bluuebunny/crossref_metadata_2025_split huggingface dataset:
Biselyngbyaside, isolated from marine cyanobacteria, inhibits osteoclastogenesis and induces apoptosis in mature osteoclasts
Authors: Yonezawa Takayuki , Mase Naomi , Sasaki Hiroaki , Teruya Toshiaki , Hasegawa Shin‐ichi , Cha Byung‐Yoon , Yagasaki Kazumi , Suenaga Kiyotake , Nagai Kazuo , Woo Je‐Tae 
Published: June 2011

AbstractThe mass and function of bones depend on the maintenance of a complicated balance between osteoclast‐mediated bone resorption and osteoblast‐mediated bone formation. An inhibitor of osteoclast differentiation and/or function is expected to be useful for treatment of bone lytic diseases such as osteoporosis, rheumatoid arthritis, and tumor metastasis into bone. Biselyngbyaside is a recently isolated macrolide compound from marine cyanobacteria Lyngbya sp. that shows wide‐spectrum cytotoxicity toward human tumor cell lines. In this study, we investigated the effects of biselyngbyaside on osteoclast differentiation and function. Biselyngbyaside inhibited receptor activator of nuclear factor‐κB ligand (RANKL)‐induced osteoclastogenesis in mouse monocytic RAW264 cells and primary bone marrow‐derived macrophages at a low concentration. Similarly, biselyngbyaside suppressed osteoblastic cell‐mediated osteoclast differentiation in cocultures. In the RANKL‐induced signaling pathway, biselyngbyaside inhibited the expression of c‐Fos and NFATc1, which are important transcription factors in osteoclast differentiation. In mature osteoclasts, biselyngbyaside decreased resorption‐pit formation. Biselyngbyaside also induced apoptosis accompanied by the induction of caspase‐3 activation and nuclear condensation, and these effects were negated by the pancaspase inhibitor z‐VAD‐FMK. Taken together, the present findings indicate that biselyngbyaside suppresses bone resorption via inhibition of osteoclastogenesis and induction of apoptosis. Thus, biselyngbyaside may be useful for the prevention of bone lytic diseases. J. Cell. Biochem. 113: 440–448, 2012. © 2011 Wiley Periodicals, Inc.
Essential role of maternal UCHL1 and UCHL3 in fertilization and preimplantation embryo development
Authors: Mtango Namdori R. , Sutovsky Miriam , Susor Andrej , Zhong Zhisheng , Latham Keith E. , Sutovsky Peter 
Published: June 2011

AbstractPost‐translational protein modification by ubiquitination, a signal for lysosomal or proteasomal proteolysis, can be regulated and reversed by deubiquitinating enzymes (DUBs). This study examined the roles of UCHL1 and UCHL3, two members of ubiquitin C‐terminal hydrolase (UCH) family of DUBs, in murine fertilization and preimplantation development. Before fertilization, these proteins were associated with the oocyte cortex (UCHL1) and meiotic spindle (UCHL3). Intracytoplasmic injection of the general UCH‐family inhibitor ubiquitin‐aldehyde (UBAL) or antibodies against UCHL3 into mature metaphase II oocytes blocked fertilization by reducing sperm penetration of the zona pellucida and incorporation into the ooplasm, suggesting a role for cortical UCHL1 in sperm incorporation. Both UBAL and antibodies against UCHL1 injected at the onset of oocyte maturation (germinal vesicle stage) reduced the fertilizing ability of oocytes. The subfertileUchl1gad−/−mutant mice showed an intriguing pattern of switched UCH localization, with UCHL3 replacing UCHL1 in the oocyte cortex. While fertilization defects were not observed, the embryos from homozygousUchl1gad−/−mutant females failed to undergo morula compaction and did not form blastocysts in vivo, indicating a maternal effect related to UCHL1 deficiency. We conclude that the activity of oocyte UCHs contributes to fertilization and embryogenesis by regulating the physiology of the oocyte and blastomere cortex. J. Cell. Physiol. 227: 1592–1603, 2012. © 2011 Wiley Periodicals, Inc.
Potential effect of resistin on the ET‐1‐increased reactions of blood pressure in rats and Ca2+ signaling in vascular smooth muscle cells
Authors: Chuang Tung‐Yueh , Au Lo‐Chun , Wang Li‐Chun , Ho Low‐Tone , Yang De‐Ming , Juan Chi‐Chang 
Published: June 2011

