bluuebunny/crossref_metadata_2025_split huggingface dataset:
The response in floodplain respiration of an alpine river to experimental inundation under different temperature regimes
Authors: Simčič Tatjana , Mori Nataša , Hossli Christian , Robinson Christopher T. , Doering Michael 
Published: June 2015

AbstractThe respiratory potential [i.e. electron transport system activity (ETSA)] of soils and sediments from five floodplain habitats (channel, gravel, islands, riparian forest and grassland) of the Urbach River, Switzerland, and actual respiration rate (R) of the same samples exposed to experimental inundation were measured. Measurements were carried out at three incubation temperatures (4°C, 12°C and 20°C), and ETSA/R ratios (i.e. exploitation of the overall metabolic capacity) were investigated to better understand the effects of temperature and inundation on floodplain functional heterogeneity. Furthermore, ETSA/R ratios obtained during experimental inundation were compared with ETSA/R ratios from field measurements to investigate the exploitation in total metabolic potential at different conditions. Lowest ETSA and R were measured in samples from channel and gravel habitats, followed by those from islands. Substantially higher values were measured in soils from riparian forest and grassland. Both ETSA and R increased with increasing temperature in samples from all habitats, while the ETSA/R ratio decreased because of a rapid response in microbial community respiration to higher temperatures. The metabolic capacity exploitation (i.e. ETSA/R) during experimental inundation was lowest in predominantly terrestrial samples (riparian forest and grassland), indicating the weakest response to wetted conditions. Comparison of experimentally inundated and field conditions revealed that in rarely flooded soils, the metabolic capacity was less exploited during inundation than during non‐flooded conditions. The results suggest high sensitivity in floodplain respiration to changes in temperature and hydrological regime. ETSA/R ratios are considered good indicators of changes in metabolic activity of floodplain soils and sediments, and thus useful to estimate the impact of changes in hydrological regime or to evaluate success of floodplain restoration actions. Copyright © 2015 John Wiley & Sons, Ltd.
The influence of mesh topology in the abdominal wall repair process
Authors: De Maria Carmelo , Burchielli Silvia , Salvadori Claudia , Santoro Vito , Montemurro Francesca , Orsi Gianni , Vozzi Giovanni 
Published: June 2015

AbstractThe tissue integration and the formation of adhesions in the repair of abdominal wall defects are principally led to the topology and the mechanical properties of implanted prosthesis. In this study we analyzed the influence of the topology of the meshes for abdominal wall repair, made of polypropylene (PP), evaluating its ability to prevent and to minimize the formation of adhesions, and to promote tissue ingrowth. Two series of in vivo studies were performed. In the first, two types of PP meshes, a lightweight macroporous mesh (LWM) and a heavyweight microporous mesh (HWM) were compared with determine the optimal porosity for tissue integration. In the second, a composite mesh, Clear Mesh Composite (CMC), made of a LWM sewn on a PP planar smooth film, was compared with a PP planar film, to demonstrate how two different topologies of same material are able to induce different tissue integration with the abdominal wall and different adhesion with internal organs. In both studies, the prostheses were implanted in Wistar rats and histological analysis and mechanical characterization of tissue coupled with the implants were performed. LWM showed better host tissue ingrowth in comparison to HWM. CMC prosthesis showed no adhesions to the viscera and no strong foreign body reaction, moreover its elasticity and anisotropy index were more similar to that of natural tissue. These results demonstrated that the surface morphology of PP surgical meshes allowed to modulate their repair ability. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 104B: 1220–1228, 2016.
Visible light crosslinking of methacrylated hyaluronan hydrogels for injectable tissue repair
Authors: Fenn Spencer L. , Floreani Rachael 
Published: June 2015

