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Serum biochemical analysis was undertaken to study the pathophysiological details of emaciation disease of the tiger puffer fish Takifugu rubripes ( Temminck and Schlegel). Serum parameters were measured by biochemical analysis using automated dry chemistry and gas chromatography/mass spectrometry ( GC/ MS). Serum concentrations of albumin, amylase, calcium, creatinine, glucose and total protein were significantly lower in the emaciated fish when compared with those of normal fish. Regression analyses found close correlation between concentrations of total protein, albumin, amylase, glucose and progress of the disease. In contrast, serum alanine aminotransferase increased significantly in emaciated fish indicating liver function disorder. Further, GC/ MS metabolic profiling of the puffer serum showed that the profile of the emaciated fish was distinct to that of non-infected control. The serum content of amino acids including glycine, 5-oxo-proline and proline, and ascorbic acid, fumaric acid and glycerol increased significantly in serum in moderately emaciated fish. The serum glucose, linolenic acid and tyrosine level decreased significantly in the late phase of the disease. Our results clearly show that prolonged intestinal damage caused by myxosporean infection impairs absorption of nutrients, resulting in extreme emaciation. [ABSTRACT FROM AUTHOR]

The effect of metal cations, Na+, K+, Ca2+, Mg2+, Zn2+, and Ni2+, on oxide film structure and morphology changes during immersion corrosion tests of 3003 aluminum alloy in model tap waters was investigated by surface analysis techniques including Auger electron spectroscopy (AES), X-ray photoelectron spectroscopy (XPS), and scanning electron microscopy. The hardness of metal cations based on the hard and soft acids and bases (HSAB) concept was applied to explain the effect on the passive oxide film structure. Numerous nano-sized pits were observed after 86.4 ks immersion in model tap water, and nano-sized corrosion products were also observed especially in specimens immersed in K+ containing solutions. The AES and XPS results showed that hard metal cations like Zn2+ and Ni 2+ were included in the oxide films, while soft metal cations were not included in the oxide films. The results are in good agreement with those which could be expected from the HSAB hardness of the metal cations. Copyright © 2013 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

The prolactin response to nemonapride, a new antipsychotic drug, was studied in 27 schizophrenic inpatients (12 males, 15 females). The daily dose of nemonapride was 18 mg/day, and the duration of treatment was 3 weeks. Plasma prolactin concentrations were measured by enzyme immunoassay. Nemonapride treatment significantly (p <0·01) increased prolactin concentrations at each week in both genders. The Δprolactin (the mean concentration during 3 weeks minus the pretreatment concentration) was significantly (p <0·01) greater in females (mean± SD, 81·6±57·8 ng/ml) than males (34·9±19·8 ng/ml). The present study thus shows that nemonapride treatment markedly increases prolactin concentrations in schizophrenic patients, with greater responses in females than males, suggesting a strong D2 receptor blockade property of the drug. © 1997 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

The steady-state serum kinetics of zotepine, an antipsychotic drug, were studied in 59 psychiatric in-patients receiving 50-500 mg/day (mean 215 mg/day) of the drug. There was a 26-fold inter-individual variation in the concentration/dose ratios (C/D ratios: ng/ml/mg/kg), which ranged from 2.4 to 62.2 (mean 13.2). The smokers (n = 37) had significantly lower C/D ratios (mean ±SD: 9.7 ± 7.0 vs 19.0 ± 15.5,p <0.01), while the patients co-administered benzodiazepines (n = 14) had significantly higher C/D ratios (19.6 ± 12.5 vs 11.2 ± 10.9, p< 0.01) than the others. There was no significant relationship between the C/D ratios and age or gender. In the 24 cases where the dose was fixed at 100 mg/day in the first week and at 200 mg/day for the next 3 weeks, no significant difference was found in the mean C/D ratios during the 4 weeks. The present study thus suggests a large inter-individual variation in the metabolism of zotepine, and that smoking enhances, and co-administration of benzodiazepines inhibits, the metabolism. Age and gender do not affect the kinetics of the drug. The results also suggest no dose-dependent kinetics and no enzyme-inducing effect of the drug. [ABSTRACT FROM AUTHOR]

A 67-year-old schizophrenic woman developed neuroleptic malignant syndrome (NMS). She had mild diabetes mellitus, which had been controlled with diet therapy only. Upon the onset of NMS, hyperglycemia of up to 490 mg/dl developed. The hyperglycemia persisted during the NMS episode despite insulin treatment, and subsided only after the symptoms of NMS disappeared. The present report suggests that hyperglycemia may develop as a symptom of NMS, especially in patients with pre-existing impaired glucose tolerance, and that blood glucose should be monitored during NMS episodes. [ABSTRACT FROM AUTHOR]

