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Biomedical subjects

K Yoshimura

Publications and source records attributed to K Yoshimura.

At least 343 records · Page 19Linked to original sources
PubMed1993

[Renal or perirenal malignant lymphoma: report of three cases].

We report three cases of renal or perirenal malignant lymphoma. The patients were a 69-year-old woman presenting with lumbago, a 43-year-old man with fever and erythema, and a 69-year-old woman with general malaise. In each case, renal or perirenal tumor was discovered by abdominal ultrasound. Biopsy and microscopic examination revealed the diagnosis of non-Hodgkin's malignant lymphoma. The computerized tomography patterns of the cases were different from each other; "direct invasion" in the first case, "solitary nodule" in the second case, and "engulfment" in the third case. Chemotherapy and/or radiation therapy were performed. Only the third case is still alive at present. The computerized tomography pattern of renal or perirenal malignant lymphoma was classified into five groups; I) multiple nodules, II) solitary nodule, III) engulfment, IV) direct invasion, V) diffuse infiltration. This classification should be useful in making an accurate and early diagnosis.

Adult↗
PubMed1993

Intestinal protection against Strongyloides ratti and mastocytosis induced by administration of interleukin-3 in mice.

Information about interleukin-3 (IL-3) effects in vivo is limited compared with the in vitro effects. We found that a repetitive injection of a low dose of recombinant IL-3 induced protection against intestinal worms of Strongyloides ratti in C57BL/6 mice. When mice were injected i.p. with different doses of recombinant IL-3 twice a day from day -5 to day -1 and infected orally with larvae recovered from the head of infected rats on day 0, worm recovery from the small intestine was markedly reduced by a total of 10(4) U IL-3 or more on day 2 post-infection. The number of intestinal mucosal mast cells (MMC) was increased by the protective dose of IL-3. The IL-3 treatment, however, was ineffective in protecting mice against tissue migrating larvae, as assessed by recovery from the head. The protective effect of IL-3 on intestinal worms was observed within 6 hr post oral infection, suggesting little concern with antigen-specific immune responses. The effective dose of IL-3 treatment increased the number of MMC progenitors five times in the spleen and the mesenteric lymph nodes. An MMC-specific protease, MMCP-1, was secreted 200 times more than in controls in the intestinal lumen by the IL-3 treatment. The IL-3 treatment induced no protection or mastocytosis in mast cell-deficient W/Wv mice. These results suggest that the IL-3-induced intestinal protection against S. ratti is mediated by MMC.

Animals↗
PubMed1993

[Study of pathophysiology of pulmonary circulation in polycythemia using scintigraphy].

In order to evaluate the pathophysiology of pulmonary circulation in polycythemia, Tl-201 myocardial scintigraphy and perfusion lung scintigraphy with 99m-Tc MAA were performed in 19 cases with polycythemia including polycythemia rubra vera and in 11 cases with secondary polycythemia due to pulmonary diseases. Tl-201 lung uptake, right ventricular visualization and pulmonary perfusion impairment were studied. In the 19 cases, Tl-201 lung uptake was observed in all cases and 54.5% of them showed moderate lung uptake. The grade of right ventricular visualization was moderate in one case and slight in 16 cases; right ventricular hypertrophy was shown in 89.5% of all cases by Tl-201 scintigraphy, only one of which showed right ventricular hypertrophy on electrocardiography. Abnormalities of lung perfusion consisted of scattered small areas of hypoperfusion in 36.8%, peripheral hypoperfusion in 78.9% and uneven distribution of pulmonary perfusion in 94.7%. The degree of hypoperfusion was slightly related to decrease in FEV1.0%, V25 and PaO2 and increase in circulating blood volume and peripheral red blood cell counts. Abnormalities of pulmonary function consisted of increased RV/TLC in 50.0%, increased CV/VC in 35.7% and decreased V25 in 36.8%. Arterial blood gases showed hypoxemia in 57.1%, the degree of which was slightly related to increase in RV/TLC and CV/VC and decrease in V25. Cases of secondary polycythemia due to pulmonary diseases showed more marked right ventricular visualization, pulmonary perfusion impairment and abnormalities of various kinds of pulmonary function than polycythemia rubra vera cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[A case of bronchogenic squamous cell carcinoma associated with Swyer-James syndrome].

