bluuebunny/crossref_metadata_2025_split huggingface dataset:
Elevated NRD1 metalloprotease expression plays a role in breast cancer growth and proliferation
Authors: Choong Lee‐Yee , Lim Shen‐Kiat , Chen Yunhao , Loh Marie‐Chiew‐Shia , Toy Weiyi , Wong Chow‐Yin , Salto‐Tellez Manuel , Shah Nilesh , Lim Yoon‐Pin 
Published: July 2011

AbstractUnderstanding the molecular etiology of cancer and increasing the number of drugs and their targets are critical to cancer management. In our attempt to unravel novel breast‐cancer associated proteins, we previously conducted protein expression profiling of the MCF10AT model, which comprises a series of isogenic cell lines that mimic different stages of breast cancer progression. NRD1 expression was found to increase during breast cancer progression. Here, we attempted to confirm the relevance of NRD1 in clinical breast cancer and understand the functional role and mechanism of NRD1 in breast cancer cells. Immunohistochemistry data show that NRD1 expression was elevated in ductal carcinoma in situ and invasive ductal carcinomas compared with normal tissues in 30% of the 26 matched cases studied. Examination of NRD1 expression in tissue microarray comprising >100 carcinomas and subsequent correlation with clinical data revealed that NRD1 expression was significantly associated with tumor size, grade, and nodal status (P < 0.05). Silencing of NRD1 reduced MCF10CA1h and MDA‐MD‐231 breast‐cancer‐cell proliferation and growth. Probing the oncogenic EGF signaling pathways revealed that NRD1 knock down did not affect overall downstream tyrosine phosphorylation cascades including AKT and MAPK activation. Instead, silencing of NRD1 resulted in a reduction of overall cyclin D1 expression, a reduction of EGF‐induced increase in cyclin D1 expression and an increase in apoptotic cell population compared with control cells. © 2011 Wiley‐Liss, Inc.
THE EFFECTS OF HIV MEDICATIONS ON THE QUALITY OF LIFE OF OLDER ADULTS IN NEW YORK CITY
Authors: Brent Robert J. 
Published: July 2011

SUMMARYA three‐equation model is used to estimate the multiple effects of antiretroviral medications (ARVs) on the quality of life (QoL) of the elderly with HIV in New York City. The transmission mechanism involves the ARVs having a direct effect on QoL via the side effects of the medications and two other effects (one indirect and one reverse) both working through feelings of depression. On a scale of 0 to 100, ARVs raise the QoL by 1 percentage point. This was because there was a large positive indirect effect of ARVs on QoL of 28 percentage points via the reduction in depression, which offsets both the 24 percentage‐point reduction due to the direct effect and the 3 percentage‐point decline from the reverse effect. Now, QoL effects can be applied to the additional life years generated by ARVs to form the quality adjusted life years outcome measure for use in economic evaluations of ARVs. Copyright © 2011 John Wiley & Sons, Ltd.
Five New Biflavonoids from Daphne aurantiaca
Authors: Liang Shuang , Shen Yun‐Heng , Tian Jun‐Mian , Feng Yi , Xiong Zhi , Zhang Wei‐Dong 
Published: July 2011

AbstractFive new biflavonoids, 1–5, were isolated from the stem bark of Daphne aurantiaca. The structures were elucidated as 2,2″‐bisteppogenin (1), 2,2″‐bisteppogenin 7‐O‐β‐glucopyranoside (2), 2′′′‐dehydroxy‐2,2″‐bisteppogenin (3), 2′′′‐dehydroxy‐2,2″‐bisteppogenin 7‐O‐β‐glucopyranoside (4), and 7‐methoxyneochamaejasmin B (5) on the basis of spectral analyses.
Stereoselective Total Synthesis of Rugulactone
Authors: Das Biswanath , Srinivas Yallamalla , Sudhakar Chithaluri , Raghavendar Reddy Parigi 
Published: July 2011

