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Biomedical subjects

H Yoshida

Publications and source records attributed to H Yoshida.

At least 1,189 records · Page 66Linked to original sources
PubMed1995

[Whole mediastinal irradiation with or without entire hemithoracic irradiation for invasive thymoma].

We retrospectively reviewed the case histories of 45 patients with invasive thymoma who underwent postoperative or definitive radiotherapy. Patients in stage II or stage III were classified according to the treatment volume as follows: a) those who received irradiation confined to the primary tumor site with a generous margin (involved field group, n = 17) and b)those who received prophylactic whole mediastinal irradiation with or without entire hemithoracic irradiation (prophylactic group, n = 21). Seven recurrences were observed among the involved field group, while all patients in the prophylactic group were relapse-free and alive after a median follow-up interval of 50 months. Major side effects were observed in two patients who received entire hemithoracic irradiation. One developed severe pneumonitis resulting in lung fibrosis that required hospitalization, while the other developed nephrotic syndrome of unknown cause. We conclude that whole mediastinal irradiation with or without entire hemithoracic irradiation can be used as a treatment of choice for postoperative invasive thymoma.

Adult↗
PubMed1995

Cloning of rat lysosomal acid lipase cDNA and identification of the mutation in the rat model of Wolman's disease.

Lysosomal acid lipase (LAL) is a hydrolase essential for the intracellular degradation of cholesteryl esters and triglycerides. We previously reported a rat model of Wolman's disease (Wolman rat) that is deficient for LAL activity. In this study, we cloned rat LAL (RLAL) cDNA and investigated abnormal LAL gene expression in the Wolman rat. We cloned the RLAL gene from a cDNA library made from normal rat liver mRNA using the human LAL cDNA as a probe, subcloned the RLAL cDNA into pBlueScript vector, and sequenced it. Next, we constructed a cDNA library from a Wolman rat liver, and used the RLAL cDNA as a probe to isolate the Wolman RLAL cDNA for comparison. The normal RLAL cDNA contains 3150 bp including an 1194 bp open reading frame and three poly A signals at the 3' end. The deduced amino acid sequence contained 397 amino acids, showed 79.9% homology with human LAL, and had the same functional domains at the same sites as human LAL. Northern blot analysis revealed that the RLAL mRNA from normal rat was 3.2 kb in length, while the RLAL mRNA from Wolman rat was only 1.4 kb. Nucleotide sequence analysis showed that Wolman rat LAL cDNA had the same sequence as a RLAL cDNA from the 5'-untranslated region to nt 1101, followed by a 60 bp replacement from nt 1102 to nt 1161 with poly A signal and a 3' 1.8 kb deletion. The deduced amino acid sequence demonstrated the substitution of 367Ile to Asn, 368Pro to stop codon, and deletion of the C-terminal 29 amino acids. Genomic Southern blot analysis disclosed a large deletion at the 3' end of the gene. These results identify the molecular defect in the Wolman RLAL, and suggest that the C-terminus of RLAL is essential for the activity and/or stability of the enzyme.

Amino Acid Sequence↗
PubMed1995

[Comparative studies on activities of antimicrobial agents against causative organisms isolated from urinary tract infections (1993). III. Secular changes in susceptibility].

Susceptibilities of Enterococcus faecalis, Staphylococcus aureus, Citrobacter spp., Enterobacter spp., Escherichia coli, Klebsiella spp., Proteus mirabilis, Pseudomonas aeruginosa and Serratia spp. isolated from patients with urinary tract infections (UTIs) in 10 hospitals during June 1993 to May 1994 to various antimicrobial agents were compared with those in the same period of previous years according to a classification, uncomplicated UTIs, complicated UTIs without indwelling catheter, and complicated UTIs with indwelling catheter. The susceptibilities of E. faecalis to chloramphenicol decreased. As for S. aureus, susceptible strains to minocycline (MINO) decreased in complicated UTIs. As for Citrobacter spp., and Enterobacter spp., their susceptibilities were not observed an obvious change. Against E. coli, the activities of cefotiam decreased in complicated UTIs, and aminoglycosides decreased. As for Klebsiella spp., susceptible strains to aminoglycosides decreased. The susceptibilities of P. mirabilis to all drugs except aminoglycosides and MINO were good. The susceptibilities of P. aeruginosa to quinolones isolated from complicated UTIs with indwelling catheter increased, but susceptible strains to aminoglycosides decreased. The susceptibilities of Serratia spp. to MINO has decreased. These data should be considered in clinical treatment of various urinary tract infections.

