Search PubMed⌕ Search

Biomedical subjects

A Yoshida

Publications and source records attributed to A Yoshida.

At least 559 records · Page 31Linked to original sources
PubMed1993

Effect of vasoactive intestinal peptide, somatostatin, and substance P on spontaneous IgE and IgG4 production in atopic patients.

The effect of vasoactive intestinal peptide (VIP), somatostatin (SOM), and substance P (SP) on spontaneous human IgE and IgG4 production in atopic patients was studied. In cultures of mononuclear cells (MNC), VIP inhibited both IgE and IgG4 production without affecting IgM, IgA, IgG1, IgG2, or IgG3 production. In contrast, SOM inhibited only IgE production whereas SP inhibited only IgG4 production without affecting production of other isotypes or other IgG subclasses. The effect of neuropeptides was specific because each was specifically blocked by a corresponding neuropeptide antagonist. To achieve the effect noted above, neuropeptides must be added at the start of the culture. IFN-alpha and IFN-gamma were found to inhibit both IgE and IgG4 production whereas prostaglandin E2 (PGE2) inhibited only IgE production. However, the inhibition of IgE and IgG4 production by neuropeptides could not have been mediated by IFN-alpha, IFN-gamma, or PGE2 because the addition of anti-IFN-alpha, anti-IFN-gamma, and indomethacin, respectively, did not reverse the inhibition. In contrast to their effects on MNC, neuropeptides did not affect production of either IgE or IgG4 by purified B cells; the addition of either T cells or monocytes to B cells had no effect on this. However, neuropeptides were effective in inhibiting IgE and IgG4 production by B cells cultured together with both T cells and monocytes. Depletion of sIgE+ and sIgG4+ B cells resulted in abrogation of IgE and IgG4 production, respectively. However, stimulation of sIgE- B cells with IL-4 plus anti-CD 40 mAb induced IgE production, which was inhibited by VIP and SOM, but not SP, in the presence of both T cells and monocytes. These results suggest that neuropeptides inhibited spontaneous IgE and IgG4 production by interaction with sIgE+ and sIgG4+ B cells in a T cell- and monocyte-dependent fashion. In addition, VIP and SOM also inhibited IgE production by modulating switching induced by IL-4 plus anti-CD 40 mAb in a T cell- and monocyte-dependent fashion.

Humans↗
PubMed1993

Synaptic connections of a periodontal primary afferent neuron within the subnucleus oralis of the cat.

The central axon of a primary afferent neuron that responded to light mechanical stimulation of the lower premolar teeth in a fast adapting fashion was intra-axonally injected with horseradish peroxidase in the cat. The labeled terminals within the rostrodorsomedial (Vo.r) and dorsomedial (Vo.dm) parts of subnucleus oralis were examined electron microscopically. The labeled ending had pale axoplasm, contained clear spherical synaptic vesicles, and formed multiple synapses with dendrites and/or unlabeled axonal endings with pleomorphic vesicles (P-endings). In these synaptic contacts, the labeled primary ending was presynaptic to dendrites and postsynaptic to P-endings. Labeled endings simultaneously synapsing with both dendrites and P-endings were more frequent in Vo.dm (28%) than in Vo.r (8.3%).

Animals↗
PubMed1993

The TSH-dependent potassium channel in a cloned rat thyroid cell line.

We found a TSH-dependent K+ channel in the membrane of a rat thyroid cell line (FRTL-5 cell). This K+ channel is activated by extracellular application of the thyroid stimulating hormone (TSH). Treatment of dibutyryladenosine cyclic monophosphate (Bt2 cAMP) also activated the TSH-dependent K+ channel. Intracellular application of protein kinase A activates this K+ channel without the presence of free Ca2+. These findings indicate that the thyroid K+ channel is activated through the TSH-cAMP-protein kinase A system. This is the first report of a polypeptide hormone activated K+ channel and it should be useful for examining the effects of this K+ channel on thyroid cell functions.

Amino Acid Sequence↗
PubMed1993

Comparison of pig cornea preservation solutions using quantitative 31P NMR spectroscopy.

We compared the abilities of three solutions (bicarbonate-free glucose-phosphate Ringer's solution (EP II), lactated Ringer's solution and physiologic saline solution) to preserve pig cornea by measuring phosphate metabolites with 31P NMR spectroscopy. EP II preserves corneal viability better than others, and preserving extracted cornea also is better than preserving the whole eye.

Animals↗
PubMed1993

Diverse polymorphism within a short coding region of the human aldehyde dehydrogenase-5 (ALDH5) gene.

Human aldehyde dehydrogenase-5 gene (originally named as ALDHX) is expressed in liver and testis. The ALDH5 does not contain introns in the coding sequence for 517 amino acid residues. Within a short nucleotide region of the gene, the following three nucleotide changes were found in high frequencies, i.e., a silent C<-->T at nucleotide (nt) 183, C<-->T at nt 257 associated with a Val<-->Ala substitution, and T<-->G at nt 320 associated with a Arg<-->Leu substitution. The frequency of C at nt 183 is 81% in Caucasians and 65% in Japanese, and the difference is statistically not significant. The frequency of C at nt 257 is 76% in Caucasians and 55% in Japanese, and the difference is statistically significant (P = 0.02). The frequency of T at nt 320 is 71% in Caucasians, while it is only 27% in Japanese. The racial difference at nt 320 is highly significant (P < 0.001). No significant difference was found in the genotypes of the three nucleotide positions between alcoholic and nonalcoholic Caucasians within the limited numbers of subjects examined.

