[Treatment of acute pancreatitis].
Explore the source record for details and available documents.
Acute Disease↗
Biomedical subjects
K Kataoka
Publications and source records attributed to K Kataoka.
Re-evaluation of ischemia-induced neuronal damage in hippocampal regions in the normothermic gerbil.
It has not been discussed whether transient forebrain ischemia of 5-min duration, which is a model frequently used to evaluate pharmacological protection against ischemic injury, is an optimal model in the CA1 field of this animal whose brain temperature is maintained at normothermic levels. The temperature of the brain during an ischemic insult strongly affects the extent of the resulting neuronal injury. If the brain temperature is not regulated, it usually falls in the gerbil by 2 degrees-4 degrees C during 5-min ischemia. However, the brain temperature during ischemic insult was not regulated in many previous studies. In the present study, the effects of transient (1 to 5 min) forebrain ischemia on the development of neuronal degeneration in hippocampal regions of the gerbil whose brain temperature was maintained at 37 degrees C were examined. In the CA1 field of the hippocampus, transient ischemia of 3- and 4-min duration caused almost the same maximal damage (88%-91% neuronal loss) as observed in the gerbils subjected to 5-min ischemia. Transient ischemia of 2- and 2.5-min duration provoked substantial neuronal damage in 25% and 55% of experimental gerbils, respectively. These results indicate that 5-min bilateral forebrain ischemia is more than is necessary to examine ischemia-induced neuronal degeneration in hippocampal CA1 field of the gerbil whose brain temperature is maintained at normothermic levels. In the normothermic gerbil brain, an ischemic period of 3-min already induces extensive neuronal death in the CA1 and, thus, constitutes a sensitive model to evaluate faint protective effects of drugs against ischemic injury in the normothermic gerbil.
Animals↗
Development of gap junctions between gastric surface mucous cells during cell maturation in rats.
The development of gap junctions in rat gastric surface mucous cells during their maturation were examined by indirect immunofluorescence and freeze-fracture methods. Monoclonal antibody against liver gap junction protein stained in large spots along the intercellular junctions between mature gastric surface mucous cells. On the other hand, relatively small fluorescent spots were present over the immature surface mucous cells. The freeze-fracture method showed many large irregular gap junctions between mature surface mucous cells. In immature surface mucous cells, the gap junctions were less developed than those of mature cells, and small gap junctions were occasionally associated with tight junctional strands. Quantitatively, the gap junctions in mature cells were larger and more numerous than those in immature cells. These findings show that gap junctions develop during the maturation of surface mucous cells and suggest that the intercellular communication mediated by gap junctions between gastric surface mucous cells plays an important role in the regulation of cell differentiation and in tissue homeostasis.
Animals↗
Isolation of the avian transforming retrovirus, AS42, carrying the v-maf oncogene and initial characterization of its gene product.
A novel avian transforming retrovirus was isolated from a chicken musculoaponeurotic fibrosarcoma. This virus (called AS42) induces tumors histopathologically indistinguishable from the original sarcoma after a long latent period when inoculated into newborn chickens. AS42 also exhibits a weak transforming activity when infected into chicken embryo fibroblasts (CEF). This virus is replication-defective and associated with a helper virus of subgroup A (called ASAV). An AS42-specific protein of about 100 kDa was immunoprecipitated from lysates of AS42-transformed CEF with antiserum directed against avian retrovirus virion proteins. Molecular analysis of the genomic structure of the AS42 virus has revealed that this 100-kDa protein represents a novel oncogene, v-maf of cellular origin, which is fused with a part of the viral gag gene (Nishizawa et al., Proc. Natl. Acad. Sci. USA 86, 7711-7715, 1989). Interestingly, some size variation was observed among the gag-maf fusion proteins found in individual clones of transformed CEF. Consistent with this observation, Southern blot analyses and nucleotide sequence determination of several independent isolates of proviral DNA indicated that this virus segregates multiple forms of deletion mutants, probably through homologous recombinations among the repetitive sequences present within the v-maf coding region.
Animals↗
Acidic fibroblast growth factor delays in vitro ischemia-induced intracellular calcium elevation in gerbil hippocampal slices: a sign of neuroprotection.
