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Biomedical subjects

J Nishimura

Publications and source records attributed to J Nishimura.

At least 127 records · Page 7Linked to original sources
PubMed1997

Outcome study of bilateral lateral rectus recession for intermittent exotropia in children.

PURPOSE: This paper reports an outcome study of 52 consecutive children treated by bilateral lateral rectus recession for intermittent exotropia over a 9 year period (1981-90) with a minimum follow up of 6 months. METHODS: Successful alignment was defined as the absence of any postoperative intermittent or constant tropia in any position of gaze. The study examined the variables that might be predictive of successful alignment. The charts were abstracted for age at initial surgery, quantity of initial deviation, initial refraction, motor alignment at 1 week and 6 months, final alignment, secondary surgery results and the incidence of a monofixation syndrome result. RESULTS: Motor tests demonstrated that 32 (62%) of the patients were successfully aligned by the initial procedure performed for a mean of 25 prism diopters of preoperative deviation while viewing distant targets at a mean age of 4 years 8 months, followed for a mean of 4 years, 4 months. The incidence of undercorrections and overcorrections were approximately equal in quantity suggesting that the current surgical dosage was adequate, but the age at initial surgery, initial deviation, initial refraction and 1 week postoperative alignment results were not predictive of success. Alignment at 6 months, however, was highly correlated with successful alignment by the end of the study (p = 0.002). Secondary surgery was performed for 11 patients and 5 patients were found to have a monofixation syndrome result. CONCLUSION: Successful alignment was achieved in the majority of children treated for intermittent exotropia by an initial bilateral lateral rectus recession. However, 20% of the patients received secondary surgery for a residual deviation, and the study confirmed a previously reported 10% incidence of monofixation syndrome result in children surgically treated for this type of strabismus.

Child↗
PubMed1996

Expression of rho A and rho kinase mRNAs in porcine vascular smooth muscle.

It has recently been indicated that rho A and rho kinase may be involved in the mechanism for the increase in Ca2+ sensitivity in smooth muscle myofilaments. In the present study, we investigated the mRNA expression of rho A and rho kinase in porcine vascular smooth muscle cells (aorta, coronary artery, pulmonary artery, and pulmonary vein). In reverse transcription-polymerase chain reaction (RT-PCR) experiments, using total RNA from these tissue specimens and the primers designed in the conserved regions of each mRNA in human and bovine, rho A and rho kinase mRNAs were detected in all of these smooth muscle cells. An analysis of these PCR products by direct sequencing indicated that they were derived from each mRNA. The finding that both rho A and rho kinase mRNAs were expressed in the various porcine vascular smooth muscle cells strongly supports the idea that these proteins are involved in the mechanism dealing with the increase in Ca2+ sensitivity in the myofilaments of vascular smooth muscle cells.

Amino Acid Sequence↗
PubMed1996

Expression of calponin mRNA in porcine aortic endothelial cells.

Using reverse transcription polymerase chain reaction (RT-PCR), we determined the expression of the mRNAs for basic calponin isoforms, namely h1 and h2 forms, in the porcine aortic endothelial cells (PAECs) and aortic smooth muscle cells (PASMCs). The mRNAs for both h1 and h2 calponin isoforms were expressed in PAECs as well as in PASMCs. However, the expression of h2 isoform mRNA was more abundant than h1 isoform in PAECs, while h1 isoform was more abundant than h2 in PASMCs. These findings indicated the existence of calponin mRNA and the predominance of h2 over h1 calponin isoform in PAECs. It is suggested that h2 as well as h1, calponin isoform might have a physiological role in vascular endothelial cell. This is the first report which describes the existence of calponin h2-dominant cells.

Animals↗
PubMed1996

P2U purinergic activation leads to the cell cycle progression from the G1 to the S and M phases but not from the G0 to G1 phase in vascular smooth muscle cells in primary culture.