AbstractThe stereoselective synthesis of the naturally occurring dihydropyranone rugulactone has been accomplished starting from 3‐phenylpropan‐1‐ol employing Maruoka allylation and ring‐closing metathesis as the key steps.
Asymmetric Total Synthesis of Stagonolide G
Authors: Ramesh Dasari , Rajaram Singanaboina , Prabhakar Peddikotla , Ramulu Udugu , Kumar Reddy Dorigondla , Venkateswarlu Yenamandra 
Published: July 2011

AbstractA simple asymmetric total synthesis of stagonolide G (1) is described. Asymmetric dihydroxylation, regioselective epoxide ring opening, and vinyl Grignard reactions are involved in generating the stereogenic centers C(4) and C(8), followed by Grubbs‐II‐catalyzed ring‐closing metathesis (RCM).
Three New Steroidal Glycosides from the Roots of Cynanchum auriculatum
Authors: Lu Yu , Xiong Hui , Li Teng Hong , Zhong Yang Guang , Nan Mei Zhi 
Published: July 2011

AbstractThree new C21 steroidal glycosides with a cinnamoyl group at C(12) and a 2‐methylbutanoyl group at C(20), and a straight sugar chain at C(3), namely cyanoauriculosides C–E (1–3, resp.), together with three known steroidal derivatives, were isolated from the roots of Cynanchum auriculatum (Asclepiadaceae). Their structures were determined by spectroscopic analyses and chemical methods. The known constituents were identified as wilfoside K1N (4), cynanauriculoside II (5), and auriculoside IV (6).
Synthesis of 2‐Oxopyridine‐Fused 1,3‐Diazaheterocyclic Compounds via a Three‐Component Reaction
Authors: Alizadeh Abdolali , Mikaeili Azadeh , Firuzyar Tahereh , Ahmadi Mahdi 
Published: July 2011

AbstractAn efficient and simple route for the preparation of 2‐oxopyridine‐fused 1,3‐diazaheterocyclic compounds via a three component reaction is described. It involves the reaction between alkylenediamines 1, 1,1‐bis(methylsulfanyl)‐2‐nitroethene, and alkyl prop‐2‐ynoates 2 in refluxing THF (Table). The structures were corroborated by spectroscopic (IR, 1H‐ and 13C‐NMR, and EI‐MS) and elemental analyses. A plausible mechanism for this type of cyclization is proposed (Scheme).
Suppression by heat shock protein 20 of hepatocellular carcinoma cell proliferation via inhibition of the mitogen‐activated protein kinases and AKT pathways
Authors: Matsushima‐Nishiwaki Rie , Adachi Seiji , Yoshioka Takashi , Yasuda Eisuke , Yamagishi Yasumasa , Matsuura Junya , Muko Masato , Iwamura Rutsu , Noda Takahiro , Toyoda Hidenori , Kaneoka Yuji , Okano Yukio , Kumada Takashi , Kozawa Osamu 
Published: July 2011

AbstractHeat shock protein (HSP) 20, one of the low‐molecular weight HSPs, is known to have versatile functions, such as vasorelaxation. However, its precise role in cancer proliferation remains to be elucidated. While HSP20 is constitutively expressed in various tissues including the liver, we have previously reported that HSP20 protein levels in human hepatocellular carcinoma (HCC) cells inversely correlate with the progression of HCC. In this study, we investigated the role of HSP20 in HCC proliferation. The activities of extracellular signal‐regulated kinase (ERK), c‐jun N‐terminal kinase (JNK), and AKT were negatively correlated with the HSP20 protein levels in human HCC tissues. Since HSP20 proteins were hardly detected in HCC‐derived cell lines, the effects of HSP20 expression were evaluated using human HCC‐derived HuH7 cells that were stably transfected with wild‐type human HSP20 (HSP20 overexpressing cells). In HSP20 overexpressing cells, cell proliferation was retarded, and the activation of the mitogen‐activated protein kinases (MAPKs) signaling pathways, including the ERK and JNK, and AKT pathways, as well as cyclin D1 accumulation induced by either transforming growth factor‐α (TGFα) or hepatocyte growth factor, were significantly suppressed compared with the empty vector‐transfected cells (control cells). Taken together, our findings strongly suggest that HSP20 suppresses the growth of HCC cells via the MAPKs and AKT signaling pathways, thus suggesting that the HSP20 could be a new therapeutic target for HCC. J. Cell. Biochem. 112: 3430–3439, 2011. © 2011 Wiley Periodicals, Inc.
FLRT2 promotes cellular proliferation and inhibits cell adhesion during chondrogenesis
Authors: Xu Y. , Wei K. , Kulyk W. , Gong S.‐G. 
Published: July 2011