Using microfluorometry, effects of acidic fibroblast growth factor (aFGF) on the in vitro ischemia-induced intracellular calcium elevation were investigated in gerbil hippocampal slices at 35 degrees C. When slices were superfused with hypoxic and glucose-free medium, the mean latency of the in vitro ischemia-induced calcium elevation was 209 +/- 51 s. The addition of aFGF in medium (25 micrograms/l) delayed the calcium elevation throughout the experiments: the mean latency was 541 +/- 94 s. This retardation in calcium elevation may be indicative of neuroprotective nature of aFGF.
Animals↗
Selective vulnerability of hippocampal CA1 neurons cannot be explained in terms of an increase in glutamate concentration during ischemia in the gerbil: brain microdialysis study.
Ischemia-induced selective neuronal injury to field CA1 is not attributable to selective glutamate release in field CA1 during ischemia. Excessive release of glutamate has been proposed to play a major role in ischemia-induced selective neuronal death in field CA1 of the hippocampus. It is well known that, following carotid arterial occlusion of 5 min duration in the gerbil, the pyramidal neurons in field CA1 show delayed neuronal death, whereas the neurons in field CA3 do not show any neuronal degeneration. In the present study, we measured the levels of released glutamate during ischemia in field CA1 and field CA3, separately, and evaluated whether there are subregional differences in the concentration of released glutamate which could be a satisfactory explanation for the selective vulnerability of hippocampal neurons to ischemia. Extracellular glutamate levels were significantly increased during ischemia in both field CA1 and field CA3. No significant differences were detected in the time-course of change in glutamate release and the levels of glutamate between field CA1 and field CA3. This result indicates that the increased glutamate levels do not play a pivotal part in the detrimental effect of glutamate during 5-min ischemia. Some differentiated post-synaptic organization may act as a crucial factor in the development of ischemia-induced selective neuronal death in the gerbil hippocampus.
Analysis of Variance↗
Functional changes in thalamic relay neurons after focal cerebral infarct: a study of unit recordings from VPL neurons after MCA occlusion in rats.
We evaluated neuronal and histological changes of thalamic neurons 1, 4, 7, and 14 days after middle cerebral artery (MCA) occlusion in rats. After the somatosensory evoked potentials (SEPs) were measured from the cerebral cortex, the thalamic relay neuronal activities were recorded with a glass microelectrode following repetitive electrical stimulation of the contralateral forepaw at frequencies ranging from 1 to 50 Hz. In approximately 95% of the occluded rats, the ipsilateral somatosensory cortex and/or the subcortical somatosensory pathway developed infarct, resulting in SEP loss. We evaluated unit data from rats with abolished SEPs. The average firing rate of the nucleus ventralis posterolateralis (VPL) neurons in response to 25 stimulations at 30 Hz was significantly reduced to 0.1 spike/stimulus 1 day after MCA occlusion. In sham-operated rats, the same stimulation produced 0.7 spike/stimulus. The firing rate recovered to 0.4 spike/stimulus at 30-Hz stimulation 4 and 7 days after occlusion. This was followed by resuppression (0.1 spike/stimulus) 14 days after occlusion. Histological study revealed some abnormal neurons in the ipsilateral thalamus 7 days after occlusion. We were unable to find normal-shaped neurons in the VPL 14 days after occlusion. The present study demonstrates that cortical infarct produces functional and morphologic changes that gradually and progressively affect the ipsilateral thalamus, although incomplete transient recovery of somatosensory transmission may occur.
Animals↗
Effects of propentofylline on hypoxia-hypoglycemia-induced calcium accumulation in gerbil hippocampal slices.
The xanthine derivative propentofylline (HWA 285) has been reported to show protective effects against neuronal damage induced by cerebral ischemia. In the present study, microfluorometry was used to investigate the effect of propentofylline on the hypoxia-hypoglycemia-induced intracellular calcium accumulation in gerbil hippocampal slices. When slices were superfused with hypoxic-hypoglycemic medium that did not contain propentofylline, an acute increase in calcium accumulation was detected 75-200 s (mean latency of 123 s) after the beginning of hypoxia-hypoglycemia. When slices were superfused with hypoxic-hypoglycemic mediums that contained 10 microM, 100 microM, and 1 mM propentofylline, the latency of the acute increase in calcium accumulation was prolonged in all subregions of the hippocampus in a dose-dependent manner: mean latencies in field CA1 were 146, 168, and 197 s after hypoxia-hypoglycemia, respectively. This retardation in calcium accumulation may be involved in the mechanisms by which propentofylline diminishes ischemic injury.
