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Increased plasma homocysteine (Hcy) levels have been widely documented in patients with overt hypothyroidism; however, the significance of Hcy level changes in patients with subclinical hypothyroidism (SCH) remains controversial. The aim of this meta-analysis was to determine the Hcy status in patients with SCH compared with euthyroid subjects. We searched PubMed, Embase, and Cochrane Library databases prior to December 2019 to identify eligible studies and assessed the quality of selected studies using the Newcastle-Ottawa Quality Assessment Scale. Publication bias was evaluated by Begg’s test and Egger’s test. Meta-regression analysis was conducted to investigate the source of heterogeneity. A likely source of heterogeneity was the year of the study. All statistical analyses were performed with RevMan 5.3 and Stata 12.0 software. Our meta-analysis of twelve observational studies with 684 patients showed that those with SCH aged between 18 and 65 years old were associated with a slightly increased plasma Hcy level compared with euthyroid controls. The pooled result of the weighted mean difference (WMD) of increased tHcy levels was 1.16 μmol/l (95% CI: 0.51, 1.82; p=0.0005). The Hcy level in patients with SCH aged between 18 and 65 years old is significantly increased compared to euthyroid controls.

Long‐term abuse of ketamine causes ketamine‐induced cystitis. The functional alterations of bladder epithelial cells in microenvironment during cystitis remain poorly understood. Here, we explored extracellular vesicles (EV) alteration in ketamine‐induced toxicity. To simulate the high‐concentration ketamine environment in vivo, we established an in vitro model of high ketamine using human uroepithelial cells (SV‐HUC‐1). Cell viability and proliferation were assessed to evaluate the effects of various concentrations (0, 0.25, 0.5, 1, 2, 4 and 8 mmol/L) of ketamine on SV‐HUC‐1 cells. The cell supernatant cultured at a concentration (0, 1, 2, 4 mmol/L) of ketamine was selected for EV extraction and identified. Subsequently, we assessed different groups (ketamine, ketamine plus EV blocker, EV, EV plus extracellular vesicles blocker) of oxidative stress and expression of inflammation. Last, luciferase reporter assay was performed to study the transcriptional regulation of EV on the NF‐kB and P38 pathway. The results of our study suggested that treatment with 0, 1, 2 or 4 mmol/L ketamine altered the morphology and secretion capacity of extracellular vesicles. As the concentration of ketamine increased, the average particle size of EV decreased, but the crest size, particle concentration and EV protein increased. Moreover, after the addition of EV blocker, EV secreted at different concentrations were blocked outside the cell membrane, and the degree of oxidative stress decreased. Our study provided evidence that ketamine alters the secretion of EV by directly stimulating cells in inflammation microenvironment and EV play significant roles in intercellular signal communication and the formation of KIC.EV

Objective: The present study aimed to evaluate the association between hematocrit (HCT) levels and all-cause mortality in geriatric hip fractures. Methods: Older adult patients with hip fractures were screened between January 2015 and September 2019. The demographic and clinical characteristics of these patients were collected. Linear and nonlinear multivariate Cox regression models were used to identify the association between HCT levels and mortality. Analyses were performed using EmpowerStats and the R software. Results: A total of 2589 patients were included in this study. The mean follow-up period was 38.94 months. Eight hundred and seventy-five (33.8%) patients died due to all-cause mortality. Linear multivariate Cox regression models showed that HCT level was associated with mortality (hazard ratio [HR] = 0.97, 95% confidence interval [CI]: 0.96–0.99, p = 0.0002) after adjusting for confounding factors. However, the linear association was unstable and nonlinearity was identified. A HCT level of 28% was the inflection point for prediction. A HCT level of 28% was not a risk factor for mortality (HR = 0.99, 95% CI: 0.97–1.01, p = 0.3792). We found that the nonlinear association was very stable in the propensity score-matching sensitivity analysis. Conclusions: The HCT level was nonlinearly associated with mortality in geriatric hip fracture patients and could be considered a predictor of mortality in these patients. Registration: ChiCTR2200057323.

