bluuebunny/crossref_metadata_2025_split huggingface dataset:
Association of the metabolic syndrome with depression and anxiety in Japanese men: A 1‐year cohort study
Authors: Takeuchi Takeaki , Nakao Mutsuhiro , Nomura Kyoko , Inoue Mariko , Tsurugano Shinobu , Shinozaki Yasuko , Yano Eiji 
Published: October 2009

AbstractBackgroundRecent studies on the association between the metabolic syndrome (MetS) and depression have reported conflicting findings. This 1‐year cohort study aims to evaluate the association of MetS with the development of both depression and anxiety.MethodsThe cohort comprised 956 Japanese male employees of an enterprise (mean age, 42.7 years; SD, 10.2 years). MetS was diagnosed according to the International Diabetes Federation criteria. The psychological conditions of depression and anxiety were assessed in 2 successive years by using the profile of mood states (POMS) questionnaire and by conducting clinical interviews as per the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM‐IV). We evaluated the temporal and dose‐response relationships between MetS and the development of depression and anxiety, controlling for potential confounding factors like age and lifestyle‐related factors.ResultsWe identified a positive relationship between MetS at baseline and new‐onset depression in the subsequent year (OR 2.14, 95% CI 1.10–4.17). Of the five MetS components examined, only waist circumference was significantly related to new‐onset depression (OR 2.08, 1.23–3.50). Trend analysis revealed a significant positive trend of association between the number of MetS components identified and new‐onset depression (Ptrend < 0.01), but not between Mets and new‐onset anxiety.ConclusionsOur results suggest that MetS is a predictive factor for the development of depression, and that waist circumference largely contributes to the association between MetS and depression. Copyright © 2009 John Wiley & Sons, Ltd.
Curcumin induces the tolerogenic dendritic cell that promotes differentiation of intestine‐protective regulatory T cells
Authors: Cong Yingzi , Wang Lanfang , Konrad Astrid , Schoeb Trenton , Elson Charles O. 
Published: October 2009

AbstractThe gut is home to a large number of Treg, with both CD4+ CD25+ Treg and bacterial antigen‐specific Tr1 cells present in normal mouse intestinal lamina propria. It has been shown recently that intestinal mucosal DC are able to induce Foxp3+ Treg through production of TGF‐β plus retinoic acid (RA). However, the factors instructing DC toward this mucosal phenotype are currently unknown. Curcumin has been shown to possess a number of biologic activities including the inhibition of NF‐κB signaling. We asked whether curcumin could modulate DC to be tolerogenic whose function could mimic mucosal DC. We report here that curcumin modulated BM‐derived DC to express ALDH1a and IL‐10. These curcumin‐treated DC induced differentiation of naïve CD4+ T cells into Treg resembling Treg in the intestine, including both CD4+CD25+ Foxp3+ Treg and IL‐10‐producing Tr1 cells. Such Treg induction required IL‐10, TGF‐β and retinoic acid produced by curcumin‐modulated DC. Cell contact as well as IL‐10 and TGF‐β production were involved in the function of such induced Treg. More importantly, these Treg inhibited antigen‐specific T‐cell activation in vitro and inhibited colitis due to antigen‐specific pathogenic T cells in vivo.
Monocyte and neutrophil recruitment during oral Salmonella infection is driven by MyD88‐derived chemokines
Authors: Rydström Anna , Wick Mary Jo 
Published: October 2009

AbstractOral Salmonella infection recruits phagocytes to Peyer's patches (PP) and MLN. The chemokines induced in infected PP and MLN, the cellular sources during infection and the TLR signaling pathways involved in vivo are not known. Here, we show that CCL2, CXCL9 and CXCL2 mRNA are up‐regulated in PP and MLN coincident with the first arrival of monocytes and neutrophils. Laser capture microdissection microscopy revealed that chemokine mRNA up‐regulation was differently distributed in PP. Despite this, recruited monocytes and neutrophils formed inflammatory cell clusters throughout PP. Monocytes and neutrophils purified from infected mice preferentially produced CXCL2 and small amounts of CCL2, and neutrophils from infected mice migrated towards CXCL2 and CCL3. Furthermore, phagocyte recruitment to PP and MLN was intact in mice lacking TLR4 alone and when signaling through TLR4 and TLR5 was simultaneously absent; however, recruitment was compromised in MyD88−/− and more so in MyD88−/−TLR4−/− double knockout mice. Phagocyte release into the blood, however, was only marginally reduced in MyD88−/−TLR4−/− mice. Defective phagocyte recruitment to PP and MLN of MyD88−/−TLR4−/− mice was paralleled by low chemokine induction. These data provide insight into the chemokines and TLR signaling pathways that orchestrate the early phagocyte response to oral Salmonella infection.
Treg suppress CTL responses upon immunization with HSP gp96
Authors: Liu Zhen , Li Xinghui , Qiu Lipeng , Zhang Xiaojun , Chen Lizhao , Cao Sheng , Wang Fusheng , Meng Songdong 
Published: October 2009