Animals↗
Detection and partial purification of ischaemia-related neurotrophic activity in the periinfarcted brain tissue.
In the rat model of middle cerebral artery (MCA) occlusion, axons originating from the ipsilateral cortical and thalamic neurons are injured by ischaemia. The cortical neurons survive thereafter without retrograde degeneration, but thalamic neurons slowly die because of retrograde degeneration. The fate of these two neurons is remarkably different and may be related to neurotrophic activity induced by ischaemia. We detected ischaemia-related neurotrophic activity, and partially purified the factor. Tissue samples were obtained from the cortex adjacent to the infarction and contralateral corresponding site at 4, 8 and 12 days after occlusion of the MCA. They were homogenated with a culture medium and ultracentrifuged. The supernatant was obtained and used for neurotrophic assay. Foetal cortical neurons were obtained from 17 days rat embryo and cultured. Neurotrophic activity was assayed by applying tissue extract to the culture medium. Application of periischaemic cortical extract obtained at 8 and 12 days after ischaemia improved neuronal survival by 50% and 200% as compared to contralateral cortical extract, respectively. The activity was not detectable at 4 days after ischaemia. The neurotrophic activity disappeared by heating the extract at 90 degrees C for 10 min. We fractionated the extract by saturated ammonium sulphate precipitation, followed by gel-filtered with Superose 12 column. The neurotrophic activity was detected in the precipitation of 30 to 60% saturation fraction of ammonium sulphate. With gel-filtration we separated neurotrophic activity in several fractions, which included marker proteins of 8, 22 and 30 kilodaltons. The activities were only detected in the lesioned side but not in the contralateral side.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Various factors associated with the manifestation of influenza-like illness.
A survey enrolling 814 schoolchildren was conducted immediately after a peak epidemic in the 1988-1989 influenza season and then a case-control study for influenza-like illness (ILI) was carried out using information concerning illness onset and usual lifestyle. Based on the analysis of the correlations among symptoms and actions taken due to symptoms, cases were defined as those with fever greater than or equal to 38 degrees C and subsequent absenteeism and medical consultation during peak epidemic; within this, mild-ILI (MILI) was defined as fever greater than or equal to 38 degrees C and less than 39 degrees C, and severe-ILI (SILI) as fever greater than or equal to 39 degrees C. Controls were defined as those with no symptoms (NS) during that period. Adjusted odds ratios (OR) were obtained through an unconditional logistic regression model between the MILI (80) or SILI (48) and NS (196) groups from among respondents (803). For MILI, increased risks were observed for easily-inflamed tonsils (OR = 3.0, 95% CI: 1.7-5.4); and larger family size (1.9, 1.1-3.4); with decreased risks for higher school grades (0.4, 0.2-0.9); frequent intake of vegetables or fruits other than green/yellow vegetables (0.5, 0.3-1.0); and larger room space per capita (0.4, 0.2-0.9). For SILI, there were increased risks for easily-inflamed tonsils (3.8, 1.8-8.1) and history of doctor-diagnosed asthma (2.9, 1.2-6.7); and decreased risks for higher grades (0.2, 0.1-0.6), frequent intake of milk or dairy products (0.3, 0.1-0.6) and vaccination (0.3, 0.1-0.8).
Case-Control Studies↗
Flow cytometric analysis on perforin induction in peripheral blood mononuclear cells with interleukin-2 or OK-432.