Purpose Breast cancer (BC) survivors have a lifelong risk of developing lymphedema . This study investigated the prevalence of BC-related arm lymphedema among Chinese BC survivors diagnosed in the last 10 years and examined the demographic and clinical variables as well as lifestyle factors associated with lymphedema status. Methods In this cross-sectional study, women with BC (N = 866) who had been diagnosed and followed up in the previous 10 years were recruited from the outpatient clinic of 4 general hospitals and one cancer association in China between August 2018 and October 2019. Lymphedema status was determined using the Norman telephone questionnaire as the patient-reported occurrence of hand/lower arm/upper arm swelling. Multiple logistic regression was used to identify risk factors for lymphedema. Results The median time from BC diagnosis was 4.0 years (interquartile range, 2.0–5.0 years). 81.4% of the patients had undergone mastectomy . The prevalence of arm lymphedema among BC survivors was 49.0%. Age ≥50 years, monthly income modified radical mastectomy , postsurgical wound infection, chemotherapy, and radiotherapy were associated with an increased risk of BC-related arm lymphedema, whereas exercise of the affected arm, engagement in active physical activity, and timely reporting of symptoms of infection to a physician decreased the risk (P Conclusions Arm lymphedema is a common complication for postoperative BC survivors within 10 years. It is essential to identify patients at risk of lymphedema based on demographic, clinical, and lifestyle factors and implement interventions targeting modifiable lifestyle behaviors-eg, active physical activity during the postoperative period .

Codoping is an effective method to improve the photoelectrochemical performance of anatase TiO2. In this work, through performing extensive hybrid density functional theory calculations, we explore the (Zn + S) and (Cd + S) codoping effects on the electronic structures and photocatalytic activities of anatase TiO2. Theoretical results clearly reveal that the coupling of the incorporated S dopant with the second-nearest neighboring O atom assisted by the acceptor metals leads to the fully occupied and delocalized intermediate bands within the band gap, which originate from the S O antibonding states (π∗). This kind of metal-assisted S O coupling can not only effectively reduce the band gap of TiO2, but also prevent the recombination of the photogenerated carriers. Moreover, the visible light absorption of anatase TiO2 is significantly enhanced via codoping, and both the reduction and oxidation potentials of water lie within the band gap of the (Zn + S) and (Cd + S) codoped anatase TiO2, which are desirable for photocatalytic water splitting. These theoretical findings imply that the metal-assisted S O coupling is an effectively approach to engineer the band structures and the visible light photoelectrochemical performance of semiconductors photocatalysts.

The rare earths are important modifier in copper alloy. This paper did research about the effect of Ce on microstructures and mechanical properties of HMn64-8-5-1.5 brass. The addition of Ce can refine the matrix grain of as-cast and extruded HMn64-8-5-1.5 brass, reduce the size and quantity of big hard phase , and contribute to the extraction of tiny hard phase, such as Mn5Si3 phase. When given tensile stress, hard phases can produce crack initiations. The addition of rare earth Ce can increase the number of hard phase and thus produce more crack initiations, so that the mechanical properties of HMn64-8-5-1.5 brass can be reduced.

This study investigated the efficiency and mechanisms of Cd

The pancreatic adenocarcinoma remains the most aggressive human malignancy with an extremely low 5-year overall survival. Postoperative gemcitabine could significantly delay recurrence after complete resection of pancreatic cancer. However, the underlying mechanisms are not fully understood. The chemo-resistance factors against gemcitabine still need further characterizations. Here we studied the mechanism of gemcitabine-induced pancreatic cancer cell death by focusing on mammalian sterile 20-like kinase 1 (MST1) and cyclophilin D (Cyp-D). We found that MST1 and Cyp-D expressions were significantly lower in gemcitabine-resistant pancreatic cancer tissues and cell lines. In vitro, gemcitabine activated MST1 through reactive oxygen species (ROS) production, which was prevented by antioxidant n-acetyl-cysteine (NAC). We found that gemcitabine-activated MST1 translocated to mitochondria and formed a complex with the local protein Cyp-D. Gemcitabine-induced cell death was alleviated by MST1 or Cyp-D shRNA silencing, but was aggravated by MST1 or Cyp-D over-expression. Further, cyclosporin A (CsA), the Cyp-D inhibitor, prevented gemcitabine-induced MST1/Cyp-D mitochondrial complexation and cancer cell death. We suggest that gemcitabine-induced death of pancreatic cancer cells requires MST1/Cyp-D mitochondrial complexation.

