Seroprevalence of human herpesvirus 8 in Okinawa, Japan.
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Adult↗
Biomedical subjects
M Satoh
Publications and source records attributed to M Satoh.
Enhanced GM3 expression, associated with decreased invasiveness, is induced by brefeldin A in bladder cancer cells.
We reported previously that non-invasive bladder cancer expresses high level of GM3 ganglioside, whereas invasive tumors have low levels. Since glycosphingolipid synthesis in Golgi is modified greatly by a macrocyclic lactone isolated from fungi, brefeldin A (BFA), we studied effects of BFA on expression of glycosphingolipids and on invasiveness of bladder cancer cell lines. Only GM3 synthesis in invasive tumors was greatly enhanced upon treatment with BFA; synthesis of other glycosphingolipids with lacto-series type 2 or globo-series structure in both invasive and non-invasive tumors was not changed. Invasiveness of bladder cancer cells was greatly decreased in association with the great increase of GM3 synthesis induced by BFA treatment. Level of sialyl-Lex expressed in invasive cell line YTS1, which provides the adhesive property of the cells to E-selectin, was unchanged upon BFA treatment. All the bladder cancer cell lines, regardless of invasiveness, highly express tetraspanin CD9. GM3 has been implicated as a co-factor of CD9 in control of tumor cell motility. Down-regulation of CD9 is associated with metastatic properties of tumor cells and survival of patients with colonic cancer. Therefore, enhanced synthesis of GM3 induced by BFA, causing decrease of invasiveness in bladder cancer, is ascribable to the capability of GM3 to interconnect integrin with CD9, in analogy to colonic cancer and perhaps many other types of cancer.
Antibodies, Monoclonal↗
[Continuous epidural administration of droperidol for the prevention of postoperative nausea].
Continuous antiemetic effect of epidural droperidol was evaluated by prospective, double-blinded study using 145 ASA physical status I-II patients undergoing major gynecological surgery. All patients received bolus epidural infusion of buprenorphine at the end of the operation and continuous epidural infusion of buprenorphine for 48 hours. Patients were divided into 3 groups, 49 patients of Group I received placebo, 50 patients of Group II received only bolus doses of droperidol 2.5 mg and the remaining 46 patients of Group III received continuous epidural infusion of droperidol 10 mg in 48 hours. Visual analogue scales for nausea, the incidence of emetic episodes and side effects were evaluated at 3 hr, 24 hr and 48 hr postoperatively. The scores for nausea were significantly lower in Group III (P < 0.05) compared with Group I 24 hr after the operation. The incidence of emesis was significantly lower in Group III (P < 0.05) as compared with Group I and II 48 hr after the operation. Extrapyramidal side effects and sedative effects were not observed in any patients. The continuous epidural administration of droperidol is effective in prevention of postoperative nausea and vomiting and the effect lasts during its infusion with no side effects.
Analgesia, Epidural↗
[Persistent left-sided superior vena cava diagnosed after flow-directed pulmonary artery catheterization; report of a case].
We describe a case of persistent left-sided superior vena cava discovered after insertion of a pulmonary artery (PA) catheter. The diagnosis was suggested by chest X-ray after PA catheter placement and was subsequently confirmed by an echocardiograph. A 68-year-old man was admitted to our ICU because of septic shock induced by MRSA enterocolitis. In order to monitor the hemodynamic state of the patient, a PA catheter was inserted through the left subclavian vein after placement of a central venous and flexible double lumen catheters through the right internal jugular and subclavian veins, respectively. A chest X-ray showed the PA catheter passing along the left border of the heart. An echocardiograph showed the PA catheter passing through the coronary sinus into the pulmonary artery. Anesthesiologists and intensivists should be aware of the occurrence of left-sided superior vena cava in order not to mistake catheters placed in it as being in the arterial circulation or malpositioned outside of the venous circulation.
Catheterization, Swan-Ganz↗
[Questionnaires on patient-controlled analgesia to the nursing staff in the surgical ward].
Thirty-one nurses in the surgical ward engaged in delivering postoperative analgesia using patient-controlled analgesia (PCA) were asked to complete questionnaires on postoperative analgesia and PCA. Ninety-seven per cent of respondents agreed that the postoperative analgesia is beneficial for postoperative recovery, and answered that the desirable goal in postoperative analgesia is "no pain at rest". Not only "pain at movement" or "pain on coughing", but also "decreased conscious level while analgesia is achieved" were selected as undesirable conditions during postoperative course. Although no one had learned the concept of PCA in their nursing schools, 94 per cent of respondents approved PCA as a method for postoperative analgesia. Seventy seven per cent responded that PCA is effective in the pain relief during position change, pulmonary physiotherapy and induced early ambulation. In addition, 65 per cent of respondents chose PCA as a method for postoperative analgesia when they receive thoraco-abdominal surgery. On the other hand, some problems on pain management using PCA, such as taking care of patients' ambulation with carrying a PCA pump, extra time for instruction of PCA and extra support for patients' psychological state were listed. In conclusion, these results suggest that PCA is accepted as an excellent method for postoperative analgesia among our nurses in the surgical ward, and education in postoperative pain management including PCA is required in nursing school as well as after graduation.
