture under normoxia. The cells were then exposed to hypoxia for 14 hours with or without EGCG, after which they were reoxygenated for 72 hours in a humidified oxygenated CO(2) incubator at 37 degrees C. Apoptosis, lactate dehydrogenase (LDH), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were evaluated according to the manufacturer's instructions. The H/R induced apoptosis in the islets that was reduced in dose-dependent manner by EGCG treatment. The viability of islets exposed to H/R was assessed by LDH release. H/R reduced viability compared with the controls, while the viability of the islets improved upon EGCG treatment. The secretion of insulin was also decreased by H/R, as well as the dose dependent EGCG protective ability on insulin secretion. The content of 8-OHdG in islets from H/R was also reduced by EGCG. Our results indicated that apoptosis and the decline in insulin secretion by H/R were inhibited by EGCG treatment. EGCG may be considered useful for protection of islets from oxidative injury associated with the transplantation procedure.
Animals↗
Comparison between human-telomerase reverse transcriptase mRNA and alpha-fetoprotein mRNA as a predictive value for recurrence of hepatocellular carcinoma in living donor liver transplantation.
OBJECTIVE: In this study we compared the potential roles of preoperative human-telomerase reverse transcriptase (h-TERT) mRNA versus alpha-fetoprotein (AFP) mRNA expression in the peripheral blood as a tool to predict prognosis and tumor recurrence after living donor liver transplantation (LDLT) in hepatocellular carcinoma (HCC) patients. PATIENTS AND METHODS: We examined 14 patients with unresectable HCC who underwent LDLT. Six patients displayed stage IVA HCC that deviated from the Milan criteria, while the rest of the patients fell within the limitations of the Milan criteria. We analyzed the relationship between preoperative h-TERT mRNA or AFP mRNA expression in the peripheral blood and survival without recurrence. RESULTS: There was no significant difference between the survival curves without recurrence of those patients who did versus did not meet the Milan criteria. There was also no significant difference between the survival curves without recurrence among patients with positive versus negative AFP mRNA expression. However, there was a significant difference (P = .005) between the survival curves without recurrence of those patients with positive preoperative h-TERT mRNA expression versus those who either had an initially negative preoperative h-TERT mRNA or who converted from positive to negative after neoadjuvant immunochemotherapy. CONCLUSIONS: h-TERT mRNA seemed to prove more valuable than AFP mRNA not only to assess preoperative treatment modalities and postoperative patient surveillance, but also to evaluate prospective LDLT patients with HCC. Moreover, use of h-TERT mRNA could potentially expand the indications for transplantation to patients outside the Milan criteria.
Carcinoma, Hepatocellular↗
Enhancement of erythrocyte antioxidants by green and black tea polyphenols during 7,12-dimethylbenz[a]anthracene-induced hamster buccal pouch carcinogenesis.
We evaluated the comparative chemopreventive efficacy of green tea polyphenols (polyphenon-E) and black tea polyphenols (polyphenon-B) on 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch (HBP) carcinogenesis. Lipid peroxidation, reduced and oxidized glutathione (GSH and GSSG, respectively), and the GSH-dependent enzymes glutathione peroxidase and glutathione S-transferase in the erythrocytes were used as biomarkers of chemoprevention. Enhanced lipid peroxidation in erythrocytes of DMBA-treated animals was accompanied by a significant decrease in the antioxidant status. Dietary administration of polyphenon-E and -B to DMBA-treated animals significantly decreased the extent of lipid peroxidation and enhanced the levels of GSH, GSH/GSSG ratio, and activities of GSH-dependent enzymes. Our study provides evidence that polyphenon-B is more effective in inhibiting HBP carcinogenesis than polyphenon-E by enhancing the antioxidant status, suggesting that polyphenon-B may have a major impact in the chemoprevention of oral cancer.
9,10-Dimethyl-1,2-benzanthracene↗
Black tea polyphenols protect against 7,12-dimethylbenz[a]anthracene-induced hamster buccal pouch carcinogenesis.