In this paper, we propose an all-digital, cyclic and synthesizable TDC architecture, which may be used as a core block in ADPLLs to replace the analog block as a phase/frequency detector and a charge pump. Traditional designs of the DVFS scheme for multidomain power management are based on a conventional analog PLL to generate the dynamic voltage and frequency in which the use of a digital TDC eliminates the need for current sources in conventional analog PLLs.

Heterogeneous Fenton-like process using fly ash as a catalyst was studied to degrade n-butyl xanthate form aqueous solution. The different reaction parameters on the degradation efficiency of the process were investigated. The fly ash/H2O2 catalyst possesses a high oxidation activity for n-butyl xanthate degradation in aqueous solution. It is found that both the dosage of catalyst and initial solution pH significantly affect the n-butyl xanthate conversion efficient. The results indicate that by using 1.176 mmol/L H2O2 and 1.0 g/L fly ash catalyst with mass fraction of 4.14% Fe(III) oxide at pH 3.0, almost 96.90% n-butyl xanthate conversion and over 96.66% COD removal can be achieved within 120 min with heterogeneous catalysis by fly ash. CS2 as an intermediate of n-butyl xanthate oxidation. Finally, it is demonstrated that the fly ash/H2O2 catalytic oxidation process can be an efficient method for the treatment of n-butyl xanthate containing wastewater.

Coffee is one of the most popular beverages in the world. Several studies consistently show that coffee drinkers with chronic liver disease have a reduced risk of cirrhosis and a lower incidence of hepatocellular carcinoma regardless of primary etiology. With the increasing prevalence of non-alcoholic fatty liver disease (NAFLD) worldwide, there is renewed interest in the effect of coffee intake on NAFLD severity and positive clinical outcomes. This review gives an overview of growing epidemiological and clinical evidence which indicate that coffee consumption reduces severity of NAFLD. These studies vary in methodology, and potential confounding factors have not always been completely excluded. However, it does appear that coffee, and particular components other than caffeine, reduce NAFLD prevalence and inflammation of non-alcoholic steatohepatitis. Several possible mechanisms underlying coffee's hepatoprotective effects in NAFLD include antioxidative, anti-inflammatory, and antifibrotic effects, while a chemopreventive effect against hepatocarcinogenesis seems likely. The so-far limited data supporting such effects will be discussed, and the need for further study is highlighted.

We investigated possible candidates for a compensated half-metal (CHM) with a double perovskite structure A 2 CrRu(Os)O 6 (A = Si, Ge, Sn, and Pb). Electronic structures and magnetic properties were analyzed using the accurate full-potential linear augmented plane wave method within the generalized gradient approximation (GGA). The compensated magnetism can be divided into half-metallic antiferromagnets (HM-AF) and antiferromagnetic insulator (AF-Is) based on their zero magnetic moments. A 2 CrRuO 6 (A = Si, Ge, Sn, and Pb) is a potential candidate for HM-AF, and Sn 2 CrOsO 6 and Pb 2 CrOsO 6 can be classified as AF-Is. The HM-AF and AF-Is states are both attributed to the superexchange and generalized double exchange mechanism. When the GGA + U calculation is taken into account, all A 2 CrRu(Os)O 6 (A = Si, Ge, Sn, and Pb) states become unconventional AF-Is because the two AF state-coupled ions consisted of two different elements and the two spin-resolved densities of states were no longer the same. Further experimental confirmation will be done for the possible CHM of A 2 CrRuO 6 (A = Si, Ge, Sn, and Pb), Sn 2 CrOsO 6 , and Pb 2 CrOsO 6 .