Swyer-James syndrome is considered to be a relatively uncommon disease entity presenting with unilateral hyperlucent lung due to hypoplasia of a pulmonary artery and bronchiectasis of the affected lung. Association of bronchogenic carcinoma with Swyer-James syndrome has not apparently been reported in any previous literature, except for one Japanese case. In the present paper, we describe a 48-year-old male individual, who developed poorly differentiated squamous cell carcinoma of the right upper lobe bronchus after he had been diagnosed to have Swyer-James syndrome with unilateral hyperradiancy of the left lung. It is suggested that the bronchial epithelium of the unaffected lung in Swyer-James syndrome is likely to be more exposed to extrinsic carcinogens than that of the affected, underventilated lung, hence resulting in a higher risk of developing bronchogenic carcinoma.

Carcinoma, Squamous Cell↗
PubMed1993

[Uveitis in human T-lymphotropic virus type I (HTLV-I) carriers--1. A seroepidemiological study].

A seroepidemiological study was carried out to find out if human T-lymphotropic virus type I (HTLV-I) was closely associated with uveitis in two hospitals: one in an area where HTLV-I was highly prevalent (Miyakonojo, Miyazaki) and the other in an area where HTLV-I was less prevalent (Kurume). In the highly prevalent HTLV-I area, the seroprevalence in patients with idiopathic uveitis (78/206, 37.9%) was significantly higher than in patients with non-uveitic ocular diseases (73/380, 19. 2%) or in patients with uveitis with defined etiologies (8/80, 10.0%). A more striking finding was that the seroprevalence in the younger group (20-49 years) with idiopathic uveitis in the area was 40/82 (48.8%), but only 9/114 (7.9%) in the other two reference groups. The odds of contracting idiopathic uveitis for HTLV-I infected persons was estimated at 11.0 in the younger group, and 2.0 in the older group. Similar observations were recorded even in the less prevalent area (Kurume). These data thus suggest that HTLV-I infection is a risk factor for idiopathic uveitis.

Adult↗
PubMed1993

[Uveitis in human T-lymphotropic virus type I (HTLV-I) carriers--2. An analysis of clinical features].

The clinical features of human T-lymphotropic virus type (HTLV-I) uveitis, an idiopathic uveitis in HTLV-I seropositive patients, were analyzed in a hospital located in an area where HTLV-I was endemic (Miyakonojo, Miyazaki). A total of 61 patients (25 males and 31 females) with HTLV-I uveitis were the subjects of the analysis. Intermediate uveitis with moderate to severe vitreous opacities accompanied by mild iritis and retinal vasculitis was the most characteristic feature, and was observed in the majority of the patients (66% of all or 84% in young adult patients between 20 and 49 years of age). The uveitis affected one eye in 57% and both eyes in 43% of the patients, with subacute onset of floaters and foggy vision. The uveitis responded well to therapy with topical or systemic corticosteroids, but recurred in many cases. A significant number of patients (15% of all and 25% of female patients) had a previous history of Graves' disease with hyperthyroidism.

Adult↗
PubMed1993

[Mechanism of parasite killing by eosinophils in parasitic infections].

Eosinophils kill a variety of helminth parasites and some protozoan parasites in vitro by antibody- or complement-dependent mechanisms. Nevertheless, direct evidence of in vivo parasite killing by eosinophils is scanty. In Angiostrongylus cantonensis infection in non-permissive hosts, however, the intracranial worms are killed by eosinophils in the cerebrospinal fluid, indicating that the cells are associated, not only with the protective immunity against helminthic infections, but also with the innate resistance of the non-permissive host. Moreover, eosinophils could be probably involved in the damage of host tissues, e.g., loss of Purkinje cells in the cerebellum of mice infected with A. cantonensis. A variety of basic proteins derived from eosinophil granules, such as MBP, ECP, EDN (= EPX) and EPO, and possibly active oxygen products, may be involved in the killing of parasites.

Animals↗
PubMed1993

[Right ventricular visualization by Tl-201 myocardial scintigraphy in chronic obstructive pulmonary disease].

