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H Moriuchi

Publications and source records attributed to H Moriuchi.

At least 19 recordsLinked to original sources
PubMed2001

Lidocaine potentiates atrial natriuretic peptide-induced relaxation of bovine tracheal smooth muscle.

The effect of lidocaine on the changes in tension and guanosine 3',5'-cyclic monophosphate (cGMP) content induced by atrial natriuretic peptide (ANP) and nitric oxide (NO) was examined in bovine tracheal smooth muscle preparations contracted with methacholine (0.3 microM). Lidocaine (10 microM) did not affect the methacholine-induced tensions, whereas 100 microM lidocaine significantly (P<0.01) attenuated methacholine-induced ones. Treatment of the tracheal preparations with lidocaine (10 and 100 microM) significantly (P<0.05) augmented the relaxant responses to ANP, whereas the same procedure did not alter the responses to sodium nitroprusside, (+/-)-(E)-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexeneamide (NOR 3) or 8-bromo-cGMP. Lidocaine (100 microM) enhanced cGMP accumulation induced by ANP (0.1 microM) but not by sodium nitroprusside (0.3 microM). In contrast, mexiletine (100 microM), another class Ib antiarrhythmic, did not affect ANP- and sodium nitroprusside-induced relaxations. These results suggest that lidocaine augments ANP-induced relaxation and cGMP accumulation, probably by modulating activation mechanism of particulate guanylyl cyclase.

Animals↗
PubMed2001

Condition of microcephaly, growth retardation, joint contractures, atopic dermatitis, and mental retardation in two Japanese sisters: a new autosomal recessive MCA/MR syndrome?

We report on two sisters in a family with a hitherto undescribed MCA/MR condition characterized by growth retardation, severe microcephaly, a peculiar facies, congenital contractures of the interphalangeal and patellar joints, atopic dermatitis, and growth and developmental delay. The disorder in the family we describe is similar to but clearly distinguished from tricho-rhino-phalangeal syndromes or Bavinck syndrome. We propose that the condition in the sisters represents a new autosomal recessive MCA/MR syndrome.

Abnormalities, Multiple↗
PubMed2001

Spontaneous in vivo reversion of an inherited mutation in the Wiskott-Aldrich syndrome.

The Wiskott-Aldrich syndrome (WAS) is an X-linked primary immunodeficiency disease, arising from mutations of the WAS-protein (WASP) gene. Previously, we have reported that mononuclear cells from WAS patients showed lack/reduced of the intracellular WASP (WASP(dim)) by flow cytometric analysis, and analysis of WASP by flow cytometry (FCM-WASP) was useful for WAS diagnosis. In this study, we report a WAS patient who showed the unique pattern of FCM-WASP. The patient had the small population of normal expression of WASP (WASP(bright)) mononuclear cells together with the major WASP(dim) population. The WASP(bright) cells were detected in T cells, not in B cells or in monocytes. Surprisingly, the molecular studies of the WASP(bright) cells revealed that the inherited mutation of WASP gene was reversed to normal. His mother was proved as a WAS carrier, and HLA studies and microsatellite polymorphic studies proved that the WASP(bright) cells were derived from the patient himself. Therefore, we concluded that the WASP(bright) cells were resulted from spontaneous in vivo reversion of the inherited mutation. Furthermore, the scanning electron microscopic studies indicated that WASP-positive cells from the patient restored the dense microvillus surface projections that were hardly observed in the WASP(dim) cells. This case might have significant implications regarding the prospects of the future gene therapy for WAS patients.

Adult↗
PubMed2001

A milk protein lactoferrin enhances human T cell leukemia virus type I and suppresses HIV-1 infection.

Human T cell leukemia virus type I (HTLV-I) and HIV-1, causative agents of adult T cell leukemia/lymphoma and AIDS, respectively, are transmitted vertically via breast milk. Here we demonstrate that lactoferrin, a milk protein that has a variety of antimicrobial and immunomodulatory activities, facilitates replication of HTLV-I in lymphocytes derived from asymptomatic HTLV-I carriers and transmission to cord blood lymphocytes in vitro. Transient expression assays revealed that lactoferrin can transactivate HTLV-I long terminal repeat promoter. In contrast, lactoferrin inhibits HIV-1 replication, at least in part, at the level of viral fusion/entry. These results suggest that lactoferrin may have different effects on vertical transmission of the two milk-borne retroviruses.

Adjuvants, Immunologic↗
PubMed2001

Role of K+ channels in N-acetylprocainamide-induced relaxation of bovine tracheal smooth muscle.

