bluuebunny/crossref_metadata_2025_split huggingface dataset:
The protective role of peroxisome proliferator‐activated receptor γ coactivator‐1α in hyperthyroid cardiac hypertrophy
Authors: Xu Wei , Hou Dongxia , Jiang Xiangrui , Lu Zhiyuan , Guo Ting , Liu Yuan , Wang Dongjin , Zen Ke , Yu Bo , Zhang Chen‐Yu 
Published: November 2011

AbstractHeart failure is a major cause of death throughout the world. Hyperthyroidism has been shown to induce cardiac hypertrophy, which is a contributing factor to heart failure. However, the mechanism underling effect of thyroid hormone is not completely clear. The present study investigates the role of peroxisome proliferator‐activated receptor (PPAR) γ coactivator‐1α (PGC‐1α) in cardiac hypertrophy induced by Triiodothyronine (T3). We investigated PGC‐1α mRNA expression in rat hearts exposed to T3 in vivo and ex vivo. Surprisingly, we found that the extended periods of T3 treatment led to an increase in PGC‐1α expression compared to shorter treatment times, which resulted in a reduction of PGC‐1α expression. Mechanistic studies showed that suppression of PGC‐1α by small interfering RNA in cardiomyocytes amplified the cellular hypertrophic response to T3 stimulation, whereas overexpression of PGC‐1α was protective. Furthermore, we presented evidence to show that T3 decreased PGC‐1α expression via p38 mitogen‐activated protein kinases (MAPK) pathway. Our studies also revealed that overexpression of PGC‐1α in cardiomyocytes inhibited basal and T3‐induced p38 MAPK phosphorylation. These data indicate for the first time that PGC‐1α plays protective role in T3‐induced cardiac hypertrophy and that hypertrophic growth induced by T3 involves a regulatory pathway between PGC‐1α and p38 MAPK. J. Cell. Physiol. 227: 3243–3253, 2012. © 2012 Wiley Periodicals, Inc.
Proteotoxic stress of cancer: Implication of the heat‐shock response in oncogenesis
Authors: Dai Chengkai , Dai Siyuan , Cao Junyue 
Published: November 2011

AbstractOrganisms frequently encounter a wide variety of proteotoxic stressors. The heat‐shock response, an ancient cytoprotective mechanism, has evolved to augment organismal survival and longevity in the face of proteotoxic stress from without and within. These broadly recognized beneficial effects, ironically, contrast sharply with its emerging role as a culprit in the pathogenesis of cancers. Here, we present an overview of the normal biology of the heat‐shock response and highlight its implications in oncogenic processes, including the proteotoxic stress phenotype of cancer; the function of this stress response in helping cancer survive and adapt to proteotoxic stress; and perturbation of proteome homeostasis in cancer as a potential therapeutic avenue. J. Cell. Physiol. 227: 2982–2987, 2012. © 2011 Wiley Periodicals, Inc.
Evidence of vitamin D and interferon‐β cross‐talk in human osteoblasts with 1α,25‐dihydroxyvitamin D3 being dominant over interferon‐β in stimulating mineralization
Authors: Woeckel V.J. , Koedam M. , van de Peppel J. , Chiba H. , van der Eerden B.C.J. , van Leeuwen J.P.T.M. 
Published: November 2011

AbstractIt is well established that 1α‐25‐dihydroxyvitamin D3 (1,25D3) regulates osteoblast function and stimulates mineralization by human osteoblasts. The aim of this study was to identify processes underlying the 1,25D3 effects on mineralization. We started with gene expression profiling analyses of differentiating human pre‐osteoblast treated with 1,25D3. Bioinformatic analyses showed interferon‐related and ‐regulated genes (ISG) to be overrepresented in the set of 1,25D3‐regulated genes. 1,25D3 down‐regulated ISGs predominantly during the pre‐mineralization period. This pointed to an interaction between the vitamin D and IFN signaling cascades in the regulation of osteoblast function. Separately, 1,25D3 enhances while IFNβ inhibits mineralization. Treatment of human osteoblasts with 1,25D3 and IFNβ showed that 1,25D3 completely overrules the IFNβ inhibition of mineralization. This was supported by analyses of extracellular matrix gene expression, showing a dominant effect of 1,25D3 over the inhibitory effect of IFNβ. We identified processes shared by IFNβ‐ and 1,25D3‐mediated signaling by performing gene expression profiling during early osteoblast differentiation. Bioinformatic analyses revealed that genes being correlated or anti‐correlated with interferon‐induced protein with tetratricopeptide repeats 1 (IFIT1) were associated with osteoblast proliferation. In conclusion, the current study demonstrates a cross talk between 1,25D3 and IFNβ in osteoblast differentiation and bone formation/mineralization. The interaction is complex and depends on the process but importantly, 1,25D3 stimulation of mineralization is dominant over the inhibitory effect of IFNβ. These observations are of potential clinical relevance considering the impact of the immune system on bone metabolism in conditions such as rheumatoid arthritis. J. Cell. Physiol. 227: 3258–3266, 2012. © 2011 Wiley Periodicals, Inc.
Apert syndrome mutant FGFR2 and its soluble form reciprocally alter osteogenesis of primary calvarial osteoblasts
Authors: Suzuki Hiroyuki , Suda Naoto , Shiga Momotoshi , Kobayashi Yukiho , Nakamura Masataka , Iseki Sachiko , Moriyama Keiji 
Published: November 2011

