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Biomedical subjects

T Sakata

Publications and source records attributed to T Sakata.

At least 397 records · Page 22Linked to original sources
PubMed1989

Effect of sodium saccharin and calcium saccharin on urinary parameters in rats fed Prolab 3200 or AIN-76 diet.

The effects of the salt form of saccharin and of diet on urinary ion levels have been studied in rats. Sodium saccharin (NaS) or calcium saccharin (CaS) was fed at a level of 5% in either Agway Prolab 3200 diet or AIN-76 diet to male, 5-wk-old F344 rats for 10 wk. The AIN-76 diet contained considerably less calcium, sodium and potassium than the Prolab 3200 diet, and smaller amounts of these ions were eliminated over 24 hr in the urine of rats fed the AIN-76 diet. Although food consumption was less in the groups fed AIN-76, total urinary saccharinate ion excretion with either saccharin salt was comparable with, or even higher than, that excreted by rats fed either salt in the Prolab 3200 diet. Rats fed Prolab 3200 eliminated approximately equal amounts of saccharinate ion in the faeces and urine. Rats fed AIN-76 eliminated about 10-20 times as much saccharin in the urine as in the faeces. Total saccharin excretion (faecal and urinary) was not influenced by the salt form. Water intake and urine volume were lower in rats fed control AIN-76 diet in comparison with those fed Prolab 3200, and were increased above the control level in groups fed saccharin in the AIN-76 diet. Urine electrolyte levels and osmolality were lower in the groups fed AIN-76. In general, NaS administration in either diet resulted in increased urinary sodium compared with controls, and the pH was at, or above, the level of control rats. CaS resulted in increased urinary calcium and decreased pH. There were marked diurnal variations in the urinary excretion of the various electrolytes, pH, and urine volume over a 24-hr period in all rats. This diurnal variation was more pronounced in the rats fed the Prolab 3200 diet. These results indicate that NaS and CaS have marked effects on the excretion of urinary electrolytes, and that these effects are influenced by diet.

Animal Feed↗
PubMed1989

Exogenous expression of mouse interferon gamma cDNA in mouse neuroblastoma C1300 cells results in reduced tumorigenicity by augmented anti-tumor immunity.

To examine the influence of interferon gamma (IFN-gamma) on tumorigenicity, we established constitutively IFN-gamma-producing cell lines from a malignant mouse neuroblastoma, C1300, by retroviral transfer of a mouse IFN-gamma cDNA. The gene-transferred cells generally showed an enhanced high-level expression of the major histocompatibility complex class I antigens at the cell surface and the transcription levels, irrespective of their IFN-gamma-producing potential. Although in vitro cell growth of these cells was unaffected by the IFN-gamma production, their s.c. tumor growth in syngeneic A/J mice was dependent upon levels of IFN-gamma production; tumors induced by a low-producer line grew well at a rate similar to those induced by the parental one, but tumor growth of a high-producer line was strongly suppressed. This apparent tumor suppression was abolished by simultaneous i.p. injection of anti-Lyt2.2 and/or anti-IFN-gamma monoclonal antibodies, and subsequently large tumors of the high producer were generated. Anti-asialoganglioside GM1 antibodies allowed the high-producer line to induce a substantial but only transient tumor growth, whereas other antibodies, such as anti-Lyt2.1, anti-IFN-beta, and anti-activated macrophage, had no such effect. The mice immunized with the high-producer line were resistant to tumor growth of the parental cells but permitted another kind of A/J tumor line, Sa-1, to induce remarkable tumors. These results indicate that the reduced tumorigenicity of the IFN-gamma high-producer line was due to the augmented specific anti-tumor immunity, in which cytotoxic T lymphocytes seemed to play a decisive role, probably as a result of the immunomodulatory effects of the IFN-gamma derived from the tumor.

Animals↗
PubMed1989

The effects of acetaminophen, antipyrine and phenacetin on rat urothelial cell proliferation.

