bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of forest cover on peak flow and sediment discharge—an integrated field and modelling study in central–southern Chile
Authors: Birkinshaw Stephen J. , Bathurst James C. , Iroumé Andrés , Palacios Hardin 
Published: November 2010

AbstractAn integrated field and modelling study was carried out on the 35‐ha La Reina catchment, Chile, to test the hypothesis that the effect of forest cover on flood peaks becomes less important as the size of the hydrological event increases. Meteorological and discharge data were measured at the catchment before and after the pine plantation that covered 80% of the catchment area was logged. Analysis of the measured response of the catchment provides support for the hypothesis but is not conclusive. Therefore, modelling of the catchment using 1000 years of generated rainfall data representative of the current conditions was carried out for the forested and logged states. The simulations show that the absolute difference in discharge between the two cases remains approximately constant as the discharge increases: thus as a percentage of discharge it decreases. This relative convergence appears to become significant at return periods of greater than approximately 10 years. Tests with different hypothetical soil depths for the forested and logged catchments show an absolute convergence in discharge between the two cases for shallow soils and no convergence for deep soils. Sediment transport simulations show that forest cover provides a clear benefit in protecting the soil from erosion. Copyright © 2010 John Wiley & Sons, Ltd.
Investigation of the impacts of vegetation distribution and evaporative cooling on synthetic urban daytime climate using a coupled LES—LSM model
Authors: Huang Hsin‐Yuan , Margulis Steven A. , Chu Chia Ren , Tsai Hsiao‐Chung 
Published: November 2010

AbstractLocal flow properties and regional weather or climate are strongly affected by land‐atmosphere interactions of momentum and scalars within the daytime convective boundary layer (CBL). In this study, we investigate the impact of green space scale on the daytime atmospheric boundary layer (ABL) over a synthetic urban domain using a recently developed large‐eddy simulation‐land surface model (LES–LSM) framework. With the use of realistic soundings as initial conditions, a series of numerical experiments over synthetic urban surfaces with varied scale of vegetated area is performed. Simulated micrometeorological properties, surface fluxes, basic CBL characteristics, and cloud distribution are analysed. The results show reference‐level air potential temperature and specific humidity as well as surface fluxes over green space are significantly affected by the scale of green space in the urban domain. The surface organization due to vegetated area scale also has impacts on horizontally averaged scalar and momentum profiles; however, the magnitude in this study is smaller than the results of a previous study using a set of offline surface fluxes as the lower boundary condition for LES. In addition, even though this study only performs a daytime diurnal cycle, the impact of green space scale on cloud distribution in simulations is significant. The cases with more organized green space yield lower‐elevated cumulus cloud and larger‐cloud cover fraction, which impacts the energy budget at the top of boundary layer and, in turn, could lead to additional surface cooling with respect to longer‐term weather and climate. Copyright © 2010 John Wiley & Sons, Ltd.
Macrophage and dendritic cell phenotypic diversity in the context of biomaterials
Authors: Kou Peng Meng , Babensee Julia E. 
Published: November 2010

AbstractMacrophages (Mϕ) and dendritic cells (DCs) are critical antigen presenting cells that play pivotal roles in host responses to biomaterial implants. Although Mϕs have been widely studied for their roles in the inflammatory responses against biomaterials, the roles that DCs play in the host responses toward implanted materials have only recently been explored. DCs are of significant research interest because of the emergence of a large number of combination products that cross‐traditional medical device boundaries. These products combine biomaterials with biologics, including cells, nucleic acids, and/or proteins. The biomaterial component may evoke an inflammatory response, primarily mediated by neutrophils and Mϕs, whereas the biologic component may elicit an immunogenic immune response, initiated by DCs involving lymphocyte activation. Control of Mϕ phenotypic balance from proinflammatory M1 to reparative M2 is a goal of investigators to optimize the host response to biomaterials. Similarly, control of DC phenotype from proinflammatory to toleragenic is of interest in vaccine delivery and tissue engineering/transplantation situations, respectively. This review discusses the interconnection between innate and adaptive immunity, the comparative and contrasting phenotypes and roles of Mϕs and DCs in immunity, their responses to biomaterials and the strategies to modulate their phenotype for applications in tissue engineering and vaccine delivery. Furthermore, the collaboration between and unique roles of DCs and Mϕs needs to be addressed in future studies to gain a more complete picture of host responses toward combination products. © 2010 Wiley Periodicals, Inc. J Biomed Mater Res Part A:, 2010.
Biomimeticity in tissue engineering scaffolds through synthetic peptide modifications—Altering chemistry for enhanced biological response
Authors: Sreejalekshmi Kumaran G. , Nair Prabha D. 
Published: November 2010

