bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Lateral Dorsal Cutaneous Branch of the Sural Nerve
Authors: Fansa Ashraf M. , Smyth Niall A. , Murawski Christopher D. , Kennedy John G. 
Published: June 2012

Background: Fractures of the proximal fifth metatarsal are one of the most common forefoot injuries encountered by orthopaedic surgeons in sports medicine. The percutaneous surgical approach to Jones fracture fixation and corresponding anatomy has received little attention in the literature to date. Purpose: To describe in detail the location of the lateral dorsal cutaneous nerve (LDCN) and its branches relative to the base of the fifth metatarsal and to the standard lateral approach. Study Design: Descriptive laboratory study. Methods: Ten fresh-frozen cadaveric foot specimens were used for this study. Specimens were dissected at the lateral aspect of the foot over the proximal fifth metatarsal, and the LDCN and its branches were identified. The distance of the LDCN to the superior border of the peroneus brevis tendon (PBT) was measured relative to standard reference points in all specimens, and the presence of an anastomotic branch was noted. A set of vertical and horizontal reference lines were also constructed to determine whether the LDCN or its branches would be compromised by a standard lateral approach. Results: The LDCN was superficial (ie, lateral) and inferior to the superior border of the PBT in all specimens and at all reference points. A bifurcation of the LDCN was present in 8 specimens, located an average of 18 mm posterior and 11 mm dorsal to the base of the fifth metatarsal. The dorsolateral branch and dorsomedial branch of the LDCN each intersected with the base of the fifth metatarsal horizontal line and vertical line, respectively, indicating potential compromise of the nerve with a standard lateral surgical approach. Conclusion: The standard lateral approach to the base of the fifth metatarsal carries a higher risk for surgical injury to the LDCN. A “high and inside” approach that remains superior to the superior border of the PBT is anatomically safe and may decrease the chance of intraoperative nerve injury and irritation postoperatively.
Publication of Sports Medicine–Related Randomized Controlled Trials Registered in ClinicalTrials.gov
Authors: Chahal Jaskarndip , Tomescu S. Sebastian , Ravi Bheeshma , Bach Bernard R. , Ogilvie-Harris Darrell , Mohamed Nizar N. , Gandhi Rajiv 
Published: June 2012

Background: There is increasing evidence that a significant proportion of randomized trials in medicine, and recently in orthopaedics, do not go on to publication. Purpose: The objectives of this study were (1) to determine publication rates of randomized controlled trials in sports medicine that have been registered with ClinicalTrials.gov (CTG) and (2) to compare the registration summaries of randomized trials on CTG with final published manuscripts on pertinent methodological variables. Study Design: Systematic review. Methods: Two independent investigators searched ClinicalTrials.gov for all closed and completed trials related to sports medicine until June 2009 using a text search strategy. The authors then searched for publications resulting from these registered trials in peer-reviewed journals that are indexed with MEDLINE and/or EMBASE as of February 2012 based on study authors and key words provided in the study protocol. Details of primary outcomes and secondary outcomes, study sponsors, and sample size were extracted and compared between registrations and publications. Results: Of 34 closed and completed trials registered on CTG, there were 20 resultant publications in peer-reviewed journals (58.8%). There was no significant relationship between source of funding and rate of publication ( P > .05). The authors found a discrepancy between the CTG registration summary and the manuscript in at least one methodological variable (primary/secondary outcomes, inclusion/exclusion criteria, sample size) in 16 of 20 (80.0%) articles and a discrepancy in the primary outcome in 8 of 20 (40.0%) published trials. Conclusion: Although registration of sports medicine trials in CTG does not consistently result in publication or disclosure of results at 32 months from the time of study completion, observed publication rates are higher than in other orthopaedic subspecialties. Changes are also frequently made to the final presentation of eligibility criteria and primary and secondary outcomes that are not reflected in the registered trial data.
Effects of commercial formulations of deltamethrin and/or thiacloprid on thyroid hormone levels in rat serum
Authors: Şekeroğlu V , Şekeroğlu Z Atlı , Demirhan ES 
Published: June 2012

