bluuebunny/crossref_metadata_2025_split huggingface dataset:
Development of visual contour integration in children with migraine without aura
Authors: Braunitzer Gábor , Rokszin Alice , Kóbor Jenő , Nagy Attila , Sztriha László , Benedek György 
Published: June 2011

Introduction: As migraine attacks pose insult to cerebral circulation and ion homeostasis, migraine has the potential to interfere with the development of different brain structures, producing functional deficits. It is known that visual contour integration (CI) is a function with a protracted development. Therefore, we sought to establish whether migraine interferes with its development. Methods: Forty-eight migraineurs (without aura) and 48 age- and sex-matched controls participated in the study, divided into three cohorts by age. Stimuli were presented on cards with a contour consisting of Gabor patches embedded in random noise. Difficulty was varied by the manipulation of relative noise density. The task was to identify and show the contour. Results: A significant difference was found between the performance of migraineurs and controls in the 10–14-year-old and 15–18-year-old cohorts ( p < 0.05). Development between all three cohorts was significant in the control group ( p < 0.017), while it was not significant in migraineurs between 6 and 14 years. Correlation between age and CI threshold was stronger in controls than in migraineurs. Conclusion: Children with paediatric migraine exhibited a less marked development in the Gabor patch-based CI task.
Characterization of Subchondral Bone Repair for Marrow-Stimulated Chondral Defects and Its Relationship to Articular Cartilage Resurfacing
Authors: Chen Hongmei , Chevrier Anik , Hoemann Caroline D. , Sun Jun , Ouyang Wei , Buschmann Michael D. 
Published: June 2011

Background Microfracture and drilling are bone marrow–stimulation techniques that initiate cartilage repair by providing access to cell populations in subchondral bone marrow. This study examined the effect of hole depth and of microfracture versus drilling on subchondral bone repair and cartilage repair in full-thickness chondral defects. Hypotheses Repaired subchondral bone does not reconstitute its native structure and exhibits atypical morphologic features. Drilling deeper induces greater bone remodeling and is related to improved cartilage repair. Study Design Controlled laboratory study. Methods Trochlear cartilage defects debrided of the calcified layer were prepared bilaterally in 16 skeletally mature rabbits. Drill holes were made to a depth of 2 mm or 6 mm and microfracture holes to 2 mm. Animals were sacrificed 3 months postoperatively, and joints were scanned by micro–computed tomography before histoprocessing. Bone repair was assessed with a novel scoring system and by 3-dimentional micro–computed tomography and compared with intact controls. Correlation of subchon-dral bone features to cartilage repair outcome was performed. Results Although surgical holes were partly repaired with mineralized tissue, atypical features such as residual holes, cysts, and bony overgrowth were frequently observed. For all treatment groups, repair led to an average bone volume density similar to that of the controls but the repair bone was more porous and branched as shown by significantly higher bone surface area density and connectivity density. Deeper versus shallower drilling induced a larger region of repairing and remodeling subchondral bone that positively correlated with improved cartilage repair. Conclusion Incomplete reconstitution of normal bone structure and continued remodeling occurred in chondral defects 3 months after bone marrow stimulation. Deep drilling induced a larger volume of repairing and remodeling bone, which appeared beneficial for chondral repair. Clinical Relevance Bone marrow stimulation does not reconstitute normal bone structure. Strategies that increase subchondral bone involvement in marrow stimulation could further benefit cartilage repair.
Surgical Trends in Bankart Repair
Authors: Owens Brett D. , Harrast John J. , Hurwitz Shepard R. , Thompson Terry L. , Wolf Jennifer Moriatis 
Published: June 2011