AbstractResistin and endothelin‐1 (ET‐1) are upregulated in people with type II diabetes mellitus, central obesity, and hypertension. ET‐1 signaling is involved in Ca2+‐contraction coupling and related to blood pressure regulation. The aim of this study is to investigate the role of resistin on ET‐1‐increased blood pressure and Ca2+ signaling. The blood pressure and cytosolic Ca2+ of vascular smooth muscle cells (VSMCs) of Sprague–Dawley rats were detected. The data demonstrated that resistin accelerated and prolonged ET‐1‐induced increases in blood pressure and had significant effects on ET‐1‐increased Ca2+ reactions. Resistin‐enhanced ET‐1‐increased Ca2+ reactions were reversed by blockers of store‐operated Ca2+ entry (SOCE) and extracellular‐signal‐regulated kinase (ERK). The endogenous expression of Orai and stromal interaction molecular (STIM) were characterized in the VSMCs. Furthermore, resistin‐enhanced ET‐1 Ca2+ reactions and the resistin‐dependent activation of SOCE were abolished under STIM1‐siRNA treatment, indicating that STIM1 plays an important role in resistin‐enhanced ET‐1 Ca2+ reactions in VSMCs. Resistin appears to exert effects on ET‐1‐induced Ca2+ increases by enhancing the activity of ERK‐dependent SOCE (STIM1‐partcipated), and may accelerate and prolong ET‐1‐increased blood pressure via the same pathway. J. Cell. Physiol. 227: 1610–1618, 2012. © 2011 Wiley Periodicals, Inc.
Absence of MCP‐1 leads to elevated bone mass via impaired actin ring formation
Authors: Sul Ok‐Joo , Ke Ke , Kim Woon‐Ki , Kim Song‐Hee , Lee Sang‐Chul , Kim Hyun‐Ju , Kim Shin‐Yoon , Suh Jae‐Hee , Choi Hye‐Seon 
Published: June 2011

AbstractMonocyte chemoattractant protein‐1 (MCP‐1) is associated with various inflammatory diseases involving bone loss, and is expressed along with its receptor by bone marrow‐derived macrophages (BMM), which are osteoclast (OC) precursors. To investigate the role of MCP‐1 in bone remodeling, we compared MCP‐1‐knockout (KO) mice with wild‐type (WT) mice. The absence of MCP‐1 increased bone mass and lowered serum collagen type I fragments (CTX‐1) and TRACP 5b, but had no significant effect on the N‐terminal propeptide of type I procollagen, suggesting that OCs are primarily responsible for the bone phenotype observed in the absence of MCP‐1. MCP‐1 deficiency resulted in reduced numbers and activity of OCs in vitro. It also led to a reduced level of c‐Fms and receptor activator of nuclear factor‐κB receptor and impaired actin ring formation. Activation of ERK, Akt, Rac1, and Rho upon M‐CSF stimulation was also reduced and our evidence suggests that the aberrant actin ring formation was partly due to reduced activation of these molecules. Our findings point to a role of osteoclast MCP‐1 in regulating bone remodeling. The higher bone mass in the femurs of MCP‐1‐KO mice could be, at least in part, due to decreased osteoclastogenesis and bone resorption resulting from aberrant M‐CSF signaling in OCs. J. Cell. Physiol. 227: 1619–1627, 2012. © 2011 Wiley Periodicals, Inc.
The RhoA‐Rok‐myosin II pathway is involved in extracellular matrix‐mediated regulation of prolactin signaling in mammary epithelial cells
Authors: Du Jyun‐Yi , Chen Meng‐Chi , Hsu Tsai‐Ching , Wang Jen‐Hsing , Brackenbury Lisa , Lin Ting‐Hui , Wu Yi‐Ying , Yang Zhihong , Streuli Charles H. , Lee Yi‐Ju 
Published: June 2011