We examined the relaxant effects of N-acetylprocainamide, the major hepatic metabolite of procainamide, on bovine tracheal smooth muscle, focusing on the possible involvement of K+ channels. N-acetylprocainamide produced a concentration-dependent and full inhibition of the tension development elicited by methacholine (0.3 or 1 microM). The potency of N-acetylprocainamide in diminishing methacholine-elicited tension development was one-half of that of procainamide. By comparison, N-acetylprocainamide inhibited high-K+ (40 mM)-induced contraction more potently than procainamide though both inhibitions were largely reduced when compared to those against methacholine-induced contraction. Iberiotoxin (30 nM), Ba(2+) (1 mM) or a combination of both agents significantly attenuated the relaxant effect of N-acetylprocainamide on methacholine-induced contraction, whereas apamin (100 nM), 4-aminopyridine (300 microM), and glibenclamide (10 microM) did not affect it. These results suggest that N-acetylprocainamide, similar to procainamide, elicits tracheal smooth muscle relaxation mainly through the activation of plasma membrane K+ channels.

Acecainide↗
PubMed2001

Mexiletine inhibits pharmacological actions of salbutamol through blockade of beta2-adrenoceptors in bovine tracheal smooth muscle.

We examined the effects of mexiletine, a class Ib antiarrhythmic drug, on the changes in tension and adenosine 3',5'-cyclic monophosphate (cAMP) content induced by salbutamol and forskolin in bovine tracheal smooth muscle. Salbutamol (0.0001-1 microM) produced concentration-dependent relaxation in bovine tracheal smooth muscle contracted with methacholine (0.3 microM). Mexiletine (5-500 microM) caused the rightward shifts of concentration-response curves for the relaxant responses to salbutamol in a concentration-dependent manner. Mexiletine (5, 50 or 500 microM) did not change basal cAMP levels, whereas it concentration-dependently attenuated the salbutamol (0.1 microM)-induced cAMP accumulation. On the other hand, mexiletine (500 microM) did not change the concentration-response curves for the relaxant responses to forskolin (0.001-10 microM). Mexiletine slightly but significantly (P<0.05) increased forskolin (1 microM)-induced cAMP accumulation. In radioligand binding experiments, mexiletine concentration-dependently displaced the specific binding of [125I]cyanopindolol to beta-adrenoceptors on bovine tracheal smooth muscle membranes. By contrast, lidocaine, another class Ib antiarrhythmic drug, did not change the binding of [125I]cyanopindolol. These results demonstrate that mexiletine prevents the binding of beta2-adrenoceptor agonists to their receptors and thereby suppresses manifestation of subsequent pharmacological responses.

Adrenergic beta-Antagonists↗
PubMed2001

Severe cervical kyphosis in osteopathia striata with cranial sclerosis: case report.

We report a 29-month-old girl with osteopathia striata with cranial sclerosis (OS-CS), who showed several unusual manifestations, including short stature, muscular hypotonia, short lingual frenulum, an accessory ear and a granuloma at the oral edge. The most unusual distressing finding was severe cervical kyphosis with a dysplastic cervical spine. MRI revealed impingement of the upper spinal cord. To clarify the mode of inheritance of this disease in this patient, we performed a methylation-specific PCR analysis. It eventually showed random inactivation of X-chromosomes, suggesting an autosomal dominant trait.

Bone Diseases, Developmental↗
PubMed2001

Epidemiological and clinical studies of West syndrome in Nagasaki Prefecture, Japan.

Recent advances in diagnostic and therapeutic techniques may have changed incidence and etiologies of West syndrome (WS). We performed a retrospective epidemiological study of WS that occurred in 47 children in Nagasaki Prefecture during a recent 10-year period from 1989 to 1998. The incidence of WS was 3.1/10,000 live births. Thirty-nine patients (83%) had symptomatic WS, in which the prenatal causes were most frequent, followed by low-birth weight (LBW) infants, perinatal and postnatal. Such high frequency of LBW may have been due to a relative increase in survivors of premature babies because of recent advances in perinatal care. The brain computerized tomography/magnetic resonance imaging performed in 41 patients revealed congenital brain malformation (10 patients), destructive brain disorders (13 patients), and no structural abnormalities (18 patients). The seizure outcome was worse in the symptomatic WS than in the cryptogenic WS. The developmental outcome was very poor in both symptomatic and cryptogenic WS. The mean developmental quotient (DQ) in all patients was 25, and only four patients (11%) had a normal DQ (>70). DQ was lower in patients with developmental delay before the onset of WS, symptomatic group, relapse and/or persistence of seizure. Developmental delay seen in WS patients seems to be related to the two major factors, that is, underlying brain abnormalities and the persistent seizures as a result of the former. Therefore, every effort should be made to control seizures, including medical and early surgical treatment, as well as prevention of brain damage through perinatal care.