The regulation of the cell cycle by extracellular UTP was investigated in rat aortic smooth muscle cells in primary culture (VSMCs) by means of an immunocytochemical analysis of cell cycle-specific nuclear antigens. UTP induced a rise in the cytosolic Ca2+ concentration ([Ca2+]i) of VSMCs, which was desensitized by pretreatment with ATP, but not with 2-methylthioATP nor alpha, beta-methyleneATP. The incubation of serum-deprived G0 cells with platelet derived growth factor (PDGF) induced cell cycle progression into the G1 phase without any further progression into the S and M phases, while none of the nucleotides had any effect on the cell cycle of the G0 cells. The incubation of the PDGF-pretreated cells at the G1 phase with 2-methylthioATP or alpha, beta-methyleneATP had no effect on the cell cycle of G1 cells, while the incubation of the G1 cells with UTP, ATP, and ATP gamma S stimulated cell cycle progression into the S and M phases. These results thus indicate that P2U purinergic activation mediates a [Ca2+]i transient and a progression growth factor effect of nucleotides in VSMCs.

Adenosine Triphosphate↗
PubMed1996

P2U receptor is linked to cytosolic Ca2+ transient and release of vasorelaxing factor in bovine endothelial cells in situ.

1. With the use of front-surface fluorimetry and fura-2-loaded strips of bovine aortic valve, we characterized the [Ca2+]i transients induced in endothelial cells in situ using a non-selective purinergic agonist (adenosine 5'-triphosphate (ATP)), and selective agonists for P2X (alpha, beta-methylene ATP), P2Y (2-methylthio-ATP (2MeSATP)) and P2U (uridine 5'-triphosphate (UTP)) purinoceptors and an unrelated agonist bradykinin (BK). 2. Double staining with fura-2 and acetylated low-density lipoprotein labelled with 1,1'-dioctadecyl-3,3,3',3'-tetramethyl-indo-carbocyanine perchlorate showed that the fura-2 fluorescence arose exclusively from a single monolayer of endothelial cells covering the surface of the valvular strips. 3. All nucleotides (ATP, UTP and 2MeSATP) induced an elevation of the intracellular Ca2+ concentration ([Ca2+]i), with an initial transient peak and a subsequent lower sustained elevation. Blockade of the Ca2+ influx with 1 mM Ni2+ did not affect the peak levels of the [Ca2+]i transients, whereas it abolished the sustained increases in [Ca2+]i induced by these nucleotides. 4. The potency order of these nucleotides was 2MeSATP > ATP > UTP, while the order of the maximum responses was UTP = ATP > 2MeSATP. alpha, beta-Methylene ATP (up to 1 mM) had only a minimal effect. 5. Prolonged exposure to ATP or UTP, at concentrations giving a maximum response, desensitized the responses to ATP, UTP and 2MeSATP, but not to BK. Prolonged exposure to 2MeSATP at concentrations giving a maximum response did not desensitize the responses to UTP or BK, but did desensitize those to ATP and 2MeSATP. Prolonged exposure to BK did not induce heterologous desensitization to any of the three nucleotides. 6. [Ca2+]i elevation in valvular endothelial cells induced by UTP was associated with the relaxation of adjacent vascular medial strips precontracted with U-46619, the stable analogue of thromboxane A2. 7. We conclude that: (1) the peak elevation of the [Ca2+]i transient induced by these nucleotides is independent of extracellular Ca2+, which therefore suggests the release of intracellular Ca2+ and, (2) mature endothelial cells in situ, in a valvular preparation, have a common receptor for ATP and UTP (nucleotide or P2U receptor), which coexists with the P2Y receptor. Thus we propose that the activation of the nucleotide receptor, P2U, induces [Ca2+]i elevation in endothelial cells in situ, and thus leads to the release of vasorelaxing factors.

Adenosine Triphosphate↗
PubMed1996

Endothelin-1 and angiotensin II act as progression but not competence growth factors in vascular smooth muscle cells.

