Systemic and hepatic circulatory responses caused by head tilting in liver transplanted pigs.
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Biomedical subjects
Publications and source records attributed to T Sakaguchi.
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Gastric acid secretion induced by tetragastrin was examined after glucose injection into the portal vein in rats. The enhancement of acid secretion caused by gastrin was inhibited by glucose injection into the portal vein, and the acid response was dose dependent. The acid response due to portal glucose injection was not reproduced when the hepatic vagal branch was sectioned. These findings suggest that the portal glucose signal modulates gastric acid secretion controlled by gastrin.
The cyclicity and intensity of gastric motility were examined following glucose injection into the nucleus of the vagus nerve (X) or into the nucleus of the solitary tract (SOL) in anesthetized rats. Enhanced gastric motility caused by insulin administration was influenced by 4 mM glucose (500 nl) injected into the X; glucose provoked a shift in the cyclicity power spectrum without any change in intensity. The peak power spectrum shifted from 4.0-5.0 cpm to 2.0-3.0 cpm, but not significant change in the cyclicity power spectrum was seen when the same dose of glucose was injected into the SOL. It was also noted that the power spectrum response to 4 mM glucose injection into the X was not modified when 4 mM glucose was injected into the SOL simultaneously. The results suggest that the medullary glucose signal in the X differentially modulates the cyclicity of gastric motility independent of the SOL.
The effect of omeprazole on liver regeneration was studied in rats following partial (65 per cent) hepatectomy. Omeprazole 0.2 mg/kg increased the relative liver weight (weight of liver as a proportion of body-weight) and mitotic index (P < 0.05). There was no difference in food and water intake. The serum gastrin concentration was significantly higher in animals receiving omeprazole 0.2 mg/kg than in controls (P < 0.05). Omeprazole administration induced an increase in the level of serum alkaline phosphatase (P < 0.05) but had no effect on serum albumin, glutamic-pyruvic transaminase and total bilirubin levels. Omeprazole stimulates liver regeneration after partial hepatectomy and this regeneration may be mediated by gastrin.
We have detected fibroblast growth factor receptor (FGFR) gene expression in the focal ischemia model. The FGFR gene expression in neurons can be explained by neuronal network disturbances, but the mechanism of astroglial gene expression remains uncertain. We speculated that blood-borne edema fluid may activate gene expression of astroglias. To prove this hypothesis, we compared the pattern's of gene expression of FGFR and distribution of edema fluid by using serial tissue sections of the middle cerebral artery (MCA) ischemia. The left MCA of twenty-four male Wistar rats were occluded, and sacrificed 1, 3, 4, 7 and 14 days later by transcardiac perfusion and fixation. The tissues were sliced thinly to 14 microns sections. Part of the tissue sections was used for in situ hybridization for rat FGFR with [35S]labeled RNA probes. The other part of the sections was used for immunostaining for albumin, immunoglobulin G (IgG) and IgM. The FGFR mRNA expression was evident in the lesion-side hemisphere. In the cortex, neurons mainly expressed FGFR gene in the cortex, whereas astroglias and capillary endothelium expressed FGFR in the corpus callosum and internal capsule. The albumin distributed cortex and white matter of the lesion-side and it extended to the contralateral side. The IgG distributed mainly in the lesion-side white matter, and in part extended to the contralateral side. The IgM only distribute to the infarcted area. When we compared topographical distribution of FGFR in the white matter and pattern of albumin, IgG and IgM distribution, pattern of IgG distribution correlated well to the area of FGFR expression.(ABSTRACT TRUNCATED AT 250 WORDS)
Gastric acid outputs caused by glucose injection into the lateral hypothalamic area (LHA) were examined in insulin hypoglycemia with or without estradiol-17 beta (EST) administration in bilaterally ovariectomized (OV) female rats. The basal level of acid output was higher in OV rats without EST than in OV rats with EST. When acid response was expressed as the percentage change, glucose injection into the LHA decreased acid output in a dose-dependent fashion in OV rats, while, in OV rats with EST, glucose injection into the LHA also reduced acid output without dose dependency. It was also noted that the threshold concentration of glucose that induced an acid response was lower in OV rats without EST than in OV rats with EST. These findings suggest that glucose-sensitive neurons responsible for gastric acid secretion can be modulated by estrogen at the LHA level.