AbstractTissue engineering hydrogels are primarily cured in situ using ultraviolet (UV) radiation which limits the use of hydrogels as drug or cell carriers. Visible green light activated crosslinking systems are presented as a safe alternative to UV photocrosslinked hydrogels, without compromising material properties such as viscosity and stiffness. The objective of this study was to fabricate and characterize photocrosslinked hydrogels with well‐regulated gelation kinetics and mechanical properties for the repair or replacement of soft tissue. An anhydrous methacrylation of hyaluronan (HA) was performed to control the degree of modification (DOM) of HA, verified by 1H‐NMR spectroscopy. UV‐activated crosslinking was compared to visible green light activated crosslinking. While the different photocrosslinking techniques resulted in varied crosslinking times, comparable mechanical properties of UV and green light activated crosslinked hydrogels were achieved using each photocrosslinking method by adjusting time of light exposure. Methacrylated HA (HA‐MA) hydrogels of varying molecular weight, DOM, and concentration exhibited compressive moduli ranging from 1 kPa to 116 kPa, for UV crosslinking, and 3 kPa to 146 kPa, for green light crosslinking. HA‐MA molecular weight and concentration were found to significantly influence moduli values. HA‐MA hydrogels did not exhibit any significant cytotoxic effects toward human mesenchymal stem cells. Green light activated crosslinking systems are presented as a viable method to form natural‐based hydrogels in situ. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 104B: 1229–1236, 2016.
Conditional Deletion of Indian Hedgehog in Limb Mesenchyme Results in Complete Loss of Growth Plate Formation but Allows Mature Osteoblast Differentiation
Authors: Amano Katsuhiko , Densmore Michael J , Lanske Beate 
Published: June 2015

ABSTRACT

Indian hedgehog (Ihh) is widely recognized as an essential factor for proper skeletal development. Previous in vivo studies using mutant Ihh mouse models were limited by perinatal lethality or carried out after a growth plate formed. Thus the important role of Ihh in mesenchymal cell differentiation has not been investigated. In this study, we established Prx1-Cre;Ihhfl/fl mice to ablate Ihh specifically in limb mesenchyme to allow us to observe the phenotype continuously from prenatal development to 3 weeks of age. Mutant mice displayed severe limb abnormalities characterized by complete lack of secondary ossification center and growth plate, indicating an essential role for Ihh in the development of these structures. Interestingly, we discovered that osteoblast differentiation and bone formation could occur in conditions of deficient Ihh. This is a novel finding that has not been observed because of the early lethality of previous Ihh mutants. Mature osteoblasts expressing osteocalcin could be detected in the center of mutant bones at postnatal day 10 (P10). Osteoclasts and blood vessel formation were also present, suggesting active bone remodeling. Histomorphometric analyses show a significant increase in osteoclast number with no major changes in bone formation rate at 3 weeks of age. Mutant long bones in the limbs were deformed, with cortices comprised of irregular woven bone. Also, there was a marked decrease in gene expression of osteoblastic and osteocytic markers. Moreover, mutant long bones displayed bone dysplasia in which we observed increased osteoclast activity and partially reduced osteoblastic and osteocytic differentiation that lead ultimately to loss of bone structures at 3 weeks of age. In summary, our data show for the first time, the presence of mature osteoblasts in long bones of the limbs despite the complete loss of growth plate formation due to Ihh deficiency. These data indicate an important function for Ihh in regulating limb mesenchymal cell differentiation. © 2015 American Society for Bone and Mineral Research.
Alternative NF-κB Regulates RANKL-Induced Osteoclast Differentiation and Mitochondrial Biogenesis via Independent Mechanisms
Authors: Zeng Rong , Faccio Roberta , Novack Deborah V 
Published: June 2015

ABSTRACT

Mitochondrial biogenesis, the generation of new mitochondrial DNA and proteins, has been linked to osteoclast (OC) differentiation and function. In this study we used mice with mutations in key alternative NF-κB pathway proteins, RelB and NF-κB–inducing kinase (NIK), to dissect the complex relationship between mitochondrial biogenesis and osteoclastogenesis. In OC precursors lacking either NIK or RelB, receptor activator of NF-κB ligand (RANKL) was unable to increase mitochondrial DNA or oxidative phosphorylation (OxPhos) protein expression, which was associated with lower oxygen consumption rates. Transgenic OC precursors expressing constitutively active NIK showed normal RANKL-induced mitochondrial biogenesis (OxPhos expression and mitochondria copy number) compared to controls, but larger mitochondrial dimensions and increased oxygen consumption rates, suggesting increased mitochondrial function. To deduce the mechanism for mitochondrial biogenesis defects in NIK-deficient and RelB-deficient precursors, we examined expression of genes known to control this process. PGC-1β (Ppargc1b) expression, but not PGC-1α, PPRC1, or ERRα, was significantly reduced in RelB–/– and NIK–/– OCs. Because PGC-1β has been reported to positively regulate both mitochondrial biogenesis and differentiation in OCs, we retrovirally overexpressed PGC-1β in RelB–/– cells, but surprisingly found that it did not affect differentiation, nor did it restore RANKL-induced mitochondrial biogenesis. To determine whether the blockade in osteoclastogenesis in RelB-deficient cells precludes mitochondrial biogenesis, we rescued RelB–/– differentiation via overexpression of NFATc1. Mitochondrial parameters in neither WT nor RelB-deficient cultures were affected by NFATc1 overexpression, and bone resorption in RelB–/– was not restored. Furthermore, NFATc1 co-overexpression with PGC-1β, although allowing OC differentiation, did not rescue mitochondrial biogenesis or bone resorption in RelB–/– OCs, by CTX-I levels. Thus, our results indicate that the alternative NF-κB pathway plays dual, but distinct, roles in controlling the independent processes of OC differentiation and OC mitochondrial biogenesis. Furthermore, the inability of PGC-1β to drive mitochondrial biogenesis in OCs without RelB indicates a cell-type specificity in mitochondria regulation. © 2015 American Society for Bone and Mineral Research.
Numb Protects Human Renal Tubular Epithelial Cells From Bovine Serum Albumin‐Induced Apoptosis Through Antagonizing CHOP/PERK Pathway
Authors: Ding Xuebing , Ma Mingming , Teng Junfang , Shao Fengmin , Wu Erxi , Wang Xuejing 
Published: June 2015