The direct effects of endothelin-1 and angiotensin II on cell cycle progression were investigated in rat aorta smooth muscle cells in primary culture. The phase of the cell cycle was determined by an immunocytochemical analysis of cell cycle-specific nuclear antigens. The primary cultured cells were synchronized in the G0 phase (100%) by serum deprivation for 24 h. Endothelin-1 (0.1 microM) or angiotensin II (1 microM) had no effect on the cell cycle of G0 cells, whereas platelet-derived growth factor (PDGF) stimulated the entry of the G0 cells into the G1 phase (100%) without a further progression to the S and M phases. Endothelin-1 or angiotensin II stimulated the progression of the PDGF-pretreated G1 cells to the S and M phases. Fura-2 microfluorometry revealed that, between the G0 and G1 cells, there were no differences in the extent and time course of cytosolic Ca2+ elevations induced by endothelin-1 or angiotensin II, which suggested that endothelin-1 and angiotensin II receptors and their signaling pathways regulating cytosolic Ca2+ remained intact in these cell phases. We thus conclude that endothelin-1 and angiotensin II require the prior G0/G1 transition induced by a competence growth factor such as PDGF to exert their mitogenic effects. These results suggest the important role of endothelin-1 and angiotensin II in atherosclerosis as promoters (progression growth factors), but not as initiators.

Angiotensin II↗
PubMed1996

Expression of EVI1 and the Retinoblastoma genes in acute myelogenous leukemia with t(3;13)(q26;q13-14).

The EVI1 DNA-binding protein gene on chromosome 3q26 has been reported to be activated in some leukemia cells with alterations in 3q26. We present an acute myelogenous leukemia (AML) patient with a rare chromosomal translocation, t(3;13)(q26.2;q13-14). By reverse transcription-polymerase chain reaction, we detected active transcription of the EVI1 gene in the patient's leukemia cells. The retinoblastoma susceptibility (Rb) gene, a tumor-suppressor gene, is located at chromosome 13ql4 and is within the other translocation breakpoint in this patient. The expression of the Rb gene product was found to be substantially decreased in the patient's leukemia cells by Western blotting. Southern blot analysis, however, revealed no gross abnormalities of the Rb gene. Although it is unlikely that the Rb gene is directly involved in this translocation, the loss of the Rb gene product combined with the activation of the EVI1 gene may have led to the development of leukemia.

Asian People↗
PubMed1996

Natural killing activities in chronic liver diseases and hepatocellular carcinoma.

Previously we proposed a new analysis of natural killing activity, for comparison, employing an individual effector/target cell ratio according to the peripheral number of effector cells. Using this analysis, we studied natural killing activities in chronic liver diseases and hepatocellular carcinoma (HCC). The activity in chronic persistent hepatitis remained nearly at the level of the nonactivated state, but that was significantly elevated in chronic active hepatitis. The activity in liver cirrhosis (LC) of Child's A or B grade was at the level of a nonactivated or reduced-activity state, while LC patients with impaired general conditions showed significantly elevated activities. In HCC, each of which was accompanied by LC in our cases, the activity appeared to be associated with the progression of HCC. Thus, natural killing activity showed a close relationship with the condition of chronic liver diseases.

Adolescent↗
PubMed1996

Infective endocarditis caused by Campylobacter fetus after allogeneic tooth transplantation: a case report.

A patient developed infective endocarditis caused by Campylobacter fetus. He gave a history of recent dental extraction and allogeneic tooth transplantation. He was treated with various antibodies to which the organism was said to be sensitive, but it was not until the transplanted tooth was removed that he started to improve. The mode of infection was thought to be blood borne through the open tooth socket from the raw chicken that he ate regularly.

Animals↗
PubMed1996

Direct inhibitory effect of chlorpromazine on smooth muscle of the porcine pulmonary artery.

