bluuebunny/crossref_metadata_2025_split huggingface dataset:
Progressive ankylosis protein (ANK) in osteoblasts and osteoclasts controls bone formation and bone remodeling
Authors: Kim Hyon Jong , Minashima Takeshi , McCarthy Edward F , Winkles Jeffrey A , Kirsch Thorsten 
Published: February 2010

Abstract
The progressive ankylosis gene (ank) encodes a transmembrane protein that transports intracellular inorganic pyrophosphate (PPi) to the extracellular milieu. ank/ank mice, which express a truncated nonfunctional ANK, showed a markedly reduced bone mass, bone-formation rate, and number of tartrate-resistant acid phosphatase–positive (TRAP+) multinucleated osteoclasts. ANK function deficiency suppressed osteoblastic differentiation of ank/ank bone marrow stromal cells, as indicated by the decrease in the expression of bone marker genes, including osterix, reduced alkaline phosphatase activity, and mineralization. Runx2 gene expression levels were not altered. Conversely, overexpression of ANK in the preosteoblastic cell line MC3T3-E1 resulted in increased expression of bone marker genes, including osterix. Whereas runx2 expression was not altered in ANK-overexpressing MC3T3-E1 cells, runx2 transcriptional activity was increased. Extracellular PPi or Pi stimulated osteoblastogenic differentiation of MC3T3-E1 cells or partially rescued delayed osteoblastogenic differentiation of ank/ank bone marrow stromal cells. A loss of PPi transport function ANK mutation also stimulated osteoblastogenic differentiation of MC3T3-E1 cells. Furthermore, ANK function deficiency suppressed the formation of multinucleated osteoclasts from ank/ank bone marrow cells cultured in the presence of macrophage colony-stimulating factor and receptor activator of nuclear factor-κB ligand. In conclusion, ANK is a positive regulator of osteoblastic and osteoclastic differentiation events toward a mature osteoblastic and osteoclastic phenotype. © 2010 American Society for Bone and Mineral Research
Leptin stimulates fibroblast growth factor 23 expression in bone and suppresses renal 1α,25-dihydroxyvitamin D3 synthesis in leptin-deficient ob/ob Mice
Authors: Tsuji Kiyomi , Maeda Toyonobu , Kawane Tetsuya , Matsunuma Ayako , Horiuchi Noboru 
Published: February 2010

Abstract
Leptin is the LEP (ob) gene product secreted by adipocytes. We previously reported that leptin decreases renal expression of the 25-hydroxyvitamin D3 1α-hydroxylase (CYP27B1) gene through the leptin receptor (ObRb) by indirectly acting on the proximal tubules. This study focused on bone-derived fibroblast growth factor 23 (FGF-23) as a mediator of the influence of leptin on renal 1α-hydroxylase mRNA expression in leptin-deficient ob/ob mice. Exposure to leptin (200 ng/mL) for 24 hours stimulated FGF-23 expression by primary cultured rat osteoblasts. Administration of leptin (4 mg/kg i.p. at 12-hour intervals for 2 days) to ob/ob mice markedly increased the serum FGF-23 concentration while significantly reducing the serum levels of calcium, phosphate, and 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3]. Administration of FGF-23 (5 µg i.p. at 12-hour intervals for 2 days) to ob/ob mice suppressed renal 1α-hydroxylase mRNA expression. The main site of FGF-23 mRNA expression was the bone, and leptin markedly increased the FGF-23 mRNA level in ob/ob mice. In addition, leptin significantly reduced 1α-hydroxylase and sodium-phosphate cotransporters (NaPi-IIa and NaPi-IIc) mRNA levels but did not affect Klotho mRNA expression in the kidneys of ob/ob mice. Furthermore, the serum FGF-23 level and renal expression of 1α-hydroxylase mRNA were not influenced by administration of leptin to leptin receptor–deficient (db/db) mice. These results indicate that leptin directly stimulates FGF-23 synthesis by bone cells in ob/ob mice, suggesting that inhibition of renal 1,25(OH)2D3 synthesis in these mice is at least partly due to elevated bone production of FGF-23. © 2010 American Society for Bone and Mineral Research
Near-infrared fluorescent probe traces bisphosphonate delivery and retention in vivo
Authors: Kozloff Kenneth M , Volakis Leo I , Marini Joan C , Caird Michelle S 
Published: February 2010

