Job stress and temperaments in female nurses.

BACKGROUND: According to previous studies, temperament predicts a large share of the variance in job stress. It may be necessary for mental health practitioners to offer intervention strategies in accordance with individual temperament. AIMS: To investigate the relationship between job stress and temperament among nurses in a general hospital and to provide insight into personality traits influencing their mental or physical health. METHODS: A questionnaire survey of nurses in a general hospital. Work stress was measured using the Japanese version of the Effort-Reward Imbalance (ERI) scale. Temperament was assessed by a Japanese version of Temperament Evaluation of Memphis, Pisa, Paris and San Diego-Autoquestionnaire (TEMPS-A). Hierarchical multiple regression analysis was used to determine the independent contribution of temperament to effort-reward ratio and over-commitment. RESULTS: Response rate was 48% (326/685). Temperament predicted part of the variance of the four ERI ratios (effort-reward ratio 26%; effort-esteem ratio 27%; effort-promotion ratio 26%; and effort-security ratio 18%) and also of over-commitment (38%). Depressive temperament influenced all four ERI ratios and over-commitment. Anxious temperament influenced only over-commitment. CONCLUSIONS: Nurses with depressive or anxious temperaments should be identified, monitored for signs of job stress and offered interventions to prevent adverse physical and mental effects.

Fibre type-specific expression patterns of myosin heavy chain genes in adult torafugu Takifugu rubripes muscles.

Comprehensive in silico studies, based on the total fugu genome database, which was the first to appear in fish, revealed that torafugu Takifugu rubripes contains 20 sarcomeric myosin heavy chain (MYH) genes (MYH genes) (Ikeda et al., 2007). The present study was undertaken to identify MYH genes that would be expressed in adult muscles. In total, seven MYH genes were found by screening cDNA clone libraries constructed from fast, slow and cardiac muscles. Three MYH genes, fast-type MYH(M86-1), slow-type MYH(M8248) and slow/cardiac-type MYH(M880), were cloned exclusively from fast, slow and cardiac muscles, respectively. Northern blot hybridization substantiated their specific expression, with the exception of MYH(M880). In contrast, transcripts of fast-type MYH(M2528-1) and MYH(M1034) were found in both fast and slow muscles as revealed by cDNA clone library and northern blot techniques. This result was supported by in situ hybridization analysis using specific RNA probes, where transcripts of fast-type MYH(M2528-1) were expressed in fast fibres with small diameters as well as in fibres of superficial slow muscle with large diameters adjacent to fast muscle. Transcripts of fast-type MYH(M86-1) were expressed in all fast fibres with different diameters, whereas transcripts of slow-type MYH(M8248) were restricted to fibres with small diameters located in a superficial part of slow muscle. Interestingly, histochemical analyses showed that fast fibres with small diameters and slow fibres with large diameters both contained acid-stable myofibrillar ATPase, suggesting that these fibres have similar functions, possibly in the generation of muscle fibres irrespective of their fibre types.

Effort-reward imbalance and depressive state in nurses.

BACKGROUND: The mental health of nurses is an important issue. AIMS: To examine relationships between effort-reward imbalance (ERI) and depression and anxiety in nurses of a Japanese general hospital. METHODS: A self-report survey was conducted among 406 nurses. Work stress was measured using a Japanese version of the ERI scale. Depression and anxiety were assessed by an item of the QOL-26. Logistic regression analysis was used to determine the independent contribution of the effort-reward ratios or overcommitment to the depressive state. RESULTS: Both higher effort-money ratio and higher overcommitment significantly correlated with the depressive state (OR: 2.75; 95% CI: 1.34-5.66 and OR: 1.27; 95% CI: 1.15-1.41, respectively). CONCLUSIONS: These findings suggest that in addition to effort-money ratio, overcommitment at work is an especially important issue that may be able to be managed in health promotion services for nurses in general hospitals.