Event-related potential (ERP) is a reliable neuroelectric measure of brain activity that helps to confirm the assessment of mental status and cognitive impairment. Many studies have reported that alcoholics show a significantly lower ERP P300 amplitude than the norm. In the present study, ERP P300 waves were measured to evaluate the effect of citric acid on cognitive function during excessive alcohol consumption in healthy adults. Five volunteers were selected through clinical interview, physical examination, and psychiatric assessment for participation in this study. In a double-blind placebo-controlled before-after design, each subject was treated with 5 ml/kg body weight alcohol, 5 ml/kg body weight alcohol and 1 mg citric acid, or a placebo on three separate occasions, one week apart. ERP P300, blood biochemical indicators, blood alcohol concentrations (BACs) and acetaldehyde concentrations were assessed. Repeated measure analysis of variance (ANOVA) with a within-subjects factor was used to evaluate differences in blood biochemical indicators, BACs, blood acetaldehyde concentrations, and ERP P300 in the three sessions of assessments. Several blood biochemical indicators showed significant differences between treatments, including the levels of cholinesterase (CHE), total bile acid (TBA), triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), and glycylproline dipeptidyl aminopeptidase (GPDA). BACs after consumption of alcohol alone or citric acid with alcohol were significantly higher compared to those after placebo treatment (P

Objective: Inflammatory bowel diseases (IBDs) are idiopathic, chronic, and inflammatory intestinal disorders. The two main types, ulcerative colitis (UC) and Crohn’s disease (CD), sometimes mimic each other and are not readily distinguishable. The purpose of this study was to present a series of hospitalized cases, which could not initially be classified as a subtype of IBD, and to try to note roles of the terms indeterminate colitis (IC) and inflammatory bowel disease unclassified (IBDU) when such a dilemma arises. Methods: Medical records of 477 patients hospitalized due to IBD, during the period of January 2002 to April 2009, were retrospectively studied in the present paper. All available previous biopsies from endoscopies of these patients were reanalyzed. Results: Twenty-seven of 477 IBD patients (5.7%) had been initially diagnosed as having IBDU. Of them, 23 received colonoscopy and histological examinations in our hospital. A total of 90% (9/10) and 66.7% (4/6) of patients, respectively, had a positive finding via wireless capsule endoscopy (CE) and double-balloon enteroscopy (DBE). The barium-swallow or small bowel follow-through (SBFT) was performed on 11 patients. Positive changes were observed under computer tomographic (CT) scanning in 89.5% (17/19) of patients. Reasonable treatment strategies were employed for all patients. Conclusions: Our data indicate that IBDU accounts for 5.7% of initial diagnoses of IBD. The definition of IBDU is valuable in clinical practice. For those who had no clear clinical, endoscopic, histological, or other features affording a diagnosis of either UC or CD, IBDU could be used parenthetically.

OBJECTIVE: The aim of this study was to investigate the prevalence of nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome (MS) in subjects who underwent a routine health checkup. We intended to establish a clinical association between NAFLD and MS as well as to compare the diagnostic criteria of MS based on the definitions set forth by the International Diabetes Federation (IDF), the US National Cholesterol Education Program Adult Treatment Panel III (2001) (NCEP/ATP-III) and the Metabolic Syndrome Study Group of Chinese Diabetes Society (CDS). METHODS: Weight, height, waist circumference, hip circumference, percentage of body fat, blood pressure and ultrasound of liver were performed on subjects undergoing routine health checkup. Serum triglyceride, total cholesterol, high density lipoprotein cholesterol and fasting plasma glucose level were measured. RESULTS: A total of 2394 subjects were included in this analysis and 437 had NAFLD. The prevalence of MS in the whole sample according to IDF, NCEP/ATP-III and CDS definitions was 11.11%, 8.48% and 5.30%, respectively. The total degree of agreement between IDF, NCEP/ATP-III and CDS definition was 87.76%. The prevalence of MS in NAFLD subjects is much higher than that in non-NAFLD subjects. The prevalence of NAFLD in MS subjects is also much higher than that in non-MS subjects. CONCLUSION: The prevalence of MS varied depending on the diagnostic criteria used. NAFLD was strongly associated with the MS, although it remains unknown whether NAFLD is a cause or effect of MS.