AbstractApert syndrome is characterized by craniosynostosis and syndactyly, and is predominantly caused by mutation of either S252W or P253W in the fibroblast growth factor receptor (FGFR) 2 gene. In this study, we characterized the effects of one of the mutations (S252W) using primary calvarial osteoblasts derived from transgenic mice, Ap‐Tg and sAp‐Tg, that expressed an Apert‐type mutant FGFR2 (FGFR2IIIc‐S252W; FGFR2IIIc‐Ap), and the soluble form (extracellular domain only) of the mutant FGFR2 (sFGFR2IIIc‐Ap), respectively. Compared to WT‐derived osteoblasts, osteoblasts from Ap‐Tg mouse showed a higher proliferative activity and enhanced differentiation, while those from sAp‐Tg mouse exhibited reduced potential for proliferation and osteogenic differentiation. When transplanted with β‐tricalcium phosphate (β‐TCP) granules into immunodeficient mice, Ap‐Tg‐derived osteoblasts showed a higher bone forming capacity, whereas sAp‐Tg‐derived osteoblasts were completely deficient for this phenotype. Phosphorylation of extracellular signal‐regulated kinase (ERK), MEK, PLCγ, and p38 was increased in Ap‐Tg‐derived osteoblasts, whereas phosphorylation of these signaling molecules was reduced in sAp‐Tg‐derived osteoblasts. Interestingly, when these experiments were carried out using osteoblasts from the mice generated by crossing Ap‐Tg and sAp‐Tg (Ap/sAp‐Tg), which co‐expressed FGFR2IIIc‐Ap and sFGFR2IIIc‐Ap, the results were comparable to those obtained from WT‐derived osteoblasts. Taken together, these results indicate that osteoblasts expressing FGFR2IIIc‐Ap proliferate and differentiate via highly activated MEK, ERK, and p38 pathways, while these pathways are suppressed in osteoblasts expressing sFGFR2IIIc‐Ap. Our findings also suggest that altered FGFR2IIIc signaling in osteoblasts is mostly responsible for the phenotypes seen in Apert syndrome, therefore these osteoblast cell lines are useful tools for investigating the pathogenesis of Apert syndrome. J. Cell. Physiol. 227: 3267–3277, 2012. © 2011 Wiley Periodicals, Inc.
Potential role of prolactin in antipsychotic‐mediated association of schizophrenia and type 2 diabetes
Authors: Oberweis Brandon , Gragnoli Claudia 
Published: November 2011

AbstractIt remains unclear why atypical antipsychotics confer a risk for hyperglycemia compared to typical antipsychotics. Atypical antipsychotics antagonize dopamine receptors‐2 (D2) and serotonin (5‐HT) receptors‐2, while typical antipsychotics antagonize only D2 receptors. We aimed at elucidating the mechanistic differences between the role of typical and atypical antipsychotics on prolactin levels and glucose regulation. A Medline search was conducted during 2010 using the search terms type 2 diabetes (T2D), typical/atypical antipsychotics, schizophrenia, prolactin, and serotonin. We discuss the effect of typical and atypical antipsychotics on prolactin levels and glucose regulation. Given that prolactin is under negative control by dopamine and positive control by serotonin, typical antipsychotics induce elevations in prolactin, while atypical antipsychotics do not. Research studies show protective effects of prolactin on T2D. We hypothesize that the difference in induction of T2D between typical and atypical antipsychotics is due to the antipsychotic receptor binding mediated effect in changes in prolactin levels. J. Cell. Physiol. 227: 3001–3006, 2012. © 2011 Wiley Periodicals, Inc.
TGF β‐1 administration during Ex vivo expansion of human articular chondrocytes in a serum‐free medium redirects the cell phenotype toward hypertrophy
Authors: Narcisi R. , Quarto R. , Ulivi V. , Muraglia A. , Molfetta L. , Giannoni P. 
Published: November 2011

