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Biomedical subjects

Y Morimoto

Publications and source records attributed to Y Morimoto.

At least 217 records · Page 12Linked to original sources
PubMed1998

[Percutaneous transhepatic portal vein embolization for hepatocellular carcinoma].

We report on the significance of percutaneous transhepatic portal vein embolization (PTPE) for hepatocellular carcinoma based on the results in 111 patients who underwent PTPE in our hospital. All patients tolerated the procedure without major complications, although transient elevations in serum transaminase levels were noted. Immediately after PTPE, the portal pressure increased. Portal venous flow at the main portal trunk decreased, but the flow in the nonembolized part of the liver increased. PTPE produced regenerative hypertrophy in the nonembolized part of the liver, which was mainly predicted by the volume of the embolized area and the morphological score of the hepatitis or cirrhosis. PTPE increased the safety of subsequent hepatectomy and expanded the indications for hepatectomy. PTPE is also useful as a type of multiplicative therapy for hepatocellular carcinoma.

Carcinoma, Hepatocellular↗
PubMed1998

[Cardiopulmonary cerebral resuscitation and acidosis].

It is still controversial whether sodium bicarbonate is effective for the correction of acidemia during cardiopulmonary resuscitation (CPR). To resolve this issue, we must clarify the influence of acidosis accompanied by cardiac arrest on the cardiac and cerebral resuscitability. The influence of acidosis on cardiac resuscitability The factors which determine the cardiac resuscitability during asystole or ventricular fibrillation are the presser response to administered catecholamines and the threshold of defibrillation. However, there is still no evidence that acidosis inhibits these factors during CPR. Recent reports suggested that CO2 itself impaired cardiac resuscitability rather than acidosis. On the other hand, our study using isolated perfused rat hearts proposed that the effect of acidosis is not still eliminated. The influence of acidosis on the cerebral resuscitability There are two contrary opinions. One is that acidosis deteriorates the cerebral damage after resuscitation. The other is that acidosis is rather protective against the cerebral damage. In the studies which support the latter opinion, the evaluation of the effect of reperfusion is lacking. Accordingly, any factors which develop during the reperfusion phase may be enhanced by acidosis. These findings indicate that the influence of acidosis accompanied by cardiac arrest is complicated and that it includes many unresolved questions. Until we clarify these questions, we can not conclude that the correction of acidemia is necessary during CPR.

Acid-Base Equilibrium↗
PubMed1998

[Carbon monoxide in the expiratory gas during laparoscopic surgery].

One of the complications of laparoscopic surgery is carbon monoxide (CO) production under the use of electrocautery. We experienced a case in which high levels of CO were detected in the expiratory gas. An 80-year old, 33 kg female was scheduled for laparoscopic nephrectomy. Anesthesia was induced with thiopental and vecuronium and maintained with nitrous oxide 60% in oxygen and isoflurane. The concentrations of CO in the anesthetic circuit were examined with CO sensor (XC-341, Shinkosumosudenshi, Tokyo). The CO concentrations were not detected at the start of operation. About 140 minutes after carbon dioxide pneumoperitoneum, the CO concentration increased up to 170 ppm accompanying a high Paco level. The high concentrations, however, decreased immediately after ending of pneumoperitoneum. The HbCO levels were unchanged. Subcutaneous emphysema was noted at the end of surgery. This is because CO is more absorbable in the subcutaneous tissue than in the peritoneal cavity. We consider that CO was absorbed in subcutaneous emohysema during pneumoperitoneum and exhausted in the expiratory gas. When subcutaneous emphysema occurred during laparoscopic surgery, we should be aware of absorption of CO.

Aged↗
PubMed1998

Possible mechanisms of vascular relaxation induced by pulsed-UV laser.