AbstractBisphosphonate use has expanded beyond traditional applications to include treatment of a variety of low-bone-mass conditions. Complications associated with long-term bisphosphonate treatment have been noted, generating a critical need for information describing the local bisphosphonate-cell interactions responsible for these observations. This study demonstrates that a fluorescent bisphosphonate analogue, far-red fluorescent pamidronate (FRFP), is an accurate biomarker of bisphosphonate deposition and retention in vivo and can be used to monitor site-specific local drug concentration. In vitro, FRFP is competitively inhibited from the surface of homogenized rat cortical bone by traditional bisphosphonates. In vivo, FRFP delivery to the skeleton is rapid, with fluorescence linearly correlated with bone surface area. Limb fluorescence increases linearly with injected dose of FRFP; injected FRFP does not interfere with binding of standard bisphosphonates at the doses used in this study. Long-term FRFP retention studies demonstrated that FRFP fluorescence decreases in conditions of normal bone turnover, whereas fluorescence was retained in conditions of reduced bone turnover, demonstrating preservation of local FRFP concentration. In the mandible, FRFP localized to the alveolar bone and bone surrounding the periodontal ligament and molar roots, consistent with findings of osteonecrosis of the jaw. These findings support a role for FRFP as an effective in vivo marker for bisphosphonate site-specific deposition, turnover, and long-term retention in the skeleton. © 2010 American Society for Bone and Mineral Research
Taking vitamin D with the largest meal improves absorption and results in higher serum levels of 25-hydroxyvitamin D
Authors: Mulligan Guy B , Licata Angelo 
Published: February 2010

Abstract
Many patients treated for vitamin D deficiency fail to achieve an adequate serum level of 25-hydroxyvitamin D [25(OH)D] despite high doses of ergo- or cholecalciferol. The objective of this study was to determine whether administration of vitamin D supplement with the largest meal of the day would improve absorption and increase serum levels of 25(OH)D. This was a prospective cohort study in an ambulatory tertiary-care referral center. Patients seen at the Cleveland Clinic Foundation Bone Clinic for the treatment of vitamin D deficiency who were not responding to treatment make up the stugy group. Subjects were instructed to take their usual vitamin D supplement with the largest meal of the day. The main outcome measure was the serum 259(OH)D level after 2 to 3 months. Seventeen patients were analyzed. The mean age (±SD) and sex (F/M) ratio were 64.5 ± 11.0 years and 13 females and 4 males, respectively. The dose of 25(OH)D ranged from 1000 to 50,000 IU daily. The mean baseline serum 25(OH)D level (±SD) was 30.5 ± 4.7 ng/mL (range 21.6 to 38.8 ng/mL). The mean serum 25(OH)D level after diet modification (±SD) was 47.2 ± 10.9 ng/mL (range 34.7 to 74.0 ng/mL, p &lt; .01). Overall, the average serum 25(OH)D level increased by 56.7% ± 36.7%. A subgroup analysis based on the weekly dose of vitamin D was performed, and a similar trend was observed.
Thus it is concluded that taking vitamin D with the largest meal improves absorption and results in about a 50% increase in serum levels of 25(OH)D levels achieved. Similar increases were observed in a wide range of vitamin D doses taken for a variety of medical conditions. © 2010 American Society for Bone and Mineral Research
Splice variant specific increase in Ca2+/calmodulin‐dependent protein kinase 1‐gamma mRNA expression in response to acute pyrethroid exposure
Authors: Harrill Joshua A. , Knapp Geremy W. , Crofton Kevin M. 
Published: February 2010

AbstractIn mammals, pyrethroids are neurotoxicants that interfere with ion channel function in excitable neuronal membranes. Previous work demonstrated increases in the expression of Ca2+/calmodulin‐dependent protein kinase 1‐gamma (Camk1g) mRNA following acute deltamethrin and permethrin exposure. In the rat, this gene is expressed as two distinct splice variants,Camk1g1andCamk1g2. The present study tests the hypothesis that changes inCamk1gmRNA expression in the rat following acute pyrethroid exposure are due to a specific increase in theCamk1g1splice variant and not theCamk1g2splice variant. Long‐Evans rats were acutely exposed to permethrin, deltamethrin, or corn oil vehicle. Frontal cortex was collected at 6 h postdosing. In addition, rats were exposed to permethrin (100 mg/kg) or deltamethrin (3 mg/kg), and frontal cortex was collected at 1, 3, 6, 9, 12, or 24 h along with time‐matched vehicle controls. Expression ofCamk1g1andCamk1g2mRNA was measured by quantitative real‐time RT‐PCR and quantified using the 2‐Δ ΔCTmethod. Dose‐dependent increases inCamk1g1mRNA expression were observed for both pyrethroids at 6 h. In addition, a dose‐dependent increase inCamk1g2was observed at 6 h although it was very small in magnitude. The increases inCamk1g1expression for deltamethrin and permethrin peak between 3 and 6 h postexposure and returns to control levels by 9 h. There was no increase in CAMK1G1 protein as measured with Western blots. The present data demonstrate that pyrethroid‐induced changes inCamk1gare driven mainly by increased expression of theCamk1g1splice variant. © 2010 Wiley Periodicals, Inc. J Biochem Mol Toxicol 24:174–186, 2010; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20324
Young mothers' involvement in a prenatal and postpartum support program
Authors: Wen Xiaoli , Korfmacher Jon , Hans Sydney L. , Henson Linda G. 
Published: February 2010