AbstractIn mammary epithelial cells (MECs), prolactin‐induced signaling and gene expression requires integrin‐mediated cell adhesion to basement membrane (BM). In the absence of proper cell–BM interactions, for example, culturing cells on collagen‐coated plastic dishes, signal propagation is substantially impaired. Here we demonstrate that the RhoA‐Rok‐myosin II pathway accounts for the ineffectiveness of prolactin signaling in MECs cultured on collagen I. Under these culture conditions, the RhoA pathway is activated, leading to downregulation of prolactin receptor expression and reduced prolactin signaling. Enforced activation of RhoA in MECs cultured on BM suppresses prolactin receptor levels, and prevents prolactin‐induced Stat5 tyrosine phosphorylation and β‐casein expression. Overexpression of dominant negative RhoA in MECs cultured on collagen I, or inhibiting Rok activity, increases prolactin receptor expression, and enhances prolactin signaling. In addition, inhibition of myosin II ATPase activity by blebbistatin also exerts a beneficial effect on prolactin receptor expression and prolactin signaling, suggesting that tension exerted by the collagen substratum, in collaboration with the RhoA‐Rok‐myosin II pathway, contributes to the failure of prolactin signaling. Furthermore, MECs cultured on laminin‐coated plastic have similar morphology and response to prolactin as those cultured on collagen I. They display high levels of RhoA activity and are inefficient in prolactin signaling, stressing the importance of matrix stiffness in signal transduction. Our results reveal that RhoA has a central role in determining the fate decisions of MECs in response to cell–matrix interactions. J. Cell. Physiol. 227: 1553–1560, 2012. © 2011 Wiley Periodicals, Inc.
Bounded transversals in multipartite graphs
Authors: Berke Robert , Haxell Penny , Szabó Tibor 
Published: June 2011

AbstractTransversals in r‐partite graphs with various properties are known to have many applications in graph theory and theoretical computer science. We investigate f‐bounded transversal s (or f‐BT), that is, transversals whose connected components have order at most f. In some sense we search for the sparsest f‐BT‐free graphs. We obtain estimates on the smallest maximum degree that 3‐partite and 4‐partite graphs without 2‐BT can have and provide a greatly simplified proof of the best known general lower bound on the smallest maximum degree in f‐BT‐free graphs. © 2011 Wiley Periodicals, Inc. J Graph Theory.
Treatment of inpatient hyperglycemia beginning in the emergency department: A randomized trial using insulins aspart and detemir compared with usual care
Authors: Bernard Jennifer B. , Munoz Christina , Harper Jaime , Muriello Michael , Rico Edward , Baldwin David 
Published: June 2011

AbstractOBJECTIVE:We examined the impact of an aspart insulin protocol for treatment of hyperglycemia in the emergency department (ED) coupled with rapid initiation of a detemir‐aspart insulin protocol for patients admitted to the hospital.RESEARCH DESIGN AND METHODS:ED patients with type 2 diabetes mellitus and a blood glucose (BG) ≥ 200 mg/dL were randomized to intervention (INT) or usual care (UC). INT patients (n = 87) received aspart every 2 hours when BG > 200 mg/dL, and if admitted, began daily detemir in the ED. UC patients (n = 89) were treated per hospital physicians.RESULTS:The initial ED BG was 304 ± 76 mg/dL. The final ED BG differed: 217 ± 71 mg/dL for INT patients versus 257 ± 89 mg/dL for UC patients (P < .01). No INT patients and 3 UC patients had a BG < 50 mg/dL (P = .5). ED length of stay (LOS) was similar: 5.4 ± 1.8 hours for INT patients versus 4.9 ± 1.9 hours for UC patients (P = .06). Sixty‐nine percent from each group were admitted. Admission BG was 184 ± 74 mg/dL for INT patients versus 224 ± 93 mg/dL for UC patients (P < .01). Patient‐day weighted mean glucose was 163 ± 39 mg/dL for INT patients versus 202 ± 39 mg/dL for UC patients (P < .01). One INT patient and 6 UC patients had a BG < 50 mg/dL (P = .11). Hospital LOS was similar: 2.7 ± 2.0 versus 3.1 ± 1.9 days, respectively (P = .58).CONCLUSIONS:An aspart insulin protocol safely lowers BG levels in the ED without prolonging LOS. During hospitalization, a detemir‐aspart protocol achieves significantly better glycemic control compared with guideline‐driven use of NPH‐aspart or glargine/detemir‐aspart (usual care) without increasing hypoglycemia. Standardization of insulin protocols in the ED and hospital settings leads to improvement in overall glycemic control with greater safety and efficacy than usual care. Journal of Hospital Medicine 2011. © 2011 Society of Hospital Medicine
Frequently asked questions by hospitalists managing pain in adults with sickle cell disease
Authors: Smith Wally R. , Jordan Lanetta B. , Hassell Kathryn L. 
Published: June 2011