AbstractCell‐based cartilage resurfacing requires ex vivo expansion of autologous articular chondrocytes. Defined culture conditions minimize expansion‐dependent phenotypic alterations but maintenance of the cells' differentiation potential must be carefully assessed. Transforming growth factor β‐1 (TGF β‐1) positively regulates the expression of several cartilage proteins, but its therapeutic application in damaged cartilage is controversial. Thus we evaluated the phenotypic outcomes of cultured human articular chondrocytes exposed to TGF β‐1 during monolayer expansion in a serum‐free medium. After five doublings cells were transferred to micromass cultures to assess their chondrogenic differentiation, or replated in osteogenic medium. Immunocytostainings of micromasses of TGF‐expanded cells showed loss of aggrecan and type II collagen. Positivity was evidenced for RAGE, IHH, type X collagen and for apoptotic cells, paralleling a reduction of BCL‐2 levels, suggesting hypertrophic differentiation. TGF β‐1‐exposed cells also evidenced increased mRNA levels for bone sialoprotein, osteopontin, matrix metalloproteinase‐13, TIMP‐3, VEGF and SMAD7, enhanced alkaline phosphatase activity and pyrophosphate availability. Conversely, SMAD3 mRNA and protein contents were reduced. After osteogenic induction, only TGF‐expanded cells strongly mineralized and impaired p38 kinase activity, a contributor of chondrocytes' differentiation. To evaluate possible endochondral ossification progression, we seeded the chondrocytes on hydroxyapatite scaffolds, subsequently implanted in an in vivo ectopic setting, but cells failed to reach overt ossification; nonetheless, constructs seeded with TGF‐exposed cells displayed blood vessels of the host vascular supply with enlarged diameters, suggestive of vascular remodeling, as in bone growth. Thus TGF‐exposure during articular chondrocytes expansion induces a phenotype switch to hypertrophy, an undesirable effect for cells possibly intended for tissue‐engineered cartilage repair. J. Cell. Physiol. 227: 3282–3290, 2012. © 2011 Wiley Periodicals, Inc.
Sonographic evaluation of peripheral nerve injuries following the Wenchuan earthquake
Authors: Tang Peifu , Wang Yuexiang , Zhang Lihai , He Chunqing , Liu Xianfei 
Published: November 2011

AbstractPurpose.To analyze retrospectively the sonographic characteristics of the peripheral nerve injuries (PNIs) resulted from Wunchuan earthquake.Methods.The sonographic images of 38 patients with surgically proved PNIs were reviewed and compared with the surgical findings.Results.A total of 78 nerves in 38 patients were found injured in surgery, which included 16 median nerves in the forearm (20.5%), 6 ulnar nerves in the forearm or arm (7.7%), 8 radial nerves in upper limb (10.0%), 8 sciatic nerves (10.3%) in gluteal region, 17 tibial nerves in the leg (21.8%), and 23 peroneal nerves (29.5%). The most common injured nerve in the lower extremity was the peroneal nerve (29.5%) and in upper extremity was the median nerve (20.5%). Sonography correctly diagnosed 72 earthquake‐related nerve injuries (92.3%), which included 5 complete disruption (6.4%), 4 partial disruption (5.1%), 63 nerve entrapment (88.5%, included 1 entrapment by bone calus, 38 entrapments by the scar tissue, 13 entrapments by the thickened muscle or tendinous arch, and 11 entrapment in the narrowed osteofibrous tunnels).Conclusions.Nerve entrapment injury was the common sonographic finding in earthquake‐related PNI. © 2011 Wiley Periodicals, Inc. J Clin Ultrasound, 2011;
In vitro assays for vesper mice (Calomys laucha) sperm using heterologous substrates from nonrodent species
Authors: Corcini Carine D. , Stephan Mariângela H.L. , Colares Élton P. , Santos Elisa C.S. , Varela Antonio S. , Bongalhardo Denise C. , Lucia Thomaz 
Published: November 2011