AbstractThe involvement of 124 young mothers in a doula support program was measured in two dimensions—quantity of program contact and quality of mother–doula helping relationship. The study examined each dimension's differential associations with maternal outcomes, as well as the moderating effects of mother characteristics on these associations. Quantity of program contact was related to the quality of helping relationship, especially when rated by doulas. Both quantity and quality of involvement predicted the maternal outcomes, although not always in the expected direction. For mothers with limited vocabulary skills and better connections with the baby's father, program contact was more likely to promote positive birth experiences. A negative association between program contact and parenting behaviors was observed among mothers who were less mature or had less positive social relationships. The study suggests the multidimensionality of program involvement and the complexity of interactions between program and participant factors in producing program outcomes. © 2010 Wiley Periodicals, Inc.
Measuring perceived procedural justice and coercion among persons with mental illness in police encounters: the Police Contact Experience Scale
Authors: Watson Amy C. , Angell Beth , Vidalon Theresa , Davis Kristin 
Published: February 2010

AbstractDespite increased recent attention to improving the quality of encounters between police officers and people with serious mental illness, there are no measures available for assessing how consumers perceive their interactions with police officers. Drawing upon conceptual frameworks developed within social psychology, this study reports the development and testing of a new measure, the Police Contact Experience Scale (PCES), which yields indicators of procedural justice and coercion as evaluated by persons with mental illness in relation to specific encounters with the police. The PCES was administered to 154 individuals with mental illness that had police contact within the prior 12 months. Rasch rating scale analysis supported construct validity of a 10‐item procedural justice and a 5‐item coercion scale. Correlational analysis supported convergent validity for both scales. © 2010 Wiley Periodicals, Inc.
Predictors of family participation in a multiple family group intervention for aggressive middle school students
Authors: Quinn William H. , Hall Dan B. , Smith Emilie P. , Rabiner David 
Published: February 2010

AbstractThe authors examine predictors of family participation in the G.R.E.A.T. Families Program of the Multisite Violence Prevention Project (MVPP), a four‐site collaboration examining student, teacher, and family interventions for middle school students. Teachers recruited two cohorts of sixth grade students, recognized as being aggressive and influential with their peers, and their families into a voluntary, 15‐session weekly program. Among the 643 families that consented (66%), the mean number of sessions attended was 8.13, with almost half (48.3%) attending 11 or more sessions. Linear mixed models (LMMs) were developed to predict the number of sessions attended based on a cluster of demographic variables and scales designed to measure aggression, problem behaviors, family factors, and other psychosocial constructs. Three of the nine clusters held significance when associated with attendance: level of aggression as rated by the child (negative association), parent–child bond (negative association), and level of child victimization (positive association). Somewhat surprisingly, the variance component due to interventionist turned out to be small and to constitute a nonsignificant component of the overall variability in attendance. Results suggest that family recruitment for multiple family group programs can be achieved with substantial effort and that resources available for recruitment might be differentially applied across families based on predictors of attendance. © 2010 Wiley Periodicals, Inc.
Implementation of the Communities That Care prevention system by coalitions in the Community Youth Development Study
Authors: Arthur Michael W. , Hawkins J. David , Brown Eric C. , Briney John S. , Oesterle Sabrina , Abbott Robert D. 
Published: February 2010

AbstractAlthough advances in prevention science over the past two decades have produced a growing list of tested and effective programs and policies for preventing adolescent delinquency and drug use, widespread dissemination and high‐quality implementation of effective programs and policies in communities has not been achieved. The Community Youth Development Study (CYDS) is a randomized, community‐level trial of the Communities That Care (CTC) system for promoting science‐based prevention in communities. This study compares 12 community prevention coalitions implementing the CTC system in 12 intervention communities as part of the CYDS to prevention coalitions located in the 12 control communities. As hypothesized, the CYDS coalitions implemented significantly more of the CTC core intervention elements, and also implemented significantly greater numbers of tested, effective prevention programs than the prevention coalitions in the control communities. Implications of the findings for efforts to achieve widespread dissemination of effective prevention programs, policies, and practices are discussed. © 2010 Wiley Periodicals, Inc.
Profilin‐1 overexpression inhibits proliferation of MDA‐MB‐231 breast cancer cells partly through p27kip1 upregulation
Authors: Zou Li , Ding Zhijie , Roy Partha 
Published: February 2010