Tl-201 myocardial scintigraphy was performed in 130 patients with chronic obstructive pulmonary disease (COPD) to evaluate right ventricular hypertrophy, and the clinical significance of this method was studied. Tl-201 uptake ratio of the right ventricle, which represents the ratio of total counts of the right ventricle to counts of the administered dose of Tl-201, was higher in COPD, especially in pulmonary emphysema and B type COPD by Burrows classification than in controls. The grade of visualization of the right ventricle by visual assessment (RVV) was marked (+3) in only a few cases and moderate (+2) in many cases (more than 80%) in all diseases except bronchial asthma. The incidences of right ventricular hypertrophy by electrocardiogram, right-sided heart failure and marked dyspnea (Hugh-Jones 4.5) were very low in cases with RVV grade +2 and very high in cases with +3. The grade of RVV was related to the severity of pulmonary perfusion impairment, although in diffuse panbronchiolitis the RVV was relatively slight compared with the impairment of perfusion. May parameters of pulmonary function such as %VC, FEV1.0%, RV/TLC, V25, %DLCO, Raw, delta N2 and PaO2 showed abnormal values in patients with RVV grade of (+2) or (+3) in all diseases except bronchial asthma. In COPD, Tl-201 myocardial scintigraphy seems to be useful for assessment of right ventricular overloading, and for follow-up observation and differentiation between cor pulmonale and right ventricular hypertrophy secondary to cardiac diseases by observing Tl-201 uptake of the lung and left ventricle.

Humans↗
PubMed1993

[Identical twins with atypical benign partial epilepsy].

Female identical twins with atypical absence in waking state and partial seizures in sleep state were reported. During atypical absence the EEGs of both cases showed bursts in bilateral parietal and temporal regions during waking state and almost continuous diffuse spike-waves during sleep. Phenytoin was effective to discontinue the seizures in both cases. These findings were compatible to atypical benign partial epilepsy first reported by Aicardi et al. A possibility of genetic cause of this disorder may be considered.

Child↗
PubMed1992

Tumor necrosis factor modulation of expression of the cystic fibrosis transmembrane conductance regulator gene.

Based on the knowledge that expression of the cystic fibrosis transmembrane conductance regulator (CFTR) gene can be modulated at the transcriptional level, and that the CFTR gene promoter contains sequences homologous to elements in other promoters that respond to tumor necrosis factor-alpha (TNF), we evaluated the hypothesis that TNF might modulate CFTR gene expression in epithelial cells. Studies with HT-29 cells, a colon epithelium-derived tumor cell line known to express the CFTR gene, demonstrated that TNF downregulated CFTR mRNA transcript levels in a dose- and time-dependent fashion. Interestingly, nuclear run-on analyses demonstrated that TNF did not affect the rate of transcription of CFTR gene, but exposure of the cells to TNF did modify the stability of CFTR mRNA transcripts, resulting in a mRNA half-life that was reduced to 65% of the resting level. These observations suggest that CFTR gene expression can be modulated by TNF, at least in part, at the posttranscriptional level.

Blotting, Northern↗
PubMed1992

Uveitis associated with human T-cell lymphotropic virus type I.

Seroepidemiologic, clinical, and virologic studies were performed to determine whether human T-cell lymphotropic virus type I was closely associated with uveitis in two hospitals. One hospital was in an endemic area of the virus (Miyakonojo, Miyazaki) and the other hospital was in a less endemic area (Kurume). In the endemic area, the seroprevalence of the virus in patients with uveitis without defined causes (35.4%, 62 of 175 patients) was significantly higher than that in patients with nonuveitic ocular diseases (16.1%, 42 of 261 patients), or in patients with uveitis with defined causes (10.3%, eight of 78 patients). The seroprevalence in younger patients (20 to 49 years of age) with uveitis without defined causes in the area was 44.8% (30 of 67 patients), whereas it was only 9.3% (ten of 107 patients) in the other two groups. A similar observation was recorded even in the less endemic area (Kurume). Because the seroprevalence of the virus in the general population is known to be low in younger patients and to increase with age, these findings were interpreted to indicate that the association of human T-cell lymphotropic virus type I with uveitis was significant. Most patients, particularly those aged 20 through 49 years, had an intermediate uveitis characterized by a moderate inflammation in the vitreous body accompanied by an iritis and retinal vasculitis. The ocular symptoms in the patients differed from those of other types of uveitis common in Japan (Behçet's disease, Vogt-Koyanagi-Harada's disease, and toxoplasmosis, for example).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Expression of the cystic fibrosis transmembrane conductance regulator gene can be regulated by protein kinase C.