AbstractPain is the predominant medical presentation to hospitalists for patients with sickle cell disease (SCD). Dramatic treatment gains of SCD in childhood have resulted in more adults now requiring hospitalization than children. This has created new challenges to improve the quality of hospital care for SCD. The evidence base for pain management in SCD is lacking. We therefore offer some evidence and our informed opinion to answer frequently asked questions (FAQs) about pain management by hospitalists caring for adults with SCD. The most common questions center around defining a crisis; selecting and managing opioids; distinguishing between opioid tolerance, physical dependence, and addiction or misuse; determining appropriateness of discharge; and avoiding lengthy or recurrent hospitalizations. Journal of Hospital Medicine 2011. © 2011 Society of Hospital Medicine.
Work motivation and organizational citizenship behaviors
Authors: Barbuto John E. , Story Joana S.P. 
Published: June 2011

AbstractThis study tested the relationship between employees' sources of work motivation and their display of organizational citizenship behaviors. Two hundred thirty‐nine employees from 38 locations of four companies in the agricultural industry completed the Motivation Sources Inventory and were rated by their leaders in organizational citizenship behaviors. Results showed significant positive relationships between individuals' self‐concept internal motivations and organizational citizenship behaviors. Results also showed significant negative relationships between instrumental and self‐concept external motivations and organizational citizenship behaviors. A hierarchical regression with each of the significant covariates accounted for 12% of the total variance in organizational citizenship behavior. These results indicate that employees' sources of motivation offer some explanation of their organizational citizenship behaviors. Implications for future research and practice are discussed.
Epilogue
Authors: Browde Beth 
Published: June 2011

AbstractIn the corporate world, leadership development programs are standard fare. Such programs often include well‐defined competencies and performance metrics, as well as regularly scheduled feedback and mentoring sessions, especially for those employees designated “high potential” performers.Not so in the public sphere. There are no defined career paths or standardized training curricula for heads of
state. There are, however, requisite competencies for effective public sector leadership. As Gardner (1990) observed, “Leadership is not a mysterious activity. It is possible to describe the tasks that leaders perform....[But] we have barely scratched the surface in our efforts toward leadership development” (p. xix).The learning curve is steep for a newly elected leader, and fraught with potential landmines. Speaking with
the candor of someone no longer seeking public office, former UK Prime Minister Tony Blair said recently, “When I came to office, prime minister was the only job I'd ever held; I'd never been a government minister before....The business of running a government is like anything else: You get better the longer you do it. And there are lessons out there that, had they come to me in an identifiable form, would have been useful to know” (talk given on December 16, 2010b).Both Gardner and Blair are emphatic that leadership is not something one is born with but something learned
over time. And as Blair (2010a) put it, “Government is a race between expectations and capability.”In the essays that follow, several leadership coaches discuss the unique challenges and effective approaches
they are using to help government leaders build the competencies that will enable them to govern effectively—and win that race between their constituents's expectations and their own capabilities.
Photofragmentation of the K‐shell excited perfluorocyclobutane: anisotropies in the fragments and breakdown pathways
Authors: Okada K. , Suemitsu A. , Terashima T. , Iwasaki Y. , Tamenori Y. , Suzuki I. H. , Nagaoka S. , Tabayashi K. 
Published: June 2011