AbstractProfilin‐1 (Pfn1), a ubiquitously expressed actin‐binding protein, has gained interest in epithelial‐derived cancer because of its downregulation in expression in various adenocarcinoma. Pfn1 overexpression impairs tumorigenic ability of human breast cancer xenografts thus suggesting that Pfn1 could be a tumor‐suppressor protein. The objective of the present study was to determine how Pfn1 overexpression affects cell‐cycle progression of breast cancer cells. We show that Pfn1 overexpression in MDA‐MB‐231 breast cancer cells causes cell‐cycle arrest in G1 phase and dramatically reduced proliferation in culture. Pfn1 overexpression results in increased protein stability of p27kip1 (p27—a major cyclin‐dependent kinase inhibitor) and marked elevation in the overall cellular level of p27. Proliferation defect of Pfn1 overexpressers can be partly rescued by silencing p27 expression thus suggesting a critical role of p27 in Pfn1‐induced growth inhibition of MDA‐MB‐231 cells. Finally, Pfn1 overexpression was found to sensitize MDA‐MB‐231 cells to apoptosis in response to cytotoxic stimulus thus suggesting for the first time that survival of breast cancer cells can also be negatively influenced by Pfn1 upregulation. These findings may provide novel insights underlying Pfn1's tumor‐suppressive action. J. Cell. Physiol. 223:623–629, 2010. © 2010 Wiley‐Liss, Inc.
Both superficial and deep zone articular chondrocyte subpopulations exhibit the crabtree effect but have different basal oxygen consumption rates
Authors: Heywood Hannah K. , Knight Martin M. , Lee David A. 
Published: February 2010

AbstractIn the absence of in vivo measurements, the oxygen concentration within articular cartilage is calculated from the balance between cellular oxygen consumption and mass transfer. Current estimates of the oxygen tension within articular cartilage are based on oxygen consumption data from full‐depth tissue samples. However, superficial and deep cell subpopulations of articular cartilage express intrinsic metabolic differences. We test the hypothesis that the subpopulations differ with respect to their intrinsic oxygen consumption rate. Chondrocytes from the full cartilage thickness demonstrate enhanced oxygen consumption when deprived of glucose, consistent with the Crabtree phenomena. Chondrocyte subpopulations differ in the prevailing availability of oxygen and glucose, which decrease with distance from the cartilage–synovial fluid interface. Thus, we tested the hypothesis that the oxygen consumption of each subpopulation is modulated by nutrient availability, by examining the expression of the Crabtree effect. The deep cells had a greater oxygen consumption than the superficial cells (Vmax of 6.6 compared to 3.2 fmol/cell/h), consistent with our observations of mitochondrial volume (mean values 52.0 vs. 36.4 µm3/cell). Both populations expressed the Crabtree phenomena, with oxygen consumption increasing ∼2.5‐fold in response to glycolytic inhibition by glucose deprivation or 2‐deoxyglucose. Over 90% of this increase was oligomycin‐sensitive and thus accounted for by oxidative phosphorylation. The data contributes towards our understanding of chondrocyte energy metabolism and provides information valuable for the accurate calculation of the oxygen concentration that the cells experience in vivo. The work has further application to the optimisation of bioreactor design and engineered tissues. J. Cell. Physiol. 223:630–639, 2010. © 2010 Wiley‐Liss, Inc.
BMP‐3 promotes mesenchymal stem cell proliferation through the TGF‐β/activin signaling pathway
Authors: Stewart Aaron , Guan Haiyan , Yang Kaiping 
Published: February 2010