Abuse of combination analgesics containing phenacetin, antipyrine (phenazone) and caffeine have been associated with urinary tract tumors. Phenacetin and antipyrine have been shown to be promoters of urinary tract carcinogenesis and antipyrine is also a weak urinary tract carcinogen. Acetaminophen, the main metabolite of phenacetin, is one of the most commonly used analgesics in the USA. In the present study, the dose-related effect on the cell proliferation of the urothelium was evaluated in male Sprague-Dawley rats by autoradiography. Nine groups of twenty, 6-week old rats were treated with 0.5%, 1.0% or 1.5% of acetaminophen, antipyrine or phenacetin in the diet. A tenth group of rats received control diet without added chemicals. Ten rats from each group were killed after each of 6 and 12 weeks of feeding. There was a dose-related increase in the labeling index in the urothelium of the bladder and kidney, particularly after 6 weeks of drug administration. In particular, the 1.0% and 1.5% dose levels of antipyrine and phenacetin showed a marked proliferative effect on the urothelium. In the bladder after 6 weeks, the labeling indices were significantly increased. After 12 weeks, although numerically increased, the indices were not statistically significant. In the renal pelvic urothelium the labeling index was significantly increased in antipyrine and phenacetin treated rats at doses of 1.0% and 1.5%. After 12 weeks the majority of rats treated with 1.5% antipyrine and phenacetin had labeling indices greater than or equal to 2-fold than the control rats both in the kidney and bladder. The increased labeling indices were associated with urothelial hyperplasia, in particular after 6 weeks. In the rats treated with antipyrine there were significant degenerative changes in the urothelial cells expressed as marked vacuolization. The vacuolization is considered to be a toxic effect and the beginning of cell death. Thus cell death with regeneration may be responsible for the increased labeling index in the antipyrine groups. High doses of antipyrine were also associated with renal papillary necrosis in 50% of the rats.

Acetaminophen↗
PubMed1989

Stereospecific feeding modulation by endogenous organic acid gamma-lactone in rats.

Stereospecificity of 3,4-dihydroxybutanoic acid gamma-lactone (3,4-DB) and 2,4,5-trihydroxypentanoic acid gamma-lactone (2,4,5-TP) in their effects on feeding behavior and humoral factors was assessed by infusion into the rat third cerebroventricle. Initial transient food intake was most potently affected by infusion of 2.50 mumol of the 2S,4S-stereoisomer of 2,4,5-TP (80%) at 1100 h. Among the others, 2.50 mumol of the 2R,4S-isomer was somewhat potent in feeding elicitation (20%). Feeding induced by these isomers was not accompanied by periprandial drinking. Ambulation increased with elicitation of feeding. During the first dark period after infusion at 1940 h, 2.50 mumol of the 3S-isomer of 3,4-DB decreased food intake, including reduced meal size, and prolonged postprandial intermeal interval, but the 3R-isomer did not. Potent hypoglycemia with hyperinsulinemia was caused by the 2S,4S-isomer of 2,4,5-TP, and the S-isomer of 3,4-DB caused responses that were reciprocal to those to 2,4,5-TP. The remaining isomers did not affect feeding or humoral factors. The results suggest that the S- or S,S-stereo-isomer of the endogenous organic acid gamma-lactones may be important in modulating food intake through the hypothalamus.

4-Butyrolactone↗
PubMed1989

Neuronal histamine modulates feeding behavior through H1-receptor in rat hypothalamus.

