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Biomedical subjects

T Sakaguchi

Publications and source records attributed to T Sakaguchi.

At least 19 recordsLinked to original sources
PubMed1995

Neural discharge can be modulated by carotid arterial injection of gastrin-17 in rat hypothalamic paraventricular nucleus.

Neural discharge in the hypothalamic paraventricular nucleus (PVN) was examined after gastrin-17 injection into the carotid artery in anesthetized rats. Neural discharge was increased by gastrin-17 injection into the carotid artery close to the cranium, and the response due to the gastrin was dose-dependent. No discharge response was seen when gastrin was injected into the jugular vein. These results suggest that gastrin circulating in the arterial blood can penetrate the blood brain barrier, and modulate neural PVN activity which is responsible for gastric acid secretion.

Animals↗
PubMed1995

8-Hydroxyadenine (7,8-dihydro-8-oxoadenine) induces misincorporation in in vitro DNA synthesis and mutations in NIH 3T3 cells.

An oligodeoxyribonucleotide containing 8-hydroxyadenine (OH8Ade) was chemically synthesized and single- and double-stranded c-Ha-ras gene fragments with OH8Ade at the second position of codon 61 were prepared. The single-stranded ras gene fragment was used as a template for in vitro DNA synthesis with the Klenow fragment of Escherichia coli DNA polymerase I, Taq DNA polymerase, rat DNA polymerase beta and mouse DNA polymerase alpha. The former two enzymes exclusively incorporated dTMP opposite OH8Ade. The DNA polymerases alpha and beta misinserted dGMP, and dAMP and dGMP, respectively. The c-Ha-ras gene was constructed using the double-stranded ras gene fragment containing OH8Ade and was transfected into NIH 3T3 cells. The gene with OH8Ade induced focus formation, indicating that OH8Ade elicited point mutations in cells. When c-Ha-ras genes present in transformed cells were analyzed, an A-->G transition and an A-->C transversion were detected. These results indicate that OH8Ade induced misincorporation in in vitro DNA synthesis and mutations in mammalian cells.

3T3 Cells↗
PubMed1995

Phylogenetic analysis of a novel sulfate-reducing magnetic bacterium, RS-1, demonstrates its membership of the delta-Proteobacteria.

Most of the 16S ribosomal RNA gene of a sulfate-reducing magnetic bacterium, RS-1, was sequenced, and phylogenetic analysis was carried out. The results suggest that RS-1 is a member of the delta-Proteobacteria, and it appears to represent a new genus. RS-1 is the first bacterium reported outside the alpha-Proteobacteria that contains magnetite inclusions. RS-1 therefore disrupts the correlation between the alpha-Proteobacteria and possession of magnetite inclusions, and that between the delta-Proteobacteria and possession of greigite inclusions. The existence of RS-1 also suggests that intracellular magnetite biomineralization is of multiple evolutionary origins.

Bacteria↗
PubMed1995

Gastric acid secretion caused by gastrin-17 injection into both sides of the hypothalamic paraventricular nucleus in rats.

Gastric acid outputs were examined after gastrin-17 (gastrin) injection into either side of the hypothalamic paraventricular nucleus (PVN) or both sides of the PVN in bilaterally adrenalectomized rats. The acid output increased when 40 pM gastrin was unilaterally injected (10 s, 500 nl) into the PVN through a 28-gauge stainless steel tube. The acid output was also increased when 80 pM gastrin was iontophoretically injected (2 min, -50 nA) into the PVN through a glass tube. An additive increase in the acid output was elicited when an effective concentration of gastrin was simultaneously injected into both sides of the PVN. It was also noted that there was a significant increase in acid output when an ineffective concentration of gastrin was simultaneously injected into both sides of the PVN. Almost the same magnitude of acid response due to PVN gastrin was reproduced in normoglycemia, but it was diminished in hyperglycemia. These results suggest that PVN neurons sensitive to gastrin form a neural circuit in both sides of the nucleus, and the circuit acts to potentiate the stimulation of gastric acid which is dependent on the glycemic condition.

Animals↗
PubMed1995

Control of motor and secretory functions of the stomach by a portal glucose signal.

D-glucose solution injected into the portal vein influences efferent tonic activities of the vagal nerve innervating the stomach. This suggested the existence of a neural connection between hepatic vagal branch afferents and gastric vagal efferents in the brain. Considering this observation together with findings indicating that electrical stimulation of the proximal cut end of the hepatic vagal branch changes acidity in the gastric perfusing fluid or pressure within the stomach, it has been presumed that hepatic afferent signals related to glucose may regulate the motor or secretory function of the stomach through a change in central nervous activity. Recently active interaction between the portal and medullary glucose signals in gastric function was discovered, and analysis of the characteristic features of the system is in progress.

Animals↗
PubMed1995

Correlation between anti-ubiquitin immunoreactivity and region-specific neuronal death in N-methyl-D-aspartate-treated rat hippocampal organotypic cultures.