This study was designed to examine the mechanism of vasorelaxation induced by pulsed-UV laser. Luminal diameters of rat femoral arteries were measured prior to and following krypton-fluoride excimer laser irradiation of 248 nm in wavelength. The diameter was enlarged to 1.3 times the preirradiated size at 1 or 10 Hz irradiation when the fluence was over 2.0 mJ/pulse/mm2, while the diameter reached 1.8 times at 100 Hz with a fluence of 0.8 mJ/pulse/mm2. Vasorelaxation by the 100 Hz irradiation was inhibited when the artery was pretreated with methylene blue but was enhanced with superoxide dismutase. Pathological analysis revealed an ablation crater and vacuole formation in the vessel at 1 or 10 Hz irradiation, but these changes were not remarkable in the 100 Hz-exposed sample. These findings suggest that vasorelaxation induced by the pulsed UV irradiation at 1 or 10 Hz results from structural alteration of vascular smooth muscle by the ablation crater or vacuolization. On the other hand, a possible mechanism of vasorelaxation at the 100 Hz irradiation is partially related to nitric oxide.

Animals↗
PubMed1998

Human colon cancer cells express the functional Fas ligand.

Fas ligand (FasL) belongs to the TNF superfamily. It is induced in activated lymphocytes and eliminates Fas-positive lymphocytes, resulting in the down-regulation of immune responses. FasL has also been detected in tissues other than lymphoid cells. We investigated the expression and function of FasL on human colon cancer cells. FasL mRNA was detected by RT-PCR in all six colon cancer cell lines tested and was not found on fibroblasts. FasL protein was detected in DLD-1, LoVo, HCT-116 and RPMI 4788 cells by immunohistochemical staining. DLD-1, LoVo and WiDr were cytotoxic against mouse T lymphoma cells which were transfected with human Fas receptor cDNA. The cytotoxicity was significantly enhanced by phorbol 12-myristate 13-acetate (PMA) and ionomycin. Our data suggest that the FasL expressed in human colon cancer cells may be regulated by endogenous factors in the microenvironment of the host and facilitates the escape from the host immune system.

Apoptosis↗
PubMed1998

[Anesthesia for fourteen cases of auto-renal transplantation].

We experienced anesthetic management of 14 cases of auto-renal transplantation. The causative diseases are stenosis (n = 7) and aneurysm of the renal artery (n = 5) as well as renal cancer (n = 2). The mean time intervals for operation, anesthesia, and clamping of the renal artery were 10 h 54 min, 12 h 42 min and 4 h 14 min, respectively. In the patients whose serum creatinine values were above 1 mg.dl-1 within the 3rd postoperative day, time intervals for operation and anesthesia were significantly longer than in the patients whose serum creatinine values remained below 1 mg.dl-1. The water balance in the former patients was significantly positive in comparison with the latter patients. The auto-renal transplantation is a highly invasive surgery so that proper fluid management and sufficient urination seem to be especially important for the perioperative management of patients of this category.

Adult↗
PubMed1997

Novel combination therapy for human colon cancer with adenovirus-mediated wild-type p53 gene transfer and DNA-damaging chemotherapeutic agent.

Alteration of the wild-type (wt) p53 gene by mutation, deletion or re-arrangement is a major factor in the development of human colon cancer. Recent studies have demonstrated that p53 might be an essential component of the apoptotic pathway triggered by DNA-damaging stimuli such as chemotherapeutic agents and ionizing radiation. We examined the anti-tumor effects of adenovirus-mediated wt-p53 gene transfer in combination with a chemotherapeutic drug on the human colon cancer cell line WiDr, which is homozygous for a mutation in the p53 gene. Treatment with the chemotherapeutic drug cisplatin following infection with a replication-deficient, recombinant adenoviral vector expressing wt-p53 (termed AdCMVp53) significantly suppressed the growth of WiDr cells compared to single treatments alone. To evaluate the in vivo efficacy of AdCMVp53 and cisplatin given sequentially, WiDr cells were inoculated s.c. in nu/nu mice. After 3 days, AdCMVp53 was injected s.c. into the area where tumor cells were implanted, followed by i.p. administration of cisplatin. Analysis of initial growth inhibition at 21 days demonstrated a profound therapeutic cooperativity, though administration of either AdCMVp53 or cisplatin alone was followed only by a slowing of growth. Our results suggest that gene therapy using wt-p53-expressing adenovirus in combination with a chemotherapeutic DNA-damaging drug could be a useful strategy for treating human colon cancer.