BACKGROUND: Chlorpromazine has been widely used by anesthesiologists to take advantage of its anesthesia-potentiating and vasorelaxing actions. However, the mechanisms of vasorelaxation induced by chlorpromazine are still not fully understood. METHODS: Using front-surface fluorometry of fura-2 and porcine pulmonary arterial strips, we investigated the effects of chlorpromazine on the intracellular Ca2+ concentration ([Ca2+]i) and force of vascular smooth muscle. The affinities of chlorpromazine and other neuroleptics to vascular alpha(1)-adrenergic receptors were then determined by a radio-ligand binding study. RESULTS: Chlorpromazine (as much as 1 microM) inhibited both the elevation of [Ca2+]i and force in pulmonary arterial smooth muscle induced by 80 mM K+-depolarization and 1 microM norepinephrine in a concentration-dependent manner. The extent of inhibition by chlorpromazine in norepinephrine-induced contraction was much greater than that in 80 mM K+-induced contraction. In contrast, as much as 1 microM chlorpromazine had no effect on the increases in [Ca2+]i or force induced by U46619, a thromboxane A2 analogue. Chlorpromazine also had no effect on the intracellular Ca2+ release induced by U46619. In a radio-ligand displacement study, chlorpromazine, haloperidol, phentolamine, trifluoperazine, and imipramine inhibited the specific binding of [3H]prazosin to the porcine aortic membranes, in this order of potency. CONCLUSIONS: Chlorpromazine induces vasorelaxation through an alpha-adrenergic blocking action as well as a calcium antagonistic action; the former action may, therefore, play a major role in chlorpromazine-induced vasorelaxation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

Case report: primary splenic non-Hodgkin's B cell lymphoma in a patient with chronic hepatitis C.

A case of primary splenic lymphoma in a patient with chronic hepatitis C is reported. A 69-year-old man with chronic hepatitis C was admitted to Fukuoka City Hospital for evaluation of an enlarging splenic tumour. In the spleen, ultrasonographic examination revealed a hypoechoic tumour and computed tomography demonstrated a non-enhancing low density area measuring 7 cm in diameter; coeliac angiography revealed a hypovascular tumour. Gallium scintigraphy showed uptake of the radioisotope in the splenic tumour. A splenectomy was performed and the morphological and immunohistochemical findings of this tumour were compatible with those of non-Hodgin's B cell lymphoma. Recently, cases of malignant B cell lymphoma associated with hepatitis C virus infection have been reported. Lymphotropism of hepatitis C virus may play a pathological role in the development of non-Hodgkin's lymphoma. We emphasize the importance of considering lymphoma in the differential diagnosis of extrahepatic disorders during the course of chronic hepatitis C virus infections.

Aged↗
PubMed1996

The mechanism of relaxation induced by atrial natriuretic peptide in the porcine renal artery.