AbstractOne of the earliest events during chondrogenesis is the formation of condensations, a necessary pre‐requisite for subsequent differentiation of a chondrogenic phenotype. Members of the Fibronectin Lecucine Rich Transmembrane (FLRT) proteins have been shown to be involved in cell sorting and neurite outgrowth. Additionally, FLRT2 is highly expressed at putative sites of chondrogenic differentiation during craniofacial development. In this study, we demonstrate that FLRT2 plays a role in mediating cell proliferation and cell–cell interactions during early chondrogenesis. Clones of stable transfectants of a murine chondroprogenitor cell line, ATDC5, were established in which FLRT2 was knocked down or overexpressed. Cells in which FLRT2 was knocked down proliferated at a slower rate compared to control wild‐type ATDC5 cells or those containing a non‐coding shRNA. In addition, FLRT2 knockdown cells formed numerous lectin peanut agglutinin (PNA) stained aggregates and exhibited higher expression of the cell adhesion molecule, N‐cadherin. In an in vitro wound healing assay, fewer FLRT2 knockdown cells appeared to migrate into the defect. Surprisingly, the FLRT2 knockdown cells demonstrated increased formation of Alcian blue‐stainable extracellular matrix, suggesting that their reduced aggregate formation did not inhibit subsequent chondrogenic differentiation. The opposite trends were observed in ATDC5 clones that overexpressed FLRT2. Specifically, FLRT overexpressing cells proliferated faster, formed fewer PNA‐positive aggregates, accumulated increased Alcian blue‐positive matrix, and migrated faster to close a wound. Collectively, our findings provide evidence for a role of FLRT2 in enhancing cell proliferation and reducing intercellular adhesion during the early stages of chondrogenesis. J. Cell. Biochem. 112: 3440–3448, 2011. © 2011 Wiley Periodicals, Inc.
Mammary adipocytes bioactivate 25‐hydroxyvitamin D3 and signal via vitamin D3 receptor, modulating mammary epithelial cell growth
Authors: Ching Stephen , Kashinkunti Soumya , Niehaus Matthew D. , Zinser Glendon M. 
Published: July 2011

AbstractThe vitamin D3 receptor (VDR) is present in all microenvironments of the breast, yet it is hypothesized to signal through the epithelium to regulate hormone induced growth and differentiation. However, the influence or contribution of the other microenvironments within the breast that express VDR, like the breast adipose tissue, are yet to be investigated. We hypothesized that the breast adipocytes express the signaling components necessary to participate in vitamin D3 synthesis and signaling via VDR, modulating ductal epithelial cell growth and differentiation. We utilized human primary breast adipocytes and VDR wild type (WT) and knockout (KO) mice to address whether breast adipocytes participate in vitamin D3‐induced growth regulation of the ductal epithelium. We report in this study that breast primary adipocytes express VDR, CYP27B1 (1α‐hydroxylase, 1α‐OHase), the enzyme that generates the biologically active VDR ligand, 1α,25‐dihydroxyvitamin D3 (1,25D3), and CYP24 (24‐hydroxylase, 24‐OHase), a VDR‐1,25D3 induced target gene. Furthermore, the breast adipocytes participate in bioactivating 25‐hydroxyvitamin D3 (25D3) to the active ligand, 1,25D3, and secreting it to the surrounding microenvironment. In support of this concept, we report that purified mammary ductal epithelial fragments (organoids) from VDR KO mice, co‐cultured with WT breast adipocytes, were growth inhibited upon treatment with 25D3 or 1,25D3 compared to vehicle alone. Collectively, these results demonstrate that breast adipocytes bioactivate 25D3 to 1,25D3, signal via VDR within the adipocytes, and release an inhibitory factor that regulates ductal epithelial cell growth, suggesting that breast adipose tissue contributes to vitamin D3‐induced growth regulation of ductal epithelium. J. Cell. Biochem. 112: 3393–3405, 2011. © 2011 Wiley Periodicals, Inc.
Downregulation of p57kip2 promotes cell invasion via LIMK/cofilin pathway in human nasopharyngeal carcinoma cells
Authors: Chow Shu‐Er , Wang Jong‐Shyan , Lin Ming‐Rung , Lee Chien Lin 
Published: July 2011