Deltamethrin (DEL) and thiacloprid (THIA) are the two commonly used synthetic insecticides applied either separately or as a mixture. The aim of this study was to assess thyroid stimulating hormone (TSH) and the serum levels of thyroid hormones exposure to these compounds in rats. The animals were orally gavaged with a single dose of DEL (15 mg/kg), THIA (112.5 mg/kg) or DEL + THIA (15 + 112.5 mg/kg) for 24 h (acute treatments) or DEL (3 mg/kg per day), THIA (22.5 mg/kg per day) or DEL + THIA (3 + 22.5 mg/kg per day) for 30 days (subacute treatments). Although all independent and combined treatments with DEL and THIA changed the levels of TSH, these alterations were not significant. Statistically significant increases in free triiodothyronine (FT3) and free thyroxine (FT4) serum hormone levels were observed in the independent treatment with THIA and the combined treatment with DEL and THIA for 30 days. The results of this study suggest that in vivo exposure to subacute treatments of commercial formulations of THI and mixture of DEL + THIA increased serum FT3 and FT4 levels in rats. Further studies are required to determine the effects of endocrine disruptors and potential health risks of these insecticides in human, especially in children because of the importance of these hormones during growth and development.
Perceptions of psychiatry of old age amongst psychiatry registrars in Australia and New Zealand
Authors: Flynn Brendan , Couzin-Wood Colin , Macfarlane Stephen 
Published: June 2012

Objective: To assess the perceptions of psychiatry registrars of their training experience in Psychiatry of Old Age (POA), and whether factors such as clinical exposure and stage of training correlate with these perceptions. Method: Royal Australian and New Zealand College of Psychiatrists (RANZCP) registrars were surveyed in September 2009. Demographic information, POA exposure and responses to 14 statements related to registrar experience were collected. Results: From 978 surveys sent, 226 responses were complete enough to be analysed. Themes that emerged included a high level of enjoyment of a POA rotation, favourable views of supervision, the challenging nature of managing medical co-morbidities and concerns regarding the teaching of cognitive assessment. In general, type or duration of POA exposure and demographic variables were not correlated with a significant difference in perceptions of the field. Conclusion: These data may be useful in addressing a shortfall of trainees in POA, which has implications for the health of older Australasians. It may inform service providers and the RANZCP of factors that could be modified or optimised to encourage registrars to consider subspecialty training in the area.
Psychiatry and online social media: potential, pitfalls and ethical guidelines for psychiatrists and trainees
Authors: Frankish Katherine , Ryan Christopher , Harris Anthony 
Published: June 2012

Objective: This paper proposes ethical guidelines for psychiatrists and psychiatry trainees when interacting with social media. Methods: A three-stage process was followed in the development of these guidelines. A literature review provided situations and possible broad rules as to how social media could be ethically engaged. A roundtable discussion by a panel of invited psychiatrists, psychiatry trainees, psychologists, e-health practitioners, lawyers and consumers was held to discuss the situations and to better formulate the ethical principles upon which psychiatrists could act. These vignettes and principles were then broadly discussed at a seminar held at the 2011 RANZCP Congress. Finally, this paper was circulated to the original invitees for final comment. Results: A set of recommendations for working with social media were developed. Conclusions: The new social media provides important avenues for communication, education and treatment. These avenues pose ethical and practical dilemmas that can be resolved by the application of established ethical principles. Practical recommendations for navigating social media are proposed.
Relationship between angiotensin-converting enzyme gene insertion/deletion polymorphism, angiographically defined coronary artery disease and myocardial infarction in patients with type 2 diabetes mellitus
Authors: Narne Parimala , Ponnaluri Kamakshi C , Singh Shailender , Siraj Mohammed , Ishaq Mohammed 
Published: June 2012