Background and Aims: The aim of the present study is to elucidate whether endoplasmic reticulum stress involved in the course of lipogenesis in fatty acids induced hepatic steatosis and the potential effect of metformin on endoplasmic reticulum stress. Methods: HepG2 cells were exposed to different types of culture media. After incubation for 24 h, cells were harvested to evaluate cell survival rate and lipid level among different groups. Moreover, reverse transcriptase polymerase chain reaction and western blot for glucose-regulated protein-78 (GRP78), sterol response element-binding protein-1c (SREBP1c) and fatty acid synthase (FAS) were applied. Results: The levels of triglyceride (TG), mRNA of FAS, mRNA and protein of GRP78 and SREBP1c significantly increased in the free fatty acids (FFA)-induced hepatic steatosis group. Then, HepG2 cells with hepatic steatosis induced by FFA were treated by metformin, levels of TG, GRP78 mRNA, SREBP1c mRNA and FAS mRNA as well as GRP78 and SREBP1 protein levels were partially decreased but without significant differences. Conclusion: Endoplasmic reticulum stress might be involved in lipogenesis in fatty acids-induced hepatic steatosis. Therefore, endoplasmic reticulum stress might serve as a novel target in the pathogenesis and therapy of non- alcoholic fatty liver disease.

A simple, efficient, one-pot method has been developed for the synthesis of tetrahydro-4H-chromene derivatives by concurrent reaction of aryl aldehydes, active methylene compounds, and 1,3-cyclohexanedins using a catalytic amount of lithium bromide in aqueous media. The present approach offers several advantages such as shorter reaction times, good yields, low cost, recycling of the catalyst, and simple workup.

The study of intestinal intraepithelial γδ lymphocytes has been hindered by the difficulty of isolating a population of pure cells representative of their in vivo phenotype and function. Here, we describe a procedure for the purification of small intestinal intraepithelial γδ T lymphocytes in BALB/c mice, including extraction and purification of intraepithelial lymphocytes (IELs) followed by separation of γδ T cells from IELs by magnetic activated cell sorting (MACS). The small intestinal IEL isolation protocol reported here is a less time-consuming with high purity and high yields. One-step Percoll purification of IELs using a 40%-70% discontinuous Percoll gradient is less laborious yet sufficient to get exact profiles during phenotypic analysis of cell subsets. IELs obtained after two-step Percoll centrifugation using 30% Percoll, followed by a 40%-70% discontinuous Percoll gradient, are fit to purify γδ T cells by MACS. Small intestinal IELs produce much more IFN-γ and TGF-β1 than sorted γδ T cells upon stimulation with plate-bound anti-CD3ε mAb. γδ T cells secret moderate amounts of TGF-β1 and minimal amounts of IFN-γ. Purification of γδ T cells is helpful in investigating the phenotype and function of intestinal mucosal γδ T cells.

Background/Aims To explore the unique microRNA expression pattern of nonalcoholic fatty liver disease in a rat model, and search for targets of certain dysregulated microRNAs. Methods Microarray and stem-loop RT-PCR were utilized to detect dysregulated microRNAs in a rat model. Significance Analysis of Microarray, Prediction Analysis of Microarray and clustering analysis were implemented to calculate significantly aberrantly expressed microRNAs. TargetScan, miRanda and PicTar were jointly used to predict targets of microRNAs. Results Confirmed by Significance Analysis of Microarray and predicted by Prediction Analysis of Microarray, portfolios of 27 and 21 microRNAs were selected as an accurate molecular signature in distinguishing steatosis and steatohepatitis from normal rat liver. Besides, a panel of microRNA-target pairs that may be involved in lipid and glucose metabolism and inflammation process was delineated. Conclusion This is by far the first report on the dysregulated microRNAs expression pattern in nonalcoholic fatty liver disease. The successful differentiation of steatosis and steatohepatitis from normal liver hints to the potential of using lists of dysregulated microRNAs for diagnosis, though many problems need to be solved. Besides, these data will guide further studies of the contribution of microRNAs to the pathogenesis of nonalcoholic fatty liver disease while disease-specific microRNAs might become potential targets for therapeutic intervention.