Dietary chemoprevention has emerged as a cost-effective approach for cancer control. We evaluated the chemopreventive effects of black tea polyphenols (Polyphenon-B) administration during the preinitiation phase of 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch (HBP) carcinogenesis. The expression of proliferating cell nuclear antigen (PCNA) in the buccal pouch and the concentration of lipid peroxides, protein carbonyl, and the antioxidant status in the buccal pouch, liver and erythrocytes were used as biomarkers of chemoprevention. All the hamsters painted with DMBA alone for 14 weeks developed buccal pouch carcinomas associated with increased expression of PCNA, diminished lipid and protein oxidation, and enhanced antioxidant status. In the liver and erythrocytes of tumor-bearing animals, enhanced oxidation of lipids and proteins was accompanied by compromised antioxidant defenses. Dietary administration of Polyphenon-B effectively suppressed DMBA-induced HBP carcinogenesis as revealed by decreased incidence of tumours and PCNA expression. In addition, Polyphenon-B modulated lipid and protein oxidation and enhanced the antioxidant status in the pouch, liver, and erythrocytes. We suggest that Polyphenon-B exerts its chemopreventive effects by inhibiting cell proliferation in the target tissue and modulating the oxidant-antioxidant status in the target as well as in host tissues.
Animals↗
Comparative evaluation of the chemopreventive efficacy of green and black tea polyphenols in the hamster buccal pouch carcinogenesis model.
OBJECTIVES: To evaluate the comparative chemopreventive efficacy of green tea polyphenols (Polyphenon-E) and black tea polyphenols (Polyphenon-B) on 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch (HBP) carcinogenesis. DESIGN AND METHODS: Hamsters were divided into 6 groups. Animals in group 1 served as controls. Animals in groups 2 and 3 were administered 0.05% Polyphenon-E and B, respectively, in the diet. The right buccal pouches of animals in groups 4-6 were painted with 0.5% DMBA three times a week for 14 weeks. While group 4 received no further treatment, hamsters in groups 5 and 6 received diet containing 0.05% Polyphenon-E and B, respectively. The status of carcinogen-metabolising enzymes, lipid peroxidation and glutathione-dependent antioxidants in the buccal pouch and liver, as well as the frequency of bone marrow micronuclei were used as biomarkers. RESULTS: Application of DMBA induced HBP carcinomas, increased genotoxicity with an imbalance in carcinogen-metabolising enzymes and the cellular redox status. Inhibition of HBP carcinomas by Polyphenon-E and B was associated with a significant decrease in phase I enzymes, modulation of lipid peroxidation and enhanced antioxidant and phase II enzyme activities. CONCLUSION: The greater efficacy of Polyphenon-B in inhibiting HBP carcinogenesis suggests that it may have a major impact in the chemoprevention of oral cancer.
9,10-Dimethyl-1,2-benzanthracene↗
Surgical procedures for decompression of excessive shear stress in small-for-size living donor liver transplantation--new hepatic vein reconstruction.
We have reported that acute elevation of portal pressure, reflecting wall shear stress of sinusoidal endothelial cells, triggers liver regeneration after partial hepatectomy and that excessive portal hypertension induces liver failure. For prevention of excessive shear stress in small-for-size living donor liver transplantation (LDLT), we developed a new hepatic vein reconstruction to expand the anastomotic site. Fourteen adult patients, who underwent LDLT, were divided into two groups: previous end-to-end hepatic vein reconstruction in nine patients (group P) and the new method in five patients (group N). The outside middle and left hepatic veins of the graft were incised and enlarged to 40 mm. The vena cava was cut 40 mm longitudinally. The graft was positioned a quarter turn counterclockwise with the hepatic vein of the graft anastomosed end-to-side to the vena cava longitudinally. Postoperative portal pressures and serum total bilirubin levels of these two groups showed portal pressure in group N to rapidly decrease below 25 cm H2O following LDLT. No cases showed posttransplanted hyperbilirubinemia above 10 mg/dL in group N; however, all cases were small-for-size grafts. Moreover, serum total bilirubin levels in group N were significantly lower than those in group P. This procedure is simple despite not using a venous patch. If the hepatic vein is narrow or obstructed, such as in Budd-Chiari syndrome, the procedure is applicable. Even in small-for-size grafts, excessive tension did not occurred at the portal vein or hepatic artery anastomoses. Moreover, it is possible to avoid outflow block and posttransplanted hyperbilirubinemia.
Adult↗
Comparison of the vector systems for gene transduction into rat dendritic cells and peritoneal exudate cells.
