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Biomedical subjects

S Baba

Publications and source records attributed to S Baba.

At least 739 records · Page 41Linked to original sources
PubMed1988

[Combined immuno-radio-chemotherapy of head and neck non-Hodgkin's lymphoma].

Twenty-one previously untreated cases, who underwent the same protocol at our department from January 1984 until December 1986, were investigated. The following results were obtained. Non-Hodgkin's lymphoma accounted for 10.5% of all the head and neck malignant tumors at our department. The age range was from 23 to 76 years of age and had a peak in the forties. Fourteen were male and seven were female. According to the stage distribution, six cases were stage I (28.6%), nine were stage II (42.9%), four were stage III (19.0%) and two were stage IV (9.5%). Stage I and II accounted for 71.4%. By site grouping, palatine tonsil and nasal cavity accounted for 38.1%, respectively. Surgical therapy was presumably useful for a solitary lesion which resisted all conservative therapies. By combined therapy with radiotherapy, VAPE-Chemotherapy and OK-432-immunotherapy, the survival rates were 100% (stage I), 77.8% (Stage II), 50% (stage III) and 50% (stage IV). The mean survival rate was 76.2%.

Adult↗
PubMed1987

Acute suppression of endogenous testosterone levels by exogenous testosterone in normal men.

The effect of exogenous testosterone on endogenous plasma testosterone was studied in normal men. Intramuscularly administered testosterone-19,19,19-d3 rapidly appeared in the systemic circulation in large amounts. Endogenous plasma testosterone was suppressed to near-castrate levels. The suppressed level began to rise between 6 and 10 h, and reached a preinjection level at 24 h after the injection. Plasma LH decreased with a concomitant decrease in endogenous testosterone and began to rise as soon as plasma total testosterone returned to physiological levels.

Adult↗
PubMed1987

[Coupling of guanine nucleotide inhibitory protein to somatostatin receptors on rat pancreatic acinar membranes].

To investigate whether somatostatin receptors couple to guanine nucleotide inhibitory protein, Ni, on rat pancreatic acinar membranes, the effects of guanine nucleotide analogs or pretreatment of acini with islet activating protein (IAP), pertussis toxin on labeled somatostatin binding were examined. Guanine nucleotides reduced labeled somatostatin binding to acinar membranes up to 80%, with rank order of potency being guanyl-5'-yl imidodiphosphate (Gpp(NH)p) greater than GTP greater than GDP greater than GMP. Scatchard analysis of the labeled somatostatin binding revealed that the decrease in somatostatin binding caused by Gpp(NH)p was due to the decrease in the maximum binding capacity without a significant change in the binding affinity. The inhibitory effect of Gpp(NH)p was partially abolished in the absence of Mg2+ and Na+ also reduced labeled somatostatin binding. Furthermore, inhibitory effects of 100mM Na+ and Gpp(NH)p were additive in reducing labeled somatostatin binding. A half maximal inhibitory concentration of Gpp(NH)p was decreased to 10(-7)M in the presence of 100mM Na+ and 5mM Mg2+ as compared to 10(-6)M in the presence of 5mM Mg2+ alone. Results therefore suggest that Gpp(NH)p requires Mg2+ for Ni activation and Na+ increases sensitivity of Ni to guanine nucleotide analogs. When pancreatic acini were treated for 4 hours with varying concentrations of IAP, which has been shown to uncouple Ni-mediated communication between inhibitory receptors and adenylate cyclase catalytic unit, subsequent labeled somatostatin binding to the acinar membranes was decreased in a dose dependent manner. These results indicate that somatostatin receptors on pancreatic acinar membranes couple to guanine nucleotide inhibitory protein, Ni and thus somatostatin probably functions in the pancreas to regulate intracellular signal transduction via Ni.

Adenylate Cyclase Toxin↗
PubMed1987

Proglumide has access to brain and antagonizes the central satiety effect of cholecystokinin octapeptide in the dog.

Intra-third cerebroventricularly administered cholecystokinin octapeptide (CCK-8) decreased food intake through central mechanisms in the dog. Proglumide, administered intravenously, did enter into cerebrospinal (ventricular) fluid, and partially, but significantly, reversed this effect. CR1409, one of the newly synthesized glutaramic derivatives, blocked CCK-8-induced satiety more strongly than proglumide. These results indicate that systemic proglumide and CR1409 result in antagonism of the central CCK receptor for satiety in the dog.