A family of cAMP-binding proteins that directly activate Rap1.

cAMP (3',5' cyclic adenosine monophosphate) is a second messenger that in eukaryotic cells induces physiological responses ranging from growth, differentiation, and gene expression to secretion and neurotransmission. Most of these effects have been attributed to the binding of cAMP to cAMP-dependent protein kinase A (PKA). Here, a family of cAMP-binding proteins that are differentially distributed in the mammalian brain and body organs and that exhibit both cAMP-binding and guanine nucleotide exchange factor (GEF) domains is reported. These cAMP-regulated GEFs (cAMP-GEFs) bind cAMP and selectively activate the Ras superfamily guanine nucleotide binding protein Rap1A in a cAMP-dependent but PKA-independent manner. Our findings suggest the need to reformulate concepts of cAMP-mediated signaling to include direct coupling to Ras superfamily signaling.

Rap2 as a slowly responding molecular switch in the Rap1 signaling cascade.

Rap2 is a member of the Ras family of GTPases and exhibits 60% identity to Rap1, but the function and regulation of Rap2 remain obscure. We found that, unlike the other Ras family proteins, the GTP-bound active form exceeded 50% of total Rap2 protein in adherent cells. Guanine nucleotide exchange factors (GEFs) for Rap1, C3G, Epac (or cyclic AMP [cAMP]-GEF), CalDAG-GEFI, PDZ-GEF1, and GFR efficiently increased the level of GTP-Rap2 both in 293T cells and in vitro. GTPase-activating proteins (GAPs) for Rap1, rap1GAPII and SPA-1, stimulated Rap2 GTPase, but with low efficiency. The half-life of GTP-Rap2 was significantly longer than that of GTP-Rap1 in 293T cells, indicating that low sensitivity to GAPs caused a high GTP/GDP ratio on Rap2. Rap2 bound to the Ras-binding domain of Raf and inhibited Ras-dependent activation of Elk1 transcription factor, as did Rap1. The level of GTP-Rap2 in rat 3Y1 fibroblasts was decreased by the expression of v-Src, and expression of a GTPase-deficient Rap2 mutant inhibited v-Src-dependent transformation of 3Y1 cells. Altogether, Rap2 is regulated by a similar set of GEFs and GAPs as Rap1 and functions as a slowly responding molecular switch in the Rap1 signaling cascade.

Endoscopic endonasal excision of nasal chondromesenchymal hamartoma with intracranial extension.

INTRODUCTION: Nasal chondromesenchymal hamartoma (NCMH) is an extremely rare benign hamartoma of the sinonasal tract, predominantly involving infants and young children. METHODS: We report the case of a 3-year-old boy of NCMH with extension to anterior skull base. RESULTS: The tumor was completely resected piece by piece via an endonasal endoscopic approach. There is no recurrence 3 years after operation. CONCLUSIONS: We reported the case of NCMH extending to skull base was successfully resected by endonasal endoscopic approach.

The novel sequences of major plasma apolipoproteins in the eel Anguilla japonica.

cDNAs encoding major plasma apolipoproteins (apo) were cloned from the eel Anguilla japonica liver and their nucleotide sequences determined. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed that eel lipoproteins contain apolipoproteins of 28 kDa and 14 kDa as major components. Each of the two apolipoproteins showed two isoforms having different isoelectric points as demonstrated by two-dimensional electrophoresis. The two 28 kDa components had different N-terminal amino acid sequences, whereas the two 14 kDa components had an identical one. Then cDNA clones encoding these apolipoproteins were isolated from a cDNA library constructed from the eel liver. An acidic 28 kDa component (28 kDa-1) consisted of 259 amino acids including a putative signal peptide of 27 residues, whereas a basic 28 kDa component (28 kDa-2) was composed of 260 amino acids containing a putative signal peptide of 23 residues. The tandem repeating units, which are characteristic of apolipoproteins, for 28 kDa-1 showed 27.8% identity to that of porcine apoA-IV, although mammalian apoA-IV is about 40 kDa and much larger than 28 kDa-1. However, the repeating units of 28 kDa-2 showed 52.5% identity to that of Atlantic salmon apoA-I. The 14 kDa apolipoprotein consisted of 142 amino acids containing a putative signal peptide of 20 residues. It has a novel sequence differing from apolipoproteins of other vertebrates. The transcriptional expressions of 28 kDa-1, 28 kDa-2, and 14 kDa components were all restricted to the liver, except for the transcripts of 28 kDa-2 which were also slightly expressed in the intestine.

