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J Horiguchi

Publications and source records attributed to J Horiguchi.

At least 109 records · Page 6Linked to original sources
PubMed1990

[Sleep-wake complaints in Parkinson's disease].

We analyzed the questionnaires concerning sleep-wake complaints in 1,575 Parkinsonian patients and 2,509 controls of 945 office workers and 1564 seniors living at home. The questionnaire included 20 contents. The Parkinsonian patients complained of sleep-wake disturbances more frequently than the controls in initiation disturbance, frequent awakenings in night, early morning awakening, day time sleepiness, usage of sleep pills, parasomnias, restless legs symptoms, nocturnal myoclonus, snoring, apnea episodes and dyspnea in night (chi-square method). The incidences of restless legs symptoms and nocturnal myoclonus increased significantly with worsening of physical symptoms in the Parkinsonian patients (p less than 0.01).

Aged↗
PubMed1989

Successful treatment with clonazepam for neuroleptic-induced akathisia.

Twenty-one patients with severe neuroleptic-induced akathisia resistant to antiparkinsonian medications were treated with oral clonazepam in an open trial. All the patients reported subjective improvement. We suggest that clonazepam is effective in managing neuroleptic-induced akathisia.

Adolescent↗
PubMed1989

Effect of clonazepam on neuroleptic-induced oculogyric crisis.

Fourteen patients with neuroleptic-induced oculogyric crisis resistant to antiparkinsonian drugs were treated with oral clonazepam. The neuroleptic-induced oculogyric crisis was completely inhibited by clonazepam in 10 patients, moderately inhibited in 2, slightly inhibited in 1, and not changed in 1. We suggest that clonazepam is useful in managing neuroleptic-induced oculogyric crisis.

Adult↗
PubMed1989

Role of arachidonic acid metabolism in transcriptional induction of tumor necrosis factor gene expression by phorbol ester.

The treatment of human HL-60 promyelocytic leukemia cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with induction of tumor necrosis factor (TNF) transcript. The study reported here has examined TPA-induced signaling mechanisms responsible for the regulation of TNF gene expression in these cells. Run-on assays demonstrated that TPA increases TNF mRNA levels by transcriptional activation of this gene. The induction of TNF transcripts by TPA was inhibited by the isoquinolinesulfonamide derivative H7 but not by HA1004, suggesting that this effect of TPA is mediated by activation of protein kinase C. TPA treatment also resulted in increased arachidonic acid release. Moreover, inhibitors of phospholipase A2 blocked both the increase in arachidonic acid release and the induction of TNF transcripts. These findings suggest that TPA induces TNF gene expression through the formation of arachidonic acid metabolites. Although indomethacin had no detectable effect on this induction of TNF transcripts, ketoconazole, an inhibitor of 5-lipoxygenase, blocked TPA-induced increases in TNF mRNA levels. Moreover, TNF mRNA levels were increased by the 5-lipoxygenase metabolite leukotriene B4. In contrast, the cyclooxygenase metabolite prostaglandin E2 inhibited the induction of TNF transcripts by TPA. Taken together, these results suggest that TPA induces TNF gene expression through the arachidonic acid cascade and that the level of TNF transcripts is regulated by metabolites of the pathway, leukotriene B4 and prostaglandin E2.

Arachidonic Acid↗
PubMed1989

Posttranscriptional stabilization of c-fms mRNA by a labile protein during human monocytic differentiation.