AbstractBiomimetic and bioactive biomaterials are desirable as tissue engineering scaffolds by virtue of their capability to mimic natural environments of the extracellular matrix. Biomimeticity has been achieved by the incorporation of synthetic short peptide sequences into suitable materials either by surface modification or by bulk incorporation. Research in this area has identified several novel synthetic peptide segments, some of them with cell‐specific interactions, which may serve as potential candidates for use in explicit tissue applications. This review focuses on the developments and prospective directions of incorporating short synthetic peptide sequences onto scaffolds for tissue engineering, with emphasis on the chemistry of peptide immobilization and subsequent cell responses toward modified scaffolds. The article provides a decision‐tree‐type flow chart indicating the most probable cellular events on a given peptide‐modified scaffold along with the consolidated list of synthetic peptide sequences, supports as well as cell types used in various tissue engineering studies, and aims to serve as a quick reference guide to peptide chemists and material scientists interested in the field. © 2010 Wiley Periodicals, Inc. J Biomed Mater Res Part A:, 2011.
PDGF‐induced proliferation in human arterial and venous smooth muscle cells: Molecular basis for differential effects of PDGF isoforms
Authors: Li Li , Blumenthal Donald K. , Terry Christi M. , He Yuxia , Carlson Mary L. , Cheung Alfred K. 
Published: November 2010

AbstractPlatelet‐derived growth factor (PDGF) has been implicated in the pathogenesis of arterial atherosclerosis and venous neointimal hyperplasia. We examined the effects of PDGF isoforms on smooth muscle cells (SMCs) from arterial and venous origins in order to further understand the differential responsiveness of these vasculatures to proliferative stimuli. Serum‐starved human arterial and venous SMCs exhibited very different proliferative responses to PDGF isoforms. Whereas, proliferation of arterial SMCs was strongly stimulated by PDGF‐AA, venous SMCs showed no proliferative response to PDGF‐AA, but instead demonstrated a significantly greater proliferative response to PDGF‐BB than arterial SMCs. Part of this difference could be attributed to differences in PDGF receptors expression. There was a 2.5‐fold higher (P < 0.05) density of PDGF receptor‐α (PDGF‐Rα) and a 6.6‐fold lower (P < 0.05) density of PDGF‐Rβ expressed on arterial compared to venous SMCs. Concomitant with an increased proliferative response to PDGF‐AA in arterial SMCs was a marked PDGF‐Rα activation, enhanced phosphorylation of ERK1/2 and Akt, a transient activation of c‐Jun NH2‐terminal kinase (JNK), and a significant reduction in expression of the cell‐cycle inhibitor p27kip1. This pattern of signaling pathway changes was not observed in venous SMCs. No phosphorylation of PDGF‐Rα was detected after venous SMC exposure to PDGF‐AA, but there was enhanced phosphorylation of ERK1/2 and Akt in venous SMCs, similar to that seen in the arterial SMCs. PDGF‐BB stimulation of venous SMC resulted in PDGF‐Rβ activation as well as transactivation of epidermal growth factor receptor (EGF‐R); transactivation of EGF‐R was not observed in arterial SMCs. These results may provide an explanation for the differential susceptibility to proliferative vascular diseases of arteries and veins. J. Cell. Biochem. 112: 289–298, 2011. © 2010 Wiley‐Liss, Inc.
Hepatitis C virus E2 protein induce reactive oxygen species (ROS)‐related fibrogenesis in the HSC‐T6 hepatic stellate cell line
Authors: Ming‐Ju Hsieh , Yih‐Shou Hsieh , Tzy‐Yen Chen , Hui‐Ling Chiou 
Published: November 2010