Aims: Globular glial tauopathy (GGT) is a new category within the 4‐repeat tauopathies that is characterised neuropathologically by tau‐positive globular glial inclusions (GGIs), namely, globular oligodendrocytic and astrocytic inclusions (GOIs and GAIs). Occurrence of tau‐positive neuronal cytoplasmic inclusions (NCIs) is also a feature. GGT is classified into three pathological subtypes (Types I, II and III). We studied the tau pathology in 6 cases of GGT (Type II, n = 3; Type III, n = 3), with special reference to GAIs and NCIs. Methods: Neuropathological examinations were conducted, along with immunohistochemistry, morphometry and three‐dimensional imaging, and biochemical and genetic analysis of tau. Results: The cortical GAIs in Type II and those in Type III were distinguishable from each other. In the motor cortex, GAIs were much more numerous in Type III than in Type II. Prominent occurrence of perikaryal globular structures was a feature of GAIs in Type III. By contrast, prominent occurrence of radiating process‐like structures was a feature of GAIs in Type II. Overall, the GAIs were significantly smaller in Type III than in Type II. NCIs were divisible into three subgroups in terms of shape: diffuse granular, thick cord‐like, and round/horseshoe‐shaped structures. In all cases, NCIs were a feature of the upper and lower motor neurons. Interestingly, the round/horseshoe‐shaped NCIs were observed only in Type III cases. Conclusions: These findings, which characterised GAIs and NCIs, indicated that Type II and Type III constitute two distinct pathological subtypes, and also further strengthen the concept of GGT as a distinct entity. [ABSTRACT FROM AUTHOR]

Aim: Surgery for colorectal cancer located in the splenic flexure is difficult to perform because of the complex anatomy. Recently, in addition to the middle colic artery and left colic artery (LCA), the accessory middle colic artery (AMCA) has been recognized as a feeding artery for the left‐sided colon. This study aimed to evaluate the vascular anatomy of the splenic flexure focusing on the AMCA in a large number of patients. Method: A total of 734 patients who underwent CT before surgery for colorectal cancer were enrolled. We retrospectively evaluated the vascular anatomy using both two‐ and three‐dimensional CT angiography. Results: The AMCA existed in 36.4% of the cases (n = 267). In many cases, it originated from the superior mesenteric artery (n = 228, 85.4%). The AMCA had a common trunk with the transverse pancreatic artery in 54 patients (20.2%). The frequency of the presence of the AMCA was associated with the branching pattern of the LCA, and was more frequent when the LCA was absent (P < 0.001). Conclusion: The presence of the AMCA is not rare and the AMCA has some branching patterns; therefore, recognizing it preoperatively and intra‐operatively is important, being especially careful when the LCA is absent. [ABSTRACT FROM AUTHOR]

Aim Ulcerative colitis ( UC) is considered to be a disease of continuous mucosal inflammation extending proximally from the rectum. However, appendiceal orifice inflammation ( AOI) is a skip lesion with segments of continuous involvement from the rectum. The aim of this study was to examine the clinical characteristics and clinical course, particularly focused on proximal extension, of UC in patients with AOI. Method A retrospective evaluation of patients with UC who underwent total colonoscopy at the Department of Surgical Oncology, The University of Tokyo, from 2004 to 2014. The degree of AOI was graded endoscopically as follows: 0 (no inflammation); 1 (slight oedema); 2 (moderate inflammation); and 3 (marked inflammation). A total of 189 patient records were reviewed retrospectively. The presence of AOI was analysed with regard to the clinical information of each patient, and its association with proximal extension of proctitis or left-sided colitis was evaluated. Results Of 189 patients with UC who underwent total colonoscopy at our institution, 92 were diagnosed with pancolitis, 50 with left-sided colitis and 47 with proctitis. Endoscopic findings of AOI were observed in 26 patients, including 11 (12.0%) with pancolitis, six (12.0%) with left-sided colitis and nine (19.1%) with proctitis. During follow up, proximal extension of the disease occurred in all nine patients with proctitis AOI. Conclusion AOI is more frequently observed in patients with proctitis. Our results showed correlations between AOI and subsequent proximal extension of mucosal inflammation in patients with proctitis. [ABSTRACT FROM AUTHOR]