The c-fms proto-oncogene encodes a transmembrane glycoprotein that is closely related or identical to the receptor for the monocyte colony-stimulating factor CSF-1. The present studies examined the mechanisms responsible for the regulation of c-fms gene expression during human monocytic differentiation. Levels of c-fms mRNA were undetectable in HL-60 promyelocytic leukemia cells, while 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced monocytic differentiation of these cells was associated with the appearance of these transcripts. Run-on transcription assays demonstrated that the c-fms gene was transcriptionally active in uninduced HL-60 cells and that the rate of transcription was unchanged after TPA treatment. These findings suggested that c-fms mRNA levels in HL-60 cells are controlled by posttranscriptional mechanisms. The half-life of c-fms transcripts in TPA-induced HL-60 cells was found to be at least 6 h, while inhibition of protein synthesis with cycloheximide (CHX) decreased this half-life to 4 h. Moreover, inhibition of protein synthesis was associated with decreases in c-fms mRNA levels and a block in the induction of c-fms transcripts by TPA. These findings indicated that the c-fms transcript is stabilized by a labile protein. In contrast to HL-60 cells, c-fms mRNA is constitutively expressed in resting human monocytes and is down-regulated by treatment of these cells with TPA. Run-on assays demonstrated that TPA-induced downregulation of c-fms mRNA levels in monocytes occurred at the posttranscriptional level. Moreover, the results demonstrate that levels of c-fms mRNA are regulated posttranscriptionally by a labile protein. In this regard, the half-life of the c-fms transcript was 6.1 h in monocytes, while treatment of these cells with CHX decreased the half-life to 30 min. Furthermore, this effect of CHX occurred in the absence of changes in the rate of c-fms gene transcription. Together, these findings indicate that c-fms gene expression is regulated at a posttranscriptional level both in HL-60 cells induced to differentiate along the monocytic lineage and in human monocytes. The findings also indicate that levels of c-fms mRNA are regulated by the synthesis of a labile protein which is involved in stabilization of the c-fms transcript.

Cell Differentiation↗
PubMed1989

[Intellectual impairments in patients with Parkinson's disease--a proposal of the subgroups of the disease].

The severity of intellectual impairments of the 89 patients with Parkinson's disease was evaluated with Osaka Intelligence Scale for the Aged (OISA). They were divided into three groups; normal, slightly impaired, and demented using three discriminative functions of OISA. Their motor disabilities were rated on the Hoehn and Yahr's functional classification scale. EEG, psychotic symptoms such as visual hallucination and "leibhaftige Bewusstheit (K. Jaspers)", medications and prognosis for life were also examined. There was no significant correlation between the duration of the illness and the degree of their intellectual impairments. There were two specific subgroups among our samples; a group of patients who were demented rapidly after their onsets of parkinsonism, and a group of patients whose intelligence was preserved for a long period. The age of onset of the former group was older than the latter. The duration from the onset to death in the former was shorter than the latter. The former group of the patients exhibited psychotic symptoms and EEG abnormalities more frequently. The severity of motor disability and medication did not differ between two groups.

Adult↗
PubMed1988

CSF-1 and C-FMS gene expression in human carcinoma cell lines.

The macrophage-specific colony stimulating factor CSF-1 is required for the growth and differentiation of monocytes. The cell surface receptor for CSF-1 is identical to the product of the c-fms proto-oncogene. The present studies have monitored CSF-1 and c-fms expression in human carcinoma cell lines. Two of three human ovarian carcinoma cell-lines expressed multiple species of CSF-1 mRNA. Furthermore, detection of CSF-1 transcripts was associated with secretion of CSF-1 protein that was increased after phorbol ester treatment. CSF-1 mRNA was also detectable in 4 breast and 2 lung carcinoma cell lines. In contrast, c-fms expression was found only in SK-Br-3 breast carcinoma cells. Similar studies in 2 human choriocarcinoma cell lines demonstrated the presence of c-fms, but not CSF-1, transcripts. While phorbol ester treatment was associated with increased c-fms mRNA levels in choriocarcinoma cells, this agent had no effect on CSF-1 expression. These findings indicate that: 1) CSF-1 expression is frequent in human ovarian, breast and lung carcinoma cells; and 2) coexpression of the CSF-1 and c-fms genes, as found in monocytes is infrequent in malignant epithelial and choriocarcinoma cell lines.

Blotting, Northern↗
PubMed1988

Transcriptional and posttranscriptional regulation of CSF-1 gene expression in human monocytes.

Regulation of CSF-1 gene expression was investigated in human monocytes. CSF-1 transcripts were at low or undetectable levels in resting monocytes. However, in monocytes treated with 12-O-tetradecanoylphorbol-13-acetate (TPA), CSF-1 mRNA was increased by 3 h and reached maximal levels by 12 h of drug exposure. When nuclear run-on assays were used, CSF-1 gene transcription was also at low or undetectable levels in resting monocytes but was activated after TPA exposure. TPA-treated monocytes exposed to actinomycin D further demonstrated that the half-life of the CSF-1 mRNA is 0.9 h. The results also demonstrated that the protein synthesis inhibitor, cycloheximide (CHX), increases CSF-1 mRNA levels in both resting and TPA-treated monocytes. These effects of CHX occurred in the absence of detectable increases in CSF-1 gene transcription. Moreover, treatment of monocytes with CHX and actinomycin D demonstrated that inhibition of protein synthesis is associated with stabilization of the CSF-1 transcript. Taken together, these findings indicated that CSF-1 gene expression is controlled at both transcriptional and posttranscriptional levels in human monocytes.