Background: Arthroscopic Bankart repair emerged in the 1990s as a minimally invasive alternative to open repair. The optimal technique of surgical stabilization of the unstable glenohumeral joint remains controversial. Hypothesis: A review of the American Board of Orthopaedic Surgery (ABOS) data would show a trend toward an increasing number of arthroscopic versus open Bankart procedures. Study Design: Descriptive epidemiology study. Methods: A query of the ABOS database for all cases of open or arthroscopic Bankart repair from 2003 through 2008 was performed, as the CPT (Current Procedural Terminology) codes for arthroscopic repair were introduced in 2003. All cases coded with CPT codes for arthroscopic Bankart repair (29806) or open Bankart repair (23455) were reviewed. Additional data were obtained on the surgeons (year of procedure, geographic location, fellowship training, subspecialty examination area) as well as the patients (age, gender, follow-up length, complications, objective outcome measures [pain, deformity, function, and satisfaction]). Results: From 2003 to 2008, a total of 4562 Bankart repair cases were reported, composing 8.6% of the total number of shoulder surgery cases in the ABOS database. From 2003 to 2005, 71.2% of Bankart repairs were arthroscopic, compared with 87.7% between 2006 and 2008 ( P < .0001). Surgeons having obtained subspecialty training in sports medicine performed the majority (65.3%) of Bankart repairs. Over the entire period, sports-trained surgeons also performed a higher proportion of arthroscopic repairs (84.1%) compared with surgeons without this training (71.9%) ( P < .0001). However, by 2008 both non-fellowship–trained and sports medicine fellowship–trained surgeons performed arthroscopic repair in 90% of cases. Surgeons in the Northeast region performed a significantly greater proportion of arthroscopic Bankart repairs (84.7%) than did surgeons in other regions (78.6%) ( P < .0001) from 2003 to 2008. The most commonly reported complications were nerve palsy/injury and dislocation, with a rate of nerve injury of 2.2% in the open group compared to 0.3% in the arthroscopic group ( P < .0001), and dislocation rate of 1.2% with open stabilization compared with 0.4% arthroscopically ( P = .0039). Conclusion: Review of the ABOS data shows a trend toward arthroscopic shoulder stabilization over time, with the use of open repair declining. Reported complications were lower overall in the arthroscopic stabilization group when compared with open surgeries.
Aliskiren reduces prorenin receptor expression and activity in cultured human aortic smooth muscle cells
Authors: Ferri Nicola , Greco Carolina Magdalen , Maiocchi Giuseppe , Corsini Alberto 
Published: June 2011

Introduction: The recent discovery of a specific receptor for renin/prorenin (PRR) has added new interest to the potential pharmacological actions of aliskiren, the first direct renin inhibitor. Materials and methods: In the present study, to gain new insights into the pharmacological properties of aliskiren, we investigated the effect of aliskiren on PRR expression and activity in cultured human smooth muscle cells (HSMCs). Results: Co-incubation of HSMCs with angiotensinogen (ANG) (1.5× 10-7M) and prorenin (10-8–10-7M) resulted in an efficient production (within 4h) of angiotensin I, almost completely inhibited by 10-5M aliskiren (-86.0 ± 14.0%). In HSMCs stimulated with both ANG and prorenin, a 24h incubation with aliskiren (10-6–10-5M) resulted in a concentration-dependent reduction of PRR mRNA levels (IC50 4.6 × 10-6M). The cell surface expression of PRR determined by flow cytometry analysis was also reduced after incubation with aliskiren in a concentration-dependent manner. The lower levels of PRR were associated with a reduced expression of TGF-β, PAI-1 and type I collagen mRNA. Conclusions: These results suggest a direct pharmacological action of aliskiren on PRR expression and its signalling pathway in HSMCs. This reported action of aliskiren may reveal a new scenario of the pharmacological properties of aliskiren.
Hypoglycaemia is more frequent in type 2 diabetic patients with co-morbid vascular disease: an analysis of the DiaRegis registry
Authors: Gitt Anselm K , Bramlage Peter , Binz Christiane , Krekler Michael , Plate Tanja , Deeg Evelin , Tschöpe Diethelm ,   (for the DiaRegis Study Group)
Published: June 2011