Introduction: The insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been implicated in the pathogenesis of cardiovascular diseases. The objective of the present study was to investigate the influence of ACE gene I/D polymorphism on the development and progression of coronary artery disease (CAD) and myocardial infarction (MI) in type 2 diabetic (T2DM) patients. Materials and Methods: We screened 283 T2DM patients, inclusive of 160 patients with angiographically defined CAD, 73 patients with MI, 89 patients without MI and 121 T2DM individuals with no evidence of CAD for ACE gene I /D polymorphism. Results: There was no significant difference in the distribution of genotypes and alleles of ACE gene I/D polymorphism between T2DM+CAD and T2DM (non-CAD) groups. However, a significant association of this polymorphism with MI in T2DM+CAD patients ( p=0.024) was observed. Further analysis revealed that the frequencies of the DD and ID genotypes increased with the number of stenosed coronary vessels ( p=0.026). The DD genotype and the D allele were more frequent in the subgroup of T2DM patients with multivessel CAD ( p=0.01) than in individuals with single vessel stenosis. Conclusions: These findings reveal a significant relationship between ACE gene I/D polymorphism, multivessel CAD and also the occurrence of MI in T2DM individuals with significant coronary stenoses in our population.
Association of polymorphisms in prolylcarboxypeptidase and chymase genes with essential hypertension in the Chinese Han population
Authors: Wu Yanrui , Yang Hongju , Yang Benguan , Yang Ke , Xiao Chunjie 
Published: June 2012

Introduction: The prolylcarboxypeptidase (PRCP) gene encodes a membrane protein that acts on angiotensin II (Ang II) and kallikrein to release vasoactive peptides. The chymase (CMA1) gene is important for Ang II generation. Therefore, the two genes might be involved in the pathogenesis of essential hypertension (EH). Materials and Methods: Eleven tag single nucleotide polymorphisms (SNPs) in the PRCP gene and four tag SNPs and G-1903A (rs1800875) polymorphism in the CMA1 gene were genotyped in the Chinese Han population ( n=1020) using a polymerase chain reaction-restriction fragment length polymorphism method. Results: In the PRCP gene, single site analyses indicated that the rs7104980 G allele was a susceptible factor for EH (adjusted odds ratio (OR)=1.98, 95% confidence interval (CI) 1.62–2.43, p=0.3×10-10). The protective effect of Hap3 GAGCACTAACA was observed without carrying the susceptible rs7104908 G allele (OR=0.67, 95% CI 0.56–0.81, p=0.3×10-4) by haplotype analyses. In the case of the CMA1 gene, no associations with EH were found through single site analyses. However, haplotype analyses showed that Hap16 TTTA significantly increased the risk of EH with OR=3.15 ( p=0.0002) which may be driven by interaction with a nearby SNP combination. Conclusions: The present results indicated PRCP rs7104980 can be considered as a marker for EH and Hap3 GAGCACTAACA (PRCP) and Hap16 TTTA (CMA1) might be associated with EH in Chinese Han population.
Living with diabetes on Buffalo, New York’s culturally diverse West Side
Authors: Kahn Linda S , Vest Bonnie M , Karl Renée , Tumiel-Berhalter Laurene , Taylor Robert , Schuster Roseanne C , Glaser Kathryn , Danakas Alexandra , Fox Chester H 
Published: June 2012

Objectives: This study explores the perceptions, attitudes, and beliefs that inform how people live with diabetes in a high poverty, ethnically diverse neighborhood with a growing population of refugees. The specific research objective was to examine participants’ explanations of how their diabetes began, understandings about the illness, description of symptoms, as well as physical and emotional reactions to the diagnosis. Methods: Qualitative design using semi-structured interviews. The transcripts were analyzed using an immersion–crystallization approach. Results: Thirty four individuals diagnosed with diabetes for at least 1 year participated. The sample included 14 refugees (from Somalia, Sudan, Burma, or Cuba), eight Puerto Ricans, six non-Hispanic Caucasians, six African-Americans, and two Native Americans. Three broad themes were identified across ethnic groups: (a) the diagnosis of diabetes was unexpected; (b) emotional responses to diabetes were similar to Kubler-Ross’s stages of grief; (c) patients’ understanding of diabetes focused on symptoms and diet. Conclusions: Patients were frequently stunned by the diagnosis of diabetes, and expressed emotions associated with the stages of grief including denial, anger, bargaining, depression, and acceptance. Our findings suggest that clinicians might consider addressing the patients’ emotions or grief reaction as an early priority to promote acceptance as a first step to self-management.
Contrasting acute graft-versus-host disease effects of Tim-3/galectin-9 pathway blockade dependent upon the presence of donor regulatory T cells
Authors: Veenstra Rachelle G. , Taylor Patricia A. , Zhou Qing , Panoskaltsis-Mortari Angela , Hirashima Mitsuomi , Flynn Ryan , Liu Derek , Anderson Ana C. , Strom Terry B. , Kuchroo Vijay K. , Blazar Bruce R. 
Published: June 2012