Analgesia, Patient-Controlled↗
Renal toxicity caused by cisplatinum in glutathione-depleted metallothionein-null mice.
To elucidate the protective role of metallothionein (MT) and glutathione (GSH) in renal toxicity caused by cisplatinum (cis-DDP), we examined the sensitivity of GSH-depleted MT-null mice to the renal toxicity of cis-DDP. Blood urea nitrogen and creatinine values in the serum, and histopathological change in the kidney were utilized as indicators of nephrotoxicity caused by cis-DDP. Although cis-DDP exerted renal toxicity in MT-null mice and wild-type mice, the toxicity was more conspicuous in the MT-null mice than in the wild-type mice. Moreover, renal toxicity caused by cis-DDP was enhanced significantly by a decrease in the renal GSH level by buthionine sulfoximine (BSO) pretreatment in both kinds of mice. The cis-DDP-caused nephrotoxicity that was enhanced by BSO-mediated GSH depletion was much more severe in the MT-null mice than in the wild-type mice. However, preadministration of zinc sulfate cancelled the BSO-enhanced, cis-DDP-dependent renal toxicity in the wild-type mice, but not in the MT-null mice. In the present study, we found that MT and GSH play an important, cooperative role in detoxification of severe kidney damage caused by cis-DDP. Moreover, the renal MT preinduced by zinc could protect mice from cis-DDP nephrotoxicity enhanced by GSH depletion.
Animals↗
Expression of leukemia inhibitory factor receptor mRNA in sensory dorsal root ganglion and spinal motor neurons of the neonatal rat.
Previous studies have shown that the application of leukemia inhibitory factor to the proximal nerve stump prevents the degeneration of axotomized sensory neurons in the dorsal root ganglion and motor neurons in the spinal cord of newborn rats. This study investigated the expression of leukemia inhibitory factor receptor mRNA in these neurons using in situ hybridization. Leukemia inhibitory factor receptor mRNA was detected both in sensory neurons within the dorsal root ganglion and motor neurons of the cervical spinal cord. Twenty-four hours after axotomy these neurons continue to express leukemia inhibitory factor receptor mRNA. This pattern of leukemia inhibitory factor receptor expression provides a mechanism by which endogenous and exogenous leukemia inhibitory factor could act on injured sensory and motor neurons.
Animals↗
Tri-n-butyltin-induced change in cellular level of glutathione in rat thymocytes: a flow cytometric study.
Since some of organotins, accumulated in edible mollusks of aquatic environments, exert a variety of toxic actions on experimental animals, it causes concern for the health of humans. We examined the effects of tri-n-butyltin chloride (TBT) and other organotins (triethyltin chloride, trimethyltin chloride, triphenyltin chloride and tetrabutyltin) on cellular content of glutathione (GSH) in rat thymocytes using a flow cytometer to further characterize the toxicity of TBT. When the cells were incubated with TBT at concentrations of 3 nM or more for 15 min, the cellular content of GSH dose-dependently decreased. However, it completely or partly recovered until 180 min even in the continued presence of TBT. This recovery was temperature-sensitive, suggesting an involvement of metabolic process. The efficacy of TBT to decrease the cellular content of GSH was greater than those of other organotins. Results suggest that TBT and some organotins at environmentally relevant (nanomolar) concentrations significantly reduce the cellular content of GSH, suggesting that they increase the vulnerability to some biological and chemical insults.
Animals↗
Frequent hypermethylation of CpG islands and loss of expression of the 14-3-3 sigma gene in human hepatocellular carcinoma.