The mechanism of geranylgeraniol-induced apoptosis involves activation, by a caspase-3-like protease, of a c-jun N-terminal kinase signaling cascade and differs from mechanisms of apoptosis induced by conventional chemotherapeutic drugs.

In the present study, we investigated the effects of geranylgeraniol (GGO), a potent inducer of apoptosis in various lines of human tumor cells, on signal transduction cascades involved in apoptosis in human leukemia cells. GGO strongly induced the activation of c-Jun N-terminal kinase (JNK/SAPK) within 2 h in U937 and K562 cells, while neither ERK nor p38 was activated to any considerable extent during GGO-induced apoptosis. Transient expression of a constitutively active mutant form of mitogen-activated protein kinase kinase 1 (MEKK1), deltaMEKK1, or of deltaMEKK1-green fluorescent protein (GFP) in K562 cells activated JNK, but not a caspase-3-like protease, and was insufficient to induce cell death but rendered cells susceptible to GGO-induced cell death. Stable expressions of deltaMEKK1-GFP in U937 cells gave similar results. In contrast to VP-16-induced apoptosis, GGO-induced activation of JNK was almost completely inhibited by benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone (Z-DEVD) and by benzyloxycarbonyl-Asp-CH2OC[O]-2,6,-dichlorobenzene (Z-Asp), indicating that the JNK-activation step is located downstream of the caspase signaling pathway in GGO-induced apoptosis. Moreover, apoptosis induced by GGO was significantly inhibited in two lines of cells with a dominant-negative deletion mutation in c-Jun, indicating a requirement for JNK signaling. In addition, unlike the effects on other inducers of apoptosis, the activation of JNK and of the caspase-3-like protease by GGO was significantly delayed by 12-O-tetradecanoylphorbol-13-acetate (TPA), suggesting that the site of inhibition by TPA might be located upstream of the protease and JNK in the GGO-induced apoptotic signaling pathway.

Myosin subfragment-1 isoforms having different heavy chain structures from fast skeletal muscle of thermally acclimated carp.

Three heavy chain isoforms of chymotryptic myosin subfragment-1 (S1) with different molecular sizes of 96 kDa (H1), 94 kDa (H2), and 92 kDa (H3), were detected in the fast skeletal muscle from thermally acclimated carp. In total, six S1 isoforms were present, including two S1 isoforms for each heavy chain due to associated A1 and A2 light chains. H1 heavy chain was dominant in the 10 degrees C-acclimated carp and responsible for high acto-S1 Mg(2+)-ATPase activity and low thermostability. In contrast, H3 heavy chain predominating in the 30 degrees C-acclimated carp showed low acto-S1 Mg(2+)-ATPase activity and high thermostability. H2 heavy chain was found in the 10- and 20 degrees C-acclimated fish. H3 heavy chain featured three tryptic fragments with normal molecular masses of 25, 50, and 20 kDa in order from the N-terminus. However, H1 heavy chain contained an unusual, longer "20 kDa" peptide whose molecular size was estimated to be about 23 kDa.

Lower activation energy for sliding of F-actin on a less thermostable isoform of carp myosin.

We have examined the temperature-dependence of sliding velocity of fluorescent F-actin on myosins isolated from 10 degrees C- and 30 degrees C-acclimated carp. Activation energies for the sliding of F-actin were 63 and 111 kJ/mol for the 10 degrees C- and 30 degrees C-acclimated carp myosins, respectively. Arrhenius plots of the sliding velocity from 10 degrees C- and 30 degrees C-acclimated carp myosin were shown to intersect at high temperature (about 30 degrees C). The thermostability estimated by measuring the Ca(2-)-ATPase activity was less for myosin from 10 degrees C- than 30 degrees C-acclimated carp. We suggest that a less thermostable structure in cold-acclimated carp myosin results in a reduced activation energy for the contractile process, which allows the F-actin to slide fast even at low temperatures.