AbstractT-cell immunoglobulin mucin-3 (Tim-3) is expressed on pathogenic T cells, and its ligand galectin-9 (gal-9) is up-regulated in inflamed tissues. When Tim-3+ T cells encounter high gal-9 levels, they are deleted. Tim-3 is up-regulated on activated T cells during GVHD. Inhibition of Tim-3/gal-9 binding by infusion of a Tim-3-Ig fusion protein or Tim-3−/− donor T cells increased T-cell proliferation and GVHD lethality. When the Tim-3/gal-9 pathway engagement was augmented using gal-9 transgenic recipients, GVHD lethality was slowed. Together, these data indicate a potential for modulating this pathway to reduce disease by increasing Tim-3 or gal-9 engagement. Paradoxically, when Tim-3/gal-9 was inhibited in the absence of donor T-regulatory cells (Tregs), GVHD was inhibited. GVHD reduction was associated with decreased colonic inflammatory cytokines as well as epithelial barrier destruction. CD25-depleted Tim-3−/− donor T cells underwent increased activation-induced cell death because of increased IFN-γ production. To our knowledge, these studies are the first to show that although the absence of Tim-3/gal-9 pathway interactions augments systemic GVHD, concurrent donor Treg depletion paradoxically and surprisingly inhibits GVHD. Thus, although donor Tregs typically inhibit GVHD, under some conditions, such Tregs actually may contribute to GVHD by reducing activation-induced T-cell death.
Ezh2 augments leukemogenicity by reinforcing differentiation blockage in acute myeloid leukemia
Authors: Tanaka Satomi , Miyagi Satoru , Sashida Goro , Chiba Tetsuhiro , Yuan Jin , Mochizuki-Kashio Makiko , Suzuki Yutaka , Sugano Sumio , Nakaseko Chiaki , Yokote Koutaro , Koseki Haruhiko , Iwama Atsushi 
Published: June 2012

Abstract
EZH2, a catalytic component of the polycomb repressive complex 2, trimethylates histone H3 at lysine 27 (H3K27) to repress the transcription of target genes. Although EZH2 is overexpressed in various cancers, including some hematologic malignancies, the role of EZH2 in acute myeloid leukemia (AML) has yet to be examined in vivo. In the present study, we transformed granulocyte macrophage progenitors from Cre-ERT;Ezh2flox/flox mice with the MLL-AF9 leukemic fusion gene to analyze the function of Ezh2 in AML. Deletion of Ezh2 in transformed granulocyte macrophage progenitors compromised growth severely in vitro and attenuated the progression of AML significantly in vivo. Ezh2-deficient leukemic cells developed into a chronic myelomonocytic leukemia–like disease with a lower frequency of leukemia-initiating cells compared with the control. Chromatin immunoprecipitation followed by sequencing revealed a significant reduction in the levels of trimethylation at H3K27 in Ezh2-deficient leukemic cells, not only at Cdkn2a, a known major target of Ezh2, but also at a cohort of genes relevant to the developmental and differentiation processes. Overexpression of Egr1, one of the derepressed genes in Ezh2-deficient leukemic cells, promoted the differentiation of AML cells profoundly. Our findings suggest that Ezh2 inhibits differentiation programs in leukemic stem cells, thereby augmenting their leukemogenic activity.
MYH10 protein expression in platelets as a biomarker of RUNX1 and FLI1 alterations
Authors: Antony-Debré Iléana , Bluteau Dominique , Itzykson Raphael , Baccini Véronique , Renneville Aline , Boehlen Françoise , Morabito Margot , Droin Nathalie , Deswarte Caroline , Chang Yunhua , Leverger Guy , Solary Eric , Vainchenker William , Favier Rémi , Raslova Hana 
Published: June 2012