Age Distribution↗
PubMed2001

Reciprocal interactions between human T-lymphotropic virus type 1 and prostaglandins: implications for viral transmission.

Human T-lymphotropic virus type 1 (HTLV-1), the etiologic agent of adult T-cell leukemia/lymphoma, is transmitted through breast milk and seminal fluid, which are rich in prostaglandins (PGs). We demonstrate that PGE(2) upregulates the HTLV-1 long terminal repeat promoter through the protein kinase A pathway, induces replication of HTLV-1 in peripheral blood mononuclear cells (PBMC) derived from asymptomatic carriers, and enhances transmission of HTLV-1 to cord blood mononuclear cells (CBMC). Furthermore, HTLV-1 Tax transactivates a promoter for cyclooxygenase 2, a PG synthetase, and induces PGE(2) expression in PBMC or CBMC. Thus, HTLV-1 interacts with and benefits from PGs, constituents of its own vehicle for transmission.

CCAAT-Enhancer-Binding Protein-beta↗
PubMed2001

[Epidemiological and clinical study of West syndrome in Nagasaki Prefecture, Japan].

To determine the occurrence, outcome, and prognostic factors of West syndrome (WS), we performed a retrospective epidemiological study of WS occurred in 47 children (26 boys and 21 girls) in Nagasaki prefecture during a recent 10-year period from 1989 to 1998. The incidence of WS was 3.1/10,000 live births. The mean age at onset of spasm is 6.3 months (range: 2 to 12 months). Thirty-nine patients (83%) had symptomatic WS, in which the prenatal causes (patients) were most frequent, followed by low-birth weight infants (patients), perinatal (patients) and postnatal (patients). The brain CT was performed in 37 patients, and revealed congenital brain malformations (9 patients), destructive brain disorders (12 patients), and no structural abnormalities (16 patients). The seizure outcome was worse in the symptomatic WS than in the cryptogenic WS; seizure/disappeared in 39% of the former and in 75% of the latter/developmental delay before the onset of WS, relapse of WS and persistence of seizures were associated with poor seizure outcomes. Among the remaining seizures at the time of this surveillance, a tonic seizure was most frequently observed, followed by the partial seizures. Lennox-Gastaut syndrome was observed in 2 patients only. Epileptic discharge in the latest interictal EEG were diffuse in 4.3%, focal or multifocal in 60.7%, and absent in 35%, suggesting that many patients with WS had cortical epileptogenic foci. The developmental outcome was very poor in both the symptomatic and cryptogenic WS. The mean DQ in all the patients was 25, and only 4 patients (11%) had a normal DQ (> 75). DQ was lower in patients with congenital brain malformations than in those with destructive brain disorders.

Brain↗
PubMed2001

[Transitional pre-B-cell ALL].

An 18-month-old girl was referred to our hospital because of fever and pancytopenia. On admission, her bone marrow nuclear cell count was 45,000/microliter, being mostly blasts with cleaved nuclei. The leukemic cells were negative for peroxidase staining, expressed CD10, CD19, CD34 and sIg mu, and did not express sIg kappa and lambda, corresponding to a minor subpopulation of B cells known as transitional pre-B-cells (TPBs). Since TPB-ALL has been reported only infrequently, the incidence and clinical picture of this rare type of ALL are still uncertain. Extensive immunophenotypic studies to determine the expression of sIg mu, sIg kappa and lambda will provide accurate diagnosis, which is essential for effective management of this condition.

Antigens, CD19↗
PubMed2001

[Mumps].

Explore the source record for details and available documents.

Antibodies, Viral↗
PubMed2001

Developmental assessment-based surgical intervention for intractable epilepsies in infants and young children.

PURPOSE: To define the most appropriate time for surgery for medically intractable epilepsies in infants and young children. METHODS: First we examined retrospectively the changes in developmental quotients (DQs) during the clinical course and the clinical factors affecting the DQ in 39 consecutive patients younger than 15 years, who underwent surgical treatment for intractable epilepsy. Second, we examined prospectively five new patients for early detection of developmental arrest or regression by periodic developmental assessments and whether this could lead to early surgical intervention, eventually resulting in minimal developmental defects. RESULTS: Retrospective studies revealed that the DQ progressively decreased with age and that the reduction of DQ was related to continuing frequent seizures in many patients. The prospective studies demonstrated that periodic developmental assessments could detect the reduction of DQ at 5 months or later after onset of frequent seizures in three patients. In two other patients, operations were performed before reduction of DQs, and their postoperative DQ levels were normal. The post-operative recovery of DQ was complete in one patient whose operation was performed 3 months after reduction of DQ, whereas it was incomplete in two others whose operations were carried out at 12 and 14 months after reduction, respectively. Furthermore, three patients with normal developmental outcome had shorter periods between the onset of frequent seizures and the operation (< or = 7 months) than those of two patients with developmental delay (> or = 17 months). CONCLUSIONS: To minimize the developmental defects, periodic developmental assessments should be initiated when frequent seizures have occurred, and surgery should be considered as soon as possible when DQ reduction is recognized.