Fast skeletal myosin isoforms in thermally acclimated carp.

Fast skeletal myosins were isolated from carp acclimated to 10 and 30 degrees C, and their structural and enzymatic properties were compared. Myosins in 0.5 M KCl were subjected to limited proteolysis by using various proteases including alpha-chymotrypsin, trypsin, and papain, and different SDS-PAGE patterns were seen for the 10- and 30 degrees C-acclimated myosins in all cases. Myosin subfragment-1 (S1) prepared from the 10 degrees C-acclimated myosin by alpha-chymotryptic digestion in 0.12 M NaCl showed higher acto-S1 Mg(2+)-ATPase activity and lower thermostability than S1 from the warm-acclimated myosin. The peptide maps and ATP-induced spectral changes of tryptophan fluorescence also showed an obvious difference between the two types of S1. Temperature acclimation further caused changes in the rod region of myosin, since the apparent sizes of light meromyosin were different from each other for the two types of myosin. Myosin from carp acclimated to 20 degrees C showed intermediate properties between those of the 10- and 30 degrees C-acclimated myosins. Myosin isoforms might be expressed in a temperature-dependent manner to compensate for the effect of seasonal environmental temperature variation on swimming ability.

Differential scanning calorimetry of light meromyosin fragments having various lengths of carp fast skeletal muscle isoforms.

Various recombinant light meromyosin (LMM) fragments were prepared from cDNAs encoding the 10 degrees C and 30 degrees C types of myosin heavy chain isoforms predominantly expressed in fast skeletal muscles of the 10 degrees C- and 30 degrees C-acclimated carp, respectively. These included three kinds of quarter fragments, 1/4-, 2/4-, and 4/4-quarter, composed of residues 1-130, 131-270, and 401-563 from the N-terminus, respectively, as well as three halves, N-, M-, and C-half fragments, containing residues 1-301, 131-400, and 302-563, respectively, and 69K fragments of residues 1-525. Unfortunately, in spite of extensive efforts, the 3/4-quarter fragment was not expressed for both 10 degrees C and 30 degrees C types in our expression system using Escherichia coli. All the LMM fragments except for the 10- and 30-2/4 quarters for the 10 degrees C and 30 degrees C types, respectively, exhibited a typical pattern of a-helix in CD spectrometry. When these were subjected to differential scanning calorimetry (DSC), 30 degrees C-type LMM fragments were all found to be more thermostable than the 10 degrees C-type counterparts. To identify amino acid substitutions responsible for different thermostabilities between the 10 degrees C- and 30 degrees C-type LMMs, six mutant proteins were prepared, mainly focusing on substitutions in the C-terminal half of LMM, and subjected to DSC and CD analyses. For three mutants in which two residues of the 10 degrees C type were replaced by those of the 30 degrees C type, 10-S355T/T361A, 10-M415L/L417V, and 10-S535A/H536Q, the endothermic peaks in DSC increased by 1.4-2.0 degrees C from that of the original 10 degrees C type. The T(m) values for two single-residue substitutions, 10-H449R and 10-T491I, shifted 0.8 and 1.3 degrees C higher than that for the 10 degrees C-type LMM, respectively, whereas the last mutant, 10-G61V, showed no change in thermostability. The finding that the difference in T(m) values for major endothermic peaks from the 10-69K and 30-69K fragments was 4.6 degrees C, which roughly corresponds to that between the original 10 degrees C and 30 degrees C types, suggested that the eight substitutions located in the C-terminal region of the 69K fragments (residues 302-525) are major candidates for the residues responsible for the difference in thermostability between the 10 degrees C- and 30 degrees C-type LMMs.

Zinc ions prevent processing of caspase-3 during apoptosis induced by geranylgeraniol in HL-60 cells.