Anti-Bacterial Agents↗
PubMed1995

Production of platelet-activating factor by porcine brain microvascular endothelial cells in culture.

Endothelial cells produce platelet-activating factor (PAF), which is the key process in the interactions between the vascular wall and blood cells. To examine the production of PAF in brain microvasculature we have cultured brain endothelial cells and performed a comparative study with aortic endothelial cells. Fresh porcine brain was homogenized, and microvascular endothelial cells were separated by enzyme digestion. The cells were cultured in medium containing epidermal growth factor and bovine brain extract. Endothelial cells from the aorta of the same animal were cultured in a similar manner. Production of PAF was assessed by [3H]acetate incorporation into phospholipids or by radioimmunoassay. Prostacyclin was measured by radioimmunoassay of 6-ketoprostaglandin F 1 alpha. The cells produced 1760 +/- 403 and 2892 +/- 347 dpm/10(6) cells (n = 4) of PAF when stimulated with bradykinin and calcium ionophore A23187, each at 1 microM, respectively. Aortic endothelial cells produced 3911 +/- 2006 and 8052 +/- 2270 dpm/10(6) cells (n = 4), respectively, and these values were significantly higher than those in brain endothelial cells (p < 0.01, U-test). Prostacyclin production was also higher in aortic cells as compared to brain microvascular endothelial cells. In aortic endothelial cells both Ca ionophore A23187 and bradykinin significantly stimulated PMN adherence whereas in brain microvascular cells only Ca ionophore enhanced the adherence. Brain microvascular endothelial cells produce smaller amount of PAF and prostacyclin as compared to aortic endothelial cells, and this fact may imply that the functional integrity of the brain microvascular endothelium is maintained at a low level.

Animals↗
PubMed1995

[Efficacy of early administration of G-CSF after intensive chemotherapy in acute leukemia: a randomized controlled trial. Tokai Infection Study Group on Hematological Disorders].

The effect of granulocyte colony-stimulating factor (G-CSF) on neutropenia and infection was studied in a randomized trial in patients receiving intensive chemotherapy for acute leukemia. Fifty seven patients with acute leukemia (35 cases of refractory acute myeloid leukemia, 19 cases of acute lymphoblastic leukemia and 3 cases of blast crisis of chronic myeloid leukemia) were given G-CSF under either of the following two conditions; 1) Group A: starting G-CSF (200 micrograms/m2iv) administration 24 hrs after chemotherapy. 2) Group B: the same dose of G-CSF administration after a febrile episode of 38 degrees C with neutropenia (less than 1,000/microliters). Five patients were excluded from the study. Group A (27 patients) showed a shorter febrile period (2.15 +/- 2.98 days) than the 25 patients of Group B (3.40 +/- 4.78 days), but the difference was not statistically significant. Compared to Group B, Group A showed significantly early recovery of neutrophil counts as well as early recovery from documented infections. There was no evidence that early administration of G-CSF accelerates the growth of leukemic cells nor causes early relapse of acute leukemia.

Acute Disease↗
PubMed1995

A modified method for quantitative measurements of cholinergic and adrenergic sialogogue-induced salivation in mice.

A modified procedure based on that reported by Richter is described for the quantitative measurement of salivation induced by sialogogues in mice. As a new immobilizing technique for mice, the present method uses a combination of light anesthesia produced by a low dose (1.0 g/kg, i.p.) of urethane and a fixing plate, instead of deep anesthesia induced by a high dose (1.8 g/kg, i.p.) of urethane. Unlike Richter's method, the immobilizing technique described here did not potentiate the toxicity of sialogogues and hence no mice died within 48 h after the end of the experiment. This method could easily measure salivation induced by cholinergic agonists (pilocarpine and bethanechol) and adrenergic agonists (phenylephrine and isoproterenol), dose-dependently. Thus, the present method may be useful for studying salivation responses induced by various types of sialogogues under less toxic experimental conditions in mice.

Animals↗
PubMed1995

[An experience of surgery for thymolipoma in a patient with amyotrophic lateral sclerosis].