The 14-3-3 sigma gene has been implicated in G2/M cell cycle arrest by p53. Frequent inactivation of the 14-3-3 sigma gene by hypermethylation of CpG islands has recently been reported in human breast carcinoma. The aim of this study was to examine the methylation status of CpG islands of the 14-3-3 sigma gene in hepatocellular carcinoma (HCC). The methylation status of the 14-3-3 sigma gene was evaluated in four normal liver tissues and 19 paired specimens of carcinoma and adjacent non-tumorous liver tissues using bisulfite-single strand conformation polymorphism (bisulfite-SSCP), a combination of sodium bisulfite modification and fluorescence-based polymerase chain reaction (PCR)-SSCP. The 14-3-3 sigma protein expression was examined by immunohistochemical staining. Hypermethylation of CpG islands of the 14-3-3 sigma gene was detected in 89% (17/19) of the HCC tissues but not in any of the four normal liver tissues. All of the 14 methylation-positive HCC samples analysed by immunohistochemistry showed loss of 14-3-3 sigma expression, while both of the methylation-negative HCC samples retained the expression, and a significant correlation was found between methylation and loss of expression. Lower levels of methylation were detected in adjacent non-tumorous liver tissues (6/16 in cirrhotic tissues and 1/3 in chronic hepatitis tissues), but the 14-3-3 sigma expression was retained in all of these tissues. In a methylation-positive HCC cell line, HLE, 5-aza-2'-deoxycytidine (5-aza-dC)-induced demethylation of CpG islands led to reactivation of gene expression, indicating that hypermethylation plays a causal role in inactivation of the 14-3-3 sigma gene in HCC. Hypermethylation and the resulting loss of expression of the 14-3-3 sigma gene corresponds to one of the most common abnormalities reported to date in HCC, suggesting their crucial role in the development and/or progression of HCC.
14-3-3 Proteins↗
Expression of inducible nitric oxide synthase mRNA and production of nitric oxide are induced by adenosine triphosphate in cultured rat microglia.
The effect of adenosine triphosphate (ATP) on the expression of the inducible nitric oxide synthase (iNOS) mRNA and production of nitric oxide in cultured rat microglia was examined. ATP induced iNOS mRNA dose-dependently (100-1,000 microM). The induction began within 1 h after addition of ATP (100 microM) with peak expression occurring at 6 h. The release of nitric oxide to culture medium was significantly increased by the treatment with ATP (100 and 1,000 microM) for 12 and 24 h. These results indicate that ATP is a potential mediator to induce iNOS mRNA expression and NO production in microglia.
Adenosine Triphosphate↗
A chemiluminescent assay for hydroperoxide level of phosphatidylcholine hydroperoxide fraction purified by two Sep-Pak cartridges in biological samples.
A chemiluminescent assay for hydroperoxide level of phosphatidylcholine hydroperoxide (PCOOH) fraction purified from biological samples was presented. This method utilized of two Sep-Pak cartridges. A lipid soluble fraction was isolated from each homogenized tissue or blood by Folch's method. The mixture of phosphatidylcholine (PC) and PCOOH was separated from the lipid soluble fraction by a Sep-Pak silica cartridge. A Sep-Pak tC18 cartridge made complete separation of both PCOOH and PC possible. The hydroperoxide level of PCOOH fraction was quantified by the reaction with ferrous ion using 2-methyl-6-[p-methoxyphenyl]-3,7-dihydroimidazo[1,2-a]pyrazin++ +-3-one as a chemiluminescent dye. The mixture of positional isomers, 1-hexadecanoyl-2-[9, or 10-hydroperoxyl octadecanoyl]-sn-glycero-3-phosphocholine was used as an authentic standard. The good recovery rate for authentic PCOOH of 87.1 +/- 11.6% (mean +/- S.E., n = 4) was obtained by using two Sep-Pak cartridges. Linear calibration curve was obtained in the range from 2.5 to 20 nmol, and the detection limit of the standard was 10 pmol (signal-to-noise ratio > 3). This method was applied to the investigation of the lipid peroxidation induced by reperfusion of the liver with cold preservation, mimicking liver transplantation in rats. The effect of liposome-encapsulated dichloromethylene diphosphonate (LEDD), which eliminate of Kupffer cells to prevent the generation of oxygen radicals on the lipid peroxidation, was compared with the untreated group as a control. After 1 h reperfusion at 37 degrees C the hydroperoxide level obtained the liver without preservation in the untreated group was 12.4 +/- 2.4 nmol/100 mg lipid (n = 4) and levels increased significantly by prolongation of the preservation time. On the other hand, the hydroperoxide level in the LEDD treated group did not change up to 24 h preservation. These results suggest that this improved assay for hydroperoxide level of PCOOH fraction in biological samples can be applied to investigations involving lipid peroxidation because of its simplicity and accuracy.
Animals↗
Fas and Fas ligand mutations inhibit autoantibody production in pristane-induced lupus.