Adenoviridae↗
PubMed1997

Inhibitory effect of ethanol on the 5-HT3 receptor-mediated tachycardia in isolated guinea-pig atrium.

The influence of ethanol on 5-hydroxytryptamine (5-HT)-induced tachycardia mediated by 5-HT3 receptor activation in the isolated guinea-pig atrium was studied. Ethanol at 200 mM significantly inhibited 5-HT - but not isoproterenol- or histamine-induced tachycardia in the isolated guinea-pig atrium. The same inhibitory effect was observed in response to 2-propanol and chloral hydrate application. Both 2-propanol at 100 mM and chloral hydrate at 1 mM exhibited inhibitory effects on 5-HT -induced tachycardia as potent as those of ethanol at 200 mM. These alcohols did not inhibit the tachycardia induced by isoproterenol or histamine. The inhibitory effects of the alcohols seemed to be specific for 5-HT and to increase according to their lipophilicity. Our results suggest that the inhibitory effects of ethanol on 5-HT3 receptor-mediated tachycardia are related to the direct effect of ethanol on 5-HT3 receptors in the atrium.

1-Propanol↗
PubMed1997

The protein phosphatase inhibitors okadaic acid and calyculin A induce apoptosis in human osteoblastic cells.

To determine whether protein phosphorylation and dephosphorylation can affect apoptosis in osteoblastic cells, we examined the effects of okadaic acid (OA) and calyculin A (CA) on cultured human osteoblastic cells Saos-2 and MG63, and mouse osteoblastic MC3T3-E1 cells. After reaching confluence, these cells were exposed to varying concentrations of OA or CA. OA and CA induced cell death in all three cell lines in a dose- and time-dependent manner. Marked nuclear condensation and fragmentation of chromatin were also observed in these cells by using the Hoechst 33342 stain. DNA ladder formation, a hallmark of apoptosis, was detected in Saos-2 and MG63 cells, but not in MC3T3-E1 cells by treatment of OA or CA. In the Saos-2 cells, OA- and CA-induced DNA ladder formation was dose-dependent with maximal effect at concentrations of 10 and 2 nM, respectively, and was time-dependent from 14 to 48 h. DNA ladder formation in response to OA and CA was revealed by using conventional ethidium bromide staining of electrophoresed DNA without using autoradiography. Beyond the maximal effects at the respective concentrations, however, cell death did not indicate DNA laddering, suggesting that phosphatase activity may be required for ladder formation. Our results indicate that apoptosis in the cultured osteoblastic cells is induced by moderate inhibition of PP-1 or PP-2A based on the known selectivity of okadaic acid and of calyculin A.

Animals↗
PubMed1997

Role of nitric oxide in oxygen transport in rat liver sinusoids during endotoxemia.

To evaluate the role of nitric oxide (NO) in hepatic microcirculation and liver injury during endotoxemia, we studied O2 transport in the hepatic microcirculation of endotoxin-infused rats. Rats were continuously infused with Escherichia coli lipopolysaccharide (LPS) (0.8 mg/kg/h) for 7 hours. LPS increased the plasma levels of NO2- + NO3- and aspartate transaminase (AST), and decreased the bile flow rate and hepatic adenosine triphosphate (ATP) level. Hepatic microcirculation was evaluated by two methods: reflectance spectrophotometry showed a decrease in the oxygenation of hemoglobin (Hb) in the liver, and dual-spot microspectroscopy indicated that LPS administration decreased blood velocity, the oxygenation of Hb, and O2 release from sinusoids to hepatocytes. The observed decreases in the O2 transport parameters were prominent in pericentral sinusoids. All of these phenomena were further aggravated by the administration of N(w)-nitro-L-arginine methyl ester (L-NAME) (5 mg/kg/h) plus LPS, and by aminoguanidine (AMG) (5 mg/kg/h) plus LPS, and these could be reversed by the concomitant administration of L-arginine (L-Arg) (100 mg/kg/h). These results suggest that deterioration of hepatic oxygen transport and liver function induced by endotoxin can be ameliorated by NO.