ABSTRACTIn recent studies, we found that Numb is involved in oxidative stress‐induced apoptosis of renal proximal tubular cells; however, its function on ER stress‐induced apoptosis in proteinuric kidney disease remains unknown. The objective of the present study is to explore the role of Numb in urinary albumin‐induced apoptosis of human renal tubular epithelial cells (HKCs). In this study, we demonstrate that incubation of HKCs with bovine serum albumin (BSA) resulted in caspase three‐dependent cell death. Numb expression was down‐regulated by BSA in a time‐ and dose‐dependent manner. Knockdown of Numb by siRNA sensitized HKCs to BSA‐induced apoptosis, whereas overexpression of Numb protected HKCs from BSA‐induced apoptosis. Moreover, BSA activated CHOP/PERK signaling pathway in a time‐ and dose‐dependent manner as indicated by increased expression of CHOP, PERK, and P‐PERK. Furthermore, knockdown of CHOP or PERK significantly attenuated the promoting effect of Numb on BSA‐induced apoptosis, while overexpression of CHOP impaired the protective effect of Numb on BSA‐induced apoptosis. Taken together, our findings demonstrate that Numb plays a protective role on BSA‐induced apoptosis through inhibiting CHOP/PERK signaling pathway in human renal tubular epithelial cells. Therefore, the results from this study provides evidence that Numb is a new target of ER‐associated apoptotic signaling networks and Numb may serve as a promising therapeutic target for proteinuric diseases. J. Cell. Biochem. 117: 163–171, 2016. © 2015 Wiley Periodicals, Inc.
PRDM1, a Tumor‐Suppressor Gene, is Induced by Genkwadaphnin in Human Colon Cancer SW620 Cells
Authors: Kang Ho‐Bum , Lee Ha‐Reum , Jee Da Jung , Shin Su‐Hyun , Nah Seong‐Su , Yoon Sun Young , Kim Jae Wha 
Published: June 2015

ABSTRACTGenkwadaphnin (GD‐1) is isolated from the flower buds of Daphne genkwa Siebold et Zuccarini (Thymelaeaceae), and it has been used as a traditional Korean and Chinese medicine. In this study, the authors observe that GD‐1 inhibits the growth of the colon cancer cell line, SW620, through the up‐regulation of p21 expression in a PRDM1‐dependent manner. After treatment with GD‐1, the transcriptional repressor PRDM1 is prominently induced in SW620 cells. Furthermore, GD‐1 induce the phosphorylation of PKD1 and MEK and subsequently provide PRDM1 enhancement, resulting in the suppression of c‐Myc expression and the up‐regulation of p21. PKD1 knockdown using siRNA abrogates PRDM1 expression by GD‐1 and subsequently disrupts the regulation of c‐Myc and p21 expression. Treating SW620 cells with GD‐1 inhibits cell‐cycle progression and is characterized by the down‐regulation of c‐Myc followed by the up‐regulation of p21 expression. The up‐regulation of p21 by GD‐1 induces the growth arrest of the SW620 colon cancer cell line. Based on these data, the authors propose that GD‐1 has tumor‐suppressor activity that may contribute to the anti‐tumor effects of PRDM1 in colon cancer. J. Cell. Biochem. 117: 172–179, 2016. © 2015 Wiley Periodicals, Inc.
Regulation of Adipose Tissue Stem Cells Angiogenic Potential by Tumor Necrosis Factor‐Alpha
Authors: Zubkova Ekaterina S. , Beloglazova Irina B. , Makarevich Pavel I. , Boldyreva Maria A. , Sukhareva Olga Yu. , Shestakova Marina V. , Dergilev Konstantin V. , Parfyonova Yelena V. , Menshikov Mikhail Yu. 
Published: June 2015