AbstractAdipogenesis plays a key role in the pathogenesis of obesity. It begins with the commitment of mesenchymal stem cells (MSCs) to the adipocyte lineage, followed by terminal differentiation of preadipocytes to mature adipocytes. A critical, but poorly understood, component of adipogenesis involves proliferation of MSCs and preadipocytes. The present study was undertaken to examine the hypothesis that bone morphogenetic protein‐3 (BMP‐3) promotes adipogenesis using C3H10T1/2 MSCs and 3T3‐L1 preadipocytes as in vitro model systems. We demonstrated that although it did not promote the commitment of MSCs to the adipocyte lineage or the differentiation of preadipocytes to adipocytes, BMP‐3‐stimulated proliferation by threefold in both cell types. Owing to a lack of information on MSC proliferation, we then delineated the molecular mechanisms underlying BMP‐3‐stimulated MSC proliferation. We showed that BMP‐3 activated the transforming growth factor‐β (TGF‐β)/activin but not ERK1/2, p38 MAPK, or JNK signaling pathways in C3H10T1/2 cells. Furthermore, the TGF‐β/activin receptor kinase inhibitor SB‐431542 blocked BMP‐3‐stimulated proliferation. Importantly, siRNA‐mediated knockdown of the key TGF‐β/activin signaling pathway components, ActRIIB, ALK4, or Smad2, abrogated the mitogenic effects of BMP‐3 on MSCs. Together, these results demonstrate that BMP‐3 stimulates MSC proliferation via the TGF‐β/activin signaling pathway, thus revealing a novel role for this divergent and poorly understood member of the TGF‐β superfamily in regulating MSC proliferation. J. Cell. Physiol. 223:658–666, 2010. © 2010 Wiley‐Liss, Inc.
Non‐genomic rapid inhibition of Na+/H+‐exchange 1 and apoptotic immunosuppression in human T cells by glucocorticoids
Authors: Chang Ching‐Pang , Wang Shyi‐Wu , Huang Zih‐Ling , Wang Olivia Ya‐Hsuan , Huang Michael I‐Ta , Lu Li‐Ming , Tarng Der‐Cherng , Chien Chau‐Heng , Chien Eileen Jea 
Published: February 2010

AbstractGlucocorticoids (GCs) have been employed as immunosuppressive agents for many years. However, it is still unclear how GCs instantly uncouple T cells from acute stressful inflammatory. In terms of time scale, the genomic activity of the classic GC receptor cannot fulfill this role under crisis; but a rapid non‐genomic response can. In a previous study, intracellular acidification was found to be due to a rapid non‐genomic inhibition of Na+/H+‐exchange 1 (NHE1) and this event led to the immunosuppression of T cell proliferation by progesterone. The aim of this study was to examine whether there is a rapid acidification response caused by an inhibition of NHE1 activity and to explore the differential non‐genomic effect on immunosuppression of hydrocortisone and dexamethasone. The IC50 values for NHE1‐dependent pHi recovery by hydrocortisone and dexamethasone are 250 and 1 nM, respectively. Co‐stimulation of GCs with phytohemagglutinin (PHA) is able to inhibit PHA‐induced IL‐2 secretion, IL‐4 secretion, and T‐cell proliferation. Furthermore, apoptosis in PHA‐activated T cells is not induced by hydrocortisone but by dexamethasone. The mechanism of immunosuppression on proliferation by dexamethasone was found to be different of hydrocortisone and seems to involve cytotoxicity against T cells. Moreover, apoptosis induced by dexamethasone and impermeable dexamethasone–bovine serum albumin suggests that the apoptotic immunosuppression occurs through both the plasma membrane and cytoplasmic sites. The rapid inhibitory responses triggered by GCs would seem to release T cells instantly when an acute stress‐related response is needed. Nonetheless, the apoptotic immunosuppression by dexamethasone is attributable to its severe cytotoxicity. J. Cell. Physiol. 223:679–686, 2010. © 2010 Wiley‐Liss, Inc.
Competitiveness for the niche and mutual dependence of the germline and somatic stem cells in the Drosophila testis are regulated by the JAK/STAT signaling
Authors: Singh Shree Ram , Zheng Zhiyu , Wang Hong , Oh Su‐Wan , Chen Xiu , Hou Steven X. 
Published: February 2010

AbstractIn many tissues, two or more types of stem cells share a niche, and how the stem cells coordinate their self‐renewal and differentiation is poorly understood. In the Drosophila testis, germ line stem cells (GSCs) and somatic cyst progenitor cells (CPCs) contact each other and share a niche (the hub). The hub expresses a growth factor unpaired (Upd) that activates the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway in GSCs to regulate the stem cell self‐renewal. Here, we demonstrate that the JAK/STAT signaling also regulates CPCs self‐renewal. We also show that a negative regulator, the suppressor of cytokine signaling 36E (SOCS36E), suppresses JAK/STAT signaling in somatic cells, preventing them from out‐competing the GSCs. Furthermore, through selectively manipulating the JAK/STAT signaling level in either CPCs or GSCs, we demonstrate that the somatic JAK/STAT signaling is essential for self‐renewal and maintenance of both CPCs and GSCs. These data suggest that a single JAK/STAT signal from the niche orchestrate the competitive and dependent co‐existence of GSCs and CPCs in the Drosophila testis niche. J. Cell. Physiol. 223: 500–510, 2010. © 2010 Wiley‐Liss, Inc.