To clarify the physiological role of hypothalamic neuronal histamine in control of food intake, ingestive behavior and neuronal activity were investigated under blockade or diurnal fluctuation of hypothalamic neuronal histamine. Histamine H1- but not H2-receptor antagonist potently induced feeding in a dose-related manner after infusion into rat third cerebroventricle at 1100 h. Elicitation was attenuated after infusion at 1940 h when histamine content in the hypothalamus was low and was abolished after intraperitoneal pretreatment with 0.11 mmol alpha-fluoromethylhistidine (alpha-FMH), a specific suicide inhibitor of histidine decarboxylase. Electrophoretic application of a histamine H1-receptor antagonist to ventromedial hypothalamic neurons specifically suppressed activities of glucose-responding neurons that are related to food intake. The suppressive effect was also attenuated by intraperitoneal pretreatment with alpha-FMH. These results suggest that feeding induced by histamine H1-receptor antagonists is due to blockade of neuronal histamine at the site of histamine H1-receptors, at least in part, in the ventromedial hypothalamus and that diurnal fluctuation of feeding behavior may reflect circadian variation of neuronal histamine level.

Animals↗
PubMed1989

Stimulatory effect of short-chain fatty acids on epithelial cell proliferation of isolated and denervated jejunal segment of the rat.

Involvement of the mesenteric nerve in the efferent transmission of the trophic effect of short-chain fatty acids was tested in rats. A short segment of jejunum was translocated under the skin with or without its mesenteric connection maintained. A mixture of acetic, propionic, and n-butyric acids (100, 20, and 60 mM, respectively) or 0.9% NaCl (control) was injected into the caecum via an ileostomy twice a day for 14 days. Trophic effects of short-chain fatty acids were observed in jejunal and caecal segments and in the translocated jejunal segments both with and without mesenteric connection. The results suggest that short-chain fatty acids given into the hindgut lumen can indirectly stimulate the epithelial cell proliferation of a distant intestinal segment without luminal continuation to the site of administration, and this trophic effect does not require efferent transmission by nerves in the mesentery. Blood-born mediation is likely.

Acetates↗
PubMed1989

Synthesis and properties of RNA with catalytic activity.

Ribooligonucleotides, which form the self-cleavage domain of a satellite RNA of tobacco ringspot virus, were synthesized by the solid-phase phosphoramidite method using o-nitrobenzyl groups for 2'-hydroxyl protection. The oligomers were obtained in quantities sufficient for NMR measurement. Specific cleavage at an expected site was observed when the three RNA fragments were mixed in the presence of magnesium ions.

Base Sequence↗
PubMed1989

[Report of two cases of long ureteral polyps and review of literature].

Two cases of long ureteral polyps are presented. The patients were a 46-and a 40-year-old women, complaining of gross hematuria and miction pain respectively. Excretory urographies showed filling defects of right ureter and lower part of left ureter respectively. Right and left total nephroureterectomy with bladder cuff were respectively performed because of malignant possibility. The tumors removed were benign polyps, measuring 19 and 5 cm in length, respectively. The 19 cm polyp is the longest in Japan. The former case was suspected as hamartoma from müllerian duct and the latter as simple fibro-epithelial polyp.

Adult↗
PubMed1989

[A case of esophageal cancer metastatic to the kidney presenting as renal pelvic cancer].

A 50-year-old man, who had undergone operation of esophageal carcinoma 2 years earlier, was admitted with the complaints of right flank pain and macroscopic hematuria. Intravenous urogram showed right unvisualized kidney. Right retrograde pyelography showed the dilatation of calices and irregularity of middle and lower calices. Computed tomography revealed severe hydronephrosis of the right kidney. Right nephrectomy was performed under the diagnosis of either renal pelvic cancer or esophageal cancer metastatic to the kidney. Pathological examination revealed metastatic squamous cell carcinoma from esophagus. The patient was treated by radiotherapy but died 4 months after the surgical treatment. Literature on eight case of metastatic renal cancer from esophagus is reviewed.

Carcinoma, Squamous Cell↗
PubMed1989

[Usefulness of serum adenosine deaminase activity in the early diagnosis of Mycoplasma pneumonia].