AbstractHSP gp96‐based vaccines have been trialled in rodent models and, more recently, in humans. Better understanding of gp96's immunomodulatory role will help with the design of more effective strategies for treatment of cancer and infectious diseases. In this study, we monitored the activities of T cells and activation of Treg in BABL/c mice after immunization using different doses of gp96 as adjuvant. We found that co‐injection of gp96 simultaneously stimulated both CTL and Treg activity. Activation of CTL at low dose was far more pronounced than Treg activation. Treg population and suppression increased with gp96 dose, eventually abrogating the T‐cell response induced by immunization. Low‐dose cyclophosphamide treatment could restore the T‐cell responses lost after high‐dose gp96 adjuvant injection by suppression of Treg activation. We further examined the effect of different doses of gp96 or N355 peptide administration on tumor rejection. Our results provide new insights into the mechanisms of gp96‐mediated balance between regulatory and responder T cells, which may facilitate future development of an effective gp96‐based therapeutic vaccine.
Nuclear retention of IL‐1α by necrotic cells: A mechanism to dampen sterile inflammation
Authors: Luheshi Nadia M. , McColl Barry W. , Brough David 
Published: October 2009

AbstractSterile inflammation is a host response to tissue injury that is mediated by damage‐associated molecular patterns released from dead cells. Sterile inflammation worsens damage in a number of injury paradigms. The pro‐inflammatory cytokine IL‐1α is reported to be a damage‐associated molecular pattern released from dead cells, and it is known to exacerbate brain injury caused by stroke. In the brain, IL‐1α is produced by microglia, the resident brain macrophages. We found that IL‐1α is actively trafficked to the nuclei of microglia, and hence tested the hypothesis that trafficking of IL‐1α to the nucleus would inhibit its release following necrotic cell death, limiting sterile inflammation. Microglia subjected to oxygen‐glucose deprivation died via necrosis. Under these conditions, microglia expressing nuclear IL‐1α released significantly less IL‐1α than microglia with predominantly cytosolic IL‐1α. The remaining IL‐1α was immobilized in the nuclei of the dead cells. Thus, nuclear retention of IL‐1α may serve to limit inflammation following cell death.
Self‐Assembly from Two‐Dimensional Layered Networks to Tetranuclear Structures: Syntheses, Structures, and Properties of Four Copper–Thiacalix[4]arene Compounds
Authors: Bi Yanfeng , Liao Wuping , Wang Xinwu , Deng Ruiping , Zhang Hongjie 
Published: October 2009

AbstractTwo new copper–thiacalix[4]arene compounds, [CuI2Cl2(H4TC4A)](CH3OH) (1) and [CuI2Cl2(H4PTC4A)](CH3OH)(CHCl3)0.5 (2) (where H4TC4A = p‐tert‐butylthiacalix[4]arene and H4PTC4A = p‐phenylthiacalix[4]arene), were synthesized by the solvothermal method in the mixed CH3OH/CHCl3 (1:1) solvent and reassembled in air at room temperature to two other structures, [CuII4Cl3(HCO2)(TC4A)(CH3OH)2(H2O)](CHCl3)(CH3OH)2.7 (3) and [CuII4Cl4(PTC4A)(CH3OH)4] (4), respectively. All these four compounds were characterized by TG analyses, FTIR spectroscopy, and single‐crystal X‐ray diffraction analyses. Compounds 1 and 2 feature two‐dimensional layered networks, while compounds 3 and 4 are assembled by some tetranuclear units. The luminescence of compounds 1 and 2 in the solid state and magnetic properties of compound 3 were studied.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2009)
Genomic alterations in histopathologically normal breast tissue from BRCA1 mutation carriers may be caused by BRCA1 haploinsufficiency
Authors: Rennstam Karin , Ringberg Anita , Cunliffe Heather E. , Olsson Håkan , Landberg Göran , Hedenfalk Ingrid 
Published: October 2009