Adenosine Triphosphate↗
PubMed1997

KB-R7785, a novel matrix metalloproteinase inhibitor, exerts its antidiabetic effect by inhibiting tumor necrosis factor-alpha production.

It has been suggested that tumor necrosis factor-alpha (TNF-alpha) is a key mediator of insulin resistance in non-insulin-dependent diabetes mellitus (NIDDM). TNF-alpha is synthesized as a membrane-bound precursor; this is proteolytically processed to an active form by a matrix metalloproteinase (MMP)-like enzyme. In this study, we have used KKAy mice which show insulin resistance like NIDDM to investigate the effects of KB-R7785, a novel MMP inhibitor, on blood glucose and insulin levels. Subcutaneous administration of KB-R7785 at 100 mg/kg twice daily (i.e., 200 mg/kg/day) for 4 weeks resulted in a significant decrease in plasma glucose levels which was observed after 3 weeks. Oral administration of pioglitazone (20 mg/kg twice daily or 40 mg/kg/day for 4 weeks), an agent known to ameliorate insulin sensitivity, significantly decreased plasma glucose levels during the treatment period. KB-R7785, but not pioglitazone, also significantly decreased plasma insulin levels. Lipopolysaccharide (LPS) increased plasma TNF-alpha levels to a significantly greater degree in KKAy mice than in normal C57BL mice; this was inhibitable in KKAy mice by KB-R7785. In contrast, pioglitazone did not affect the LPS-induced increase in plasma TNF-alpha levels in KKAy mice. These results suggest that KB-R7785 exerts its antidiabetic effect by ameliorating insulin sensitivity through the inhibition of TNF-alpha production.

Animals↗
PubMed1997

Extracellular acidosis delays cell death against glucose-oxygen deprivation in neuroblastoma x glioma hybrid cells.

OBJECTIVE: To determine whether extracellular acidosis delays cell death against glucose-oxygen deprivation and, if so, whether this result is due to inhibition of calcium (Ca2+) influx or preservation of cellular energy state. DESIGN: Randomized, controlled, prospective study. SETTING: University research laboratory. SUBJECTS: Differentiated neuroblastoma x glioma NG108-15 cells. INTERVENTIONS: Experiment 1: cells were incubated for 8 hrs in N-(2-hydroxyethyl)piperazine-N'-2-ethanesulfonic acid-buffered medium under glucose-oxygen deprivation at pH 7.4, 6.8, 6.5, 6.2, 5.6, or 5.0. Experiment 2: cells were incubated for 8 hrs under glucose-oxygen deprivation after excluding extracellular calcium from culture medium at pH 7.4 or 6.2. Experiment 3: cells were incubated for 2, 4, 6, or 8 hrs in N-(2-hydroxyethyl)piperazine-N'-2-ethanesulfonic acid-buffered medium under glucose-oxygen deprivation at pH 7.4 or 6.2 and assayed for high-energy phosphates. MEASUREMENTS AND MAIN RESULTS: Cell viability was measured with flow cytometry after the cells were stained with fluorescein diacetate and propidium iodide. Cellular adenosine triphosphate, adenosine diphosphate, and adenosine monophosphate were analyzed with high-performance liquid chromatography. Cell viability was significantly greater at pH 6.2 than at pH 7.4 in experiment 1. By excluding extracellular calcium, a significant difference in viability between pH 7.4 and 6.2 persisted in experiment 2. Energy charge and the concentration of adenosine triphosphate were significantly greater at pH 6.2 than at pH 7.4 in the intervals preceding manifestation of a differential effect of acidosis on cell viability in experiment 3. CONCLUSIONS: Extracellular acidosis at pH 6.2 delayed cell death against glucose-oxygen deprivation. This protective effect by extracellular acidosis may be due to preservation of the cellular energy state in NG108-15 cells, although this study does not exclude the possibility that in other cell types, inhibition of calcium influx may have an effect.

Acidosis↗
PubMed1997

High-dose fentanyl does not adversely affect outcome from forebrain ischemia in the rat.