Mutations of Fas (lpr) or Fas ligand (gld) cause a limited lupus-like syndrome in B6 mice by interfering with the deletion of autoreactive B and/or T cells. A more generalized lupus syndrome reminiscent of that of MRL mice can be induced in nonautoimmune strains by pristane, which causes a nonspecific inflammatory response in the peritoneal cavity. We hypothesized that, as in MRL mice, the lpr and gld mutations might accelerate lupus in pristane-treated mice. Pristane-treated B6 mice developed anti-nRNP/Sm, Su, and ribosomal P Abs, but little anti-ssDNA or chromatin. In contrast, B6/lpr and B6/gld mice spontaneously developed anti-ssDNA/chromatin Abs, but not anti-nRNP/Sm/Su/ribosomal P. Unexpectedly, B6/lpr and B6/gld mice were highly resistant to the induction by pristane of IgM anti-ssDNA (2 wk) and IgG anti-nRNP/Sm/Su/ribosomal P autoantibodies (6 mo), suggesting that intact Fas signaling is necessary. Interestingly, pristane did not enhance IgG chromatin Ab production in B6/lpr or B6/gld mice, suggesting that it did not influence the production of autoantibodies that develop spontaneously in the setting of Fas deficiency. Pristane treatment also decreased lymphoproliferation in B6/lpr mice. Increased production of IL-12 was associated consistently with the production of anti-nRNP/Sm/Su/ribosomal P as well as anti-DNA/chromatin. In contrast, production of anti-DNA/chromatin Abs was associated with IL-6 overproduction in pristane-treated mice, but not in lpr mice. The data strongly support the idea that different subsets of autoantibodies are regulated differentially by cytokine stimulation and/or Fas signaling.
Animals↗
Modulation of adriamycin toxicity by tissue-specific induction of metallothionein synthesis in mice.
The effect of tissue specific induction of metallothionein (MT) by preadministration of metal compounds on the antitumor activity and adverse effects of adriamycin (ADR) was examined using mice bearing colon 38 adenocarcinoma. Significant increase in MT concentration was observed in the heart and bone marrow but not in the tumor tissue of the mice given bismuth (Bi) compound. Copper (Cu) increased MT in the tumor tissue but did not induce MT either in bone marrow or in the heart, whereas zinc (Zn) increased MT level in the heart and bone marrow as well as in the tumor tissue. ADR exerted cardiotoxicity, indicated by increase in lipid peroxidation in the heart, bone marrow toxicity, indicated by decrease in number of peripheral leukocytes, and antitumor activity, assessed by reduction of tumor weight, in tumor-bearing mice untreated with MT inducing metal compounds. Preadministration of Bi significantly reduced the cardiotoxicity and bone marrow toxicity without compromising the antitumor activity of ADR. Cu pretreatment did not affect the extent of cardiotoxicity and bone marrow toxicity but significantly suppressed the antitumor effect. Pretreatment with Zn markedly reduced not only the adverse side effects but also the antitumor activity. The results described above suggest that ADR toxicity can be attenuated in the tissues in which the MT level was elevated and that the tissue specific induction of MT synthesis may provide a promising regimen for cancer chemotherapy.
Animals↗
Expression of neural properties in olfactory cytokeratin-positive basal cell line.
A cytokeratin (CK)(+), horizontal basal cell (HBC)-like cell line from murine olfactory epithelium, DBC1.2, was characterized. Histochemically, it is CK14(+), CK18(-), neuron-specific tubulin (NST)(+) and capable of binding Bandeiraea simplicifolia lectin I. RT-PCR studies revealed that it expresses mRNAs for EGF receptor, NST, Pax-6, but not for Mash-1 and neurogenin-1. Retinoic acid reduced the expression of CK14 and CKs recognized by polyclonal anti-keratin antibody, whereas it induced nestin. These results suggest that DBC1.2 shares the properties of HBCs and neural cells.
Animals↗
Overexpression of mRNAs of TGFbeta-1 and related genes in fibroblasts of Werner syndrome patients.
We analyzed mRNAs that were up- or down-regulated in fibroblasts from Werner syndrome (WS) patients compared with those from normal individuals. The mRNAs from normal and WS cells were first screened by differential display, and those mRNAs that were apparently up- or down-regulated were selected except for mRNAs related to extra-cellular matrix (ECM) proteins that are already known to be up-regulated in WS fibroblasts. Then, the expression levels of these mRNAs were semiquantified by northern blot analysis, and six up-regulated and two down-regulated mRNAs were identified in WS cell lines. Among the six up-regulated mRNAs were three mRNAs that coded TGFbeta-1 and two proteins, their expressions of which were increased by TGFbeta-1. These results together with the fact that TGFbeta-1 up-regulates the expression of ECM proteins strongly suggest that TGFbeta-1 has a key role in accelerated cellular senescence of fibroblasts of WS patients.