AbstractThe members of Rho family are well known for their regulation of actin cytoskeleton to control cell migration. The Cip/kip members of cyclin‐dependent (CDK) inhibitors have shown to implicate in cell migration and cytoskeletal dynamics. p57kip2, a CDK inhibitor, is frequently down‐regulated in several malignancy tumors. However, its biological roles in human nasopharyngeal carcinoma (NPC) cells remained to be investigated. Here, we found p57kip2 has nuclear and cytoplasm distributions and depletion of endogenous p57kip2 did not change the cell‐cycle progression. Inhibition of cell proliferation by mitomycin C promoted FBS‐mediated cell migration and accompanied with the downregulation of ΔNp63α and p57kip2, but did not change the level of p27kip1, another CDK inhibitor. By using siRNA transfection and cell migration/invasion assays, we found that knockdown of p57kip2, but not ΔNp63α, involved in promotion of NPC cell migration and invasion via decrease of phospho‐cofilin (p‐cofilin). Treatment with Y‐27632, a specific ROCK inhibitor, we found that dysregulation of ROCK/cofilin pathway decreased p‐cofilin expression and induced cell migration. This change of p‐cofilin induced actin remodeling and pronounced increase of membrane protrusions. Further, silence of p57kip2 not only decreased the interaction between p57kip2 and LIMK‐1 assayed by immunoprecipitation but also reduced the level of phospho‐LIMK1/2. Therefore, this study indicated that dysregulation of p57kip2 promoted cell migration and invasion through modulation of LIMK/cofilin signaling and suggested this induction of inappropriate cell motility might contribute to promoting tumor cell for metastasis. J. Cell. Biochem. 112: 3459–3468, 2011. © 2011 Wiley Periodicals, Inc.
MYC accelerates p21CIP‐induced megakaryocytic differentiation involving early mitosis arrest in leukemia cells
Authors: Muñoz‐Alonso María J. , Ceballos Laura , Bretones Gabriel , Frade Pilar , León Javier , Gandarillas Alberto 
Published: July 2011

Abstractp21CIP is a potent cell cycle inhibitor often up‐regulated in differentiation. Protooncogene MYC induces cell growth and proliferation, inhibits differentiation and represses p21CIP. However, both molecules are involved in processes of polyploidisation, cell size increase, differentiation and senescence. It is unclear why MYC has a dual role in differentiation. We have previously shown that overexpression of p21CIP in K562 myeloid cells induces megakaryocytic differentiation with polyploidy. We have now investigated the requirements for p21CIP to block mitosis and induce differentiation in the presence of overactivated MYC. Silencing and over‐expression studies showed that p21CIP is required to induce differentiation. However, the expression of p21CIP needs to be transient to irreversibly inhibit mitosis but not DNA replication, what leads to polyploidy. Transient overexpression of p21CIP caused early down‐regulation of mitotic Cyclins and up‐regulation of G1/S Cyclins D and E, changes typical of endoreplication. Interestingly, over‐activation of MYC did not release the proliferative block imposed by p21CIP and instead, accelerated cell size increase, megakaryocytic differentiation and polyploidisation. Our data suggests that in some systems p21CIP takes part in a mitosis control driving MYC‐induced cellular growth into differentiation. J. Cell. Physiol. 227: 2069–2078, 2012. © 2011 Wiley Periodicals, Inc.
Branched‐chain amino acids prevent insulin‐induced hepatic tumor cell proliferation by inducing apoptosis through mTORC1 and mTORC2‐dependent mechanisms
Authors: Hagiwara Asami , Nishiyama Megumi , Ishizaki Sonoko 
Published: July 2011