STAT3 plays important roles in cell proliferation and survival signaling and is often constitutively activated in transformed cells. In this study, we examined STAT3 activation in endothelial cells (EC) during angiogenic activation and therapeutic angiogenesis inhibition. VEGF stimulation of cultured EC induced STAT3 phosphorylation by a VEGFR2- and Src-dependent mechanism. FGF2 but not PlGF also induced EC STAT3 activation in vitro. Activated STAT3 mediated VEGF induction of EC Bcl-2 and contributed to VEGF protection of EC from apoptosis. In vivo, p-STAT3 was absent by immunohistological staining in the vascular EC of most normal mouse organs but was present in the vessels of mouse and human tumors. Tumor vascular p-STAT3 increased as tumors were induced to overexpress VEGF, indicating that VEGF is an activator of EC p-STAT3 in vivo. Tumor vascular p-STAT3 decreased during angiogenesis inhibition by antagonists of VEGF-VEGFR signaling, VEGF Trap and SU5416, indicating that VEGF contributed to the EC STAT3 activation seen in the tumors prior to treatment and that p-STAT3 may be used to monitor therapy. These studies show that p-STAT3 is a mediator and biomarker of endothelial activation that reports VEGF-VEGFR2 activity and may be useful for studying the pharmacodynamics of targeted angiogenesis inhibitors.

Resistance of cancer cells to radiotherapy is a major clinical problem in cancer treatment. Therefore, understanding the molecular basis of cellular resistance to radiotherapy and identification of novel targets are essential for improving treatment efficacy for cancer patients. Our previous studies have demonstrated a significant role of ERp29 in breast cancer cell survival against doxorubicin-induced genotoxic stress. We here reported that ERp29 expression in the triple negative MDA-MB-231 breast cancer cells significantly increased cell survival against ionizing radiation. Methylation PCR array analysis identified that ERp29 expression increased promoter hypomethylation of the DNA repair gene, O6-methylguanine DNA-methyltransferase (MGMT), by downregulating DNA methyltransferase 1. Knockdown of MGMT in the ERp29-transfected cancer cells increased radiosensitivity, leading to a decreased post-irradiation survival. In addition, radiation treatment in the MGMT-knockdown cells elevated phosphorylation of γ-H2AX and cleavage of caspase 3, indicating that depletion of MGMT facilitates DNA double strands breaks and increases cell apoptosis. Hence, our studies prove a novel function of ERp29\MGMT in cancer cell survival against radiation. Targeting ERp29\MGMT axis may be useful for providing better treatment efficacy in combination with radiotherapy in breast cancer.

An intracerebroventricular (i.c.v.) injection of neuropeptide Y (NPY) or [Leu31, Pro34]-NPY (non-Y2 receptor agonist) given during middle cerebral artery occlusion (MCAO) increases the infarct volume and nitric oxide (NO) overproduction in the rat brain. An i.c.v. injection of NPY3-36 (non-Y1 receptor agonist) has no effects, while BIBP3226 (selective Y1 receptor antagonist) reduces the infarct volume and NO overproduction. This study examined the effects of NPY or its receptor analog on the immunoreactivity (ir) for three isoforms of NO synthase (NOS) following 1 h of MCAO and 3 h of reperfusion. Focal ischemia/reperfusion led to increased ir for neuronal NOS (nNOS) within the ipsilateral caudate putamen and insular cortex. NPY or [Leu31, Pro34]-NPY enhanced but BIBP3226 suppressed such increase in the nNOS-ir. Focal ischemia/reperfusion also led to an ipsilateral increase in extent and/or intensity of the ir for endothelial NOS (eNOS) in the caudate putamen and/or parietal cortex. NPY or [Leu31, Pro34]-NPY suppressed but BIBP3226 enhanced such change in the eNOS-ir. NPY3-36 did not consistently influence the nNOS-ir or eNOS-ir following MCAO. Specific ir for inducible NOS was undetectable. These opposing effects of NPY-Y1 receptor activation or inhibition on nNOS and eNOS may lead to harmful or beneficial consequences following ischemia/reperfusion.