Colony-Stimulating Factors↗
PubMed1988

Expression of the macrophage colony-stimulating factor and c-fms genes in human acute myeloblastic leukemia cells.

Macrophage colony-stimulating factor (CSF-1; M-CSF) is a growth factor required for growth and differentiation of mononuclear phagocytes. The effects of CSF-1 are mediated through binding to specific, high-affinity surface receptors encoded by the c-fms gene. CSF-1 and c-fms gene expression was investigated in fresh human acute myeloblastic leukemic cells by Northern blot hybridization using cDNA probes. 4.0-kb CSF-1 transcripts were detected in 10 of 17 cases of acute myeloblastic leukemia (AML), while c-fms transcripts were detected in 7 of 15. Coexpression of CSF-1 and c-fms was observed in five cases, and in five other cases neither gene was expressed. In situ hybridization demonstrated that transcripts for CSF-1 were present in 70-90% of cells in each of three cases studied while c-fms mRNA was detected in 40-70% of cells. The constitutive expression of CSF-1 transcripts was associated with production of CSF-1 protein, although detectable amounts of CSF-1 were not secreted unless the cells were exposed to phorbol ester. These results demonstrate that leukemic myeloblasts from a subset of patients with AML express transcripts for both the CSF-1 and CSF-1 receptor genes, often in the same leukemic cells in vitro.

Colony-Stimulating Factors↗
PubMed1987

Induction of tumor necrosis factor expression and resistance in a human breast tumor cell line.

Tumor necrosis factor (TNF) is a polypeptide cytokine that is cytotoxic to some but not all tumor cells. The basis for resistance to the cytotoxic effects of this agent remains unclear. We have studied the development of TNF resistance in human ZR-75-1 breast carcinoma cells. ZR-75-1 cells have undetectable levels of TNF RNA and protein. However, TNF transcripts are transiently induced in these cells by exposure to recombinant human TNF. This induction of TNF RNA is associated with production of TNF-like protein in cell lysates and culture supernatants. Stable resistance to TNF-induced cytotoxicity develops when ZR-75-1 cells are exposed to increased concentrations of TNF. The TNF-resistant cells, designated ZR-75-1R, continuously express TNF transcripts and a TNF-like protein. Furthermore, ZR-75-1R cell supernatants contain cytotoxic activity that is abrogated by polyclonal antibody against TNF. The ZR-75-1R cells also possess TNF receptors that are occupied or down-regulated by the TNF-like protein. These findings thus suggest that (i) TNF induces TNF transcripts and production of a TNF-like protein in ZR-75-1 cells and (ii) resistance to TNF-induced cytotoxicity is associated with stable TNF expression.

Breast Neoplasms↗
PubMed1987

Detection of c-fms and CSF-1 RNA by in situ hybridization.

Recent studies have demonstrated by Northern blot analysis that both the c-fms proto-oncogene and the CSF-1 gene are expressed during human monocytic differentiation. In order to examine c-fms and CSF-1 expression at the cellular level, we have applied alkaline phosphatase detection of biotinylated v-fms and CSF-1 cDNA probes in situ. Using this approach, we demonstrate that c-fms and CSF-1 transcripts are detectable in HL 60 cells induced along the monocytic lineage but not in uninduced cells. The specific detection of these transcripts is further supported by the absence of histochemical staining in RNase-treated cells and when using pBR322 plasmid without insert as the biotinylated probe. Finally, the results indicate that most of the induced HL-60 cells have detectable levels of both c-fms and CSF-1 RNA. This approach should be useful for studying expression of these genes in populations of leukemic blasts and normal hematopoietic cells.

Cell Differentiation↗
PubMed1987

Expression of the macrophage-specific colony-stimulating factor in human monocytes treated with granulocyte-macrophage colony-stimulating factor.

