Criminal offenses among discharged mentally ill individuals. Determinants of the duration from discharge and absence of diagnostic specificity.
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Adult↗
Biomedical subjects
T Inada
Publications and source records attributed to T Inada.
Expression and distribution of brain natriuretic peptide in human right atria.
OBJECTIVES: We investigated expression of brain natriuretic peptide (BNP) as well as atrial natriuretic peptide (ANP) and their genes in human right atria. Their relations with atrial pressure were also examined. BACKGROUND: The BNP plays a roll in electrolyte-fluid homeostasis such as ANP. The tissue level is reported to be elevated in the failing ventricles. However, expression and transmural distribution of BNP in the atria remain unclear. METHODS: Expression of ANP and BNP was immunohistochemically investigated in the right atrial (RA) specimens from 21 patients who had undergone cardiac surgery. The mRNA of specimens were quantitatively measured by Northern blot analysis and also evaluated by in situ hybridization. In addition, plasma levels of ANP and BNP were measured in the patients. RESULTS: The BNP immunoreactivity was diffusely seen in RA tissue of patients with mean RA pressure (mRAP) of 5 mm Hg or more, but it was noted only in the subendocardial half of the atria of those with mRAP less than 5 mm Hg. There was a significant correlation between the incidence of BNP-positive myocytes and mRAP (r = 0.850, p < 0.0001). Conversely, ANP-positive myocytes were found diffusely in all cases. In Northern blot analysis, the mRNAs levels of ANP and BNP in the atrial tissue were positively correlated with the mRAP (ANP, p = 0.775, p < 0.005 and BNP, p = 0.771, p < 0.005). In situ hybridization confirmed these findings. The mRNA levels were significantly correlated to each other (r = 0.845, p < 0.0002). Plasma ANP and BNP levels were elevated in the patients compared with that in controls; however, none were significantly correlated with the mRAP. CONCLUSIONS: Expression of BNP and BNP mRNA is augmented in the atria with increased pressure, and distributed predominantly in the subendocardial side. The level of BNP mRNA was well correlated with that of ANP mRNA. Thus, these two genes might be commonly regulated in response to atrial pressure.
Aged↗
Genetic uncoupling of the dsRNA-binding and RNA cleavage activities of the Escherichia coli endoribonuclease RNase III--the effect of dsRNA binding on gene expression.
RNase III, a double-stranded RNA-specific endonuclease, is proposed to be one of Escherichia coli's global regulators because of its ability to affect the expression of a large number of unrelated genes by influencing post-transcriptional control of mRNA stability or mRNA translational efficiency. Here, we describe the phenotypes of bacteria carrying point mutations in rnc, the gene encoding RNase III. The substrate recognition and RNA-processing properties of mutant proteins were analysed in vivo by measuring expression from known RNase III-modulated genes and in vitro from the proteins' binding and cleavage activities on known double-stranded RNA substrates. Our results show that although the point mutation rnc70 exhibited all the usual rnc null-like phenotypes, unlike other mutations, it was dominant over the wild-type allele. Multicopy expression of rnc70 could suppress a lethal phenotype of the wild-type rnc allele in a certain genetic background; it could also inhibit the RNase III-mediated activation of lambdaN gene translation by competing for the RNA-binding site of the wild-type endonuclease. The mutant protein failed to cleave the standard RNase III substrates in vitro but exhibited an affinity for double-stranded RNA when passed through poly(rI):poly(rC) columns. Filter binding and gel-shift assays with purified Rnc70 showed that the mutant protein binds to known RNase III mRNA substrates in a site-specific manner. In vitro processing reactions with purified enzyme and labelled RNA showed that the in vivo dominant effect of the mutant enzyme over the wild-type was not necessarily caused by formation of mixed dimers. Thus, the rnc70 mutation generates a mutant RNase III with impaired endonucleolytic activity but without blocking its ability to recognize and bind double-stranded RNA substrates.
Alleles↗
Inducer exclusion by glucose 6-phosphate in Escherichia coli.