Oncostatin M (OSM), a cytokine of the interleukin-6 (IL-6) family, can either promote or inhibit cell growth in various normal and tumor cells. We addressed the effects of exogenous OSM on the proliferation and invasion of human astroglioma cells. In addition, we investigated one of the possible mechanisms involved: modulation of matrix metalloproteinase (MMP) expression and enzymatic activity. We found that OSM inhibited the proliferation of two human astroglioma cell lines (CH235-MG and U87-MG), and that this effect was not due to apoptosis. The inhibitory effect of OSM on proliferation was mediated through the gp130/OSMRβ receptor complex. To extend these findings, we analyzed the effects of OSM on primary tumor cells from glioblastoma patients. OSM suppressed the proliferation of primary glioblastoma cells, but not that of normal astrocytes. Interestingly, OSM did not suppress astroglioma cell invasion. This may be due to the differential regulation of MMPs by OSM. We found that OSM inhibited the constitutive expression of MMP-2, while MMP-9 expression was enhanced in astroglioma cell lines. We conclude that OSM inhibits proliferation of human astroglioma cells and primary glioblastoma cells via the gp130/OSMRβ receptor complex. However, OSM does not affect the invasive capacity of the astroglioma cells, which may be due to the divergent effects of OSM on MMP-2 and MMP-9 expression. Collectively, these findings suggest a complex role for OSM in astroglioma biology. © 2005 Wiley-Liss, Inc.

Oncostatin M (OSM), a member of the interleukin-6 (IL-6) cytokine family, has yet to be well studied, especially in the context of the central nervous system (CNS). The biological functions of OSM are complex and variable, depending on the cellular microenvironment. Inflammatory responses and tumor development are among two of the major events that OSM is involved in. Although OSM levels remain low in the normal CNS, elevated expression occurs in pathological conditions. Therefore, it is crucial to understand the regulation of OSM to control its expression and/or its effects. Accumulating data demonstrate that OSM binds to specific receptor complexes, then activates two major signaling pathways: Janus Kinase-Signal Transducers and Activators of Transcription (JAK-STAT) and Mitogen-Activated Protein Kinase (MAPK), to regulate downstream events. In this review, we focus on the biological functions of OSM, the signaling pathways of OSM in the CNS, and OSM involvement in CNS diseases.

Aims. Thyroid dysfunction is frequently observed in patients with type 2 diabetes mellitus (T2DM), but the underlying mechanism is still poorly understood. The present study aimed to investigate whether nesfatin-1 played a role in the thyroid dysfunction in patients with T2DM.Methods. 55 euthyroid patients were enrolled in this study including 30 patients with T2DM and 25 patients with impaired glucose regulation (IGR). 30 age-matched healthy people were also included as the control. The plasma levels of nesfatin-1, thyrotropin (TSH), and glycosylated hemoglobin (HbA1c) as well as the body mass index (BMI) were comparatively analyzed among the three groups.Results. The nesfatin-1 was significantly lower in patients with T2DM than in patients with IGR and in the control. On the contrary, the TSH level was significantly higher in patients with T2DM than in patients with IGR and in the control. Simple regression analysis showed that the plasma nesfatin-1 was negatively correlated with the TSH and HbA1c levels and positively correlated with the BMI. With multiple stepwise regression analysis, the nesfatin-1 remained to be independently correlated with the TSH, BMI, and HbA1c.Conclusions. The study was suggesting a role of nesfatin-1 in thyroid dysfunction in patients with T2DM.