Aldehyde Dehydrogenase↗
PubMed1993

Hepatocellular carcinoma coexistent with adenomatous hyperplasia: report of a case.

We would like to draw attention to hepatic tumor-like lesions which frequently complicate the differential diagnosis of hepatocellular carcinoma (HCC), while considering their pathology and diagnosis by radiographic imaging. In particular, adenomatous hyperplasia is recognized as a precancerous lesion of HCC, and the relationship between adenomatous hyperplasia and the multicentric development of HCC is recognized. We observed a patient who demonstrated hyperplastic changes in both the liver cells and a well-differentiated HCC lesion adjacent to the adenomatous hyperplasia, suggesting a multicentric development of the HCC. The histopathological features of adenomatous hyperplasia are also described.

Carcinoma, Hepatocellular↗
PubMed1993

Proton magnetic resonance spectroscopy of vitreal changes in experimental streptococcal endophthalmitis.

We used magnetic resonance spectroscopy to examine endophthalmitis in rabbits inoculated with a virulent strain of Streptococcus pneumoniae. On different days after infection, the animals were sacrificed and the vitreous isolated and examined with water-suppressed proton magnetic resonance spectroscopy. A broad resonance corresponding to the methyl envelope of lipoprotein lipids appeared 2 days after infection and persisted until the eyes developed phthisis (around 10 days postinfection). This resonance was absent in the control eye and the bacterial culture; it could be used as the marker of breakdown of blood-vitreous barrier and onset of endophthalmitis-induced changes.

Animals↗
PubMed1993

Effect of trapidil on serum lipid and apolipoprotein levels in patients with ischemic heart disease.

1. Serum total cholesterol (TCH), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein (LDL-C), atherosclerotic index (AI) and apolipoprotein (apo A-I, A-II, B, C-II, C-III and E) levels were investigated in patients with ischemic heart disease before and after medication of trapidil. 2. Twenty-one patients were orally given 100 mg of trapidil, three times daily (300 mg/day). After 8 weeks' administration, serum HDL-C level increased (P < 0.01) and AI decreased (P < 0.02) significantly, whereas TCH, TG and LDL-C levels tended to decrease but not significantly. 3. Among the parameters of apolipoproteins, apo A-I, a main protein of HDL-C, was significantly increased (P < 0.05) by trapidil. 4. These results indicate that trapidil has a beneficial effect on the coronary risk profile as reflected by lipid measurements.

Aged↗
PubMed1993

5' structure and expression of human glucose-6-phosphate dehydrogenase mRNA.

The human glucose-6-phosphate (G6PD) cDNAs cloned from normal and carcinoma cells can encode 545-amino-acid residues starting from the first in-frame chain initiation codon. However, it was reported that the G6PD mRNAs of carcinoma cell lines were shorter and could encode only 515-amino-acid residues (Martini et al., 1986). We demonstrated the existence of two major G6PD mRNAs in normal reticulocytes, lymphoblasts, and hepatocytes by the primer extension analysis. The longer mRNA has a cap site at approx. nucleotide -166 and can encode 545-amino-acid residues, whereas the shorter mRNA has a cap site at approx. nucleotide -66, and encodes 515-amino-acid residues. These two naturally existing mRNAs (cDNAs) and an artificially truncated mRNA, which can encode the carboxy-terminal 479-amino-acid residues of the subunit, were expressed in the in vitro reticulocyte and wheat germ systems and in the in vivo E. coli system. All three species of mRNA (cDNA) were efficiently translated and produced proteins with the expected molecular sizes. The peptide with 515 residues formed the catalytically active enzyme, but the 545-residue protein and the 479-residue protein were catalytically inactive. The larger 545-residue protein may correspond to the larger G6PD precursor observed in the rat. The extended amino-terminal region encoded by the larger mRNA contains the -Arg-Gly-Gly-Arg-Arg-Arg-Arg-sequence, which is conserved in the nucleotide-binding protamine family.

Amino Acid Sequence↗
PubMed1993

UDP glucuronosyltransferase gene expression is involved in the stimulation of ascorbic acid biosynthesis by xenobiotics in rats.