The main mechanism causing catabolite repression by glucose and other carbon sources transported by the phosphotransferase system (PTS) in Escherichia coli involves dephosphorylation of enzyme IIA(Glc) as a result of transport and phosphorylation of PTS carbohydrates. Dephosphorylation of enzyme IIA(Glc) leads to 'inducer exclusion': inhibition of transport of a number of non-PTS carbon sources (e.g. lactose, glycerol), and reduced adenylate cyclase activity. In this paper, we show that the non-PTS carbon source glucose 6-phosphate can also cause inducer exclusion. Glucose 6-phosphate was shown to cause inhibition of transport of lactose and the non-metabolizable lactose analogue methyl-beta-D-thiogalactoside (TMG). Inhibition was absent in mutants that lacked enzyme IIA(Glc) or were insensitive to inducer exclusion because enzyme IIA(Glc) could not bind to the lactose carrier. Furthermore, we showed that glucose 6-phosphate caused dephosphorylation of enzyme IIA(Glc). In a mutant insensitive to enzyme IIA(Glc)-mediated inducer exclusion, catabolite repression by glucose 6-phosphate in lactose-induced cells was much weaker than that in the wild-type strain, showing that inducer exclusion is the most important mechanism contributing to catabolite repression in lactose-induced cells. We discuss an expanded model of enzyme IIA(Glc)-mediated catabolite repression which embodies repression by non-PTS carbon sources.
Biological Transport↗
A global repressor (Mlc) is involved in glucose induction of the ptsG gene encoding major glucose transporter in Escherichia coli.
Glucose stimulates the expression of ptsG encoding the major glucose transporter in Escherichia coli. We isolated Tn 10 insertion mutations that confer constitutive expression of ptsG. The mutated gene was identified as mlc, encoding a protein that is known to be a repressor for transcription of several genes involved in carbohydrate utilization. Expression of ptsG was eliminated in a mlc crp double-negative mutant. The Mlc protein was overproduced and purified. In vitro transcription studies demonstrated that transcription of ptsG is stimulated by CRP-cAMP and repressed by Mlc. The action of Mlc is dominant over that of CRP-cAMP. DNase I footprinting experiments revealed that CRP-cAMP binds at two sites centred at -40.5 and -95.5 and that Mlc binds at two regions centred around -8 and -175. The binding of CRP-cAMP stimulated the binding of RNA polymerase to the promoter while Mlc inhibited the binding of RNA polymerase but not the binding of CRP-cAMP. Gel-mobility shift assay indicated that glucose does not affect the Mlc binding to the ptsG promoter. Our results suggest that Mlc is responsible for the repression of ptsG transcription and that glucose modulates the Mlc activity by unknown mechanism.
Bacterial Proteins↗
Phase II study of 5-fluorouracil, pirarubicin and low-dose consecutive administration of cisplatin for advanced and recurrent gastric cancer.
BACKGROUND: The FAP regimen was modified and low-dose consecutive daily administration of cisplatin (CDDP) and continuous infusion of 5-fluorouracil (5-FU) and pirarubicin were employed to reduce the toxicity and achieve synergy. Patients with advanced and recurrent gastric cancer were treated with this regimen as early phase II trial and its efficacy and toxicity were assessed. METHODS: Twenty-nine patients with advanced or recurrent gastric cancer were treated with intravenous 5-FU, 360 mg/m2, continuous infusion, on days 1-5 and 8-12, CDDP, 10 mg/body, drip infusion, on days 1-5 and 8-12 and pirarubicin, 20 mg/body, on days 1 and 8, which was repeated every 4 weeks. RESULTS: One complete (CR) and 10 partial (PR) responses were observed. Eleven patients showed no change (NC) and seven had progressive disease (PD). The overall response rate (CR and PR) was 37.9%. The response rates of lymph node metastatic lesions and primary gastric lesions were 47 and 44%, respectively. The major toxicity was bone marrow suppression, which was well tolerated. Grade 3/4 nausea/vomiting did not occur. The median survival of all patients was 30 weeks, that of those who responded was 48 weeks and that of those showing NC or PD was 24 weeks. CONCLUSIONS: This modified FAP regimen was considered useful with a moderate response and less severe toxicity, but further investigation is necessary.
Adult↗
Propofol inhibits ketamine-induced c-fos expression in the rat posterior cingulate cortex.