AbstractBranched‐chain amino acids (BCAA) supplementation has been reported to suppress the incidence of liver cancer in obese patients with liver cirrhosis or in obese and diabetic model animals of carcinogenesis. Whether BCAA directly suppresses cell proliferation of hepatic tumor cells under hyperinsulinemic condition remain to be defined. The aim of this study was to investigate the effects of BCAA on insulin‐induced proliferation of hepatic tumor cells and determine the underlying mechanisms. BCAA suppressed insulin‐induced cell proliferation of H4IIE, HepG2 cells. In H4IIE cells, BCAA did not affect cell cycle progression but increased apoptosis by suppressing expressions of anti‐apoptotic genes and inducing pro‐apoptotic gene via inactivation of PI3K/Akt and NF‐κB signaling pathways. Further studies demonstrated that BCAA inhibited PI3K/Akt pathway not only by promoting negative feedback loop from mammalian target of rapamycin complex 1 (mTORC1)/S6K1 to PI3K/Akt pathway, but also by suppressing mTORC2 kinase activity toward Akt. Our findings suggest that BCAA supplementation may be useful to suppress liver cancer progression by inhibiting insulin‐induced PI3K/Akt and subsequent anti‐apoptotic pathway, indicating the importance of BCAA supplementation to the obese patients with advanced liver disease. J. Cell. Physiol. 227: 2097–2105, 2012. © 2011 Wiley Periodicals, Inc.
Brain‐derived neurotrophic factor induces migration of endothelial cells through a TrkB–ERK–integrin αVβ3–FAK cascade
Authors: Matsuda Shinji , Fujita Tsuyoshi , Kajiya Mikihito , Takeda Katsuhiro , Shiba Hideki , Kawaguchi Hiroyuki , Kurihara Hidemi 
Published: July 2011

AbstractBrain‐derived neurotrophic factor (BDNF) promotes the regeneration of periodontal tissue. Since angiogenesis is important for tissue regeneration, investigating effect of BDNF on endothelial cell function may help to reveal its mechanism, whereby, BDNF promotes periodontal tissue regeneration. In this study, we examined the influence of BDNF on migration in human microvascular endothelial cells (HMVECs), focusing on the effects on extracellular signal‐regulated kinase (ERK), integrin αVβ3, and focal adhesion kinase (FAK). The migration of endothelial cells was assessed with a modified Boyden chamber and a wound healing assay. The expression of integrin αVβ3 and the phosphorylation of ERK and FAK were analyzed by immunoblotting and immunofluorescence microscopy. BDNF (25 ng/ml) induced cell migration. PD98059, an ERK inhibitor, K252a, a specific inhibitor for TrkB, a high affinity receptor of BDNF, and an anti‐integrin αVβ3 antibody suppressed the BDNF‐induced migration. BDNF increased the levels of integrin αVβ3 and phosphorylated ERK1/2 and FAK. The ERK inhibitor and TrkB inhibitor also reduced levels of integrin αVβ3 and phosphorylated FAK. We propose that BDNF stimulates endothelial cell migration by a process involving TrkB/ERK/integrin αVβ3/FAK, and this may help to enhance the regeneration of periodontal tissue. J. Cell. Physiol. 227: 2123–2129, 2012. © 2011 Wiley Periodicals, Inc.
Axonal tracing of the normal and regenerating visual pathway of mouse, rat, frog, and fish using manganese‐enhanced MRI (MEMRI)
Authors: Sandvig Axel , Sandvig Ioanna , Berry Martin , Olsen Øystein , Pedersen Tina Bugge , Brekken Christian , Thuen Marte 
Published: July 2011