Neuronal degeneration appears to be associated with changes in anti-ubiquitin immunoreactivity (UIR). To elucidate the relationship between the two events, we examined the time course of changes in UIR in pyramidal neurons of hippocampal organotypic cultures following exposure to an excitotoxin, N-methyl-D-aspartate (NMDA). In nontreated cultures, weak UIR was confined to the nucleus. Exposure to 100 microM NMDA for 15 min induced degeneration of pyramidal neurons, within 24 h, in the CA1 and CA3c regions. In these neurons, the nuclear UIR was reduced, and instead, UIR developed in the cytoplasm. In response to the same procedure, CA3a,b pyramidal neurons showed slight shrinkage but otherwise virtually normal morphological features. Little perikaryal (cytoplasmic) UIR developed in CA3a,b neurons. Both degeneration and perikaryal UIR were observed in CA3a,b neurons, however, when the culture was exposed to 300 microM NMDA. Immunoblot analysis showed that changes in the amount of a ubiquitin protein conjugate (24 kDa), presumably ubiquitinated histone, are similar to those of nuclear UIR in the same time course. We propose that the changes in the expression of nuclear and perikaryal ubiquitinated proteins represent some process closely related to neuronal death.

Animals↗
PubMed1995

Expression of c-fos mRNA after cortical ablation in rat brain is modulated by basic fibroblast growth factor (bFGF) and the NMDA receptor is involved in c-fos expression.

Expression of c-fos mRNA after cortical injury was studied using the in situ hybridization technique. Strong signals for c-fos mRNA were observed immediately after cortical ablation in neurons throughout the cortex ipsilateral to the injury. However, this c-fos mRNA expression was transient and disappeared within 6 h after the injury. When basic fibroblast growth factor (bFGF; 1 micrograms) was applied to the site of ablation, c-fos mRNA signals were observed for a much longer period. Even 24 h after injury, diffuse expression of c-fos mRNA was detected throughout the cortex, being mainly confined to non-neuronal cells. Intraperitoneal injection of MK-801 (3 mg/kg), a non-competitive NMDA receptor antagonist, suppressed the expression of c-fos mRNA after cortical ablation. It suppressed both the immediate and late expression induced by cortical ablation and bFGF. The immediate expression of c-fos in neurons is likely to be due to spreading depression, while neuronal-glial interactions would be involved in the mechanism of late c-fos expression by non-neuronal cells. Our results suggest that induction of c-fos after cortical injury can be modulated by topically applied bFGF and that the N-methyl-D-aspartate (NMDA) receptor is involved in c-fos expression not only caused by injury itself but also induced by injury and bFGF. As the immediate early genes regulate secondary gene responses, the induction of c-fos may contribute to neuronal plasticity and bFGF may enhance its effect.

Animals↗
PubMed1995

[The role of emergent endoscopic retrograde pancreatography (ERP): its usefulness in the diagnosis of pancreatic injury].

To determine the therapeutic modalities for pancreatic injury (PI), it is important for the pancreatic ductal injury (DI) to be present or not. We performed ERPs in 36 patients who had positive findings in physical examinations, serum amylase levels and CT within about 13 hours after injury to diagnose the DIs early after injury and to avoid negative laparotomy. In 33 successful ERP patients (intraoperatively in 3), 22 had PIs (14 DIs) and 11 had non-PIs. Of 14 patients with DIs, 12 with main DIs and one with branch injury were treated surgically. Another patient with branch injury, who was treated conservatively, died of the complications of PI. Nineteen patients without DIs, including 8 PIs, were treated conservatively or operated for the associated abdominal injuries, who had no complications on PIs in the hospital days. Three unsuccessful ERP patients, having PIs, were also operated upon. Among 15 patients, including these 3 patients and 12 treated surgically during the era before introducing ERPs, 2 (13.3%) negative laparotomies were noted. Among 16 patients, who underwent both of ERP and operation, no negative laparotomies were noted. No complications of ERPs occurred. In conclusion, ERP is a reliable modality to detect DIs and to determine the therapeutic modalities for PIs.

Adolescent↗
PubMed1994

Enhanced gastric acid secretion induced by gastrin can be suppressed by glucose injected into the portal vein in rats.

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.

Animals↗
PubMed1994

Glucose signal in the nucleus of the vagus nerve modulates the cyclicity of gastric motility in rats.

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.

Analysis of Variance↗
PubMed1994

Liver regeneration is enhanced by omeprazole in rats following partial hepatectomy.

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.

Animals↗
PubMed1994

Blood-borne macromolecule induces FGF receptor gene expression after focal ischemia.

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)

Animals↗
PubMed1994

An interaction between glucose and estrogen in gastric acid secretion in the lateral hypothalamic area of female rats.

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.

Adrenalectomy↗
PubMed1994

A field isolate of Sendai virus: its high virulence to mice and genetic divergence form prototype strains.

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.

Animals↗