UNLABELLED: Ketamine, a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, has psychotomimetic activity. NMDA receptor antagonists cause morphological damage in the posterior cingulate cortex, which may be the brain region responsible for their psychotomimetic effects. Benzodiazepines are effective in preventing these effects through gamma-aminobutyric acid A (GABA(A)) receptor activation. We investigated the effect of propofol, which has both GABAA receptor-activating and NMDA receptor-suppressing activity, on ketamine-induced c-fos expression in the rat posterior cingulate cortex. Propofol or vehicle was continuously infused IV. Fifteen minutes later, 100 mg/kg ketamine or isotonic sodium chloride solution was injected intraperitoneally. Two hours later, brain sections were prepared, and c-fos expression was detected using immunohistochemical methods. Propofol significantly inhibited ketamine-induced c-fos expression in the posterior cingulate cortex. Propofol itself did not induce c-fos expression in this brain region. We conclude that propofol may be able to inhibit ketamine-induced psychotomimetic activity and neuronal damage. IMPLICATIONS: In the present study, we demonstrated that the clinically relevant dose of propofol significantly inhibited ketamine-induced c-fos expression in the rat posterior cingulate cortex. This finding implies that propofol may inhibit ketamine-induced psychotomimetic activity and neuronal damage.
Anesthetics, Dissociative↗
The tracheal tube with a high-volume, low-pressure cuff at various airway inflation pressures.
When the tracheal tube with a high-volume, low-pressure cuff is used, the pressure exerted by the cuff on the tracheal wall is similar to the intracuff pressure, and the pressure is claimed to be lower than the capillary perfusion pressure; however, it is not known if this is the case when a high airway pressure is required. In a randomized, cross-over design, we studied 61 patients (31 men) and measured the intracuff pressures of the tracheal tube at various airway pressures. While the lungs were inflated at five different airway pressures in turn (10, 15, 20, 25 and 30 cm H2O), the cuff of the tracheal tube was inflated with air until it prevented an airleak ('just-seal' pressure). Intracuff pressures [median (range)] at airway pressures of 10, 15, 20, 25 and 30 cm H2O were 8 (0-20), 15 (4-20), 22 (6-32), 26 (11-52) and 31 (16-54) cm H2O, respectively, for men and 6 (0-20), 11 (0-20), 15 (0-24), 21 (0-32) and 25 (1-41) cm H2O, respectively, for women. Therefore, we conclude that the pressure exerted by the cuff of the tracheal tube on the tracheal wall is unlikely to exceed the capillary perfusion pressure (arbitrarily defined as 25 mmHg or 34 cm H2O) when the airway pressure is 25 cm H2O or less, but it may exceed the capillary perfusion pressure when the airway pressure is greater than 25 cm H2O.
Anesthesiology↗
A transcultural study of psychopharmacotherapy for schizophrenia of neuroleptic treatment between Tokyo and Bali.
We made a comparison of drug treatment for the patients with schizophrenia between two psychiatric hospitals in Tokyo, Japan, and Bali, Indonesia. An initial preliminary, cross-sectional study revealed that the mean daily dose of neuroleptics was significantly higher in Tokyo than it was in Bali. A second, longitudinal, study showed that the mean neuroleptic dose for newly admitted patients in the acute phase was higher, and the number of patients receiving maintenance treatment after discharge larger in Tokyo, while the mean duration of hospitalization was shorter, and the re-admission rate 1 year after discharge lower in Bali. These findings suggest that the course of schizophrenia is more favorable in Bali. As a result of lower dose of neuroleptics, the prevalence of tardic dyskinesia was much lower in Bali than it was in Tokyo.
Adult↗
Expression of heat shock protein after ischemic preconditioning in rabbit hearts.
Previous studies have shown that preconditioning (PC) with a brief ischemic episode induces heat shock protein (HSP) in cardiac tissue. However, it is unclear when and where in the left ventricle HSP is expressed after PC. Hence, the expression of HSP was studied in rabbit hearts at various time intervals after PC using immunohistochemical methods. Rabbits were preconditioned four times with 5 min of occlusion and 5 min of reperfusion of the coronary artery and then were killed at 0, 3, 24, 48, 72 and 168 h after the PC (n=4, for each time interval). Samples were obtained from the subendocardium and subepicardium of the preconditioned and nonpreconditioned wall and these were processed to 4 microm thick cryosections. The sections were immunolabelled with mouse monoclonal IgGs against HSP 72/73. Positive immunoreactivity was observed as early as 3 h after PC, persisting up to 72 h but not detected at 168 h. HSP was expressed not only in the preconditioned myocardium but also in the remote nonpreconditioned myocardium. There was a wide variation in expression among myocytes. Expression was dominant in myocytes compared with vessel walls. It was concluded that PC induced transient and inhomogeneous expression of HSP in rabbit hearts.