1. The mechanisms underlying the relaxation of the porcine renal artery induced by atrial natriuretic peptide (ANP) were investigated, using front-surface fluorimetry with fura-2 and receptor-coupled permeabilization by alpha-toxin. 2. ANP decreased the cytosolic Ca2+ concentration ([Ca2+]i) and tension during the contraction induced by a high external K+ solution, in a concentration-dependent manner. This ANP-induced decrease in [Ca2+]i during the contraction induced by high K+ solution was composed of two phases, an initial rapid phase, followed by a maintenance phase. The initial rapid decrease in [Ca2+]i, but not the maintained decrease in [Ca2+]i, was inhibited when the tissue was treated with thapsigargin, a selective Ca2+ pump inhibitor of the sarcoplasmic reticulum. When the tissues were treated with thapsigargin and external Ca2+ was replaced by Ba2+, which cannot be transported by the Ca2+ pump, ANP did not induce a decrease in [Ba2+]i, even though the elevation of tension induced by Ba2+ was strongly inhibited. 3. In the absence of extracellular Ca2+, ANP inhibited the release of Ca2+ from the intracellular store induced by noradrenaline (NA). 4. The [Ca2+]i (abscissa scale)-tension (ordinate scale) relationship observed during the contraction induced by various concentrations of high external K+ solution was shifted downwards by the addition of 10(-8) M ANP, indicating that, at any given [Ca2+]i, the tension generated by high K+ solution was considerably inhibited by the addition of 10(-8) M ANP. The [Ca2+]i-tension curve of the contraction obtained by the cumulative application of external Ca2+ (0-3.75 mM) during depolarization with 118 mM K+ solution was shifted to the left by 3 x 10(-7) M NA. This NA-induced [Ca2+]i-tension relationship was shifted to the right by 10(-8) M ANP, indicating that the ANP-induced reduction of Ca(2+)-sensitivity operates during the contraction induced by NA. 5. In alpha-toxin-permeabilized preparations, ANP induced relaxation of tissues precontracted with a mixture of 3 x 10(-7) M Ca2+, 10(-5) M guanosine 5'-triphosphate (GTP) and 10(-6) M NA. Thus a component of ANP-induced relaxation took place by way of a reduction in the Ca2+ sensitivity of the myofilaments, independent of changes in [Ca2+]i. 6. These results indicate that ANP induces relaxation of the porcine renal artery by: (1) reducing [Ca2+]i mainly via the activation of the Ca2+ pumps located on the sarcoplasmic reticulum and sarcolemma, as well as via inhibition of agoinist-induced release of Ca2+ from the intracellular store; and (2) decreasing the Ca(2+)-sensitivity of the contractile elements.

Animals↗
PubMed1996

Dual regulation of cerebrovascular tone by UTP: P2U receptor-mediated contraction and endothelium-dependent relaxation.

1. The mechanisms of vascular tone regulation by extracellular uridine 5'-triphosphate (UTP) were investigated in bovine middle cerebral arterial strips. Changes in cytosolic Ca2+ concentration ([Ca2+]i) and force were simultaneously monitored by use of front-surface fluorometry of fura-2. 2. In the arterial strips without endothelium, UTP (0.1 microM-1 mM) induced contraction in a concentration-dependent manner. However, when the endothelium was kept intact, cumulative application of UTP (0.1-100 microM) (and only at 1 mM) induced a modest phasic contraction in arterial strips. This endothelium-dependent reduction of the UTP-induced contraction was abolished by 100 microM N omega-nitro-L-arginine (L-NOARG) but not by 10 microM indomethacin. In the presence of intact endothelium, UTP (30 microM) induced a transient relaxation of the strips precontracted with 30 nM U-46619 (a stable analogue of thromboxane A2), which was completely inhibited by pretreatment with L-NOARG but not with indomethacin. 3. In the endothelium-denuded strips, the contractile response to UTP was abolished by desensitization to either ATP gamma S or ATP (P2U receptor agonists), but not by desensitization to alpha, beta-methylene-ATP (P2x receptor agonist) or to 2-methylthio-ATP (P2Y receptor agonist). Desensitization to UTP abolished the contractile response to ATP. 4. In the endothelium-denuded artery, a single dose application of UTP induced an initial transient, and subsequently lower but sustained increase in [Ca2+]i and force. In the absence of extracellular Ca2+, UTP induced only the initial transient increases in [Ca2+]i and force, while the sustained increases in [Ca2+]i and force were abolished. UTP (1 mM) had no effect on the basic [Ca2+]i-force relationship obtained on cumulative application of extracellular Ca2+ at steady state of 118 mM K(+)-depolarization-induced contraction. 5. We conclude that in the presence of an intact endothelium, UTP-induced relaxation of preconstricted middle cerebral artery is mainly mediated indirectly, by the production of an endothelium-derived relaxing factor, but at high doses of UTP, vascular smooth muscle contraction is mediated directly via activation of P2U purinoceptor and [Ca2+]i elevation without Ca(2+)-sensitization of the contractile apparatus. UTP may thus exert a dual regulatory effect upon cerebrovascular tone, but in cases where the endothelium is impaired, it may also act as a significant vasoconstrictor.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

CPA induces a sustained increase in [Ca2+]i of endothelial cells in situ and relaxes porcine coronary artery.