Animals↗
PubMed1987

Disulfide bonds within the alpha-subunit of insulin receptors in rat liver and brain membranes.

We have characterized inter- and intrasubunit disulfide bonds of insulin receptors using reductant-treated rat liver and brain membranes. In autoradiograms of 125I-insulin cross-linked to both membranes pretreated with dithiothreitol, the intensity of affinity-labeled bands of the alpha beta-heterodimer and alpha-subunit was increased. Interestingly, labeled 120 and 110 kDa bands considered to be the alpha-subunit in partially reduced liver and brain membranes moved to 130 and 120 kDa bands under further reduced conditions, respectively. Double electrophoresis of each partially reduced band in the presence of reductants clearly demonstrates that the alpha-subunit of insulin receptors contains intrasubunit disulfide bonds.

Animals↗
PubMed1987

[The effects of carbamylation of hormones on their biological activities--with reference to 3,5,3'-L-triiodothyronine and insulin].

It has been demonstrated that the binding of cyanic acid, formed from urea which is increased in renal failure, to hemoglobin (Hb) results in the formation of HbA1. The combination of Hb and cyanic acid is called carbamylation, a nonspecific reaction between protein and cyanic acid. It is theoretically considered that like glycation, carbamylation may occur between cyanic acid and not only Hb but also various peptides and proteins. In the present study, hormones were subjected to carbamylation, and the effects of carbamylation on the biological activity of the hormones, i.e. 3,5,3'-L-triiodothyronine (T3) and insulin, were investigated. Carbamylated T3 and carbamylated insulin were synthesized in vitro, using KCNO. The carbamylated hormones were isolated by high-performance liquid chromatography (HPLC). The biological activities of carbamylated T3 and carbamylated insulin were assayed by employing the metamorphosis of tadpoles (Rana nigromaculata) and the glucose oxidation of fat cells or the receptor binding capacity of rat hepatocytes, respectively. The biological activity of carbamylated T3 was less than about 1/13 of that of T3, and the binding activity of carbamylated insulin was 1/5 of that of insulin. Therefore, carbamylation of hormones may be an important factor in the analysis of clinical conditions, especially the endocrine condition in renal failure.

Animals↗
PubMed1987

Regulation of free cytosolic Ca2+ in the isolated guinea pig gastric chief cells.

Stimulation with COOH-terminal octapeptide of cholecystokinin (CCK8) or carbachol resulted in a rapid increase in Quin-2 fluorescence of isolated guinea pig gastric chief cells, whereas histamine, vasoactive intestinal peptide, secretin or forskolin had no effect. The minimum effective dose of CCK8 or carbachol to elicit the rise in Quin-2 fluorescence was almost similar to that for pepsinogen secretion. Removal of Ca2+ from extracellular medium or Ca2+ channel blockers did not affect CCK8- or carbachol-induced increase in Quin-2 fluorescence. Moreover, following addition of CCK8, carbachol was unable to stimulate a second increase in Quin-2 fluorescence. These results suggest that CCK8 and carbachol share common Ca2+ pools and an increase in free cytosolic Ca2+ concentration may mediate CCK8- or carbachol-induced pepsinogen secretion from gastric chief cells.

Aminoquinolines↗
PubMed1987

Determination of stable isotopically substituted histidine in human plasma by gas chromatography-mass spectrometry.

A gas chromatographic-electron-impact mass spectrometric method for the determination of stable isotopically substituted histidine in human plasma has been developed. Histidine was derivatized to alpha N-trifluoroacetyl-imN-carbethoxyhistidine n-butyl ester (TCB derivative) by a three-step reaction: an initial esterification by 3 M n-butanolic hydrochloric acid, followed by trifluoroacetylation with trifluoroacetic anhydride and then ethoxycarbonylation with diethyl pyrocarbonate. Quantitation was carried out by selected-ion monitoring on the molecular ions (m/z 379, 383 and 385) of the respective TCB derivatives of histidine, [1-15N,5,beta,beta-2H3]histidine (histidine-[M + 4]) and [1,3-15N2,5,alpha,beta,beta-2H4]histidine (histidine-[M + 6]). The sensitivity, specificity, precision and accuracy of the method were demonstrated to be satisfactory for application to a pharmacokinetic study of histidine after administration of a trace amount of stable isotopically substituted histidine (histidine-[M + 4]) in humans.

Chemical Phenomena↗