Animals↗
Delayed kinking of the tracheal tube during neck flexion in a paediatric neurosurgical patient.
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Child↗
Anaesthesia in a child with deletion 13q syndrome.
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Abnormalities, Multiple↗
Hoarseness after cardiac surgery.
OBJECTIVE: To investigate the incidence, severity, and duration of hoarseness after adult cardiac surgery and to examine movement of the endotracheal tube (ETT) during neck extension for sternotomy. DESIGN: Prospective study. SETTING: University hospital. PATIENTS: Seventy-two adults undergoing elective cardiac surgery (assessment of hoarseness was completed in 68). INTERVENTIONS: An ETT with an internal diameter of 8.0 mm and 7.5 mm was used for men and women, respectively. After surgical positioning, the ETT was placed with its tip about 3 cm above the carina. MEASURES: ETT migration during positioning for sternotomy was measured using a fiberoptic bronchoscope. Hoarseness was examined at 6-12 hrs after extubation. RESULTS: The ETT moved away from the carina during surgical positioning and the migration was 11+/-6 (1-27) mm [mean+/-SD (range)]. Hoarseness occurred in 32% of the patients (22/68), of whom five (23%) were grade 1 on a four-point scale (0-3), 14 (64%) were grade 2, and three (14%) were grade 3 (aphonic). The duration of hoarseness was 4+/-3 (1-14) days, except in one patient with left vocal cord paralysis (60 days). When this patient was excluded, intubation time was an independent predictor of the severity of hoarseness (p=0.0001). CONCLUSIONS: Hoarseness after cardiac surgery is common. Most hoarseness is transient and its severity is predicted by duration of intubation. Positioning for sternotomy displaces the ETT cuff away from the carina. This may cause persistent hoarseness because displaced cuff from trachea to larynx may damage the recurrent laryngeal nerve or vocal cords.
Cardiac Surgical Procedures↗
cAMP receptor protein-cAMP plays a crucial role in glucose-lactose diauxie by activating the major glucose transporter gene in Escherichia coli.
The inhibition of beta-galactosidase expression in a medium containing both glucose and lactose is a typical example of the glucose effect in Escherichia coli. We studied the glucose effect in the lacL8UV5 promoter mutant, which is independent of cAMP and cAMP receptor protein (CRP). A strong inhibition of beta-galactosidase expression by glucose and a diauxic growth were observed when the lacL8UV5 cells were grown on a glucose-lactose medium. The addition of isopropyl beta-D-thiogalactoside to the culture medium eliminated the glucose effect. Disruption of the crr gene or overproduction of LacY also eliminated the glucose effect. These results are fully consistent with our previous finding that the glucose effect in wild-type cells growing in a glucose-lactose medium is not due to the reduction of CRP-cAMP levels but is due to the inducer exclusion. We found that the glucose effect in the lacL8UV5 cells was no longer observed when either the crp or the cya gene was disrupted. Evidence suggested that CRP-cAMP may not enhance directly the lac repressor action in vivo. Northern blot analysis revealed that the mRNA for ptsG, a major glucose transporter gene, was markedly reduced in a delta crp or delta cya background. The constitutive expression of the ptsG gene by the introduction of a multicopy plasmid restored the glucose effect in delta cya or delta crp cells. We conclude that CRP-cAMP plays a crucial role in inducer exclusion, which is responsible for the glucose-lactose diauxie, by activating the expression of the ptsG gene.
Culture Media↗
Construction of a contiguous 874-kb sequence of the Escherichia coli K-12 genome corresponding to the 50.0-68.8 min on the linkage map and analysis of its sequence features (supplement).
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Base Sequence↗
Construction of a contiguous 874-kb sequence of the Escherichia coli -K12 genome corresponding to 50.0-68.8 min on the linkage map and analysis of its sequence features.