AbstractChronic infection of hepatitis C virus (HCV) leads to hepatic fibrosis and subsequently cirrhosis, although the underlying mechanisms have not been established. Previous studies have indicated that the binding of HCV E2 protein and CD81 on the surface of hepatic stellate cells (HSCs) lead to the increased protein level and activity of matrix metallopeptidase (MMP) 2, indicating that E2 may involve in the HCV‐induced fibrosis. This study was designed to investigate the involvement of HCV E2 protein in the hepatic fibrogenesis. Results showed that E2 protein may promote the expression levels of α‐smooth muscle actin (α‐SMA) and collagen α(I). Furthermore, several pro‐fibrosis or pro‐inflammatory cytokines, including transforming growth factor (TGF)‐β1, connective tissue growth factor (CTGF), interleukin (IL)‐6 and IL‐1β, were significantly increased in E2 transfected‐HSC cell lines, while the expression of MMP‐2 are also considerably increased. Moreover, the significant increases of CTGF and TGF‐β1 in a stable E2‐expressing Huh7 cell line were also observed the same results. Further molecular studies indicated that the impact of E2 protein on collagen production related to higher production of ROS and activated Janus kinase (JAK)1, JAK2 and also enhance the activation of ERK1/2 and p38, while catalase and inhibitors specific for JAK, ERK1/2, and p38 abolish E2‐enhanced expression of collagen α(I). Taken together, this study indicated that E2 protein involve in the pathogenesis of HCV‐mediated fibrosis via an up‐regulation of collagen α(I) and oxidative stress, which is JAK pathway related. J. Cell. Biochem. 112: 233–243, 2011. © 2010 Wiley‐Liss, Inc.
Transforming growth factor‐β induces epithelial to mesenchymal transition and suppresses the proliferation and transdifferentiation of cultured human pancreatic duct cells
Authors: Shin Jeong‐Ah , Hong Oak‐Kee , Lee Hye‐Jung , Jeon Sung‐Yoon , Kim Ji‐Won , Lee Seung‐Hwan , Cho Jae‐Hyoung , Lee Jung‐Min , Choi Yoon‐Hee , Chang Sang‐Ah , Son Ho‐Young , Kim Joo‐Han , Yoon Kun‐Ho 
Published: November 2010

AbstractPancreatic duct cells are considered a potential source of β‐cell regeneration, and transforming growth factor‐β (TGF‐β) has been suggested to perform an important role in these processes, but the underlying mechanism of the signal pathways, especially in humans, remains poorly understood. To evaluate the role of TGF‐β1, pancreatic duct cells were isolated from three brain‐dead organ donors. Pancreatic cell clusters harvested after islet isolation were dispersed to single cells and cultured in monolayers, then treated with TGF‐β1. We analyzed the characteristics of the cultured cells, the TGF‐β1 intracellular signaling pathway, the proliferation, and transdifferentiation rates of the duct cells. We also evaluated the genes and protein expression patterns after TGF‐β1 treatment. After TGF‐β1 treatment, typical morphologic changes representative of EMT were observed and Erk1/2, JNK, and AKT phosphorylation, Ras downstream effectors, were increased. β cell‐specific transcription factors including PDX‐1, Beta2/NeuroD, Ist‐1, and NGN3 were markedly suppressed and the rate of transdifferentiation into β cells was also suppressed. Genomic and proteomic analyses suggested that TGF‐β1 induces marked changes in a variety of structural genes and proteins associated with EMT. In conclusion, TGF‐β1 induces EMT in cultured human pancreatic duct cells, but suppresses its proliferation and transdifferentiation into β cells. Our results are the first report of TGF‐β1 effects for EMT and ductal cell transdifferentiation and proliferation at the protein level in human pancreatic duct cells. J. Cell. Biochem. 112: 179–188, 2011. © 2010 Wiley‐Liss, Inc.
Extracellular matrix modulates insulin production during differentiation of AR42J cells: Functional role of Pax6 transcription factor
Authors: Hamamoto Kohei , Yamada Satoko , Hara Akemi , Kodera Tsutomu , Seno Masaharu , Kojima Itaru 
Published: November 2010