Abstract
RUNX1 gene alterations are associated with acquired and inherited hematologic malignancies that include familial platelet disorder/acute myeloid leukemia, primary or secondary acute myeloid leukemia, and chronic myelomonocytic leukemia. Recently, we reported that RUNX1-mediated silencing of nonmuscle myosin heavy chain IIB (MYH10) was required for megakaryocyte ploidization and maturation. Here we demonstrate that runx1 deletion in mice induces the persistence of MYH10 in platelets, and a similar persistence was observed in platelets of patients with constitutional (familial platelet disorder/acute myeloid leukemia) or acquired (chronic myelomonocytic leukemia) RUNX1 mutations. MYH10 was also detected in platelets of patients with the Paris-Trousseau syndrome, a thrombocytopenia related to the deletion of the transcription factor FLI1 that forms a complex with RUNX1 to regulate megakaryopoiesis, whereas MYH10 persistence was not observed in other inherited forms of thrombocytopenia. We propose MYH10 detection as a new and simple tool to identify inherited platelet disorders and myeloid neoplasms with abnormalities in RUNX1 and its associated proteins.
Preclinical activity of a novel CRM1 inhibitor in acute myeloid leukemia
Authors: Ranganathan Parvathi , Yu Xueyan , Na Caroline , Santhanam Ramasamy , Shacham Sharon , Kauffman Michael , Walker Alison , Klisovic Rebecca , Blum William , Caligiuri Michael , Croce Carlo M. , Marcucci Guido , Garzon Ramiro 
Published: June 2012

AbstractChromosome maintenance protein 1 (CRM1) is a nuclear export receptor involved in the active transport of tumor suppressors (eg, p53 and nucleophosmin) whose function is altered in cancer because of increased expression and overactive transport. Blocking CRM1-mediated nuclear export of such proteins is a novel therapeutic strategy to restore tumor suppressor function. Orally bioavailable selective inhibitors of nuclear export (SINE) that irreversibly bind to CRM1 and block the function of this protein have been recently developed. Here we investigated the antileukemic activity of KPT-SINE (KPT-185 and KPT-276) in vitro and in vivo in acute myeloid leukemia (AML). KPT-185 displayed potent antiproliferative properties at submicromolar concentrations (IC50 values; 100-500nM), induced apoptosis (average 5-fold increase), cell-cycle arrest, and myeloid differentiation in AML cell lines and patient blasts. A strong down-regulation of the oncogene FLT3 after KPT treatment in both FLT3-ITD and wild-type cell lines was observed. Finally, using the FLT3-ITD–positive MV4-11 xenograft murine model, we show that treatment of mice with oral KPT-276 (analog of KPT-185 for in vivo studies) significantly prolongs survival of leukemic mice (P < .01). In summary, KPT-SINE are highly potent in vitro and in vivo in AML. The preclinical results reported here support clinical trials of KPT-SINE in AML.
Polymorphisms of protein tyrosine phosphatase CD148 influence FcγRIIA-dependent platelet activation and the risk of heparin-induced thrombocytopenia
Authors: Rollin Jérôme , Pouplard Claire , Gratacap Marie-Pierre , Leroux Dorothée , May Marc-Antoine , Aupart Michel , Gouilleux-Gruart Valérie , Payrastre Bernard , Gruel Yves 
Published: June 2012

Abstract
Heparin-induced thrombocytopenia (HIT) is due primarily to IgG antibodies specific to platelet factor 4/heparin complexes (PF4/Hs) that activate platelets via FcγRIIA. CD148 is a protein tyrosine phosphatase that regulates Src kinases and collagen-induced platelet activation. Three polymorphisms affecting CD148 (Q276P, R326Q, and D872E) were studied in HIT patients and 2 control groups, with or without antibodies to PF4/Hs. Heterozygote status for CD148 276P or 326Q alleles was less frequent in HIT patients, suggesting a protective effect of these polymorphisms. Aggregation tests performed with collagen, HIT plasma, and monoclonal antibodies cross-linking FcγRIIA showed consistent hyporesponsiveness of platelets expressing the 276P/326Q alleles. In addition, platelets expressing the 276P/326Q alleles exhibited a greater sensitivity to the Src family kinases inhibitor dasatinib in response to collagen or ALB6 cross-linking FcγRIIA receptors. Moreover, the activatory phosphorylation of Src family kinases was considerably delayed as well as the phosphorylation of Linker for activation of T cells and phospholipase Cγ2, 2 major signaling proteins downstream from FcγRIIA. In conclusion, this study shows that CD148 polymorphisms affect platelet activation and probably exert a protec-tive effect on the risk of HIT in patients with antibodies to PF4/Hs.