The macrophage-specific colony-stimulating factor (CSF-1, M-CSF) regulates the survival, growth and differentiation of monocytes. We have recently demonstrated that phorbol ester induces expression of CSF-1 in human monocytes. These findings suggested that activated monocytes are capable of producing their own lineage-specific CSF. The present studies demonstrate that the granulocyte-macrophage colony-stimulating factor (GM-CSF) also induces CSF-1 transcripts in monocytes. Furthermore, we demonstrate that the detection of CSF-1 RNA in GM-CSF-treated monocytes is associated with synthesis of the CSF-1 gene product. The results thus suggest that GM-CSF may indirectly control specific monocyte functions through the regulation of CSF-1 production. These findings indicate another level of interaction between T cells and monocytes.

Colony-Stimulating Factors↗
PubMed1986

Expression of the macrophage specific colony-stimulating factor (CSF-1) during human monocytic differentiation.

We and others have previously demonstrated expression of the co-fms proto-oncogene during human monocytic differentiation. The c-fms gene has since been shown to encode for the macrophage specific colony stimulating factor (CSF-1) receptor. The present results demonstrate that both CSF-1 and c-fms transcripts are induced during monocytic differentiation of human HL-60 leukemia cells. The results further demonstrate that normal human monocytes express CSF-1 RNA and that the level of these transcripts increases upon treatment with phorbol ester. Finally, the detection of CSF-1 RNA in HL-60 cells and in monocytes is associated with production of the CSF-1 gene product. These findings would suggest that monocytes are capable of regulating their own survival, growth and differentiation through CSF-1 production.

Cell Differentiation↗
PubMedDate not supplied

Reversible pitch perception deficit caused by carbamazepine.

Carbamazepine (CBZ) is an antiepileptic drug frequently used to treat a variety of neurologic diseases or symptoms. In addition, the drug is used as a mood stabilizer in patients with affective or schizophrenic disorders. Among its adverse effects, auditory disturbance is described rarely. In this report, we describe a 25-year-old woman who noted falsely higher pitch perception after starting CBZ treatment for schizoaffective disorder. We also review the literature reporting CBZ-associated abnormal pitch perception.

Adult↗
PubMedDate not supplied

Immunohistochemical study on the expression of c-erbB-2 oncoprotein in breast cancer.

Expression of the c-erbB-2 oncogene protein was investigated by immunohistochemistry in 110 paraffin-embedded blocks of primary breast cancer. 25 (22.7%) of 110 tumors were stained positively with c-erbB-2 protein antibody. There was no correlation between c-erbB-2 immunostaining and age at diagnosis, menopausal status, hormone receptor status, tumor size, or clinical stage. The tumors with an extensive intraductal component showed a higher incidence of the c-erbB-2 expression than those without. A significantly shorter overall survival was obtained in patients with the expression of c-erbB-2 protein than in patients without. Staining of c-erbB-2 protein is an effective prognostic indicator in patients with breast cancer.

Age Factors↗
PubMedDate not supplied

Immunohistochemical fibronectin staining pattern and prognosis in invasive breast carcinoma.

Fibronectin (FN) in 99 female patients with invasive breast carcinomas (IBCs) was studied by immunohistochemistry using a monoclonal antibody to human plasma FN. Sixty-five (65.7%) of 99 IBCs were FN-positive and 34 (34.3%) were FN-negative. The FN staining pattern was not correlated with patient characteristics, such as age, tumor size, nodal involvement and estrogen receptor status. Relapse-free survival (RFS) of patients with FN-positive tumors was significantly better than that of patients with FN-negative tumors. A multivariate analysis using the Cox proportional hazards model showed that the FN staining pattern was independently correlated with RFS as well as nodal status. The results show that FN staining pattern may be an independent prognostic factor in IBCs. It is suggested that patients with FN-negative tumors should be carefully followed up, even if axillary nodal invasion is absent.

Adenocarcinoma, Mucinous↗
PubMedDate not supplied

Expression of pS2 estrogen-inducible protein in primary breast cancer.

The expression of pS2 estrogen-inducible protein was investigated using formalin-fixed, paraffin-embedded sections from 210 primary breast cancers. One hundred and three (49%) out of 210 cases were positive for pS2. A significant correlation existed between pS2 expression and hormone receptor status. Patients with pS2 expression had better overall survival and a longer survival time after the first recurrence than those without pS2 expression. By multivariate analysis, pS2 was not an independent prognostic indicator, but pS2 expression was a possible indicator for responsiveness to treatment in relapsed breast cancer patients.

Adult↗