Fentanyl citrate has properties, including agonism of the mu-opioid receptor and proconvulsant activity, that theoretically could pose adverse effects in ischemic brain. This study examined the effects of high-dose fentanyl on outcome in rats subjected to transient near-complete forebrain ischemia. Rats were anesthetized with halothane and surgically prepared for ischemia. In one group (fentanyl; n = 15), intravenous fentanyl (400 micrograms/kg followed by an infusion of 16 micrograms/kg/min for 20 min) was administered and halothane was discontinued. In the remaining rats (control: n = 15), halothane administration was continued and no fentanyl was given. Following 10 min of bilateral carotid artery occlusion and profound systemic hypotension, animals were maintained normocapnic, normothermic, and mildly hyperoxemic for 8 h. Four days later, histologic and neurologic outcomes were assessed. In another group of rats also administered halothane (uncontrolled recovery; n = 15), no attempt was made to control physiologic variables during recovery from ischemia. Fentanyl caused preischemic evidence of epileptoid activity but decreased the percentage of neurons that died in the CA1 sector of the hippocampus relative to control (p = 0.0005). Damage in the cortex or caudoputamen was not different from that in the control group. Rats with an uncontrolled recovery had decreased damage in the cortex (p = 0.005) and caudoputamen (p = 0.00015) relative to control. In this model of forebrain ischemia, fentanyl caused no worsening of histologic damage in the cortex or caudoputamen and decreased hippocampal CA1 injury despite major electroencephalographic activation in the immediate preischemic period.

Anesthesia↗
PubMed1997

Changes in T, B, and NK lymphocyte subsets during and after normal pregnancy.

PROBLEM: Pregnancy affects the maternal immune system and the clinical course of maternal diseases. Here we report the changes in the detailed lymphocyte subsets of helper T cells, suppressor T cells, CD5+ B cells, T cell receptor (TCR) alpha beta-positive T cells (T alpha beta cells), TCR alpha beta-negative T cell (T gamma delta cells), and other during and after pregnancy through to one year postpartum, and discuss the significance of the changes. METHOD: The absolute numbers of helper T cells, suppressor T cells, cytotoxic T cells, TCR alpha beta-negative T cells (T gamma delta cells), CD5- B cells, CD5+ B cells, and NK cell subsets were examined by two-color flow cytometry in peripheral blood from 51 healthy non-pregnant women, 106 healthy pregnant women, and 148 healthy postpartum women. RESULTS: In early pregnancy, the numbers of suppressor T cells and NK cells with strong cytotoxicity (NK+3 cells) increased, and the number of cytotoxic T cells decreased. In late pregnancy, the helper T cell and NK+3 cell numbers decreased. T alpha beta, CD5- B and CD5+ B cells decreased during pregnancy. After delivery, helper T cells and cytotoxic T cells increased from 1 to 4 months postpartum, and suppressor T cells increased at 7 months postpartum. TCR alpha beta-negative T cells increased at 4 to 10 months postpartum. Both CD5- and CD5+ B cells decreased further at 1 month postpartum, but CD5+ B cells increased markedly at 7 to 10 months postpartum. CONCLUSIONS: These data indicate that 1) early increases of suppressor T cells and NK+3 cells during pregnancy may be related to the mechanism to accept or reject the fetus in early pregnancy, respectively; 2) late decreases of helper T cells and NK+3 cells may be related to the maintenance of pregnancy: 3) postpartum increases of helper T cells, cytotoxic T cells, TCR alpha beta-negative T cells (T gamma delta cells), and CD5+ B cells may be related to the postpartum aggravation of autoimmune diseases; and 4) the immunological effects of pregnancy remains until about 1 year after delivery.

Adult↗
PubMed1997

A monoclonal antibody (1F3) to human glomerular epithelial cells: a new marker for renal epithelial cell injury.