AbstractPurpose:To assess optic nerve (ON) regeneration after injury by applying manganese‐enhanced MRI (MEMRI) in a study of comparative physiology between nonregenerating rat and mouse species and regenerating frog and fish species.Materials and Methods:The normal visual projections of rats, mice, frogs, and fish was visualized by intravitreal MnCl2 injection followed by MRI. Rats and mice with ON crush (ONC) were divided into nonregenerating (ONC only), and regenerating animals with peripheral nerve graft (ONC+PNG; rats) or lens injury (ONC+LI; mice) and monitored by MEMRI at 1 and 20 days post‐lesion (dpl). Frog and fish with ON transection (ONT) were monitored by MEMRI up to 6 months postlesion (mpl).Results:Signal intensity profiles of the Mn2+‐enhanced ON were consistent with ON regeneration in the ONC+PNG and ONC+LI rat and mice groups, respectively, compared with the nonregenerating ONC groups. Furthermore, signal intensity profiles of the Mn2+‐enhanced ON obtained between 1 mpl and 6 mpl in the fish and frog groups, respectively, were consistent with spontaneous, complete ON regeneration.Conclusion:Taken together, these results demonstrate that MEMRI is a viable method for serial, in vivo monitoring of normal, induced, and spontaneously regenerating optic nerve axons in different species. J. Magn. Reson. Imaging 2011;. © 2011 Wiley‐Liss, Inc.
Three‐dimensional flow‐independent balanced steady‐state free precession vessel wall MRI of the popliteal artery: Preliminary experience and comparison with flow‐dependent black‐blood techniques
Authors: Kawaji Keigo , Nguyen Thanh D. , Zou Zhitong , Reig Beatriu , Winchester Priscilla A. , Shih Andrew , Spincemaille Pascal , Prince Martin R. , Wang Yi 
Published: July 2011

AbstractPurpose:To examine the feasibility of flow‐independent T2‐prepared inversion recovery (T2IR) black‐blood (BB) magnetization preparation for three‐dimensional (3D) balanced steady‐state free precession (SSFP) vessel wall MRI of the popliteal artery, and to evaluate its performance relative to flow‐dependent double inversion recovery (DIR), spatial presaturation (SPSAT), and motion‐sensitizing magnetization preparation (MSPREP) BB techniques in healthy volunteers.Materials and Methods:Eleven subjects underwent 3D MRI at 1.5 Tesla with four techniques performed in a randomized order. Wall and lumen signal‐to‐noise ratio (SNR), wall‐to‐lumen contrast‐to‐noise ratio (CNR), vessel wall area, and lumen area were measured at proximal, middle, and distal locations of the imaged popliteal artery. Image quality scores based on wall visualization and degree of intraluminal artifacts were also obtained.Results:In the proximal region, DIR and SPSAT had higher wall SNR and wall‐to‐lumen CNR than both MSPREP and T2IR. In the middle and distal regions, DIR and SPSAT failed to provide effective blood suppression, whereas MSPREP and T2IR provided adequate black blood contrast with comparable wall‐to‐lumen CNR and image quality.Conclusion:The feasibility of 3D SSFP imaging of the popliteal vessel wall using flow‐independent T2IR was demonstrated with effective blood suppression and good vessel wall visualization. Although DIR and SPSAT are effective for thin slab imaging, MSPREP and T2IR are better suited for 3D thick slab imaging. J. Magn. Reson. Imaging 2011;. © 2011 Wiley‐Liss, Inc.
Windowed stochastic proton decoupling for in vivo 13C magnetic resonance spectroscopy with reduced RF power deposition
Authors: Xiang Yun , Shen Jun 
Published: July 2011

AbstractPurpose:To propose a strategy for reducing radiofrequency (RF) power deposition by stochastic proton decoupling based on Rayleigh's theorem.Materials and Methods:Rayleigh's theorem was used to remove frequency components of stochastic decoupling over the 3.90–6.83 ppm range. [2‐13C] or [2,5‐13C2]glucose was infused intravenously to anesthetized rats. 13C labeling of brain metabolites was detected in the carboxylic/amide spectral region at 11.7 T using either the original stochastic decoupling method developed by Ernst or the proposed windowed stochastic decoupling method.Results:By restricting frequency components of stochastic decoupling to 1.91–3.90 ppm and 6.83–7.60 ppm spectral regions decoupling power deposition was reduced by ≈50%. The proposed windowed stochastic decoupling scheme is experimentally demonstrated for in vivo 13C MRS of rat brain at 11.7 T.Conclusion:The large reduction in decoupling power deposition makes it feasible to perform stochastic proton decoupling at very high magnetic fields for human brain 13C MRS studies. J. Magn. Reson. Imaging 2011;. © 2011 Wiley‐Liss, Inc.