AbstractSmall vesper mice (Calomys laucha) may be considered as an animal model for in vitro fertilization studies, but limited data about in vitro evaluations of their sperm quality and fertility are available. The in vitro penetration (IVP) assay is used to estimate potential sperm fertility for many mammal species, but it still requires reduction in cost and labor. This study tested improvements in the IVP assay forC. lauchasperm using swine oocytes and perivitelline layers (PVL) of chicken eggs as substrates, and evaluated associations amongC. lauchasperm quality, IVP, and in vivo fertility after natural mating. In the IVP assay, gametes coincubation was carried out flat‐bottomed wells with M2, in water bath at 37°C for 2 hr.C. lauchasperm presented motility, normal morphology, membrane integrity, and acrosome integrity equal to 90.6 ± 5.6, 90.2 ± 6.6, 88.7 ± 9.6, and 90.5 ± 11.5%, respectively. The IVP rate was 39.8% in swine oocytes and 87.5% in the inner PVL. Considering in vivo fertility as the gold standard, the IVP assay in swine oocytes presented a sensitivity of 16.0% and specificity of 83.3%. The sensitivity of the IVP assay in the inner PVL was 84.0%, but the specificity was not determined because there were no true negative results. Sperm membrane integrity was correlated with parturition after natural mating (r= 0.38,P<0.01) and litter size (r= 0.54;P<0.0002).The IVP assay using swine oocytes as substrates can be performed in nearly 2 hr without gametes' coincubation in CO2.J. Exp. Zool. 317:96–102, 2012. © 2011 Wiley Periodicals, Inc.
Quinolone analogs 11: Synthesis of novel 4‐quinolone‐3‐carbohydrazide derivatives with antimalarial activity
Authors: Kurasawa Yoshihisa , Yoshida Kiminari , Yamazaki Naoki , Kaji Eisuke , Sasaki Kenji , Zamami Yoshito , Sakai Yasuhiro , Fujii Takatoshi , Ito Hideyuki 
Published: November 2011

AbstractThe reaction of the 6‐substituted 1‐methyl‐4‐quinolone‐3‐carboxylates 10a, 10b with hydrazine hydrate gave the 3‐carbohydrazides 7a, 7b, respectively, whose reaction with 2‐, 3‐, and 4‐pyridinecarbaldehydes afforded the 3‐(N2‐pyridylmethylene)carbohydrazides 8a, 8b, 8c and 9a, 9b, 9c. The Curtius rearrangement of compound 7b provided the N,N′‐bis(4‐quinolon‐3‐yl)urea 14 presumably via the 3‐carboazide 11 and then 3‐isocyanate 12. Compounds 7a, 8a, and 9a were found to possess antimalarial activity from the in vitro screening data. J. Heterocyclic Chem.,(2011).
Estimation of trends in extreme melt‐season duration at Svalbard
Authors: Kvamstø Nils Gunnar , Steinskog Dag Johan , Stephenson David B. , Tjøstheim Dag Bjarne 
Published: November 2011

AbstractA time series of monthly mean surface temperatures taken at Svalbard airport, Spitzbergen, for the period 1912–2010 was examined for changes in melt‐season length. The annual melt‐season length was constructed from daily temperature estimates based on the monthly data using smoothing splines. We argue that the changes in annual melt‐season length are linked to variability in regional sea surface temperatures, the mean Northern Hemisphere surface temperature and the North Atlantic Oscillation (NAO) index. A regression model for the melt‐season length with these three parameters as predictors, explained about 40% of the observed variance. The annual mean melt season for the period from 1912 to 2010 was estimated to be 108 days, and the linear trend was 0.17 days/year. The risk of having positive extremes in the melt season increased with increasing Northern Hemisphere surface temperature and the regional sea surface temperatures. On the basis of our study of past observations, the 100‐year return length of the melt season at Svalbard was predicted to change from the current 95% confidence interval of 131 (108, 138) days to 175 (109, 242) days with 1 °C warming of both regional sea surface temperature and the mean Northern Hemisphere surface temperature. Copyright © 2011 Royal Meteorological Society
Effects of lactic acid and glycolic acid on human osteoblasts: A way to understand PLGA involvement in PLGA/calcium phosphate composite failure
Authors: Meyer Florent , Wardale John , Best Serena , Cameron Ruth , Rushton Neil , Brooks Roger 
Published: November 2011