A 48-year-old male with amyotrophic lateral sclerosis (ALS) was revealed to have an anterior mediastinal tumor, occupying left hemithorax on a chest CT. The tumor compressed the left lower lobe, resulting in a hypoventilation, which required a continuous ventilatory support. Although ALS has poor prognosis in general, we decided to remove the tumor surgically. Because the symptoms related to ALS was limited to his extremities, indicating he could potentially reestablish his life under ventilator-free condition, when a remove of the tumor improved a hypoventilation. A remove of the tumor was performed via antero-axillar thoracotomy, and reexpansion of the left lower lobe was achieved, followed by improvement of lung function and of respiratory symptoms. Histological examination revealed that the tumor was composed of mature adipose tissue and thymic tissue, diagnosed as thymolipoma. Postoperative course was uneventful.

Amyotrophic Lateral Sclerosis↗
PubMed1994

Inhibition of the T-cell receptor-mediated signal transduction by microinjection of anti-Lck monoclonal antibody into T-cells.

Engagement of T-cell receptor (TcR)/CD3 complexes on T-cells rapidly provokes tyrosine phosphorylation of cellular proteins, which is thought to be an essential step to the following events of T-cell activation. p56lck, a member of src-related, non-receptor type protein tyrosine kinases, is expressed predominantly in lymphocytes. Accumulating data suggest that p56lck is one of the kinases responsible for TcR-mediated protein tyrosine phosphorylation. To investigate the role of p56lck in TcR-signaling in detail, we injected anti-Lck monoclonal antibody (mAb), MOL171 or MOL294, both specifically suppress Lck kinase activity in vitro, into Jurkat T-cells by the erythrocyte-ghost procedure in order to block the activity of p56lck. In Jurkat cells injected with anti-Lck mAb, intracellular Ca2+ mobilization induced by TcR-stimulation was markedly reduced in comparison with control mouse IgG-injected samples. This block of Ca2+ influx seems to be specific for TcR-signaling because anti-Lck mAb-injection did not cause significant suppression of phytohaemagglutinin-induced Ca2+ increase. Furthermore, injection of anti-Lck mAb inhibited TcR-mediated protein tyrosine phosphorylation of 100 kDa protein and phospholipase C gamma 1. These results confirm that p56lck is an indispensable element of TcR-signaling and p100 and phospholipase C gamma 1 are strongly presumed to be candidates for substrates for p56lck.

Antibodies, Monoclonal↗
PubMed1994

NMDA receptor-mediated expression of Fos protein in the rat striatum following methamphetamine administration: relation to behavioral sensitization.

In order to clarify the possible involvement of N-methyl-D-aspartate (NMDA) receptors in mediating striatal Fos protein induction and behavioral sensitization after methamphetamine administration, we examined the effects of non-competitive NMDA receptor antagonist MK-801 on these phenomena in rats. A single administration of 1.0 and 5.0 mg/kg methamphetamine resulted in a dose-dependent increase in Fos-immunoreactive cells in the medial striatum. Prior exposure to 5.0 mg/kg methamphetamine enhanced ipsilateral rotational behavior in response to subsequent methamphetamine administration in unilateral nigral-lesioned rats (sensitization). Pretreatment with 1.0 mg/kg MK-801 completely prevented both the expression of striatal Fos protein and the development of acute behavioral sensitization following a single injection of 5.0 mg/kg methamphetamine. These results suggest that NMDA receptor-mediated mechanisms contribute to the expression of striatal Fos protein associated with behavioral sensitization that follows exposure to methamphetamine.

Animals↗
PubMed1994

Bernard-Soulier syndrome Kagoshima: Ser 444-->stop mutation of glycoprotein (GP) Ib alpha resulting in circulating truncated GPIb alpha and surface expression of GPIb beta and GPIX.