AbstractMultiple biopsies of normal breast tissue from 10 BRCA1 mutation carriers have been analyzed using array‐based comparative genomic hybridization. Normal breast tissue from five age‐matched control subjects without a family history of breast cancer was included for reference purposes. We repeatedly found multiple low copy number aberrations at a significantly higher frequency in histopathologically normal tissue from BRCA1 mutation carriers than in normal control tissue. Some of these aberrations were similar across samples from different patients and linked to biological functions such as transcriptional regulation and DNA binding. We also observed a high degree of genomic heterogeneity between samples from the same patient, suggestive of tissue heterogeneity and etiological clonality in the breast epithelium. We show that neither loss of heterozygosity nor promoter methylation of the wild‐type BRCA1 allele is the predominant mechanistic origin of the observed genomic instability. Instead, we propose that haploinsufficiency of BRCA1 might be the underlying cause responsible for initiation of breast cancer in these predisposed women, making cells vulnerable to mitotic recombination. We also propose that loss of ERα expression is preceded by genetic instability in the initiation of BRCA1‐dependent tumorigenesis, indicating that the breast epithelium of BRCA1 mutation carriers may initially be estrogen‐responsive. Our results imply that genomic instability instigated by BRCA1 haploinsufficiency may be required for breast cancer initiation in BRCA1 mutation carriers. Finding molecular markers of tumor initiation and progression, for the potential use in early disease detection, may be of great clinical importance for the improved management of at‐risk women. © 2009 Wiley‐Liss, Inc.
Observed changes in streamflow at the headwaters of the Urumqi River, eastern Tianshan, central Asia
Authors: Li Zhongqin , Wang Wenbin , Zhang Mingjun , Wang Feiteng , Li Huilin 
Published: October 2009

AbstractThe runoff records of streams draining basins with between 0 and approximately 54% glacier cover, located at the headwaters of the Urumqi River in eastern Tianshan, central Asia, have been examined for the purpose of assessing climatic and glacial influences on temporal patterns of streamflow for the period 1959–2006. Runoff in the highest glacierized basin is found to be inversely correlated with the glacier mass‐balance data and increased by 165·1 × 104 m3 or 1·5 times on average from 1959 to 2006, whereas flow from a glacier‐free basin reflects precipitation changes associated with temperature that may enable either ground ice formation or ice storage release. For the basin with a glacier cover of 18·5%, the runoff increased approximately 355·4 × 104 m3 or 29·6% on average from 1983 to 2006, which underscores expected results based on glacier melt and precipitation increase, especially after 2000. This is due to several possible reasons including enhanced evaporation, groundwater percolation, increased water consumption due to plant colonization and runoff decrease from glacier basins subject to area reduction. From the measurement at Urumqi glacier No. 1 gauging station and a simple water balance model, the glacial runoff during the period 1959–2006 was calculated and found to have increased by 145·5 × 104 m3 a−1 (a factor of 2) over the 48‐year span. A significant amount of the increase occurred after 1987, particularly after 1995, and coincides with increases in both temperature and precipitation. Copyright © 2009 John Wiley & Sons, Ltd.
Nuclear receptors in head and neck cancer: current knowledge and perspectives
Authors: Schweitzer Andrea , Knauer Shirley K. , Stauber Roland H. 
Published: October 2009

AbstractDisease management of head and neck cancer has improved significantly. However, a high rate of early recurrences and metastasis still counteract improvement of long‐term survival. Hence, the quest for molecular mechanisms and key regulatory factors exploitable by targeted therapies is still ongoing. Such potential candidates may include also nuclear receptors, belonging to a superfamily of transcription factors implicated in a broad spectrum of physiological and pathophysiological processes. As dysfunction of nuclear receptor signaling contributes to a variety of proliferative diseases, they are major targets for drug discovery and hold promising potential for the development of improved anticancer treatment strategies. Several nuclear receptors have also been associated with head and neck cancer, and strategies targeting these molecules are currently tested in clinical trials. However, reports and molecular knowledge on the pathobiological relevance of nuclear receptors for cancers of the head and neck is currently rather fragmented. Hence, this review provides a general overview of nuclear receptors' molecular functions and summarizes their potential prognostic and therapeutic relevance for this tumor entity.
Maternal folate and other vitamin supplementation during pregnancy and risk of acute lymphoblastic leukemia in the offspring
Authors: Milne Elizabeth , Royle Jill A. , Miller Margaret , Bower Carol , de Klerk Nicholas H. , Bailey Helen D. , van Bockxmeer Frank , Attia John , Scott Rodney J. , Norris Murray D. , Haber Michelle , Thompson Judith R. , Fritschi Lin , Marshall Glenn M. , Armstrong Bruce K. 
Published: October 2009