It is sometimes difficult to clinically diagnose mycoplasma pneumonia at an early stage before the rise of titer of antibody to Mycoplasma pneumoniae. Mycoplasma pneumonia may be related with T-lymphocyte activity, and its inflammatory process is different from that of bacterial pneumonia. Adenosine deaminase (ADA) activity is a predominant T-lymphocyte enzyme, and its plasma activity is high in diseases in which cellular immunity is stimulated. In this study, we have investigated 31 cases with pneumonia (11 cases of mycoplasma pneumonia and 20 cases of bacterial pneumonia) within 10 days after onset to evaluate the usefulness of ADA measurement in the diagnosis of mycoplasma pneumonia. Serum ADA activity in the group of mycoplasma pneumonia was 32.1 +/- 12.0 U/l (63.9-18.8 U/l), that of non-mycoplasma pneumonia 12.5 +/- 3.3 (4.6-18.6) U/l, and that of normal control 14.0 +/- 3.4 (6.3-19.3) U/l. ADA activity of the group of mycoplasma pneumonia was significantly higher than those of non-mycoplasma pneumonia and normal control (p less than 0.001). This results suggest that serum ADA activity in patients with acute pneumonia may be useful for the early diagnosis of mycoplasma pneumonia.

Adenosine Deaminase↗
PubMed1988

Structural characteristics of endogenous sugar acids and relations to feeding modulation.

Structural specificity among short-chain organic acids for effects on feeding behavior, blood glucose and insulin was investigated by infusion of 1 exogenous and 6 endogenous derivatives into the rat third cerebral ventricle. Glyceric acid (GEA) (1.0 mumol), 3,4-dihydroxybutanoic acid gamma-lactone (3,4-DB) and 3,4,5-trihydroxypentanoic acid gamma-lactone (3,4,5-TP) (2.50 mumol) decreased food intake for, at most, 24 h. These acids depressed the size of the first meal after infusion, but did not affect latency to the first meal, eating speed, drinking or ambulation. Infusion of 2,4-dihydroxybutanoic acid gamma-lactone (2,4-DB) (1.25 mumol), 2,4,5-trihydroxypentanoic acid gamma-lactone (2,4,5-TP), and an exogenous compound, 2,4,5,6-tetrahydroxyhexanoic acid gamma-lactone (2,4,5,6-TH) (2.50 mumol), induced transient initial feeding which was not necessarily accompanied by periprandial drinking. Ambulation was concomitantly increased. Of these organic acids, 3,4-DB and 2,4,5-TP were most potent in their effects on feeding. Hyperglycemia was induced by 2.50 mumol 3,4-DB leaving insulin unaffected; 2.50 mumol 2,4,5-TP caused hypoglycemia, with a persistent but not significant rise in insulin. The results suggest that slight structural differences of endogenous organic acids, in particular the positions of hydroxyl groups on the lactone ring of 4-butanolide, may be important in feeding modulation by conveying intrinsically reciprocal signals to neurons involved in feeding and satiety.

Animals↗
PubMed1988

Augmentation of tumor targeting in a line of glioma-specific mouse cytotoxic T-lymphocytes by retroviral expression of mouse gamma-interferon complementary DNA.

As an initial approach to experiments directed toward effective adoptive immunotherapy for cancer using lymphokine genes, we transferred retrovirally a complementary DNA encoding mouse gamma-interferon (IFN-gamma) into a specific cytotoxic T-lymphocyte clone, designated E-4, against 203 glioma cells (a 20-methylcholanthrene-induced mouse glioma line) and confirmed the efficacy of IFN-gamma production from the exogenous gene on augmentation of tumor targeting. Of five, two gene-transferred subclones constitutively produced 8 to 10 times the amount of IFN-gamma as compared with the parental E-4. Correspondingly, these two subclones exhibited 2 to 3 times higher killing activity against 203 glioma than the parental cells; the enhancement of the killing activities was abrogated by an adequate addition of anti-IFN-gamma antibody. No alteration was seen after the gene transfer in cell surface phenotypes, Thy-1+, Lyt-1-, Lyt-2+,3+, and asialo-GM1-. The surface expression of a major histocompatibility complex Class I antigen, H-2Kb, was not altered remarkably, but the Class II antigen, I-Ab, was partially and slightly enhanced on the two IFN-gamma-producing sublines mentioned above on fluorescence-activated cell sorter analysis. Since it is considered that in the vicinity of the constitutively IFN-gamma producing cytotoxic T-lymphocyte cells tumor cells are exposed to a high concentration of IFN-gamma, the cells may be stimulated to induce or enhance the expression of surface antigens including major histocompatibility complex antigens as well as tumor-associated antigens relevant to immune recognition. The 203 glioma cells pretreated with IFN-gamma were more efficiently killed by both the parental E-4 and the gene-transferred sublines. Taken together, the results suggested that the augmented specific tumor-killing activity of our gene-transferred cytotoxic T-lymphocytes was ascribed to the constitutive production of IFN-gamma derived from the exogenous gene.