Base Sequence↗
Activin promotes astrocytic differentiation of a multipotent neural stem cell line and an astrocyte progenitor cell line from murine central nervous system.
The effects of activin A were investigated on the development of a multipotent neural stem cell line (MEB5) and an astrocyte progenitor cell line (AP-16) that were established from murine central nervous system (CNS). Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis demonstrated that each cell line expresses both type I and type II activin receptors and signaling molecules for activin, Smad2, Smad3, and Smad4. Activin A did not affect the proliferation of MEB5 and AP-16 cells. When each cell line was treated alone with activin A, glial fibrillary acidic protein (GFAP), a marker for astrocytes, was induced in AP-16 cells, but not in MEB5 cells. However, activin A accelerated the leukemia inhibitory factor (LIF)-induced astroglial differentiation of MEB5 cells. These results suggest that activin promotes astrocyte differentiation of CNS neural progenitors, and the competence to activin is different between multipotent stem cells and unipotent astrocyte progenitor cells.
Activin Receptors, Type I↗
Vaccination of domestic pig with recombinant paramyosin. against Schistosoma japonicum in China.
Paramyosin (PM), a myosin-like protein is a major antigen on Schistosoma japonicum (Sj). We reported that passive transfer of a monoclonal IgE SjE18varepsilon.1 which recognizes PM of Sj (SJPM), partially protected mice from challenge infection. In the present study, we developed an experimental model system of schistosomiasis japonica with domestic pigs in China and used it for the evaluation of vaccination with recombinant SJPM (rSJPM). Sixteen-week-old pigs were successfully infected by dermal penetration of 120 cercariae of a domestic strain of Sj (50-60% worm recovery 11 weeks after challenge). The pigs vaccinated with 400 UV attenuated cercariae showed a reduction of worm recovery (53%, p<0.001). The experimental groups were immunized intradermally with rSJPM and alum or TiterMax and were partially protected against the challenge infection (32-35% reduction).
Adjuvants, Immunologic↗
The alkaline single cell electrophoresis assay with eight mouse organs: results with 22 mono-functional alkylating agents (including 9 dialkyl N-nitrosoamines) and 10 DNA crosslinkers.
The genotoxicity of 22 mono-functional alkylating agents (including 9 dialkyl N-nitrosoamines) and 10 DNA crosslinkers selected from IARC (International Agency for Research on Cancer) groups 1, 2A, and 2B was evaluated in eight mouse organs with the alkaline single cell gel electrophoresis (SCGE) (comet) assay. Groups of four mice were treated once intraperitoneally at the dose at which micronucleus tests had been conducted, and the stomach, colon, liver, kidney, bladder, lung, brain, and bone marrow were sampled 3, 8, and/or 24 h later. All chemicals were positive in the SCGE assay in at least one organ. Of the 22 mono-functional alkylating agents, over 50% were positive in all organs except the brain and bone marrow. The two subsets of mono-functional alkylating agents differed in their bone marrow genotoxicity: only 1 of the 9 dialkyl N-nitrosoamines was positive in bone marrow as opposed to 8 of the 13 other alkylating agents, reflecting the fact that dialkyl N-nitrosoamines are poor micronucleus inducers in hematopoietic cells. The two groups of mono-functional alkylating agents also differ in hepatic carcinogenicity in spite of the fact that they are similar in hepatic genotoxicity. While dialkyl N-nitrosoamines produce tumors primarily in mouse liver, only one (styrene-7,8-oxide) out of 10 of the other type of mono-functional alkylating agents is a mouse hepatic carcinogen. Taking into consideration our previous results showing high concordance between hepatic genotoxicity and carcinogenicity for aromatic amines and azo compounds, a possible explanation for the discrepancy might be that chemicals that require metabolic activation show high concordance between genotoxicity and carcinogenicity in the liver. A high percent of the 10 DNA crosslinkers were positive in the SCGE assay in the gastrointestinal mucosa, but less than 50% were positive in the liver and lung. In this study, we allowed 10 min alkali-unwinding to obtain low and stable control values. Considering that DNA crosslinking lesions can be detected as lowering of not only positive but also negative control values, low control values by short alkali-treatment might make it difficult to detect DNA crosslinking lesions. In conclusion, although both mono-functional alkylating agents and DNA crosslinkers are genotoxic in mouse multiple organs, the genotoxicity of DNA crosslinkers can be detected in the gastrointestinal organs even though they were given intraperitoneally followed by the short alkali-treatment.
Alkylating Agents↗