Geranylgeraniol (GGO) at 50 microM induces apoptosis in HL-60 cells. We examined the effects of Zn2+ ions on this process. Treatment of HL-60 cells with Zn2+ ions inhibited subsequent GGO-induced fragmentation of DNA. In a cell-free system that consisted of a specific substrate for caspase-3 and a lysate of HL-60 cells that had been treated with 50 microM GGO, Zn2+ ions at concentrations above 0.1 mM inhibited the activity of caspase-3. The effect of Zn2+ ions on the processing of caspase-3 during GGO-induced apoptosis was investigated by Western blotting, which revealed that an inactive 32-kDa precursor of caspase-3 was cleaved, in response to GGO, to yield an activated 17-kDa enzyme. Treatment of HL-60 cells with Zn2+ ions inhibited the cleavage of the precursor by a protease that was induced by treatment with GGO, and inhibition of this processing was well correlated with the inhibition by Zn2+ ions of caspase-3 activity in the cell-free system. In cell-extracted cytosols, Zn2+ ions inhibited the cleavage of the 32-kDa precursor by caspase-9 (Aapf-3) that was activated by addition of cytochrome c and dATP. These results indicate that inhibition of GGO-induced apoptosis in HL-60 cells by Zn2+ ions might be due to inhibition by Zn2+ ions of the processing of a precursor to caspase-3.

Latent structures underlying schizophrenic symptoms: a five-dimensional model.

Latent structures of schizophrenic phenomenology were examined over the course of the illness in 100 newly-admitted patients. We compared the results of a confirmatory factor analysis (CFA) on ten competing models that had between zero and five dimensions using data assessed by the Positive and Negative Syndrome Scale (PANSS) at both the acute and chronic phases of the disease. The present findings did not support the two-dimensional construct of positive and negative symptoms in either the acute or the chronic phase of the illness. In the acute phase, a three- (positive, negative, and relational dimensions), four- (positive, negative, disorganization, and relational dimensions), and five-dimensional model (positive, negative, disorganization, excitement, and relational dimensions) fit the data relatively well. In contrast, in the chronic stable phase, only the five-dimensional model adequately fits the data. The present findings suggest that further investigation of the validity of the five-dimensional model over the course of the illness is necessary.

Depressive symptoms in acute schizophrenic inpatients.

Prospective and longitudinal assessment of depressive, positive, and negative symptoms were performed on 86 newly admitted schizophrenic patients. The improvement of depressive symptoms was significantly correlated with the improvement in positive symptoms, but did not correlate with the improvement in negative symptoms. However, depressive symptoms were heterogeneous. Principal components analysis was used to subdivide depressive symptoms into five factors. The improvement of the depression-anxiety factor was significantly associated with improvement of positive symptoms. On the other hand, improvement of negative symptoms was significantly related to that of the reduced activity factor. The change in hypochondriasis had a significant positive correlation with the change in positive symptoms and had a significant negative correlation with the change in negative symptoms. Changes in the other factors of depressive symptoms did not appear to be associated with changes in positive or negative symptoms. The present findings suggest that the various depressive symptoms associated with acute schizophrenia may have different pathophysiological origins.

The composition of the depressive syndrome in acute schizophrenia.

The composition of the depressive syndrome was examined at both the acute and chronic phases of schizophrenic illness in 86 newly admitted patients. A subgroup with pronounced depression was defined, and a discriminant analysis was performed using symptoms from the Hamilton Rating Scale for Depression (HRSD) as discriminant variables. At the acute phase, the following nine symptoms from the HRSD were significant: depressed mood, guilt, suicide, retardation, three types of insomnia, and two somatic symptoms. At the chronic stable phase, only four symptoms were significant: depressed mood, suicide, general somatic symptoms, and loss of weight. Initial insomnia, middle insomnia, genital symptoms, and loss of insight were poorly correlated. The positive and negative symptoms and extrapyramidal side-effects were not discriminators at either phase. These findings suggest that only certain items from the HRSD may be crucial when assessing depression in schizophrenia.

Neurohormonal control of gastrointestinal motor activity in conscious dogs.