AbstractTotal ion yield spectrum of perfluorocyclobutane (c‐C4F8) has been measured in the C and F K‐shell excitation regions. The peak assignments are presented based on angle‐resolved photofragment ion mass spectrometry. The peaks at 291.34 and 688.5 eV are found to come from the transitions from the C 1s and the F 1s to the lowest unoccupied b2σCF* orbital, respectively. A photoelectron–photoion–photoion coincidence spectrum is acquired at 700.1 eV for clarifying the breakdown pathways of c‐C4F82+. Two series of the pathways are identified; fission of F atom(s) followed by charge separation and elimination of CF2 or CF3 followed by charge separation. Copyright © 2011 John Wiley & Sons, Ltd.
Analyses of human papillomavirus genotypes and viral loads in anogenital warts
Authors: Ball Siolian L.R. , Winder David M. , Vaughan Katie , Hanna Nashat , Levy Jonathan , Sterling Jane C. , Stanley Margaret A. , Goon Peter K.C. 
Published: June 2011

AbstractCondylomata acuminata (genital warts) are the most common sexually transmitted viral diseases. These lesions are caused by infection with mucosal human papillomaviruses (HPVs). However, there is limited information on HPV strain distribution involved in the molecular pathogenesis of these lesions. To address this, the strain prevalence and the frequency of multiple HPV infections were determined in wart tissue obtained from 31 patients attending a wart clinic. These lesions were bisected and subjected to parallel DNA and mRNA extractions. HPV‐type prevalence and incidence of multiple infections were determined by the Roche Linear Array assay. qPCR compared HPV 6, 11, 16, and 18 viral loads and RT‐qPCR measured HPV 6 and 11 E6 genomic expression levels. Seventy‐one percent of these samples were infected with multiple HPVs. Only one sample was negative for HPV 6 or 11 DNA. Forty‐eight percent of samples were positive for a high risk (oncogenic) HPV. The results show that multiple infections in tissue are frequent and the subsequent analysis of HPV 6 and 11 E6 DNA viral loads suggested that other HPVs could be causing lesions. Further analysis of HPV 6/11 E6 mRNA levels showed that there was no discernable relationship between HPV 6 E6 DNA viral load and relative HPV 6 or 11 E6 mRNA levels thereby questioning the relevance of viral load to lesion causality. J. Med. Virol. 83:1345–1350, 2011. © 2011 Wiley‐Liss, Inc.
Human papillomavirus infection among women with cytological abnormalities in Switzerland investigated by an automated linear array genotyping test
Authors: Dobec Marinko , Bannwart Fridolin , Kilgus Sandra , Kaeppeli Franz , Cassinotti Pascal 
Published: June 2011

AbstractLimited data are available describing human papillomavirus (HPV) genotype distribution among females with cytological abnormalities in Switzerland. Cervical cell specimens obtained from 5,318 women were screened routinely by liquid‐based Pap smear. All specimens with cellular abnormalities were analyzed subsequently for HPV DNA by the Linear Array HPV genotyping test. Cellular abnormalities were found in 202 (3.8%) specimens, of which 150 (74.3%) were positive for high‐risk (HR) HPV. HR‐HPV was detected in 20 (60.6%; 95% CI, 43.7–75.4%) of 33 specimens with atypical squamous cells of undetermined significance compared to 98 (72.1%; 95% CI, 64–78.9%) of 136 low‐grade squamous intraepithelial lesions and 32 (97%; 95% CI, 83.4–99.9%) of 33 high‐grade squamous intraepithelial lesions. The cumulative prevalence of HR‐HPV other than HPV 16 and 18 was significantly higher than HPV 16 and/or 18 lesions with atypical squamous cells and low‐grade lesions and was comparable in high‐grade squamous intraepithelial lesions. The most common HR‐HPV genotypes were HPV 16 (15.2%), HPV 31 (12.1%), HPV 58 (12.1%), HPV 51 (9.1%), and HPV 59 (9.1%) in women with atypical squamous cells, HPV 16 (25%), HPV 51 (16.9%), HPV 52 (11.8%), HPV 31 (9.6%), and HPV 56 (8.1%) in women with low‐grade lesions (LSIL) and HPV 16 (57.6%), HPV 18 (18.2%), HPV 31 (15.2%), HPV 52 (12.1%), and HPV 58 (6.1%) in women with high‐grade lesions (HSIL). J. Med. Virol. 83:1370–1376, 2011. © 2011 Wiley‐Liss, Inc.
Comparative analysis of disease severity between genotypes IA and IIIA of hepatitis A virus
Authors: Yoon Young Kyung , Yeon Jong Eun , Kim Ji Hoon , Sim Hee Sun , Kim Jeong Yeon , Park Dae Won , Sohn Jang Wook , Chun Byung Chul , Kim Min Ja 
Published: June 2011