Child, Preschool↗
PubMed2000

Herpes simplex virus infection induces replication of human immunodeficiency virus type 1.

Genital herpes has been associated with increased efficiency of the sexual transmission and enhanced replication of human immunodeficiency virus type 1 (HIV-1). In this study we demonstrate that exposure to infectious or heat-inactivated herpes simplex virus (HSV) type 1 or 2 virions increases HIV-1 expression in macrophages at least in part by inducing NF-kappaB activity. Neutralizing antibodies to the HSV glycoprotein gB or gD markedly attenuated these virion-mediated effects on HIV-1 expression in macrophages. Thus HSV infection of macrophages that reside in genital mucosal tissue induces HIV-1 replication in these cells. Our study may have implications for the management of patients who are coinfected with the two viruses.

CD4-Positive T-Lymphocytes↗
PubMed2000

In vitro induction of HIV-1 replication in resting CD4(+) T cells derived from individuals with undetectable plasma viremia upon stimulation with human T-cell leukemia virus type I.

Microbial coinfections have been associated with transient bursts of human immunodeficiency virus (HIV) viremia in patients. In this study we investigated whether human T-cell leukemia virus type I (HTLV-I), another human retrovirus that is prevalent among certain HIV-infected populations, can induce HIV-1 replication in patients who had been successfully treated with highly active antiretroviral therapy. We demonstrate that supernatants from HTLV-I-producing MT-2 cells can induce in vitro replication of HIV-1 from highly purified, resting CD4(+) T cells obtained from individuals with undetectable plasma viremia. Depletion of proinflammatory cytokines from the supernatants reduced, but did not abrogate, the ability to induce HIV-1 replication, indicating that other factors such as HTLV-I Tax or Env also have a role. The HTLV-I-mediated effect does not require productive infection: exposure to heat-inactivated HTLV-I virions, purified Tax protein, or HTLV-I Env glycoprotein also induced expression of HIV-1. Furthermore, we demonstrate that coculture of resting CD4(+) T cells with autologous CD8(+) T cells markedly inhibits the HTLV-I-induced virus replication. Our results suggest that coinfection with HTLV-I may induce viral replication in the latent viral reservoirs; however, CD8(+) T cells may play an important role in controlling the spread of virus upon microbial stimulation.

Anti-HIV Agents↗
PubMed2000

Octamer transcription factors up-regulate the expression of CCR5, a coreceptor for HIV-1 entry.

T cell activation can induce expression of CCR5, a major coreceptor for macrophage-tropic (R5) human immunodeficiency virus type 1 (HIV-1). Here we report that overexpression of the Oct-2 transcription factor and octamer coactivator BOB.1/OBF/OCA-B, both of which are induced in T cells following T cell receptor signaling, synergistically up-regulates CCR5 promoter activity via interaction with an octamer motif on the promoter. We also show that the octamer transcription factors can increase cell surface expression of CCR5 and fusogenicity of the cells with R5 HIV-1 Env. These results suggest that octamer transcription factors may play a critical role in the induction of CCR5 expression on, and thereby susceptibility to, R5 HIV-1 of T cells following antigenic stimulation.

Base Sequence↗
PubMed2000

Class I-unrestricted noncytotoxic anti-HTLV-I activity of CD8(+) T cells.

Although it is widely believed that viral clearance is mediated principally by the destruction of infected cells by cytotoxic T cells, noncytolytic antiviral activity of CD8(+) T cells may play a role in preventing the progression to disease in infections with immunodeficiency viruses and hepatitis B virus. We demonstrate here that (1) replication of human T-lymphotropic virus type I (HTLV-I) is more readily detected from CD8(+) T-cell-depleted (CD8(-)) peripheral blood mononuclear cells (PBMCs) of healthy HTLV-I carriers than from unfractionated PBMCs, (2) cocultures of CD8(-) PBMCs with autologous or allogeneic CD8(+) T cells suppressed HTLV-I replication, and (3) CD8(+) T-cell anti-HTLV-I activity is not abrogated in trans-well cultures in which CD8(+) cells are separated from CD8(-) PBMCs by a permeable membrane filter. These results suggest that class I-unrestricted noncytolytic anti-HTLV-I activity is mediated, at least in part by a soluble factor(s), and may play a role in the pathogenesis of HTLV-I infection. (Blood. 2000;96:1994-1995)

Antiviral Agents↗