Interdigestive migrating contractions (IMC) were analyzed for their occurrence interval, duration, migrating velocity, and frequently in long term records obtained by means of chronically implanted force transducers in the main stomach and the extrinsically denervated fundic pouches or in the intact jejunum and the extrinsically denervated Thirty loop in 10 conscious dogs. Plasma immunoreactive motilin (IRM) was measured simultaneously. It was found that concomitant occurrence of IMC in the main stomach and pouch was closely associated with increase in plasma IRM concentration. On the other hand, in the extrinsically denervated jejunal loop, IMC-like contractions occurred independently of and more frequently than those in the intact jejunum and did not correlate with an increase in IRM concentration. It is concluded that gastric motor activity is under humoral control but in the jejunum, autoregulation by the intrinsic nerve plexus is more predominant than humoral factor(s).

Does motilin control interdigestive pepsin secretion in the dog?

Pepsin output in the Heidenhain pouch, plasma motilin concentration, and contractile activity in the pouch and the main stomach were investigated in five dogs. During the interdigestive state, the pepsin output was significantly increased with a cyclic increase in contractile activity in both the pouch and main stomach at approximately 100-min intervals. The plasma immunoreactive motilin (IRM) concentration fluctuated during the interdigestive state, and, peaks of IRM concentration coincided with the maximum pepsin secretory activity. Exogenous administration of motilin (0.5 micrograms/kg-hr) increased contractile activity in the main stomach and pouch quite similar to the natural interdigestive migrating contractions (IMC), and increased pepsin output significantly. Atropine pre-treatment suppressed the naturally-occurring and motilin-induced pepsin output and contractions in the pouch. It is concluded that pepsin output and contractions in the Heidenhain pouch increase in close association with the IMC in the main stomach during the interdigestive state and these cyclic motor and secretory events in the vagally denervated fundic pouch are most likely regulated by motilin through the intramural cholinergic pathway.

Simultaneous graft replacement of the ascending aorta and total aortic arch for type A aortic dissection.

We performed simultaneous graft replacement of the total aortic arch and ascending aorta for type A aortic dissection with a patent false lumen extending through the arch into the descending or abdominal aorta. During the past 7 years, this procedure was performed in 42 patients (28 men and 14 women), aged 20 to 72 years (mean age, 50 years). Nineteen patients underwent the procedure during the acute period, and 23 during the chronic period. The site of the initial intimal tear was the ascending aorta in 17 patients and the transverse aortic arch in 25 patients. Artificial graft replacement was initially accomplished by proximal anastomosis, followed by open distal anastomosis, and finally by anastomosis of each of the three arch vessels. There were 3 hospital deaths (7.1%), 1 resulting from acute dissection (5.3%) and 2 from chronic dissection (8.7%). Among the type A dissections, total arch graft replacement has been indicated in the setting of rupture of the aortic arch, arch dissection, and Marfan's syndrome. However, with increasing experience in arch reconstructions and improvement in outcome, the indications could be expanded to include all type A aortic dissections with a patent false lumen in the descending aorta.

Distribution of tritiated tetrodotoxin administered intraperitoneally to pufferfish.

Tetrodotoxin was recoil-tritiated by the 3He(n,p)3H reaction and purified by gel filtration. The [3H]tetrodotoxin gave only one spot in both cellulose acetate strip electrophoresis and thin layer chromatography. The specific toxicity of tetrodotoxin did not decrease during the recoil tritiation and the [3H]tetrodotoxin showed a specific radioactivity of 25 x 10(-6) Ci/mmole. In spite of the low specific radioactivity, the [3H]tetrodotoxin was able to be used to investigate the anatomical distribution of tetrodotoxin in pufferfish. When intraperitoneally injected into 'torafugu' puffer, [3H]tetrodotoxin accumulated in most tissues, the level being highest in the skin, followed by the liver, intestines and muscle. With time, the [3H]tetrodotoxin radioactivity level in the injected pufferfish decreased in most tissues, except for skin and gallbladder. Based on these results, the metabolism of tetrodotoxin in pufferfish is discussed.