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Biomedical subjects

H Ishida

Publications and source records attributed to H Ishida.

At least 793 records · Page 44Linked to original sources
PubMed1988

Functional expression of cloned cDNA encoding sodium channel III.

mRNA synthesized by transcription in vitro of the cloned cDNA encoding rat brain sodium channel III directs the formation of a functional sodium channel in Xenopus oocytes. The tissue distribution of the mRNAs encoding sodium channels I, II and III has been studied by blot hybridization analysis with specific probes.

Animals↗
PubMed1988

Enhanced production of interleukin-2 in patients with progressive systemic sclerosis. Hyperactivity of CD4-positive T cells?

A significant enhancement of interleukin-2 production was observed in phytohemagglutinin-stimulated peripheral lymphocytes from patients with progressive systemic sclerosis (PSS). Their Leu-3a:Leu-2a ratio was also significantly higher than normal. Moreover, Leu-3a+ cells freshly purified from PSS patients' blood produced much more interleukin-2 than did cells from normal subjects. These results suggest that T cell hyperactivity, especially among Leu-3a+ T cells, occurs in patients with PSS.

Adult↗
PubMed1988

Changes in plasma levels of prolactin and estradiol, nutrient intake, and time spent nesting during the incubation phase of broodiness in the Chabo hen (Japanese bantam).

The plasma concentrations of prolactin (PRL) and estradiol, time spent nesting, consumption of feed and water, body weight, and hematocrit were measured during egg laying, incubating, and brooding of the chicks in a Japanese strain of dwarf bantam hen, Chabo. Plasma levels of PRL increased before incubation, were maintained at high levels during incubation, and decreased rapidly at the onset of hatching the young. The concentration of estradiol decreased before incubation and was maintained at low levels when circulating levels of PRL were high. During incubation, hens spent greater than 95% of the day on the nest, reduced their daily intake of feed and water by 63 and 78%, respectively, and decreased their body weight by 19% by the end of incubation. Thus, Chabo hens show a mode of incubation behavior similar to that reported in larger chickens. The temporal changes between nutrient intake and plasma levels of PRL at the start and end of incubation behavior suggested that changes in nutrient intake may not cause changes in the concentration of PRL, whereas the association between increased levels of PRL and decreased levels of estradiol suggested that they may be causally associated. Plasma levels of PRL also appeared to be associated with time spent on the nest.

Animals↗
PubMed1988

Effect of vitamin D on gastrin and gastric somatostatin secretion from the isolated perfused rat stomach.

We have studied the role of vitamin D in the regulation of gastrin and gastric somatostatin secretion from the isolated perfused rat stomach. In Ca-deficient vitamin D-deficient rats (Ca(-)D(-) group), the basal and bombesin-stimulated gastrin and gastric somatostatin release (basal IRGa, basal IRS, sigma delta IRGa, and sigma delta IRS) all were significantly lower than in Ca-replete vitamin D-replete rats (Ca(+)D(+) group), and also lower than in Ca-replete vitamin D-deficient rats (Ca(+)D(-) group) except for the basal IRGa. In the Ca(+)D(-) group, the basal IRGa and IRS, and sigma delta IRS were not significantly lower than in the Ca(+)D(+) group. Although there was no significant impairment in basal IRGa, sigma delta IRGa in the Ca(+)D(-) group was significantly lower than in the Ca(+)D(+) control group. Thus, the gastrin and gastric somatostatin secretion from the Ca-deficient vitamin D-deficient rats were impaired. In addition, the impaired gastrin and gastric somatostatin secretions seem to be caused not only by a decrease in serum Ca but also by the reduced effect of the vitamin D on the G and gastric D cells.

Animals↗
PubMed1988

Characteristic features of insulin secretion in the streptozotocin-induced NIDDM rat model.

Male Wistar neonatal rats at age 1.5 days (Streptozotocin [STZ] group 1) and 5 days (STZ group 2) received a subcutaneous injection of 90 mg/kg STZ. After 10 weeks, the rats were subjected to an oral glucose tolerance test (OGTT) (2 g/kg) in a conscious state. The pancreas perfusion experiments were conducted 2 weeks after the OGTT. There was no statistical difference in insulin response between the STZ group 1 and the control group. On the contrary, in the STZ group 2, the plasma glucose response to OGTT showed a typical diabetic pattern, and the plasma insulin response was markedly blunted. In the isolated perfused rat pancreas, the infusion of glucose evoked a biphasic insulin secretion, but the peak insulin levels induced by 16.7 mmol/L glucose in the STZ group 1 were significantly lower than in the controls. We further investigated characteristics of insulin secretion in response to different secretagogues in these animal models using isolated islets. The insulin content of the islets of the STZ group 1 were about one half that of the control group. Insulin secretion in the STZ group 1 was impaired in response to glucose stimulation, but remained normal in response to arginine and forskolin. These results suggest that insulin secretion of non-insulin-dependent diabetes mellitus (NIDDM) rat model is selectively impaired in response to glucose stimulation, possibly due to a disorder of signaling mechanism other than adenylate cyclase.