The contiguous 874.423 base pair sequence corresponding to the 50.0-68.8 min region on the genetic map of the Escherichia coli K-12 (W3110) was constructed by the determination of DNA sequences in the 50.0-57.9 min region (360 kb) and two large (100 kb in all) and five short gaps in the 57.9-68.8 min region whose sequences had been registered in the DNA databases. We analyzed its sequence features and found that this region contained at least 894 potential open reading frames (ORFs), of which 346 (38.7%) were previously reported, 158 (17.7%) were homologous to other known genes, 232 (26.0%) were identical or similar to hypothetical genes registered in databases, and the remaining 158 (17.7%) showed no significant similarity to any other genes. A homology search of the ORFs also identified several new gene clusters. Those include two clusters of fimbrial genes, a gene cluster of three genes encoding homologues of the human long chain fatty acid degradation enzyme complex in the mitochondrial membrane, a cluster of at least nine genes involved in the utilization of ethanolamine, a cluster of the secondary set of 11 hyc genes participating in the formate hydrogenlyase reaction and a cluster of five genes coding for the homologues of degradation enzymes for aromatic hydrocarbons in Pseudomonas putida. We also noted a variety of novel genes, including two ORFs, which were homologous to the putative genes encoding xanthine dehydrogenase in the fly and a protein responsible for axonal guidance and outgrowth of the rat, mouse and nematode. An isoleucine tRNA gene, designated ileY, was also newly identified at 60.0 min.
Base Sequence↗
Selective expression of the receptor tyrosine kinase, HTK, on human erythroid progenitor cells.
HTK is a receptor tyrosine kinase of the Eph family. To characterize the involvement of HTK in hematopoiesis, we generated monoclonal antibodies against HTK and investigated its expression on human bone marrow cells. About 5% of the bone marrow cells were HTK+, which were also c-Kit+, CD34(low), and glycophorin A(-/low). Assays of progenitors showed that HTK+ c-Kit+ cells consisted exclusively of erythroid progenitors, whereas HTK- c-Kit+ cells contained progenitors of granulocytes and macrophages as well as those of erythroid cells. Most of the HTK+ erythroid progenitors were stem cell factor-dependent for proliferation, indicating that they represent mainly erythroid burst-forming units (BFU-E). During the erythroid differentiation of cultured peripheral CD34+ cells, HTK expression was upregulated on immature erythroid cells that corresponded to BFU-E and erythroid colony-forming units and downregulated on erythroblasts with high levels of glycophorin expression. These findings suggest that HTK is selectively expressed on the restricted stage of erythroid progenitors, particularly BFU-E, and that HTK is the first marker antigen that allows the purification of erythroid progenitors. Furthermore, HTKL, the ligand for HTK, was expressed in the bone marrow stromal cells. Our findings provide a novel regulatory system of erythropoiesis mediated by the HTKL-HTK signaling pathway.
Antibodies, Monoclonal↗
Effect of preoperative 5-fluorouracil on apoptosis of advanced gastric cancer.
BACKGROUND: Several studies have reported on apoptosis and the effect of anticancer chemotherapy. METHODS: We studied apoptosis induced by 5-fluorouracil (5-FU) given preoperatively to 28 patients with advanced gastric cancer and compared the findings with 101 untreated patients. The expression of bcl-2 oncoprotein, cell phase fractions, and histological chemotherapeutic effects were also compared with the apoptotic changes. RESULTS: The apoptotic and S-phase fractions in 5-FU-treated patients (apoptotic fraction: 10.46 +/- 6.93%, S-phase fraction: 17.49 +/- 11.65%) were significantly greater than those in untreated controls (apoptotic fraction: 6.56 +/- 5.06%, S-phase fraction: 12.17 +/- 6.78%). A positive correlation was observed between 5-FU-induced apoptosis and accumulation of tumor cells in the S-phase fraction. There was an inverse relationship between bcl-2 oncoprotein expression and apoptosis in 5-FU-treated patients, but no significant correlation between histological effect and apoptosis. However, two patients with significant histological effects showed no bcl-2 oncoprotein expression, whereas the histological effects were mild in all the bcl-2-positive patients. CONCLUSIONS: Apoptosis may be induced by 5-FU administered preoperatively and bcl-2 oncogene expression may suppress 5-FU-induced apoptosis.
Adenocarcinoma↗