ABSTRACTTissue regeneration requires coordinated “teamwork” of growth factors, proteases, progenitor and immune cells producing inflammatory cytokines. Mesenchymal stem cells (MSC) might play a pivotal role by substituting cells or by secretion of growth factors or cytokines, and attraction of progenitor and inflammatory cells, which participate in initial stages of tissue repair. Due to obvious impact of inflammation on regeneration it seems promising to explore whether inflammatory factors could influence proangiogenic abilities of MSC. In this study we investigated effects of TNF‐α on activity of adipose‐derived stem cells (ADSC). We found that treatment with TNF‐α enhances ADSC proliferation, F‐actin microfilament assembly, increases cell motility and migration through extracellular matrix. Exposure of ADSC to TNF‐α led to increased mRNA expression of proangiogenic factors (FGF‐2, VEGF, IL‐8, and MCP‐1), inflammatory cytokines (IL‐1β, IL‐6), proteases (MMPs, uPA) and adhesion molecule ICAM‐1. At the protein level, VEGF, IL‐8, MCP‐1, and ICAM‐1 production was also up‐regulated. Pre‐incubation of ADSC with TNF‐α‐enhanced adhesion of monocytes to ADSC but suppressed adherence of ADSC to endothelial cells (HUVEC). Stimulation with TNF‐α triggers ROS generation and activates a number of key intracellular signaling mediators known to positively regulate angiogenesis (Akt, small GTPase Rac1, ERK1/2, and p38 MAP‐kinases). Pre‐treatment with TNF‐α‐enhanced ADSC ability to promote growth of microvessels in a fibrin gel assay and accelerate blood flow recovery, which was accompanied by increased arteriole density and reduction of necrosis in mouse hind limb ischemia model. These findings indicate that TNF‐α plays a role in activation of ADSC angiogenic and regenerative potential. J. Cell. Biochem. 117: 180–196, 2016. © 2015 Wiley Periodicals, Inc.
TRPV5/V6 Channels Mediate Ca2+ Influx in Jurkat T Cells Under the Control of Extracellular pH
Authors: Tomilin Victor N. , Cherezova Alena L. , Negulyaev Yuri A. , Semenova Svetlana B. 
Published: June 2015

ABSTRACTRegulation of cytoplasmic free calcium concentration [Ca2+]i is a key factor for the maintenance of cellular homeostasis in different cell types, including lymphocytes. During T lymphocyte activation as well as production of cytokines, sustained Ca2+ influx is essential, however, it remains unclear how this influx is regulated. Previously, we reported the expression and functional activity of calcium channels TRPV5 and TRPV6 (transient receptor potential vanilloid type 5 and 6) in human leukemia Jurkat T cells. In this study, using single channel recordings, we found that activity of calcium channels TRPV5/V6 in Jurkat T cells is subject to strong control of external stimuli such as a low‐ or high‐pH stressor. We showed that extracellular acidic pH reduces the activity of TRPV5/V6 channels, whereas alkaline pH increases the activity of TRPV5/V6 channels in Jurkat T cells. Using calcium imaging, we found that Ca2+ influx in Jurkat T cells displayed sensitivity to extracellular pH, similar to that shown for the calcium channels TRPV5/V6. Double immunostaining of Jurkat T cells revealed that TRPV5 and TRPV6 channels colocalize with clathrin and the early endocytosis marker, EEA1. Moreover, we demonstrated that a specific inhibitor of clathrin‐dependent endocytosis, dynasore, blocked TRPV5/V6 activity, and Ca2+ influx into Jurkat T cells. Overall, our findings indicate that strong environmental cues may affect the intracellular calcium level in Jurkat T cells by influencing the traffic of TRPV5/V6 channels in lymphocytes. J. Cell. Biochem. 117: 197–206, 2016. © 2015 Wiley Periodicals, Inc.
The “Mechanostat Theory” of Frost and the OPG/RANKL/RANK System
Authors: Tyrovola Joanna B. , Odont XX 
Published: June 2015