Specialized antigen-presenting cells (APC), known as dendritic cells (DC), play a pivotal role in initiating primary immune responses. It has been reported that several vector systems, including adenoviral vectors, retroviral vectors, Hemagglutinating Virus of Japan (HVJ)-related vectors, and electroporation, are able to transduce genes into mouse and human DC. This has not been achieved for rat DC. To our knowledge, there is no direct evidence to support the view that the currently used vector systems are able to transduce genes into mature DC. Because most, if not all, gene transfer studies investigating DC or DC-related cell populations are carried out using heterogeneous groups of cells, it is therefore very important to determine to what extent gene transduction occurs in rat DC, and also selected mature DC (CD161a+ fully mature DC). In this study, we provide evidence that none of 4 vector systems are able to transfer genes into fully mature rat DC, which are derived from bone marrow cells (BMC), driven by Flt3/Flk2 ligand and interleukin (IL)-6, and purified by CD161a. Nevertheless, the most efficient gene transduction was observed in the developing DC progenitor cells during the long-term culture of rat BMC, and its gene expression was successfully achieved after 2 weeks of culture only with a human immunodeficiency virus (HIV)-based lentiviral vector system. The most critical time point for lentiviral gene transduction was around the 7th day from the beginning of culture with lentiviral vectors. Rat peritoneal exudate cells (PEC) and another cell line (K562) were easily transducted by adenoviral vectors and lentiviral vectors.
Adenoviridae↗
Inhibitory effects of psychotropic drugs on mexiletine metabolism in human liver microsomes: prediction of in vivo drug interactions.
Mexiletine, an anti-arrhythmic agent, is used for the control of ventricular arrhythmias and for neuropathic pain from cancer or diabetes mellitus. It is sometimes used together with psychotropic drugs in patients with depression, schizophrenia or sleep disorder. It is metabolized mainly by cytochrome P450 (CYP) 2 D 6 and, to a minor extent, by CYP1A2. To predict possible drug interactions between mexiletine and psychotropic drugs, the inhibitory effects of 14 psychotropic drugs (phenytoin, carbamazepine, fluvoxamine, paroxetine, fluoxetine, citalopram, sertraline, imipramine, desipramine, haloperidol, thioridazine, olanzapine, etizolam, and quazepam) on mexiletine metabolism in human liver microsomes were determined. Fluoxetine (Ki=0.6+/- 0.1 microM), sertraline (Ki=7.6+/- 0.8 microM) and desipramine (Ki=3.2+/- 0.5 microM) competitively inhibited the mexiletine p-hydroxylation in human liver microsomes. Thioridazine (Kis=0.5+/- 0.2 microM; Kii =3.6+/-1.6 microM) and paroxetine (Kis=1.7+/- 0.7 microM; Kii=3.6+/- 0.9 microM) exhibited a mixed-type inhibition (competitive and non-competitive) toward mexiletine p-hydroxylation in human liver microsomes. The changes of the in vivo clearance of mexiletine by the psychotropic drugs were predicted by 1+(I/Ki) using the in vitro Ki and unbound inhibitor concentrations in liver. The values were calculated as 2.4 for paroxetine, 5.5 for fluoxetine, 1.1 for sertraline, 2.8 for desipramine and 2.2 for thioridazine. In addition, paroxetine exhibited a mechanism-based inactivation with Ki=0.7 microM and Kinact=0.15 min(-1). The present study predicted the possibility of drug interactions between mexiletine and paroxetine, fluoxetine, desipramine, and thioridazine in clinical use.
Anti-Arrhythmia Agents↗
Effect of specific antigen stimulation on intraepithelial lymphocyte migration to small intestinal mucosa.
Migration of intraepithelial lymphocytes (IELs) into intestinal epithelium is not yet well understood. We established an IEL-cell line from ovalbumin (OVA) 23-3 transgenic (Tg) mice and investigated the effect of antigen stimulation on the dynamic process of IEL migration into small intestinal mucosa. The cell line was a T cell receptor (TCR) alphabeta(+) CD4(+) CD8(-) phenotype, expressing alphaEbeta7 integrin in 90% of cells. Under intravital microscopy, the lined IELs adhered selectively to the microvessels of the intestinal villus tip of the Tg mice. The accumulation of IELs was significantly inhibited by an antibody against beta7-integrin and MAdCAM-1. When IELs were stimulated with OVA, the accumulation was attenuated compared to that of resting cells, with decreased expression of alphaEbeta7 integrin. In Tg mice fed with OVA, the number of IELs which migrated in the villus mucosa was significantly smaller than in the non-fed controls. The preferential migratory capacity of IELs to villus mucosa may be altered by specific antigen stimulations.
Animals↗
Study on the rapid deswelling mechanism of comb-type N-isopropylacrylamide gels.