AbstractThe use of degradable composite materials in orthopedics remains a field of intense research due to their ability to support new bone formation and degrade in a controlled manner, broadening their use for orthopedic applications. Poly (lactide‐co‐glycolide) acid (PLGA), a degradable biopolymer, is now a popular material for different orthopedic applications and is proposed for use in tissue engineering scaffolds either alone or combined with bioactive ceramics. Interference screws composed of calcium phosphates and PLGA are readily available in the market. However, some reports highlight problems of screw migration or aseptic cyst formation following screw degradation. In order to understand these phenomena and to help to improve implant formulation, we have evaluated the effects of PLGA degradation products: lactic acid and glycolic acid on human osteoblasts in vitro. Cell proliferation, differentiation, and matrix mineralization, important for bone healing were studied. It was found that the toxicity of polymer degradation products under buffering conditions was limited to high concentrations. However, non‐toxic concentrations led to a decrease in cell proliferation, rapid cell differentiation, and mineralization failure. Calcium, whilst stimulating cell proliferation was not able to overcome the negative effects of high concentrations of lactic and glycolic acids on osteoblasts. These effects help to explain recently reported clinical failures of calcium phosphate/PLGA composites, but further in vitro analyses are needed to mimic the dynamic situation which occurs in the body by, for example, culture of osteoblasts with materials that have been pre‐degraded to different extents and thus be able to relate these findings to the degradation studies that have been performed previously. © 2011 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:864–871, 2012
Splenic hilar lymph node metastasis independently predicts poor survival for patients with gastric cancers in the upper and/or the middle third of the stomach
Authors: Zhu Guo‐lian , Sun Zhe , Wang Zhen‐ning , Xu Ying‐ying , Huang Bao‐jun , Xu Yan , Zhu Zhi , Xu Hui‐mian 
Published: November 2011

AbstractBackgroundEffectiveness of splenectomy for advanced gastric cancers occupying the upper and/or the middle third of the stomach is still in debate. The aim of the present study is to elucidate the impact of splenectomy on patient survival by investigating the pathological characteristics and prognostic significance of splenic hilar lymph node metastasis.MethodsClinicopathologic and prognostic data of 265 patients with gastric cancer in the upper and/or the middle third of the stomach who underwent the operation of en bloc resection of primary cancer and D2/D3 lymphadenectomy combined with splenectomy were retrospectively reviewed.ResultsMultivariate analysis revealed pT category, pN category, and distant lymph node metastasis independently correlated with the presence of splenic hilar lymph node metastasis. Prognoses of patients with positive splenic hilar lymph nodes were significantly poorer than that of patients with negative splenic hilar lymph nodes for the entire study population and for those who underwent R0 resection, but not for those who underwent R1‐2 resection. There was no significant difference in survival between patients who underwent R0 resection with positive splenic hilar lymph nodes and those who underwent R1‐2 resection. Splenic hilar lymph node metastasis was one of independent indicators predicting worse prognosis and the presence of distant metastasis after surgery. Subset analysis according to the TNM stage revealed there were significant differences in survival between patients with and without splenic hilar lymph node metastasis.ConclusionsSplenic hilar lymph node metastasis should be considered as one of incurable factors. Consequently, the efficiency of splenectomy aiming at prolonging survival for patients with high risk of splenic hilar lymph nodes metastasis should be questioned, although resection of invasive organs form gastric cancers has been recommended if R0 surgery could be achieved. J. Surg. Oncol. 2012; 105:786–792. © 2011 Wiley Periodicals, Inc.
Aquaporins in human breast cancer: Identification and involvement in carcinogenesis of breast cancer
Authors: Shi Zhonghua , Zhang Ting , Luo Liang , Zhao Hua , Cheng Jing , Xiang Jingying , Zhao Chun 
Published: November 2011

AbstractBackground and ObjectivesAquaporins (AQPs) play important roles in water and glycerol transport. Recently, the role of AQPs in human carcinogenesis has become an area of great interest. However, little is known about the function of AQPs in human breast cancer. The aim of this study was to investigate the expression profile of AQPs in human breast cancer and its significance.MethodsIn this study, we screened the expression profile of AQP0–12 in breast cancer tissues and corresponding normal tissues by RT‐PCR, Western blotting and immunohistochemistry.ResultsAQP1, 3–5, and 10–12 were expressed in human breast cancer and/or normal breast tissues, and AQP1 and 3–5 exhibited differential expression. AQP1 was expressed in cell membranes and its expression was higher in cancer than that in normal tissues. AQP4 was expressed in the cell membrane and cytoplasm and was detected markedly stronger in normal than in cancer tissues. AQP5 was expressed mainly in cell membranes in carcinoma tissues, but was almost absent in normal breast tissues. Expression of AQP5 was associated with cellular differentiation, lymph node invasion, and clinicopathological staging.ConclusionsThese observations suggested that several subtypes of the AQP family play a role in human breast carcinogenesis. J. Surg. Oncol. 2012; 106:267–272. © 2011 Wiley Periodicals, Inc.