AbstractAlthough hepatitis A is a major health problem worldwide, it has not yet been clarified whether or not viral factors affect the clinical characteristics. This study aimed to investigate if a genotype of hepatitis A virus (HAV) affects disease severity among adolescent and adult populations. Clinical data and specimens were collected from patients ≥16‐years‐of‐age with acute hepatitis A at two university hospitals in Korea during the two study periods: 1998 and 1999 (n = 45), and 2009 (n = 66). Nucleotide sequencing of the complete VP1 region of the HAV isolates was performed for phylogenetic analysis and genotyping. Clinical parameters related to disease severity were compared by HAV genotype to determine its clinical relevance. Of the 87 patients, 47 were male and the mean age was 29.8 ± 8.1 years. The genotype IIIA (93.0%, 53/57) was predominant in the year 2009, whereas IA (93.3%, 28/30) was the major genotype in 1998 and 1999. When comparing disease severity between the two HAV genotypes, the patients with genotype IIIA were older and had higher alanine aminotransferase (ALT) levels, prolonged prothrombin times and lower serum albumin levels. In a multivariate logistic regression model, higher ALT levels ≥ 1,000 IU/L (odds ratio [OR] 11.7, 95% confidence interval [CI] 2.5–54.0) and longer hospitalization (OR 22.49, 95%CI 4.6–132.5) were associated independently with genotype IIIA. In conclusion, this study indicates that HAV genotype might be one of the viral factors responsible for the disease severity of hepatitis A. J. Med. Virol. 83:1308–1314, 2011. © 2011 Wiley‐Liss, Inc.
Blocking p75NTR receptors alters polyinnervationz of neuromuscular synapses during development
Authors: Garcia Neus , Tomàs Marta , Santafe Manel M. , Lanuza Maria A. , Besalduch Nuria , Tomàs Josep 
Published: June 2011

AbstractHigh‐resolution immunohistochemistry shows that the receptor protein p75NTR is present in the nerve terminal, muscle cell, and glial Schwann cell at the neuromuscular junction (NMJ) of postnatal rats (P4–P6) during the synapse elimination period. Blocking the receptor with the antibody anti‐p75‐192‐IgG (1–5 μg/ml, 1 hr) results in reduced endplate potentials (EPPs) in mono‐ and polyinnervated synapses ex vivo, but the mean number of functional inputs per NMJ does not change for as long as 3 hr. Incubation with exogenous brain‐derived neurotrophic factor (BDNF) for 1 hr (50 nM) resulted in a significant increase in the size of the EPPs in all nerve terminals, and preincubation with anti‐p75‐192‐IgG prevented this potentiation. Long exposure (24 hr) in vivo of the NMJs to the antibody anti‐p75‐192‐IgG (1–2 μg/ml) results in a delay of postnatal synapse elimination and even some regrowth of previously withdrawn axons, but also in some acceleration of the morphologic maturation of the postsynaptic nicotinic acetylcholine receptor (nAChR) clusters. The results indicate that p75NTR is involved in both ACh release and axonal retraction during postnatal axonal competition and synapse elimination. © 2011 Wiley‐Liss, Inc.