The shrinking mechanism of comb-type grafted poly(N-isopropylacrylamide) gel was investigated by fluorescence spectroscopy and small-angle X-ray Scattering (SAXS). The SAXS reveals that the microdomain structure with characteristic dimension of 460A is developed in the comb-type grafted poly(N-isopropylacrylamide) gel during the shrinking process. Fluorescence spectroscopy together with SAXS observation suggests that the freely mobile characteristics of the grafted chains are expected to show the rapid dehydration to make tightly packed globules with temperature, followed by the subsequent hydrophobic intermolecular aggregation of the dehydrated graft chains. The dehydrated grafted chains created the hydrophobic cores, which enhance the hydrophobic aggregation of the networks. These aggregations of the NIPA chains contribute to an increase in void volume, which allow the gel having a pathway of water molecules by the phase separation.
Acrylamides↗
Decreased proteinuria following liver transplantation in a patient with type C liver cirrhosis complicated with nephrotic syndrome: a case report.
Type C liver cirrhosis is often associated with a nephrotic syndrome secondary to membranoproliferative glomerulonephritis. Liver transplantation in such patients may sometimes worsen viremia, causing renal dysfunction upon the introduction of immunosuppressive drugs. We present a case of a patient whose proteinuria decreased after liver transplantation. The patient was a 49-year-old male who had been followed due to chronic hepatitis type C from 1984. From 1999 he was diagnosed as having nephrotic syndrome. We performed a living related liver transplant on August 21, 2001. An intraoperative renal biopsy revealed the histology to show membranoproliferative glomerulonephritis. The volume of proteinuria was 2 to 11 g/day before surgery. After surgery it varied from 6 to 10 g/day, gradually decreasing to 1 to 2 g/day. One of the causes of reduced proteinuria may be alleviation of membranoproliferative glomerulonephritis by immunosuppression. But from the view that the recovery of the renal function followed the recovery of liver function, the major effect may have been alleviated hepatorenal syndrome.
Biopsy↗
High expression of interleukin-1beta in the corneal epithelium of MRL/lpr mice is under the control of their genetic background.
MRL/Mp mice bearing the Fas deletion mutant gene, lpr (MRL/lpr), spontaneously develop polyarthritis, sialoadenitis and dacryoadenitis, resembling rheumatoid arthritis (RA), and also corneal involvement such as keratopathy and scleritis, which is a major complication in RA patients. In this study, we found that the expression levels of IL-1beta and MMP-1 mRNAs in cornea were high in both MRL/lpr and MRL/Mp-+/+ strains of mice at an age younger than when they develop any inflammatory lesions. This was not true of other inbred strains, even those bearing the lpr gene, and also not of (NZB x NZW) F1 lupus mice. There was no significant difference in the expression of IL-1alpha and TGFbeta in cornea in these strains. Using crosses between MRL/lpr and C3H/HeJ-lpr/lpr (C3H/lpr) mice, at least the expression of IL-1beta was found to be under the control of the MRL genetic background, likely with a recessive mode of inheritance. Considering that IL-1beta in cornea was detected particularly in the epithelial layer, the high expression of IL-1beta in cornea is most likely involved in the genetic predisposition for corneal involvement and possibly also for arthritis in an MRL strain of mice.
Animals↗
Clinical and molecular analysis of Mowat-Wilson syndrome associated with ZFHX1B mutations and deletions at 2q22-q24.1.
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Adult↗
Changes in expression of the mouse homologues of KIAA genes after subchronic methamphetamine treatment.
Amphetamine abuse may be associated with adaptive changes in gene expression in the brain. In the present study, a newly developed cDNA array system comprising mouse KIAA (mKIAA) cDNA clones was used to examine the gene expression affected by chronic methamphetamine treatment. Approximately 800 mKIAA clones were blotted onto a nylon membrane and hybridized with 33P-labeled cDNA derived from mRNAs isolated from the whole brains of mice that had been treated daily with saline or methamphetamine (2 mg/kg, i.p.) for 2 weeks. The arrays displayed robust hybridization for almost all transcripts. The results obtained from five experiments were averaged, each performed with triplicate samples. Several clones were chosen as positive candidates for methamphetamine-induced changes; however, only Per2 and mKIAA0099 genes showed a significantly increased expression (P < .05). Subsequently, with the focus on the period-related proteins, the expression of these proteins in various parts of the rat brain were assessed by immunoblot analysis. Chronic administration of methamphetamine (8 mg/kg, i.p., for 10 days) caused increased Per2 protein expression in the hippocampus. Interestingly, chronic methamphetamine treatment at a lower dose (4 mg/kg, i.p., for 10 days) induced an increase in SCN circadian oscillatory protein (SCOP) expression, also in the hippocampus. These data suggest that long-lasting alterations of the period-related gene expressions in the hippocampus might play an important role in methamphetamine addiction.
Animals↗