The platelet membrane glycoprotein (GP)Ib/IX complex is composed of three polypeptides, GPIb alpha, GPIb beta, and GPIX, and functions as a platelet receptor for von Willebrand factor. All three subunits are reported to be requisite for efficient surface expression of the complex. The absence of the GPIb/IX complex on platelet membrane is the hallmark of a congenital qualitative platelet disorder, termed the Bernard-Soulier syndrome (BSS). We describe here the molecular basis of a novel variant phenotype of BSS in a female patient, designated as BSS Kagoshima. Her platelets completely lacked the surface expression of GPIb alpha, but expressed a residual amount of GPIb beta and GPIX. Unexpectedly, her platelets and plasma contained a truncated GPIb alpha polypeptide with an apparent molecular weight of 116 kD (under nonreducing conditions). The amounts of truncated protein were 23% and 60% of the normal values in platelets and plasma, respectively. The abnormal protein contained a normal amount of sialic acid as demonstrated by digestion with neuraminidase. DNA sequencing analysis showed a homozygous single nucleotide substitution from the serine codon (TCA) to a nonsense codon (TAA) at residue 444 in the GPIb alpha gene. The mutant gene generated a truncated GPIb alpha molecule lacking the transmembrane region and cytoplasmic tail. Her parents were heterozygotes for the mutation. These findings suggest that this type of truncated GPIb alpha was produced, normally glycosylated, and subsequently secreted into the plasma. Furthermore, the truncated GPIb alpha might be associated with the process of the surface expression of incomplete GPIb/IX complex, GPIb beta and GPIX.

Adult↗
PubMed1994

Effect of angiotensin-converting enzyme inhibitors on endothelium-dependent peripheral vasodilation in patients with chronic heart failure.

OBJECTIVES: This study was performed to determine whether acute inhibition of angiotensin-converting enzyme restores impaired endothelium-dependent vasorelaxation in patients with chronic heart failure. BACKGROUND: Recent reports have demonstrated that endothelium-dependent vasodilation induced by cholinergic stimuli is attenuated in the peripheral vascular bed of patients with chronic heart failure. METHODS: We examined the effects of local intraarterial infusion of enalaprilat (0.6 micrograms/min per 100 ml tissue volume) on responses initiated by acetylcholine or sodium nitroprusside in the forearm vascular bed in 8 normal subjects, 12 patients with mild heart failure (New York Heart Association functional classes I and II) and 10 patients with more advanced heart failure (functional classes III and IV). Forearm blood flow was measured by means of venous occlusion plethysmography. RESULTS: Although enalaprilat alone did not affect basal forearm blood flow, it significantly augmented the increase in forearm blood flow induced by acetylcholine in normal subjects (p < 0.01) and in those with mild heart failure (p < 0.05). However, the effect was not found in patients with more advanced heart failure. Coinfusion of enalaprilat did not enhance sodium nitroprusside-induced vasodilation in any of the groups. To explore the mechanism of the inhibitor's effect, an additional 20 patients with mild heart failure (functional class II) were pretreated with a cyclooxygenase inhibitor, acetylsalicylic acid (n = 10) or an inhibitor of nitric oxide synthesis, NG-monomethyl-L-arginine (n = 10), followed by administration of acetylcholine with or without enalaprilat. Acetylsalicylic acid reduced the converting enzyme inhibitor's effect, whereas NG-monomethyl-L-arginine failed to block the augmentation of blood flow. CONCLUSIONS: These results suggest that inhibition of angiotensin-converting enzyme potentiates endothelium-dependent vasodilation induced by cholinergic stimuli, presumably through modulation of prostaglandin metabolism, in the peripheral vasculature of patients with mild chronic heart failure.

Acetylcholine↗
PubMed1994

Abnormalities of the adenomatous polyposis coli gene in human oral squamous-cell carcinoma.

Recent studies have suggested that abnormalities in the adenomatous polyposis coli gene (APC gene) are associated with the development not only of familial adenomatous polyposis coli (FAP) but also of cancers in digestive organs. In order to elucidate whether abnormalities of the APC gene could contribute to the development of oral squamous-cell carcinoma (SCC), genomic DNAs from tumors and normal tissues of 24 unrelated Japanese patients were examined by using PCR-SSCP (polymerase chain reaction single-strand conformation polymorphism) and sequence analyses. Five novel nucleotide substitutions of the APC gene in tumor tissues were identified in 3 patients with oral SCC (12.5%), resulting in 3 amino-acid replacements or a truncation of the APC gene product. We also examined 24 tumor and 24 normal tissue samples for loss of heterozygosity (LOH) at exon 11 of the APC gene by PCR-LOH assay. In this analysis, 45.8% of samples were informative and LOH was detected in 72.7% of informative cases. The frequency of LOH in oral SCC was similar to that previously reported in esophageal SCC. These results suggest that abnormalities in the APC gene are associated with the development of human oral SCC.