Epithelial cells utilize at least two types of apical Cl- channels, the cAMP-activated cystic fibrosis transmembrane conductance regulator (CFTR) and the Ca2+/calmodulin-dependent Cl- channel. While phorbal ester (PMA) activates only CFTR-dependent Cl- secretion and the Ca2+ ionophore A23187 only the Ca2+/calmodulin-dependent Cl- secretion, PMA and A23187 share the ability to down-regulate expression of the CFTR gene at the transcriptional level. Since both PMA and A23187 can activate protein kinases, we hypothesized that protein kinase pathways may be involved in the regulation of CFTR gene expression. Exposure of HT-29 human colon carcinoma cells to the protein kinase C activator SC9 down-regulated CFTR mRNA levels in a dose-dependent fashion, similar to that seen with PMA. The reduction in CFTR transcript levels by SC9 and PMA was blocked by H7, an inhibitor of protein kinases. In a similar fashion, the down-regulation of CFTR transcript levels by A23187 was blocked by H7 as well as staurosporine, another protein kinase inhibitor. Interestingly, both H7 and staurosporine themselves increased CFTR mRNA levels. Quantification of CFTR gene transcription rate showed a reduction by SC9 (similar to that with PMA and A23187) that was prevented by H7 and that H7 by itself increased CFTR transcription. Together, these observations suggest that protein kinase pathways, likely including protein kinase C, are involved in the regulation of CFTR gene expression, with activation or inhibition of protein kinase activity down-regulating or up-regulating CFTR gene expression, respectively.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

Expression of the human cystic fibrosis transmembrane conductance regulator gene in the mouse lung after in vivo intratracheal plasmid-mediated gene transfer.

As an approach to gene therapy for the respiratory manifestations of cystic fibrosis (CF), in vivo plasmid-mediated direct transfer of the normal CF transmembrane conductance regulator (CFTR) gene to the airway epithelium was investigated in mice. To evaluate the feasibility of this strategy, pRSVL, a plasmid composed of a firefly luciferase gene driven by the Rous sarcoma virus long terminal repeat (RSV-LTR), along with cationic liposomes was instilled into the trachea of C57BI/6NCR mice. With administration of 200-400 micrograms plasmid DNA, luciferase expression could be detected in the mouse lung homogenates for at least 4 wk. With this background, a CFTR expression plasmid vector (pRSVCFTR) constructed by replacing the luciferase cDNA from pRSVL with the normal human CFTR cDNA was evaluated in vivo in mice. Intratracheal instillation of pRSVCFTR with cationic liposomes followed by analysis of mouse lung RNA by polymerase chain reaction amplification (after conversion of mRNA to cDNA) using a RSV-LTR specific sense primer and a human CFTR-specific antisense primer demonstrated human CFTR mRNA transcripts from one day to 4 wk after instillation. Further, in vivo evaluation of beta-galactosidase activity after intratracheal administration of an E. coli lacZ gene expression plasmid vector directed by the cytomegalovirus promoter (pCMV beta) demonstrated that the airway epithelium was the major target of transfer and expression of the exogenous gene. These observations demonstrate successful plasmid-mediated gene transfer to the airway epithelium in vivo. This strategy may be feasible as a form of gene therapy to prevent the pulmonary manifestations of CF.

Animals↗
PubMed1992

Transcriptional and posttranscriptional modulation of human neutrophil elastase gene expression.