Animals↗
PubMed1988

Feeding induced by blockade of histamine H1-receptor in rat brain.

Histamine antagonists were infused into the third ventricle of the cerebrum in rats. All the H1-, but none of the H2-antagonists tested, induced initial feeding during the early portion of the light phase when histamine level was highest. No periprandial drinking was observed. Ambulation increased during feeding. The effect on feeding was attenuated when brain histamine was normally low during the early portion of the dark phase, or was decreased by alpha-fluoromethylhistidine. Hypothalamic neuronal histamine may suppress food intake through H1-receptors, and diurnal fluctuations of food intake may mirror neuronal histamine levels.

Animals↗
PubMed1988

Effect of an amino group at carbon 2 of 1-deoxyglucose analogues on anorexia in the rat.

A steric hindering group at carbon 2 of 1-deoxyglucose analogues was introduced by epimerization, deoxidation and substitution of a hydroxyl group with either an acetamido or a fluoro group. Injection of this analogue into the rat third cerebroventricle attenuated the feeding suppression produced by 1-deoxyglucose. In contrast, the replacement of a hydroxyl group at carbon 2 with an amino group produced anorexia of the same magnitude as that produced by 1-deoxyglucose. Amination at carbon 2 was more potent than that at carbon 3, 4 or 6. These results indicate that an amino group at carbon 2 of the glucose molecule is important to reinforce the feeding suppression caused by 1-deoxyglucose analogues.

Animals↗
PubMed1988

Blockade of the histamine H1-receptor in the rat ventromedial hypothalamus and feeding elicitation.

All H1-, but no H2-antagonists infused into the rat third cerebroventricle, induced feeding during the early light, but not during the early dark, reflecting a concentration of hypothalamic histamine. Bilateral microinfusion identified the ventromedial hypothalamus (VMH), but not the lateral hypothalamus or the paraventricular nucleus, as a main locus for the induction of feeding by an H1-antagonist. The effect was completely abolished when brain histamine was decreased by pretreatment with alpha-fluoromethylhistidine. Hypothalamic neuronal histamine suppresses food intake, at least in part, through H1-receptors in the VMH.

Animals↗
PubMed1988

Highly efficient action of autocrine mouse interferon-gamma expressed via a retroviral vector.

Following infection with a mouse interferon-gamma (IFN-gamma)-producing retrovirus, various types of mouse cell lines began to constitutively secrete IFN-gamma in the culture medium, but the IFN-gamma production level varied according to cell type. Effects of the IFN-gamma on the IFN-gamma-producing cell itself (autocrine effects) were examined. In the IFN-gamma-producing cells, the expression of the major histocompatibility complex class I genes was augmented; this augmentation was remarkable in T cell lines tested in this work, regardless of their poor IFN-gamma production. This autocrine effect was highly efficient and could not easily be abrogated by the exogenous addition of anti-IFN-gamma antibodies. Such antibody resistance was also observed for the antiviral effect of the autocrine IFN-gamma on an IFN-gamma gene-transferred fibroblast line. These results suggest that apparently low titers of physiological IFN-gamma might exert strong in vivo autocrine and possibly paracrine effects.

Animals↗