Base Sequence↗
PubMed1994

Identification of EGF as an angiogenic factor present in conditioned medium from human salivary gland adenocarcinoma cell clones with varying degrees of metastatic potential.

We have previously shown that conditioned medium (CM) from metastasizing human salivary gland adenocarcinoma cell clones contains factor(s) that stimulate the proliferation and migration of bovine aortic endothelial (BAE) cells, and inhibit the production of collagenases by BAE cells (Azuma M. et al. (1993) Cancer Lett., 73, 85-93). To further characterize this, we evaluated the expression level of epidermal growth factor (EGF) secreted by a non-metastasizing cell clone (HSGc) and its metastasizing cell clones, and analysed the effect of EGF on the biologic behaviors of BAE cells. When the secretion of EGF by cell clones was estimated by enzyme-linked immunosorbent assay, metastasizing cell clones released a large amount of EGF as compared with HSGc. However, the number of EGF receptor was detected consistently at a level that was similar in all cell clones. With regard to the effect of EGF on the malignant potential of cell clones such as proteolytic aggressiveness, EGF did not affect the secretion of both collagenases and their inhibitor from cell clones. Alternatively, exogenous EGF stimulated the proliferation and migration of BAE cells, and inhibited the secretion of collagenases from BAE cells. Neutralization with a neutralizing antibody of EGF released into CM abolished the inhibitory effect of CM on the secretion of collagenases from BAE cells. Thus, the CM-contained factor, which is responsible for the induction of biologic behaviors of BAE cells, can be attributed to EGF.

Adenocarcinoma↗
PubMed1994

[Serial CT during arterial portography and arteriography of the liver with a triple-lumen balloon catheter].

Serial computed tomography during arterial portography (CTP) and CT during arteriography (CTA) of the liver could be performed on nine of ten patients with hepatocellular carcinoma, using triple-lumen balloon catheters (3-B-C). The 3-B-C was inserted into the common hepatic artery, and the balloon was inflated. We have injected contrast medium into the splenic artery through the side hole of the 3-B-C to perform CTP, and then into the common hepatic artery through the tip hole to perform CTA.

Adult↗
PubMed1994

Cloning and functional characterization of a third pituitary adenylate cyclase-activating polypeptide receptor subtype expressed in insulin-secreting cells.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide belonging to the vasoactive intestinal polypeptide/glucagon/secretin family. It is widely distributed in the body, and a variety of biological actions have been reported. PACAP exerts its biological effects by binding to specific receptors that are coupled to GTP-binding proteins. Recent studies have shown that there is a family of PACAP receptors (PACAPRs), and two members of this family have been identified. We report here the cloning, functional expression, and tissue distribution of a third PACAPR subtype, designated PACAPR-3. The cDNA encoding PACAPR-3 has been isolated from a mouse insulin-secreting beta-cell line MIN6 cDNA library. Mouse PACAPR-3 is a protein of 437 amino acids that has 50% and 51% identity with rat PACAP type I and type II receptors, respectively. Expression of recombinant mouse PACAPR-3 in mammalian cells shows that it binds to vasoactive intestinal polypeptide as well as PACAP-38 and -27, with a slightly higher affinity for PACAP-38, and is positively coupled to adenylate cyclase. The expression of PACAPR-3 in Xenopus oocytes indicates that calcium-activated chloride currents are evoked by PACAP and vasoactive intestinal polypeptide, suggesting that PACAPR-3 can also be coupled to phospholipase C. RNA blot analysis studies reveal that PACAPR-3 mRNA is expressed at high levels in MIN6, at moderate levels in pancreatic islets and other insulin-secreting cell lines, HIT-T15 and RINm5F, as well as in the lung, brain, stomach, and colon, and at low levels in the heart. Furthermore, insulin secretion from MIN6 cells is significantly stimulated by PACAP-38. These results suggest that the diverse biological effects of PACAP are mediated by a family of structurally related proteins and that PACAPR-3 participates in the regulation of insulin secretion.

Amino Acid Sequence↗