Aim Eukaryotic elongation factor 2 kinase ( eEF2K), also known as calmodulin (CaM)-dependent protein kinase (CaMK) III, is a unique member of CaMK family protein. We have recently found that expression of eEF2K protein increased in mesenteric artery from spontaneously hypertensive rats. As pathogenesis of hypertension is in part regulated by vascular structural remodelling via proliferation and migration of vascular smooth muscle cells (SMCs), we tested the hypothesis that eEF2K controls SMCs proliferation and migration. Methodsand results In rat mesenteric arterial SMCs, an eEF2K inhibitor, A-484954 (10 μ m), significantly inhibited platelet-derived growth factor (PDGF)-BB (10 ng mL−1)-induced SMCs proliferation as determined by a cell counting and bromodeoxyuridine incorporation assay. PDGF-BB (10 ng mL−1)-induced SMCs migration was significantly inhibited by A-484954 (10 μ m) as determined by a Boyden chamber assay. A-484954 (10 μ m) significantly inhibited PDGF-BB (10 ng mL−1)-induced phosphorylation of eEF2K, extracellular signal-regulated kinase (ERK), Akt, p38 and heat-shock protein (HSP) 27 as determined by Western blotting. It was confirmed that a CaM inhibitor, W-7 (50 μ m), inhibited PDGF-BB (10 ng mL−1)-induced phosphorylation of eEF2K. In an ex vivo mesenteric arterial ring assay, 10% foetal bovine serum-induced SMCs outgrowth was significantly inhibited by A-484954 (10 μ m). Conclusion We for the first time revealed that eEF2K mediates PDGF-BB-induced SMCs proliferation and migration through activating ERK, Akt, p38 and HSP27 signals in a CaM-dependent manner. Our results suggest eEF2K as a novel pharmaceutical target for the prevention of hypertensive cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Objective: Mesenchymal stem cells (MSC) have both self-renewal and multilineage differentiation potential, and bone marrow-derived MSC have been applied for tissue regeneration and repair. Although adipose tissue-derived MSC (ASC) have emerged as an alternative cell source, little information is available regarding the biologic difference between ASC derived from visceral and subcutaneous fat. Therefore, we aimed to compare the proliferation and gene expression profile of cultured human visceral ASC (VASC) and subcutaneous ASC (SASC), and to identify a novel gene involved in proliferation and differentiation of ASC. Materials and methods: We performed microarray analysis of cultured VASC and SASC, and investigated the role of tazarotene-induced gene 1 (TIG1), a most differentially expressed gene, in the proliferation and differentiation of ASC. Results: SASC proliferated faster than VASC for over 10 passages, and TIG1 expression was consistently up-regulated in VASC of humans, rats and mice. Overexpression of the TIG1 gene in human SASC inhibited cell proliferation, whereas knockdown of TIG1 expression by siRNA promoted cell proliferation. In addition, overexpression of the TIG1 gene in SASC enhanced their differentiation into adipocytes, and promoted up-regulation of peroxisome proliferators-activated receptor γ and CCAAT/enhancer binding protein α. On the other hand, TIG1 overexpression in SASC inhibited their differentiation into osteocytes and the expression of osteocalcin. Conclusion: TIG1 plays an important role in regulating proliferation and differentiation of ASC. [ABSTRACT FROM AUTHOR]

Recent preclinical findings that repeated treatment with methamphetamine (METH) induced an increase in tumor necrosis factor-α (TNF-α) mRNA in some brain regions and that TNF-α blocked METH neurotoxicity and rewarding effects suggest TNF-α, a multifunctional pro-inflammatory cytokine, may be involved in METH dependence. We hypothesized that genetic polymorphisms of the TNF-α gene and its receptor genes may be associated with vulnerability to METH dependence. Genetic association of -308G>A and -857C>T in the promotor region of the TNF-α gene, and 36A>G in exon 1 of the TNF receptor 1A gene (TNFR-SF1A), were analyzed in patients with METH dependence ( n= 185) and healthy controls ( n= 221) in a Japanese population. No significant association of alleles or haplotypes of the TNF-α or TNFR-SF1A genes with METH dependence was found. Neither was any significant association of clinical phenotype with METH dependence found. These results suggest that genetic variations in the TNF-α gene and its receptor genes may not be involved in individual vulnerability to METH dependence. [ABSTRACT FROM AUTHOR]

Cocaine- and amphetamine-regulated transcript (CART) was originally discovered as a peptide that increased in the rat striatum after injection of a psychostimulant drug, such as cocaine or amphetamine, and is suggested to play potential roles in drug dependence. We tested the genetic association between the CART gene and methamphetamine (METH) dependence and/or psychosis. The subjects were 203 patients with METH dependence and 239 age- and gender-matched healthy controls. Two single nucleotide polymorphisms (SNPs) of the CART gene, −156A>G and IVS1 + 224G>A, were examined . There were no significant differences in genotype and allele distributions of the polymorphisms between patients with METH dependence and/or psychosis and controls. Neither were significant differences in subgroups of clinical phenotypes, for example, age at first consumption of METH, latency to onset of psychotic symptoms after the first consumption of METH, prognosis of psychosis after therapy, complication of spontaneous relapse to a psychotic state, or multisubstance abuse status, observed. The present findings suggest that the CART gene may not play a pivotal role in the development of METH dependence and psychosis, at least in a Japanese population. [ABSTRACT FROM AUTHOR]