Animals↗
PubMed1988

Regression of line-10 hepatocellular carcinoma by a less toxic cord factor analogue combined with L18-MDP or synthetic lipid A analogues.

A transplantable hepatocarcinoma of strain 2 guinea pigs was used as an experimental model for immunotherapy of cancer. 6,6'-Dideoxy-6,6'-bis-mycoloylamino-alpha,alpha- trehalose (TDNM) was found to be more effective in producing regression of transplantable line-10 tumours than 6,6'-di-O-mycoloyl-alpha,alpha-trehalose (TDM) when combined with 6-O-stearoyl muramyldipeptide (L18-MDP). TDNM showed potent antitumour activity in combination with synthetic lipid A of Escherichia coli (compound 506), but not with the lipid A analogues (GLA-59 and 60). As with the combination of MDP derivative and lipid A analogue, MDP derivatives conjugated with GLA-60 (GMD compounds) showed no tumour regression activity of line-10 cells in guinea-pigs.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1988

Induction of tumoricidal macrophages and production of cytokines by synthetic muramyl dipeptide analogues.

The ability of various synthetic muramyl dipeptide (MDP) derivatives to induce the production of interleukin-1 (IL-1) and colony stimulating factor (CSF) in vitro and in vivo and to induce cytotoxic macrophages was studied. 6-O-L18-MDP(Me) and MDP-Lys(L18), which were potent inducers of IL-1 and CSF production and of cytotoxic macrophages, had protective activity against Sendai virus infection in mice. In contrast, 1-O-L18-(6-O-P)-MDP(Me) and 2-N-L18-MDP exhibited weak or no ability to induce IL-1 and CSF production and no induction of tumoricidal macrophages, and did not protect against infection of Sendai virus. MDP derivatives, except 2-N-L18-MDP, efficiently rendered macrophages cytotoxic against target cells in the presence of murine recombinant interferon-gamma in vitro. The derivatives that induced cytokines and cytotoxic macrophages appeared to produce anti-viral activity.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1988

Demonstration of a high affinity receptor for 1,25-dihydroxyvitamin D3 in rat pancreas.

The existence of a high affinity receptor for 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) in rat pancreas was biochemically demonstrated in this study. In order to study the properties of this putative receptor, we took advantage of the analysis of low ionic strength chromatin-localized 1,25(OH)2D3 receptor. Using this method, the susceptibility of receptor protein to enzymatic degradation was so decreased, and the contamination by plasma vitamin D binding protein (DBP) component was so efficiently eliminated that a specific, saturable binding for 1,25(OH)2D3 could be demonstrated in the saturation analysis and the peak for the receptor was consistently apparent in the sucrose density gradient analysis. The equilibrium dissociation constant (Scatchard Kd) was found to be 3.7 +/- 1.5 x 10(-10) (M), and the concentration of specific binding sites was calculated to be 1.22 +/- 0.40 (fmol/mg protein). The number of specific binding sites in the rat pancreas was only 0.44% of that present in rat intestine (277 +/- 19 (fmol/mg protein] and 6.7% of that in rat kidney (18.1 +/- 1.0 (fmol/mg]. However, when a correction is made for the 1,25(OH)2D3 receptor distribution in the tissues and expressed as the receptor concentration per receptor-containing cells, the rat pancreatic receptor level was calculated to be about 30% of the rat intestine. Sucrose density gradient sedimentation of this receptor yielded a value of 3.2 +/- 0.1 (S) for the sedimentation coefficient and this peak was displaceable by a 100-fold excess of nonradioactive 1,25(OH)2D3.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

A monoclonal antibody, KM10 reactive with human gastrointestinal cancer and its application for immunotherapy.

A monoclonal antibody, KM10 (IgG1) was produced by fusing spleen cells from a human gastric cancer cell (MKN45)-primed BALB/c mouse with the murine myeloma cell line X63-Ag8-653. The antibody reacted strongly with the plasma membrane of human gastrointestinal carcinoma. Sections of the malignant and benign tissues were tested with immunoperoxidase. All of 10 (100%) large intestinal cancers, 26 of 31 (84%) gastric cancers, 5 of 7 (71%) pancreatic cancers and all of 3 (100%) ampullary cancers reacted positively. Moderate or weak reactivity was observed with normal human tissues, hepatoma and carcinomas of mammary, thyroid and adrenal glands. According to a study of the distribution of 125I-labeled KM10 in nude mice bearing human gastric cancer, KM10 selectively localized in tumor tissue rather than normal tissue. Whole body autoradiography also supported such a selective distribution. Destruction of antigenic properties by pronase digestion demonstrated its protein nature and by Western blot analysis, it was identified as a protein with an Mr of 180-200 kd. KM10-adriamycin (ADM) conjugate was prepared via an oxidized dextran bridge and this immunoconjugate retained the binding activity against human gastric cancer. MKN45 cells were inoculated subcutaneously into athymic mice and intravenous treatment was begun when the tumor became measurable. A dose-dependent antitumor activity was observed in vivo with KM10-ADM conjugate, while this conjugate was less toxic than free ADM.