Using fura 2 fluorometry, we investigated the effect of cyclopiazonic acid (CPA), an inhibitor of Ca2+ pump adenosinetriphosphatase of the endoplasmic reticulum, on cystosolic Ca2+ concentration ([Ca2+]i) and tension in porcine aortic valvular endothelial cells and coronary arterial strips with endothelium. In normal physiological salt solution, CPA induced a sustained increase in [Ca2+]i in the valvular strips, whereas in Ca(2+)-free physiological salt solution, CPA elicited a transient elevation of [Ca2+]i. CPA(30 microM) relaxed coronary strips with endothelium precontracted by 100 nM U-46619; this relaxation was partially inhibited by N omega-nitro-L-arginine (100 microM). These results indicate that the CPA-induced increase in [Ca2+]i depends on the Ca2+ release and the Ca2+ influx in the endothelial cells in situ and that the CPA-induced endothelium-dependent decreases in [Ca2+]i and tension in the smooth muscle are due to the combined effect of N omega-nitro-L-arginine-sensitive and -resistant factors.

Animals↗
PubMed1996

Acute leukemias expressing p210-and p 190-type bcr/abl mRNAs: report of two cases and review of the literature.

We report two patients with acute leukemias who expressed two types of bcr/abl mRNA. The first case was an 8-year-old boy with acute mixed leukemia in whom the Ph1 chromosome and p210/p190 types of bcr/abl mRNAs were detected at diagnosis. The second case was a 39-year-old male with acute nonlymphocytic leukemia transformed from myelodysplastic syndrome (refractory anemia with excess of blasts). In the latter case, the p210-type mRNA appeared after leukemic transformation, and the p190-type transcript was detected only during the late stage when the Ph1 chromosome was first observed. The leukemias in these two patients were aggressive in their clinical courses. We conclude that the dual expression of p210 and p190 types of bcr/abl is a factor indicating a poor prognosis, and that, in some patients, p190-type bcr/abl may contribute to disease progression.

Acute Disease↗
PubMed1996

High prevalence of T cell receptor D delta 2(D delta)J delta rearrangement in CD7-positive early T cell acute lymphoblastic leukemia.

We have studied the molecular characteristics of the T cell receptor (TcR) genes in 16 patients with CD7+ early T cell acute lymphoblastic leukemia (T-ALL), defined as being positive for CD7 but negative for CD3/4/8, myeloperoxidase (MPO), and CD19/20. Using gene analysis, rearrangement was demonstrated in one patient for immunoglobulin heavy chain (IgH) gene, five for TcR-beta gene, and four for TcR-gamma gene. Fifteen patients (94%) had rearranged band(s) involving the joining region of the TcR-delta chain gene. In nine cases these were the only rearrangements, whereas in six cases TcR-beta and/or TcR-gamma gene rearrangements were found as well. The D delta 2(D delta)J delta 1 rearrangement was demonstrated in 87.5% (14/16) of cases. D delta 2(D delta)J delta 3 was recognized in one patient, D delta 2D delta 3 was found in three, and V(D)DJ using only V delta 2 and V delta 3 was recognized in two patients. We found no V2D delta 3, V3D delta 3, or V1(D)DJ delta rearrangement patterns. Five of nine cases with DDJ delta were positive for cytoplasmic CD3 epsilon(CyCD3 epsilon). Our data suggest that DDJ delta joining occurs at an early stage during T cell differentiation, followed by rearrangements of V delta to the DDJ delta complex. Furthermore, our findings suggest that DDJ delta recombination occurs earlier than expression of CyCD3 epsilon protein products. DDJ delta rearrangements have never been observed in non-T cell malignancies, such as precursor-B-ALL or acute myeloid leukemia. Therefore, detection of DDJ delta rearrangement in the TcR-delta locus is a useful tool to establish lineage and clonality of leukemic cells in the most immature stages of T cell development.

Antigens, CD↗