ABSTRACTFrost's great interest to elucidate the principles of action underlying skeletal deformities, during, and after growth, urged him to undertake an extensive study of the mammalian skeleton. He suggested that survival of the skeleton (but also of other tissues, such as fibrous tissue, hyaline cartilage, fibrocartilage, cementum, or dentin) requires the functional coordination of modeling and remodeling. Modeling adapts bone to overloads, by enhancing additions of new bone and by changing bone architecture, and remodeling adapts bone to underloads by removing bone next to marrow and conserving normally used bone. There exists a mechanism that monitors bone metabolism (longitudinal growth, bone modeling, and remodeling activities) in relation to mechanical usage, the “mechanostat.” Recent literature has presented new information regarding the physiological procedure of osteoclast and osteoblast activation. It has been understood that the OPG/RANKL/RANK proteinic system regulates bone metabolism by exerting biological effects on osteoblasts or osteoclasts. The same proteinic network, also regulates alveolar remodeling during tooth movement, as well as physiological root resorption and root resorption during orthodontic tooth movement. The aim of the present review is the presentation and evaluation of recent information in the field of osteoclast and osteoblast biology, as regards to the “mechanostat theory” of Frost. An attempt will be made to elucidate, whether recent data can support this remarkable theory and reveal the biological mechanisms behind it. J. Cell. Biochem. 116: 2724–2729, 2015. © 2015 Wiley Periodicals, Inc.
Risks and Benefits of Bisphosphonate Therapies
Authors: Reyes Carlen , Hitz Mette , Prieto‐Alhambra Daniel , Abrahamsen Bo 
Published: June 2015

ABSTRACTBisphosphonates are the mainstay of osteoporosis treatment but also play a fundamental role in treating other bone diseases such as Osteogenesis Imperfecta, Pagets' disease, and in the prevention of adverse skeletal effects in certain cancers such as prostate cancer or multiple myeloma. In the last decades, the refinement of bisphosphonates and an increase in the number of new bisphosphonates commercialized has altered the clinical management of these diseases. Despite differences between randomized controlled trials and observational studies, overall all bisphosphonates licensed have proven to reduce the risk of fracture through the inhibition of bone resorption. Other beneficial effects include pain reduction in bone metastasis and potentially a decrease in mortality. However, the chronic nature of most of these disorders implies long‐term treatments, which can be associated with long‐term adverse effects. Some of the adverse effects identified include an increased risk of atypical femur fractures, osteonecrosis of the jaw, gastrointestinal side effects, or atrial fibrillation. The harm/benefit thinking and the constant update regarding these medications are vital in the day‐to‐day decision‐making in clinical practices. The aims of this review are to compile the basic characteristics of these drugs and outline the most important benefits and side effects and provide a clinical context as well as a research agenda to fill the gaps in our knowledge. J. Cell. Biochem. 117: 20–28, 2016. © 2015 Wiley Periodicals, Inc.
Chondrogenic differentiation of human umbilical cord blood‐derived mesenchymal stem cells in vitro
Authors: Mostafa Ibrahim Azza , Mohamed Elgharabawi Nesrine , Mohamed Makhlouf Manal , Yahia Ibrahim Omnia 
Published: June 2015

ABSTRACTDifferent therapeutic techniques have been developed for regeneration of articular cartilage injuries, but none has provided an optimal solution to their treatment. Human umbilical cord blood‐mesenchymal Stem Cells (HUCB‐MSCs) have been considered as promising alternative cell source for cartilage repair. Objectives: Examining the success rate of MSCs isolation from HUCB as well as chondrogenic differentiation potential of HUCB‐MSCs in vitro. Materials and methods: 32 UCB samples were collected, in addition to 5 bone marrow (BM) and 5 peripheral blood (PB) samples, taken as reference controls. Samples were used for mononuclear cells isolation from which MSCs were expanded under complete aseptic conditions, were verified morphologically and through the presence of CD44 and CD105, and absence of CD34. Results: Success rate of UCB‐MSCs isolation was (25%), a rate that was lower than those of PB (40%) and BM (80%). Accordingly, certain input parameters have been recommended for successful MSCs isolation from UCB. On selecting samples in which recommended parameters were fulfilled, success rate was increased to 72%. This was together with providing optimal experiment conditions; mainly type of expansion medium, success rate reached 80%. Then, successfully expanded MSCs were subjected to chondrogenic differentiation by culturing in pelleted micromass system in presence of transforming growth factor beta‐1 and chondrogenic medium devoid of fetal bovine serum to evaluate their ability to undergo chondrogenesis. Differentiation was verified microscopically using special stains, and proved by reverse transcriptase‐polymerase chain reaction for expression of aggrecan and collagen II genes. In conclusion, in vitro differentiation into chondrocytes is possible from HUCB‐MSCs. Microsc. Res. Tech. 78:667–675, 2015. © 2015 Wiley Periodicals, Inc.