A field isolate of Sendai virus, the Hamamatsu strain, was far more virulent in mice than the prototype Z strain. The Hamamatsu strain replicated more efficiently in the mouse lung than the Z strain, causing deteriorating lung lesions. Nucleotide sequence analysis of the HN, F and M genes revealed that the Hamamatsu strain was divergent from the prototype Z, Harris and Fushimi strains.
Portal venous blood flow (PVF), hepatic arterial blood flow (HAF), and systemic arterial pressure (SAP) were examined after prostaglandin E1 (PGE1) was injected into the vena cava superior (VCS) of liver-transplanted pigs. The injection of PGE1 at 0.2 micrograms/kg/min for 2 min on the day of transplantation and 3 days later produced an increase in PVF without causing any change in HAF or SAP, the response in PVF being dose-dependent. However, no reliable change in PVF, HAF, or SAP was seen when the same dose of PGE1 was administered 7 days after transplantation. Furthermore, no significant difference was noted among the values for PVF and total hepatic blood flow (THF) during the experimented days, although the HAF value had increased markedly 3 days after transplantation. These findings suggest that PGE1 is effective in increasing PVF in the liver transplanted condition; however, the hepatic circulatory improvement attributed to this agent would be limited to the first few days following transplantation.
The understanding of the mechanisms of a functional synaptic plasticity in the hippocampus has been expanded greatly by the use of in vitro slice preparations. The question addressed in the present study was whether morphological plasticity observed in vivo can also be reproduced in hippocampal slices. In vivo, hippocampal commissural and association fibers are known to sprout and occupy synaptic sites vacated by deafferentation of the dentate gyrus (DG). In hippocampal slice preparations, the major input to the DG is eliminated, so that the DG is deafferented. Might intrinsic neurons sprout to the DG if the slice preparation is maintained for weeks? In this study hippocampal slices obtained from 6-day-old rats were cultured. Stimulation of the dentate stratum moleculare produced antidromic field potentials in the CA3 of the slices cultivated for more than 1 week. The antidromic response was not observed in CA1 pyramidal neurons. The CA3 to DG projection response was also observed in a CA3 mini-slice placed near a co-cultured whole hippocampal slice, when the DG in the latter was stimulated. Moreover, stimulation of the CA3 mini-slice induced synaptic responses in the DG of the whole-slice. The conclusion drawn is that deafferentation could induce axonal sprouting in a neuron-specific manner in hippocampal organotypic culture. This preparation would be potentially useful for the screening of chemical factors that influence sprouting of central neurons.
In a previous report we demonstrated that basic fibroblast growth factor (bFGF), as a multipotent neurotrophic factor, could prevent retrograde degeneration of the thalamic neurons after ablation of the somatosensory cortex. To elucidate the mechanism of this bFGF action, we examined changes in FGF receptor (FGFR) mRNA (flg) expression with in situ hybridization. The FGF receptor protein was detected with the immunoblotting method. The FGFR mRNA expression was found to be diffusely increased in the affected cortex. Microscopic observation indicated that FGFR mRNA was expressed in several types of cortical cells including neurons and non-neuronal cells. This increase could be observed as early as 6 hours after surgery and lasted for 48 hours. In the thalamus, however no change in FGFR mRNA signals was observed. Western blotting detected a protein immunoreactive to anti-FGFR antibody. Samples from the periablated cortex showed an increase in FGFR protein. Samples from the thalamus, however, showed no difference in FGFR protein level between the lesion side and the contralateral side. Application of exogenous bFGF in Gelfoam to the cortical ablation cavity did not show any effect on the gene expression or protein level of FGFR. These results suggest that FGFR is diffusely induced throughout the injured cortex in the early phase after injury and that bFGF may play an important role after injury. Topically applied bFGF might thus modulate cellular responses in the cortex and have a neurotrophic effect on the affected thalamic neurons.
Intragastric pressures were examined after glucose injection into the nucleus of the vagus nerve (X) of the medulla oblongata or into the portal vein (PV) or both in bilaterally adrenalectomized rats. Ten mM glucose (500 nl) injected into the X or into the PV (25 microliters) decreased gastric pressure associated with insulin-hypoglycemia. Simultaneous injection of glucose into the X and PV produced a reduction in gastric pressure in an additive manner. In addition, a significant fall in gastric pressure was seen when an ineffective concentration of glucose was injected into the X and PV simultaneously. The results suggest that the X and PV signals interact with each other to inhibit gastric motility.