Perforin is a protein present in the cytoplasmic granules of killer cells and is considered to be an important effector molecule. We assessed the perforin appearance via flow cytometry in human peripheral blood mononuclear cells stimulated in vitro for 3 days by recombinant interleukin-2 (rIL-2) or OK-432, a biological response modifier. The relationship between the lymphocyte subsets and perforin was investigated via two-color assay. CD4-positive cells had almost no perforin, and most of the CD16-positive cells did. Regarding the relationship with CD8, some of the bright positive cells (which were likely T cells) and most of the dull positive cells (likely NK cells) had perforin. Mean fluorescence was greatest in perforin-positive cells incubated with rIL-2, less in cells incubated with OK-432, and minimal in cells incubated in a medium without additives. Immunohistochemical staining with antiperforin antibody revealed that blast-transformed and enlarge cells were stained positively and that the intensity of staining of each cell alone was enhanced in cells incubated with OK-432 or rIL-2. If the fluorescence intensity of perforin-positive cells correlates with the amount of perforin in those cells, then the appearance of perforin was enhanced with OK-432, more enhanced with rIL-2, and consistent for cytotoxicity against K562 and Daudi cells. IL-2 was induced by OK-432, suggesting that the indirect effect of this IL-2 may play a role in OK-432-perforin induction. The results suggest that perforin may be an effector molecule in killer cells induced by rIL-2 or OK-432.
Cytotoxicity, Immunologic↗
Release of excitatory amino acids from cultured hippocampal astrocytes induced by a hypoxic-hypoglycemic stimulation.
An excess release of excitatory amino acids (EAA) is an important factor for postischemic brain damage. In the present communication, we demonstrate that cultured hippocampal cells release EAA after hypoxic-hypoglycemic treatment. The amounts of EAA released from astrocytes were appreciably above those released from neurons. Furthermore, the amount of aspartate released from astrocytes was comparable to that of glutamate, although the endogenous content of aspartate was one-fifth that of glutamate. The endogenous content of aspartate in astrocytes increased even after hypoxic-hypoglycemic treatment. These results suggests that ischemic neuronal death is due, at least in part, to the excitotoxicity of aspartate and glutamate derived from surrounding astrocytes.
Amino Acids↗
Characterization of muscarinic receptor subtypes on rat pancreatic acini: pharmacological identification by secretory responses and binding studies.
In order to identify subtypes of muscarinic receptor on the rat pancreas, the effects of new muscarinic receptor antagonists, [11-[[2-(diethylamino)-methyl]-1-piperidinyl]acetyl]-5, 11-dihydro-6H-pyrido[2,3-b][1,4]benzodiazepine-6-one (AF-DX 116) and 4-diphenylacetoxy-N-methylpiperadine-methiodide (4-DAMP), on amylase secretion stimulated by carbachol and binding of [3H]quinuclidinyl benzilate (QNB) were evaluated using isolated rat pancreatic acini. Atropine, pirenzepine, AF-DX 116 and 4-DAMP inhibited carbachol-stimulated amylase release in a dose-dependent manner. All these antagonists caused a concentration-dependent rightward shift of the dose-response curve for carbachol-stimulated amylase release without altering the maximal response. Schild plots revealed that pA2 values for atropine, pirenzepine, AF-DX 116 and 4-DAMP were 9.15, 6.78, 6.09 and 8.79, respectively. Every slope of Schild plots was not different from unity, suggesting that these antagonists act as competitive inhibitors. These antagonists also inhibited the binding of [3H]QNB in a dose-dependent manner. The inhibition constants were 1.21 x 10(-9) M (atropine), 1.26 x 10(-7) M (pirenzepine), 0.57 x 10(-6) M (AF-DX 116) and 2.75 x 10(-9) M (4-DAMP). Thus, the order of inhibitory potencies was atropine > or = 4-DAMP > pirenzepine > AF-DX 116. These findings suggest that 4-DAMP-sensitive M3 receptor may play an important role in the pancreatic exocrine functions.
Amylases↗
Influence of morphologic factors on calcium-containing stone formation.
Pathogenesis of urolithiasis cannot be explained only by metabolic disorder. In the present study, morphologic differences of the renal pelvic-caliceal system (PCS) were examined on both the stone and normal sides in calcium-containing stone formers. The results indicated that as compared to the normal side, the urine flow in the PCS was stagnant or not straight on the stone side even in the same individual, showing unfavorable conditions for stone formation. It is therefore considered that morphologic disorders of the urinary tract may be one of the causes for stone formation.
Adult↗
Adhesion and proliferation of bovine aortic endothelial cells on monoamine- and diamine-containing polystyrene derivatives.