In order to identify a new cell surface antigen as a potential marker of renal epithelial cell injury, we produced a monoclonal antibody (Mab), 1F3, by immunizing mice with cultured human glomerular cells. Immunofluorescence (IF) and immunoelectron microscopy (IEM) studies demonstrated that 1F3-recognizing antigen (1F3 antigen) was strongly expressed on the cell surface of glomerular podocytes and very weakly on parietal epithelial cells. 1F3 antigen was not expressed in any other cells in the normal kidney. Immunoprecipitation analysis using metabolically labeled glomeruli revealed that 1F3 recognized a 125-kD protein under reducing conditions. IF studies of biopsy specimens from patients with a variety of glomerular and tubulointerstitial diseases showed that 1F3 antigen was almost negative in cellular crescents but was strongly expressed in fibrocellular crescents. When glomerular sclerosis appeared, the expression of 1F3 antigen decreased in sclerotic areas of glomeruli. 1F3 antigen became positive in atrophic tubules that were seen in diseased kidneys. Severity of tubular atrophy correlated well with the extent of tubular expression of 1F3 antigen. These results indicate that Mab, 1F3 marks phenotypic changes of renal epithelial cells under disease conditions and may be a useful marker for progressive kidney diseases.

Animals↗
PubMed1997

Evaluation of skin permeability of drugs by newly prepared polymer membranes.

Four polymeric membranes were prepared consisting of various ratios of 2-hydroxyethyl-methacrylate/polydimethylsiloxane-methacrylate copolymer. These membranes had both lipophilic and hydrophilic domains in their copolymer networks like skin barrier. From permeation studies of the aqueous solutions or suspensions of various lipophilic and hydrophilic drugs using these membranes, a membrane having a similar drug permeability to hairless rat and human skins was selected. Permeation of indomethacin through the selected polymer membrane from simple ointment, gel and a marketed cream were then measured. About 10(2) times higher permeability was found in the polymer membrane than through excised hairless rat skin, but the rank order of the permeability through the polymer membrane among the formulations was the same through the skin membranes. These higher permeations of indomethacin were probably related to physical and chemical properties of pharmaceutical additives in the topical formulations. It is concluded that these synthetic polymer membranes may be utilized as an alternative tool to predict human or rat skin permeability of various (hydrophilic or lipophilic) drugs as well as to screen drug candidates for transdermal drug delivery.

Administration, Cutaneous↗
PubMed1997

Effects of mineral fibers on the expression of genes whose product may play a role in fiber pathogenesis.

To determine which factors are useful for the risk assessment of man-made fibers, we examined the gene expression of proinflammatory cytokines, growth factors, manganese superoxide dismutase (MnSOD), and inducible nitric oxide synthase (iNOS) in mineral fiber-exposed rats by means of reverse transcription-polymerase chain reaction (RT-PCR). Male Wistar rats received a single intratracheal instillation of either saline (control) or two types of fibers (2 mg of Union Internationale Centre le Cancer (UICC) chrysotile or alumina silicate refractory ceramic fiber [RCF]). Expression of interleukin-1 alpha (IL-1 alpha), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), platelet-deriving growth factor-A, (PDGF-A), platelet-deriving growth factor-B (PDGF-B), transforming growth factor beta 1 (TGF-beta 1), basic fibroblast growth factor (bFGF), MnSOD, and iNOS mRNA from lung and lipopolysaccharide (LPS)-stimulated alveolar macrophages (AM) were assessed by RT-PCR. Among these factors, IL-1 alpha, TNF-alpha, IL-6, bFGF, and iNOS would be the possible parameters for the risk assessment of fibers. In a follow-up study, we investigated the time course (3 days, 1 week, 1 month, and 3 months) of expression of IL-1 alpha and TNF-alpha by LPS-stimulated AM exposed to mineral fibers in vivo. Male Wistar rats were instilled intratracheally with saline or fibers (2 mg of Union Internationale Contre le Cancer UICC crocidolite or potassium octatitanate whisker [TW]). The expression of IL-1 alpha mRNA by fibers was greatest in TW, crocidolite, chrysotile, and RCF-instilled rat AM, in that order. The increase of IL-1 alpha and TNF-alpha mRNA in AM peaked at 1 month and 3 days after exposure to crocidolite or TW, respectively. The expression of IL-1 alpha by fibers (crocidolite, chrysotile, TW, and RCF) may be a good indicator of the pathologic potential of fibers.

Administration, Inhalation↗