AbstractThe Australian Study of Causes of Acute Lymphoblastic Leukemia in Children (Aus‐ALL) was designed to test the hypothesis, raised by a previous Western Australian study, that maternal folic acid supplementation during pregnancy might reduce the risk of childhood acute lymphoblastic leukemia (ALL). Aus‐ALL was a national, population‐based, multicenter case–control study that prospectively recruited 416 cases and 1,361 controls between 2003 and 2007. Detailed information was collected about maternal use of folic acid and other vitamin supplements before and during the index pregnancy. Data were analyzed using logistic regression, adjusting for matching factors and potential confounders. A meta‐analysis with the results of previous studies of folic acid supplementation was also conducted. We found weak evidence of a protective effect of maternal folate supplementation before pregnancy against risk of childhood ALL, but no evidence for a protective effect of its use during pregnancy. A meta‐analysis including this and 2 other studies, but not the study that raised the hypothesis, also found little evidence that folate supplementation during pregnancy protects against ALL: the summary odds ratios (ORs) for folate supplementation were 1.06 [95% confidence interval (CI): 0.77–1.48] with reference to no folate supplementation and 1.02 (95% CI: 0.86–1.20) with reference to no vitamin supplementation. For vitamin supplementation in general, the summary OR from a meta‐analysis of 5 studies—including Aus‐ALL—was 0.83 (95% CI: 0.73–0.94). Vitamin supplementation in pregnancy may protect against childhood ALL, but this effect is unlikely to be large or, if real, specifically due to folate.
E‐cadherin transcriptional down‐regulation by epigenetic and microRNA‐200 family alterations is related to mesenchymal and drug‐resistant phenotypes in human breast cancer cells
Authors: Tryndyak Volodymyr P. , Beland Frederick A. , Pogribny Igor P. 
Published: October 2009

AbstractThe conversion of early stage tumors into invasive malignancies with an aggressive phenotype has been associated with the irreversible loss of E‐cadherin expression. The loss of E‐cadherin expression in human tumors, including breast cancer, has been attributed to promoter CpG island hypermethylation and direct inhibition by transcriptional repressors. Recent evidence demonstrates that up‐regulation of E‐cadherin by microRNA‐200b (miR‐200b) and miR‐200c through direct targeting of transcriptional repressors of E‐cadherin, ZEB1, and ZEB2, inhibits epithelial‐to‐mesenchymal transition (EMT), a crucial process in the tumor progression. We demonstrate that microRNA miR‐200 family‐mediated transcriptional up‐regulation of E‐cadherin in mesenchymal MDA‐MB‐231 and BT‐549 cells is associated directly with translational repression of ZEB1 and indirectly with increased acetylation of histone H3 at the E‐cadherin promoter. The increase in histone H3 acetylation may be attributed to the disruption of repressive complexes between ZEB1 and histone deacetylases and to the inhibition of SIRT1, a class III histone deacetylase. These events inhibit EMT and reactivate a less aggressive epithelial phenotype in cancer cells. Additionally, disruption of ZEB1‐histone deacetylase repressor complexes and down‐regulation of SIRT1 histone deacetylase up‐regulate proapoptotic genes in the p53 apoptotic pathway resulting in the increased sensitivity of cancer cells to the chemotherapeutic agent doxorubicin.
Direct‐oxidative DNA damage and apoptosis induction in different human respiratory cells exposed to low concentrations of sodium chromate
Authors: Cavallo Delia , Ursini Cinzia Lucia , Fresegna Anna Maria , Ciervo Aureliano , Maiello Raffaele , Rondinone Bruna , D'Agata Velia , Iavicoli Sergio 
Published: October 2009