Adhesion and proliferation of bovine aortic endothelial cells on polystyrene derivatives having monoamine or diamine side chain was investigated focusing on the chemical structure of amino groups. Copolymers, SE8.5, is composed of polystyrene with 8.5 mol% of monoamine side chains, and SED8, which is with 8 mol% of diamine side chains, were estimated to contain almost the same amount of protonated amino groups in bulk composition at physiological pH (pH 7.4). There observed significant difference in cellular spreading of attached endothelial cells between these two types of copolymer surfaces. Spreading-% of attached cells on SED8 surfaces was approximately 1.6 times greater than that on SE8.5 6 h after seeding. This difference in cellular spreading influenced to subsequent cell growth. Cellular growth on each polymer surface was featured by parameter k, which corresponds to the 'rate constant' of cellular proliferation. While the k-value for SE8.5 decreased with decreasing seeding density as well as the case for polystyrene, SED8 maintained a high k-value even at low seeding density as 2 x 10(3) cells/cm2. These results suggest that cells may recognize the difference in the chemical structure of amine side chains of SE and SED copolymers.
Amines↗
The role of protonation and conformational transition of polyamine grafts in platelet retention to polyamine-graft-PHEMA copolymer surfaces.
Blood platelet retention on polyamine-graft-poly(2-hydroxyethyl methacrylate) (PHEMA) copolymer (HA) surface was investigated, focusing on pH and ionic strength of the surrounding medium to elucidate the nature of ionic interaction between platelets and HA copolymer surfaces. The conformational transition of polyamine graft chain in response to the protonation degree of amino groups was demonstrated to be an important factor influencing platelet retention on HA surfaces. When the polyamine graft chain exists in an extended conformation, protonated amino groups distribute from the matrix interface into the aqueous interior, resulting in the effective ionic interaction with platelets to increase their retention on HA copolymer surfaces. The number of protonated amino groups in polyamine portions crucially affected platelet retention. Worth noticing is that an introduction of a small but definite amount of cationic sites on the polymer surface led to significantly minimized platelet retention. It is considered that the surface property of PHEMA was drastically changed to a non-adhesive surface by introducing a small amount of protonated amino groups.
Animals↗
An interpretation of cell separation mechanism on polyamine graft copolymers.
Interaction between polyamide microcapsules having different balances of negative and positive charges on their surface, that is, different isoelectric points and copolymers with different numbers of polyamine macromer of a definite chain length grafted on poly(2-hydroxyethyl methacrylate) backbone was studied by measuring the amount adhered of the microcapsules onto the surface of copolymer-coated glass beads at different pH values. Maximum microcapsule adhesion was observed for a proper combination of microcapsule and copolymer to suggest that separation of a specified cell population from others on the surface of copolymer-coated glass beads can be explained in terms of preferential adhesion through electrostatic interaction of the specified cells with the copolymer.
Cell Separation↗
Lectin cytochemistry in the gastrointestinal tract with special reference to glycosylation in the Golgi apparatus of Brunner's gland cells.
Two hydrophilic, low temperature-embedding resins, Lowicryl K4M and LR White, were compared in lectin cytochemistry. Post-embedding staining of colloidal gold-labeled Griffonia symplicifolia agglutinin II (GSA-II) resulted in staining of the Golgi apparatus and mucous granules of mucous neck cells in the gastric fundic gland, pylorocytes, and Brunner's gland cells embedded in either resin, although it was much easier to make ultra-thin sections with LR White-embedded material than with the other. Post-fixation with uranyl acetate followed by LR White embedding improved general ultrastructure so that lectin binding sites were identified precisely. All examined lectins, soybean agglutinin (SBA), Maclura pomifera agglutinin (MPA), GSA-II, and Ulex europaeus agglutinin I (UEA-I), stained mucous granules and the Golgi apparatus, in which the staining pattern was characteristic of each lectin: cis cisternae were labeled with SBA and MPA, intermediate cisternae with GSA-II, and trans cisternae and mucous granules with SBA, GSA-II, UEA-I, and lightly with MPA. No labeling was observed in the rough endoplasmic reticulum with any lectin. These findings suggest that the Golgi apparatus is the site of O-linked glycosylation and can be divided into at least three distinct compartments with regard to the glycosylation.
Animals↗