AbstractExtracellular matrix (ECM) modulates differentiation of pancreatic β‐cells during development. However, the mechanism by which ECM proteins modulate differentiation is not totally clear. We investigated the effect of ECM proteins on differentiation β‐cells in vitro. We investigated the effect of basement membrane ECM on differentiation of AR42J cells and rat ductal cells. First, we examined the effect of reconstituted basement membrane, Matrigel on differentiation of AR42J cells induced by activin and betacellulin. Matrigel augmented insulin production and increased the expression of GLUT2, SUR1, and glucokinase. Among various transcription factors investigated, Matrigel markedly upregulated the expression of Pax6. When Pax6 was overexpressed in cells treated with activin and betacellulin, the expression of insulin was upregulated. Conversely, knockdown of Pax6 significantly reduced the insulin expression in cells cultured on Matrigel. The effects of Matrigel on insulin‐production and induction of Pax6 were reproduced partially by laminin‐1, a major component of Matrigel, and inhibited by anti‐integrin‐β1 antibody. Matrigel also enhanced the activation of p38 mitogen‐activated kinase induced by activin and betacellulin, which was inhibited by anti‐β1 antibody. Finally, the effect of Matrigel on differentiation was reproduced in rat cultured ductal cells, and Matrigel also increased the expression of Pax6. These results indicate that basement membrane ECM augments differentiation of pancreatic progenitor cells to insulin‐secreting cells by upregulating the expression of Pax6. J. Cell. Biochem. 112: 318–329, 2011. © 2010 Wiley‐Liss, Inc.
NOS inhibition synchronizes calcium oscillations in human adipose tissue‐derived mesenchymal stem cells by increasing gap‐junctional coupling
Authors: Sauer Heinrich , Sharifpanah Fatemeh , Hatry Myriam , Steffen Paul , Bartsch Caroline , Heller Regine , Padmasekar Manju , Howaldt Hans‐Peter , Bein Gregor , Wartenberg Maria 
Published: November 2010

AbstractAdipose tissue‐derived mesenchymal stem cells (ASCs) are a promising stem cell source for cell transplantation. We demonstrate that undifferentiated ASCs display robust oscillations of intracellular calcium [Ca2+]i which may be associated with stem cell maintenance since oscillations were absent in endothelial cell differentiation medium supplemented with FGF‐2. [Ca2+]i oscillations were dependent on extracellular Ca2+ and Ca2+ release from intracellular stores since they were abolished in Ca2+‐free medium and in the presence of the store‐depleting agent thapsigargin. They were inhibited by the phospholipase C antagonist U73,122, the inositol 1,4,5‐trisphosphate (InsP3) receptor antagonist 2‐aminoethoxydiphenyl borate (2‐APB) as well as by the gap‐junction uncouplers 1‐heptanol and carbenoxolone, indicating regulation by the InsP3 pathway and dependence on gap‐junctional coupling. Cells endogenously generated nitric oxide (NO), expressed NO synthase 1 (NOS 1) and connexin 43 (Cx 43). The nitric oxide NOS inhibitors NG‐monomethyl‐L‐arginine (L‐NMMA), N(G)‐nitro‐L‐arginine methyl ester (L‐NAME), 2‐ethyl‐2‐thiopseudourea, and diphenylene iodonium as well as si‐RNA‐mediated down‐regulation of NOS 1 synchronized [Ca2+]i oscillations between individual cells, whereas the NO‐donors S‐nitroso‐N‐acetylpenicillamine (SNAP) and sodium nitroprusside (SNP) as well as the soluble guanylate cyclase inhibitor 1H‐[1,2,4]oxadiazolo‐[4,3‐a]quinoxalin‐1‐one (ODQ) were without effects. The synchronization of [Ca2+]i oscillations was due to an improvement of intracellular coupling since fluorescence recovery after photobleaching (FRAP) revealed increased reflow of fluorescent calcein into the bleached area in the presence of the NOS inhibitors DPI and L‐NAME. In summary our data demonstrate that intracellular NO levels regulate synchronization of [Ca2+]i oscillations in undifferentiated ASCs by controlling gap‐junctional coupling. J. Cell. Physiol. 226: 1642–1650, 2011. © 2010 Wiley‐Liss, Inc.
Wnt5b regulates mesenchymal cell aggregation and chondrocyte differentiation through the planar cell polarity pathway
Authors: Bradley Elizabeth W. , Drissi M. Hicham 
Published: November 2010

AbstractAlthough genetic evidence has demonstrated a role for Wnt5b during cartilage and limb development, little is known about the mechanisms underlying Wnt5b‐regulated chondrocyte differentiation. We observed that Wnt5b inhibited chondrocyte hypertrophy and expression of type X collagen. In addition, Wnt5b regulated the overall size of chondrogenic cultures, suggesting that Wnt5b regulates other processes involved in cartilage development. We therefore investigated the signaling pathways by which Wnt5b influences differentiation. Wnt5b activated known calcium‐dependent signaling pathways and JNK, a component of the planar cell polarity pathway. Since the planar cell polarity pathway regulates process such as cell migration and cell aggregation that are involved in limb development, we assayed for effects of Wnt5b on these processes. We observed a marked increase chondroprogenitor cell migration with Wnt5b expression. This effect was blocked by inhibition of JNK, but not by inhibition of other Wnt5b‐responsive factors. Expression of Wnt5b also disrupted the cellular aggregation associated with mesenchymal condensation. Decreased aggregation was associated with reduced cadherin expression as well as increased cadherin receptor turnover. This increase in cadherin receptor turnover was associated with an increase in Src‐dependent beta‐catenin phosphorylation downstream of Wnt5b. Our data demonstrate that not only does Wnt5b inhibit chondrocyte hypertrophy, but document a novel role for Wnt5b in modulating cellular migration through the JNK‐dependent and cell adhesion through an activation of Src and subsequent cadherin receptor turnover. J. Cell. Physiol. 226: 1683–1693, 2011. © 2010 Wiley‐Liss, Inc.
High capacity Na+/H+ exchange activity in mineralizing osteoblasts
Authors: Liu Li , Schlesinger Paul H. , Slack Nicole M. , Friedman Peter A. , Blair Harry C. 
Published: November 2010