Wistar-Shi (genotype +/+), heterozygous Gunn (j/+) and homozygous Gunn (j/j) rats was injected intraperitoneally with 3-methylcholanthrene (3MC) dissolved in corn oil. In rats of all genotypes the hepatic concentration of UDP glucuronosyltransferase (UDPGT) mRNA was increased at 48 and 96 h after the treatment with 3MC. Hepatic activity of 4-nitrophenol UDPGT was increased by 3MC in Wistar-Shi rats and heterozygous Gunn rats but not in homozygous Gunn rats. Urinary ascorbic acid excretion increased 72 and 96 h after the injection with 3MC in Wistar-Shi and heterozygous Gunn rats but not in homozygous Gunn rats. Ninety-six hours after the injection with 3MC, the hepatic concentration of ascorbic acid in Wistar-Shi rats was 90% higher than that in the corresponding control group, whereas in heterozygous and homozygous Gunn rats the increases were 70 and 30%, respectively. Wistar-Shi rats and homozygous Gunn rats were also injected daily for 3 d with sodium phenobarbital. In rats of both genotypes, the activity and hepatic concentration of chloramphenicol-UDPGT mRNA and liver and urine ascorbic acid concentration were increased by sodium phenobarbital. The data indicate that the stimulation of the expression of both the 4-nitrophenol and chloramphenicol UDPGT genes plays a key role in the ascorbic acid biosynthesis induced by 3MC and sodium phenobarbital.

Analysis of Variance↗
PubMed1993

Arginine affects urea synthesis in rats treated with thyroid hormone.

The purpose of the present study was to determine whether the regulation of urea synthesis was mediated through the activation of N-acetylglutamate synthesis by arginine and whether the concentration of glutamate or activity of N-acetylglutamate synthetase might control N-acetylglutamate concentration when the thyroid status was manipulated. Three groups of rats were given 6-propyl-2-thiouracil (PTU, thyroid inhibitor) without triiodothyronine (T3) treatment, treated with PTU + T3 or treated with neither PTU nor T3 (control). Urinary excretion of urea, liver concentration of N-acetylglutamate and plasma concentration of arginine in rats given PTU + T3 were significantly lower than in rats given PTU alone. Liver concentration of N-acetyl-glutamate was correlated with plasma concentration of arginine (r = 0.842, P < 0.001). The activity of N-acetylglutamate synthetase and glutamate concentration in liver of the PTU + T3-treated group were significantly higher than in the group treated with PTU alone. Arginine administration (0.5 mmol/100 g body wt) elevated the liver concentration of N-acetylglutamate in all three groups. The results suggest that the greater concentration of arginine in the hypothyroid (PTU alone) rats is likely to increase the N-acetylglutamate concentration and stimulate urea synthesis.

Animals↗
PubMed1993

DNA damage and cell killing by camptothecin and its derivative in human leukemia HL-60 cells.

Camptothecin (CPT) has been recognized as a topoisomerase I (Topo I) inhibitor. However, the mechanism of cytotoxicity of this agent remains unknown. In the present study, we analyzed the kinetics of Topo I-mediated DNA single-strand breaks and internucleosomal DNA cleavage produced by CPT and its derivative, 7-ethyl-10-hydroxycamptothecin (SN-38), in HL-60 cells. DNA single-strand breaks were detected using alkaline sucrose gradient centrifugation when HL-60 cells were incubated with 10 microM CPT or 10 microM SN-38 for 30 min. These DNA single-strand breaks were rapidly repaired after drug removal, while the cytotoxic action of these drugs was sustained. Treatment of HL-60 cells with CPT or SN-38 for 3 h produced extensive degradation of DNA. Agarose gel electrophoresis showed a ladder of DNA fragments consisted of multimers of approximately 200 base pairs, characteristic of apoptosis. Interestingly, this type of DNA fragmentation was also induced within 4 h after repair of DNA single-strand breaks, and subsequently loss of cell viability was observed. When zinc ion, a potent inhibitor of endonuclease, was added to drug-free medium after treatment with CPT or SN-38, internucleosomal DNA cleavage was abolished. Furthermore, addition of zinc ion reduced the loss of cell viability. These data suggest that Topo I-mediated DNA single-strand breaks may be necessary but are not sufficient for cell death, and the endonuclease involved in induction of internucleosomal DNA cleavage may play an important role in HL-60 cell death induced by Topo I inhibitor.

Camptothecin↗
PubMed1993

Permeability of the blood-ocular barrier in adolescent and adult diabetic patients.

The permeability of the blood-ocular barrier was examined by fluorophotometry in adolescent and adult diabetic patients before the onset of retinopathy. The adolescent group consisted of 52 eyes of 52 insulin dependent diabetic patients aged 11 to 19 years and a control group of 10 eyes of 10 normal adolescents. The adult group consisted of 74 eyes of 74 non-insulin dependent diabetics and a control group of 30 eyes of 30 normal adults. The increase in lens autofluorescence in the adolescent diabetic patients compared with the controls was striking and showed a significant positive correlation (r = 0.79, p < 0.0001) with the duration of diabetes. Anterior chamber (AQ) values, an index of the permeability of the blood-aqueous barrier (BAB), increased in the adolescent diabetic patients compared with the controls and showed a significant positive correlation with glycosylated haemoglobin levels. No significant differences from the controls were observed regarding the permeability of the blood-retinal barrier (BRB). In the adult group there was no significant difference in either the permeability of the BRB or the AQ values between the diabetic and the control groups. Our results suggest that adolescent diabetic patients differ from adults in that BAB permeability is increased before the onset of retinopathy, suggesting that this is the cause of the striking increase in lens autofluorescence.

Adolescent↗