The fusion (F) protein precursor of virulent Newcastle disease virus (NDV) strains and human parainfluenza virus type 3 (HPIV3) has a multibasic amino acid sequence at the cleavage site, and intracellular cleavage activation occurs in a variety of cells. The host protease responsible for the cleavage has been proposed to be a subtilisin-like protease (subtilase) such as furin (the product of the fur gene). We found that the lymphocyte cell lines MOLT-4, Ramos and Daudi, in addition to NALM6, lacked the ability to fully cleave the F protein precursor of virulent NDV. In contrast, MT4 as well as the non-lymphocyte cell lines HeLa and Hep2 cleaved the F protein precursor efficiently. To investigate the role of subtilases in proteolytic processing, we examined the gene expression of candidate subtilases, furin, PACE4 and PC6 in these cleavage-competent and -incompetent cells. Considerable expression of the fur gene was observed in the cleavage-competent cells, but little or no expression was detected in the cleavage-incompetent cells. PACE4 and PC6 gene expression was observed in some of the cleavage-competent cells but not in the cleavage-incompetent cells. These results suggest that furin is the protease responsible for cleavage activation of the F protein of virulent NDV strains in cultured mammalian cells and the possibility is raised that PACE4 and PC6 also participate in processing in some of the cells. On the other hand, the HPIV3 F protein was cleaved efficiently in lymphocyte cells deficient in subtilases, suggesting that an unknown protease other than furin, PACE4 or PC6 may be involved in the processing.
The virulence of avian influenza viruses correlates with the sensitivity of their hemagglutinin (HA) to cellular proteases. Furin, a proprotein-processing subtilisin-related endoprotease, is a leading candidate for the enzyme that cleaves the HA of virulent avian viruses. We therefore compared the specificity of furin with those of proteases in a variety of cultured cells and in a rat Golgi fraction, using the HA cleavage mutants of a virulent avian influenza virus, A/Turkey/Ireland/1378/85 (H5N8). The results indicated similar sequence specificities among the endoproteases when purified furin was used. In experiments with the vaccinia virus expression system, overexpressed furin cleaved mutant HAs that were not recognized by the endogenous proteases, resulting in an apparent broader specificity of furin. These findings authenticate the proposed role of furin as an HA-activating protease in vivo and caution against the use of expression vectors to study protease sequence specificity.
Fifty eight cases of SBP for the latest 20 years in Japan were reviewed. General symptoms due to SBP were ascites (100%), abdominal pain (93%), jaundice (86%), fever (57%) and rebound tenderness (55%), including male/female ratio of 2.6:1. Eighty eight per cent of SBP patients had cirrhosis. Although there was no difference between bacterial spieces causing SBP in the first ten years and latter ten years, survival of short period within 2 weeks was improved from 26.7% to 71.4%. However, long survival of 6 months was very poor yet. In patients with decompensated liver function, prophylactic and early treatment of SBP were recommended for improvement of long survival in SBP patients.
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We made a diagnosis and therapeutic evaluation of herpes simplex encephalitis using polymerase chain reaction (PCR). Cerebrospinal fluids (CSF) of 24 patients suspected of meningoencephalitis were examined by PCR. HSV (herpes simplex virus) DNA was demonstrated in 3 patients, in which CSF anti-HSV antibody raised, and moreover in another patient, lacking the raise of the HSV antibody. Since this patient was considered to suffer from HSV encephalitis by clinical symptoms and findings on brain CT, this result suggests authenticity of the PCR for detection of HSV infection. HSV-DNA in the 4 patients were semi-quantitated. The amount of the DNA reduced and disappeared corresponding to their improvement of clinical symptoms and laboratory data. Thus, the present method is considered to be useful for rapid diagnosis of HSV encephalitis, and also for evaluation of effects of therapy to decide whether administration of anti-herpes drugs should be stopped.
The cyclicity and intensity of gastric motility were examined following glucose injection into the portal vein with an intragastric balloon in anesthetized rats. Enhanced gastric motility caused by insulin administration was influenced by 4 mM glucose (25 microliters) injected into the portal vein; glucose provoked a shift in the cyclicity power spectrum without any change in intensity. The peak power spectrum shifted from 4.0-5.0 cpm to 2.0-3.0 cpm. Hepatic branch vagotomy abolished the response. The results suggest that glucose signals in the hepatic vagal branch modulate the cyclicity of gastric motility.