AbstractOsteoblasts synthesize bone in polarized groups of cells sealed by tight junctions. Large amounts of acid are produced as bone mineral is precipitated. We addressed the mechanism by which cells manage this acid load by measuring intracellular pH (pHi) in non‐transformed osteoblasts in response to weak acid or bicarbonate loading. Basal pHi in mineralizing osteoblasts was ∼7.3 and decreased by ∼1.4 units upon replacing extracellular Na+ with N‐methyl‐D‐glucamine. Loading with 40 mM acetic or propionic acids, in normal extracellular Na+, caused only mild cytosolic acidification. In contrast, in Na+‐free solutions, weak acids reduced pHi dramatically. After Na+ reintroduction, pHi recovered rapidly, in keeping with Na+/H+ exchanger (NHE) activity. Sodium‐dependent pHi recovery from weak acid loading was inhibited by amiloride with the Ki consistent with NHEs. NHE1 and NHE6 were expressed strongly, and expression was upregulated highly, by mineralization, in human osteoblasts. Antibody labeling of mouse bone showed NHE1 on basolateral surfaces of all osteoblasts. NHE6 occurred on basolateral surfaces of osteoblasts mainly in areas of mineralization. Conversely, elevated HCO alkalinized osteoblasts, and pH recovered in medium containing Cl−, with or without Na+, in keeping with Na+‐independent Cl−/HCO exchange. The exchanger AE2 also occurred on the basolateral surface of osteoblasts, consistent with Cl−/HCO exchange for elimination of metabolic carbonate. Overexpression of NHE6 or knockdown of NHE1 in MG63 human osteosarcoma cells confirmed roles of NHE1 and NHE6 in maintaining pHi. We conclude that in mineralizing osteoblasts, slightly basic basal pHi is maintained, and external acid load is dissipated, by high‐capacity Na+/H+ exchange via NHE1 and NHE6. J. Cell. Physiol. 226: 1702–1712, 2011. © 2010 Wiley‐Liss, Inc.
Reduced levels of folate transporters (PCFT and RFC) in membrane lipid rafts result in colonic folate malabsorption in chronic alcoholism
Authors: Wani Nissar Ahmad , Kaur Jyotdeep 
Published: November 2010

AbstractWe studied the effect of chronic ethanol ingestion on folate transport across the colonic apical membranes (CAM) in rats. Male Wistar rats were fed 1 g/kg body weight/day ethanol (20%) solution orally for 3 months and folate transport was studied in the isolated colon apical membrane vesicles. The folate transport was found to be carrier mediated, saturable, with pH optima at 5.0. Chronic ethanol ingestion reduced the folate transport across the CAM by decreasing the affinity of transporters (high Km) for the substrate and by decreasing the number of transporter molecules (low Vmax) on the colon luminal surface. The decreased transport activity at the CAM was associated with down‐regulation of the proton‐coupled folate transporter (PCFT) and the reduced folate carrier (RFC) which resulted in decreased PCFT and RFC protein levels in the colon of rats fed alcohol chronically. Moreover, the PCFT and the RFC were found to be distributed in detergent insoluble fraction of the CAM in rats. Floatation experiments on Optiprep density gradients demonstrated the association of the PCFT and the RFC protein with lipid rafts (LR). Chronic alcoholism decreased the PCFT and the RFC protein levels in the CAM LR in accordance with the decreased synthesis. Hence, we propose that downregulation in the expression of the PCFT and the RFC in colon results in reduced levels of these transporters in colon apical membrane LR as a mechanism of folate malabsorption during chronic alcoholism. J. Cell. Physiol. 226: 579–587, 2011. © 2010 Wiley‐Liss, Inc.