Animals↗
PubMed1988

Alterations in cation homeostasis in cultured chick ventricular cells during and after recovery from adenosine triphosphate depletion.

Alterations in cation homeostasis during and after recovery from myocardial ischemia may account for some of the reversible and irreversible components of myocardial cell injury. To investigate possible mechanisms involved, we exposed cultured layers of spontaneously contracting chick embryo ventricular cells to media containing 1 mM cyanide (CN) and 20 mM 2-deoxyglucose (2-DG), and zero glucose for up to 6 h, and then allowed cultured cells to recover in serum-free culture medium for 24 h. Changes in Na, K, and Ca contents, 42K uptake and efflux, ATP content, cell water content, and lactate dehydrogenase (LDH) release were measured, and compared with changes produced by exposure to 10(-3) M ouabain and severe hypoxia. Exposure to CN and 2-DG caused marked increase in cell Na (sevenfold) and Ca (fivefold) contents, and a decrease in K content (one-fifth normal), coincident with ATP depletion to one-tenth normal levels. This produced only slight cell injury, evidenced by increased LDH release. Recovery for 24 h resulted in return to near normal values (expressed in nanomoles per milligram of protein) of Na, Ca, and ATP contents. However, there was failure of cell K content to return to normal, associated with a persistent reduced net uptake of 42K, and an increase in the rate of 42K efflux. These abnormalities in K homeostasis were associated with a decrease in cell volume and water content per milligram of protein. More marked ATP depletion (to 1/100 normal values) was produced by hypoxia plus 2-DG and zero glucose, and was associated with much more severe cell injury manifested by LDH loss. Ouabain exposure resulted in a much greater Ca gain (20-30-fold), relative to increase in Na content, than did either CN and 2-DG or hypoxia; and ouabain effects were not reversible (after a 15-fold or greater increase in Ca content was produced) and were associated with significant LDH release. We conclude that these cells are resistant to cell injury caused by moderately severe Ca overload and ATP depletion produced by exposure to CN and 2-DG. However, metabolic inhibition of ATP production produces persistent abnormalities in K homeostasis, associated with functional abnormalities.

Adenosine Triphosphate↗
PubMed1988

The number of 1,25-dihydroxyvitamin D3 receptors is decreased in both intestine and kidney of genetically diabetic db/db mice.

In previous studies on calcium homeostasis in diabetes, drug-induced diabetic rats have generally been used, and various alterations have been demonstrated in several parameters of the vitamin D-endocrine system. It is, however, still questionable whether the drug-induced diabetic rat is the most appropriate animal model for the investigation of calcium and vitamin D metabolism because of the toxicity of diabetogenic agents toward the principle organs of vitamin D metabolism, such as liver and kidney. Therefore, in the present study, we examined the strain of genetically diabetic mice, C57BL/KsJ db/db, to evaluate 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] receptors in intestine and kidney and to investigate the alterations of calcium and vitamin D metabolism. In both control and diabetic mice, intestinal and renal 1,25-(OH)2D3 receptors were demonstrated; they had a sedimentation coefficient of 3.4S. The number of specific 1,25-(OH)2D3-binding sites in intestine was 118 +/- 11 fmol/mg protein in diabetic mice, significantly lower than the value of 199 +/- 11 fmol/mg protein in controls (P less than 0.01). Moreover, the renal concentration of specific 1,25-(OH)2D3-binding sites of 34.6 +/- 7.1 fmol/mg protein in diabetic mice was also significantly reduced compared to the value of 63.3 +/- 5.7 fmol/mg protein in controls (P less than 0.01). There were no significant differences in the equilibrium dissociation constants (Kd) of intestinal and renal receptors between control and diabetic mice. Significant hypocalcemia was demonstrated in the diabetic mice (P less than 0.01), suggesting the development of a negative calcium balance. Diabetic mice showed a significant decrease in renal 24,25-(OH)2D3 production (P less than 0.02), whereas renal 1,25-(OH)2D3 production was significantly increased in the diabetic group (P less than 0.05) compared to the control value. It is probable from these results that the genetic/endogenous diabetes may be directly associated with the alterations of mineral homeostasis. The altered calcium and vitamin D metabolism in diabetic mice is suggested to be derived, at least in part, from the decreased number of the 1,25-(OH)2D3 receptors in both intestine and kidney in the diabetic state.

24,25-Dihydroxyvitamin D 3↗