It is well known that determination of temperature fields by holographic interferometry is a successful method in the measurement of thermophysics. In this paper, some practical algorithms for image reconstruction from projections are presented to produce the temperature field. Algorithms being developed include that the Radon transform integral equation is directly solved by a grid method, and that the Radon inversion formula is numerically evaluated by two-dimensional Fourier transform technique. Some examples are given to verify the validity of the above methods in practice. A heat air flow above conbustor with a rectangular hole is investigated by holographic interferometric system, and temperature distributions of two sections in the air flow field have been reconstructed by this methods.

Recent studies have shown increased immunoreactivity for neuropeptide Y (NPY) within the perilesional cortex following experimental middle cerebral artery occlusion (MCAO) or focal excitotoxic damage. Downregulation of the NPY Y1 receptor gene using an antisense oligodeoxynucleotide produced a doubling of the infarct volume, implying that NPY may mediate neuroprotection against focal ischemia. The effects of treatment with NPY on infarct volume and hemodynamic parameters were investigated in the present study. Adult male Sprague-Dawley rats were anesthetized with sodium pentobarbital to undergo right-sided endovascular MCAO for 2 h. A single dose of NPY was given via intracarotid injection (10 microg/kg) at the beginning of reperfusion, intracisternal injection (10 or 30 microg/kg) at 30 min of ischemia, or intracerebroventricular (i.c.v.) injection (10 or 70 microg/kg) at 30 min of ischemia. Control groups received the vehicle only via the same route. Body temperature was maintained constant, and hemodynamic parameters were monitored during anesthesia. Laser Doppler flowmetry was used to monitor the regional cerebral blood flow (rCBF) during ischemia and reperfusion in some rats. The rats were decapitated on day 3, and their brains were cut into 2-mm thick coronal slices before reaction with a 2% solution of 2,3,5-triphenyltetrazolium chloride to reveal the infarct. Compared to the respective control groups, NPY treatment via any method of administration increased the relative infarct volume. Suppression of rCBF was observed during reperfusion. These results indicate that peripheral or central administration of NPY impairs reperfusion following experimental MCAO and worsens the outcome of focal cerebral ischemia.

A 1/12°, 2-D barotropic tide model was used to examine the characteristics of barotropic tides and to improve the accuracy of predicting tidal sea levels and currents in the seas around Taiwan. The form ratio suggests that tides are predominantly semidiurnal in the northern reaches of the Taiwan Strait and mixed of diurnal and semidiurnal elsewhere around Taiwan. When the dominant M2 wave enters the Strait from the north, its amplitude is magnified to ~2 m in the middle, and then decreases rapidly toward the south end of the Strait. The predominance of diurnal tides along the southwest to the south coast of Taiwan is attributed to the quasi-resonance of diurnal waves in the South China Sea. The tidal range is small and tidal currents are weak off the east coast of Taiwan. Barotropic tidal energy is mostly dissipated on the shallow banks of the southwestern Strait. Results summarized from sensitivity tests on the bottom drag coefficient (CD) and horizontal eddy viscosity (AM) indicate that CD = 0.0015 - 0.00175 and AM = 150 m2 s-1 lead to the best model-data fit when compared to the observed tidal sea levels at ten reference tide-gauge stations around Taiwan. The averaged root-mean-squared (RMS) differences of the simulated tidal sea level for the six principal constituents of O1, P1, K1, N2, M2, and S2 are significantly reduced to 1.3, 0.7, 2.0, 1.6, 5.1, and 3.1 cm, respectively, compared to that calculated from a 0.5° resolution global tide harmonic constant database, NAO.99b (Matsumoto et al. 2000). The averaged RMS differences of barotropic tidal currents (U, V) for O1, K1, M2, and S2 are (0.92, 1.64), (1.17, 0.61), (3.88, 2.37), and (1.52, 1.20) cm s-1. A database of tidal sea levels and current harmonic constants, TWTIDE08, for Q1, O1, P1, K1, J1, OO1, 2N2, μ2, N2, ν2, M2, L2, T2, S2, and K2 is established with this study.