AbstractThe mechanism of Cr(VI) genotoxicity has still not been elucidated. We used Fpg‐modified comet assay to assess direct‐oxidative DNA damage on human lung (A549) and bronchial (BEAS‐2B) cells exposed to 0.1, 0.5, 1.0 and 10 μm sodium chromate for 0.5, 1 and 4 h. Moreover we evaluated apoptosis by morphological analysis and caspase‐3 activity, also after 24 h. On A549 cells a time‐dependent DNA damage, expressed as tail DNA%, beginning from 0.5 μm was found. For oxidative DNA damage an induction after 30 min to 0.5 μm decreasing with time, and a time‐dependent increase at 10 μm was found, indicating for low Cr(VI) concentration the oxidative stress as the first event followed by direct DNA damage and for the highest concentration a time‐dependent increase in oxidative DNA damage. On BEAS‐2B cells DNA damage was induced within 1 h at 0.5–10 μm, without changes with time, showing that BEAS‐2B cells are able to resist to Cr(VI) genotoxicity. Early oxidative DNA damage at 0.1 μm decreasing with time was also found. Significant apoptosis was observed by morphological analysis in A549 cells and to a lower extent in BEAS‐2B at 10 μm. The exposure to 10 μm induced caspase‐3 activity after 4 h in BEAS‐2B and after 24 h in A549 cells. The findings show a higher responsiveness of A549 cells to genotoxic effect of Cr(VI) and early transient oxidative DNA damage in BEAS‐2B. The results emphasize the suitability of this experimental model to evaluate the early genotoxic response of different cells to non‐cytotoxic concentrations of Cr(VI) on target organ. Copyright © 2009 John Wiley & Sons, Ltd.
Metal is not inert: Role of metal ions released by biocorrosion in aseptic loosening—Current concepts
Authors: Cadosch Dieter , Chan Erwin , Gautschi Oliver P. , Filgueira Luis 
Published: October 2009

AbstractMetal implants are essential therapeutic tools for the treatment of bone fractures and joint replacements. The metals and metal alloys used in contemporary orthopedic and trauma surgery are well tolerated by the majority of patients. However, complications resulting from inflammatory and immune reactions to metal implants have been well documented. This review briefly discusses the different mechanisms of metal implant corrosion in the human body, which lead to the release of significant levels of metal ions into the peri‐implant tissues and the systemic blood circulation. Additionally, this article reviews the effects of the released ions on bone metabolism and the immune system and discusses their involvement in the pathophysiological mechanisms of aseptic loosening and metal hypersensitivity in patients with metal implants. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res, 2009
Involvement of prostaglandins and histamine in nickel wire‐induced acute inflammation in mice
Authors: Hirasawa Noriyasu , Goi Yoshiaki , Tanaka Rina , Ishihara Kenji , Ohtsu Hiroshi , Ohuchi Kazuo 
Published: October 2009

AbstractThe irritancy of Nickel (Ni) ions has been well documented clinically. However, the chemical mediators involved in the acute inflammation induced by solid Ni are not fully understood. We used the Ni wire‐implantation model in mice and examined roles of prostaglandins and histamine in plasma leakage in the acute phase. The subcutaneous implantation of a Ni wire into the back of mice induced plasma leakage from 8 to 24 h and tissue necrosis around the wire at 3 days, whereas the implantation of an aluminum wire induced no such inflammatory responses. An increase in the mRNA for cyclooxygenase (COX)‐2 and HDC in cells around the Ni wire was detected 4 h after the implantation. The leakage of plasma at 8 h was inhibited by indomethacin in a dose‐dependent manner. Dexamethasone and the p38 MAP kinase inhibitor SB203580 also inhibited the exudation of plasma consistent with the inhibition of the expression of COX‐2 mRNA. Furthermore, plasma leakage was partially but siginificantly reduced in histamine H1 receptor knockout mice and histidine decarboxylase (HDC) knockout mice but not in H2 receptor knockout mice. These results suggested that the Ni ions released from the wire induced the expression of COX‐2 and HDC, resulting in an increase in vascular permeability during the acute phase of inflammation. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res, 2010
Expression of intein‐tagged fusion protein and its applications in downstream processing
Authors: Wang Lishi , Kang Jung Hye , Kim Ki Hyung , Lee E. K. 
Published: October 2009

AbstractThe conventional methods of downstream purification of a recombinant protein are not only complicated and delicate but time consuming, and need to be improved. Since the intein, the protein splicing element, was discovered, this self‐cleaving element has been exploited and applied to the purification of recombinant proteins which could significantly simplify the purification procedure. Intein has the unique property that when it is combined with an affinity tag, it enables a target protein to be purified in a single chromatographic step. This review elucidates the properties of intein (the mechanism that unravels the intein‐based protein splicing), the advantages of an intein affinity expression system, the progress of intein‐based protein purification procedures, and recent advances in the applications of intein. Further development of the intein‐based purification system may lead to the applications of this system to industrial‐scale production of recombinant proteins. Copyright © 2009 Society of Chemical Industry