Human neutrophil elastase (NE), a 29-Kd potent serine protease stored in azurophilic granules of mature neutrophils, is coded for by the NE gene, a single copy gene with 5 exons spanning a 6-kb segment of chromosome 11 at q14. With the knowledge that the NE gene expression is limited to early myeloid cell differentiation, mechanisms modulating expression of the NE gene were evaluated in the HL-60 promyelocytic leukemia cell line, a model of early bone marrow precursor cells. Consistent with the presence of NE messenger RNA (mRNA) transcripts in undifferentiated HL-60 cells, nuclear transcription run-on analyses showed that HL-60 cells actively transcribed the NE gene. However, the transcription rate of the NE gene was relatively low, only 40% of the myeloperoxidase gene, a gene expressed in parallel with NE. When induced toward the mononuclear phagocytic lineage with phorbol 12-myristate 13-acetate (PMA), HL-60 cells exhibited marked suppression of NE gene transcription, declining to 17% of the resting rate within 2 days. Induction toward mononuclear phagocytic lineage differentiation caused no change in NE mRNA transcript half-life (T1/2), but mRNA levels decreased markedly over time, with levels undetectable 1.5 days after PMA stimulation. In contrast, when induced toward the myelocytic lineage with dimethyl sulfoxide, the rate of NE gene transcription increased 1.9-fold within 5 days. Interestingly, the mRNA transcript levels increased 2.5-fold by 5 days despite the fact that induction toward myelocytic lineage differentiation was accompanied by a marked reduction of NE mRNA transcript T1/2. Together, these observations suggest that the NE gene expression during bone marrow differentiation is modulated mainly at the transcriptional level, with some posttranscriptional modulation contributing, particularly during myelocytic lineage differentiation.

Blotting, Northern↗
PubMed1992

Interaction between the calcium and cyclic AMP messenger systems in perifused rat parotid acinar cells. Possible mechanism for potentiation of amylase secretion.

Potentiation of amylase secretion induced by a combination of isoproterenol and carbamylcholine was examined in perifused rat parotid acinar cells. The time course of changes in the augmented amylase secretion induced by isoproterenol plus carbamylcholine was similar to that induced by carbamylcholine alone, but not to that caused by isoproterenol. Concentration-response analysis showed that isoproterenol increased the apparent affinity for carbamylcholine to stimulate amylase secretion with the maximum effect attained by isoproterenol plus carbamylcholine being higher than that attained by isoproterenol or carbamylcholine. 8-Bromo cyclic AMP, forskolin and 3-isobutyl-1-methylxanthine mimicked the effect of isoproterenol. Calcium ionophores (A23187 and ionomycin), but not phorbol 12,13-dibutyrate, mimicked the effect of carbamylcholine. Chelation of intracellular free calcium with 1,2-bis-[2-aminophenoxyl]-ethane-N,N,N',N'-tetraacetic acid, but not that of extracellular calcium with [ethylenebis(oxyethylenenitrile)]-tetraacetic acid (EGTA), abolished the potentiation. Calmodulin antagonists inhibited amylase secretion induced by isoproterenol plus carbamylcholine or carbamylcholine alone, but not that induced by isoproterenol alone. These results suggest that the potentiation is mainly, if not completely, caused by a coordinated interaction between the cyclic AMP system and the Ca2+ system at a step distal to second messenger generation, probably via a cyclic AMP-induced increase in the sensitivity of the Ca2+ response element to calcium.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1992

In vivo transfer of the human cystic fibrosis transmembrane conductance regulator gene to the airway epithelium.

Direct transfer of the normal cystic fibrosis (CF) transmembrane conductance regulator (CFTR) gene to airway epithelium was evaluated using a replication-deficient recombinant adenovirus (Ad) vector containing normal human CFTR cDNA (Ad-CFTR). In vitro Ad-CFTR-infected CFPAC-1 CF epithelial cells expressed human CFTR mRNA and protein and demonstrated correction of defective cAMP-mediated Cl- permeability. Two days after in vivo intratracheal introduction of Ad-CFTR in cotton rats, in situ analysis demonstrated human CFTR gene expression in lung epithelium. PCR amplification of reverse transcribed lung RNA demonstrated human CFTR transcripts derived from Ad-CFTR, and Northern analysis of lung RNA revealed human CFTR transcripts for up to 6 weeks. Human CFTR protein was detected in epithelial cells using anti-human CFTR antibody 11-14 days after infection. While the safety and effectiveness remain to be demonstrated, these observations suggest the feasibility of in vivo CFTR gene transfer as therapy for the pulmonary manifestations of CF.

Adenoviruses, Human↗