Background: Patients with type-2 diabetes are at risk for treatment- and disease-related complications. Little is known about the interrelation of hypoglycaemia and co-morbid vascular disease (VD), defined as coronary heart disease, stroke and peripheral arterial disease. Hypothesis: Hypoglycaemia is associated with co-morbid VD in diabetic patients. Methods: DiaRegis is a prospective registry that included patients with type-2 diabetes in 2009/2010. Metric variables are displayed as median and quartiles. For the comparison of patients with or without VD Odds Ratios (OR) were determined from univariate analyses and adjusted for differences in patient characteristics (multivariable analysis). Results: Data on hypoglycaemia and VD within the last 12 months were available for 3741 patients (98.2%) with a median (IQR) age of 65.9 (57.6–72.9) years; 46.7% were female. VD patients ( n = 909; 24.3%) were older (70.7 vs 63.9 years; p < 0.0001), less often female (33.6% vs 50.9%; p < 0.0001) and had had diabetes for a longer duration (6.4 vs 5.4 years; p < 0.0001). Mean cholesterol (total, HDL and LDL) was also slightly lower ( p < 0.0001). Glycaemic control (HbA1c, fasting and postprandial glucose) was comparable. VD patients received less metformin (80.7 vs 85.2%; p < 0.01) and more sulfonylureas (31.8 vs 27.6%; p < 0.05). There was an increased incidence of symptomatic hypoglycaemia with or without requiring help and with a need for medical assistance. After adjusting a number of baseline variables the rates of symptomatic hypoglycaemias with help remained significantly increased (OR 3.73 (95% CI 1.31–10.65) in patients with VD. Conclusions: As hypothesized there is a strong association between the incidence of hypoglycaemia and vascular disease at comparable glycaemic control, which confirms prior randomized controlled trial data suggesting an interrelationship between hypoglycaemia and vascular disease.
Vilazodone: a brief pharmacological and clinical review of the novel serotonin partial agonist and reuptake inhibitor
Authors: Schwartz Thomas L. , Siddiqui Umar A. , Stahl Stephen M. 
Published: June 2011

Background: Vilazodone is the latest US Food and Drug Administration approved antidepressant agent available in the USA. Its putative mechanism of antidepressant action enhances the release of serotonin across the brain’s serotonergic pathways specifically by inhibiting the serotonin transporter, similar to a selective serotonin reuptake inhibitor (SSRI), and simultaneously stimulating serotonin-1a receptors via partial agonism, similar to the anxiolytic buspirone. This combined activity in the single vilazodone agent has been termed by the authors as being a serotonin partial agonist and reuptake inhibitor or (SPARI). Methods: A MEDLINE and Internet search was conducted and the resultant preclinical and clinical evidence was reviewed . The authors attempt to review laboratory data, animal model data and human trial data to develop a translational theory on the mechanism of antidepressant action of this agent and also its adverse effect potential. Results: Randomized, controlled empirical data for vilazodone have gained it approval for treating major depressive disorder. It combines two well known pharmacodynamic mechanisms of serotonergic action into a novel agent. Although no head-to-head studies against other antidepressants have been published, the efficacy data for vilazodone appear comparable to other known antidepressants, with similar gastrointestinal side effects to SSRI or serotonin norepinephrine reuptake inhibitor (SNRI) antidepressants, but possibly with a lower incidence of sexual side effects and weight gain. Discussion: Vilazodone will lend itself to the current armamentarium in the treatment of major depressive disorder and may hold promise for patients who cannot tolerate other antidepressants. Its unique SPARI mechanism of action could also be efficacious for patients who do not respond to SSRI or SNRI antidepressant monotherapies.
RhoJ is an endothelial cell-restricted Rho GTPase that mediates vascular morphogenesis and is regulated by the transcription factor ERG
Authors: Yuan Lei , Sacharidou Anastasia , Stratman Amber N. , Le Bras Alexandra , Zwiers Peter J. , Spokes Katherine , Bhasin Manoj , Shih Shou-ching , Nagy Janice A. , Molema Grietje , Aird William C. , Davis George E. , Oettgen Peter 
Published: June 2011

AbstractERG is a member of the ETS transcription factor family that is highly enriched in endothelial cells (ECs). To further define the role of ERG in regulating EC function, we evaluated the effect of ERG knock-down on EC lumen formation in 3D collagen matrices. Blockade of ERG using siRNA completely interferes with EC lumen formation. Quantitative PCR (QPCR) was used to identify potential downstream gene targets of ERG. In particular, we identified RhoJ as the Rho GTPase family member that is closely related to Cdc42 as a target of ERG. Knockdown of ERG expression in ECs led to a 75% reduction in the expression of RhoJ. Chromatin immunoprecipitation and transactivation studies demonstrated that ERG could bind to functional sites in the proximal promoter of the RhoJ gene. Knock-down of RhoJ similarly resulted in a marked reduction in the ability of ECs to form lumens. Suppression of either ERG or RhoJ during EC lumen formation was associated with a marked increase in RhoA activation and a decrease in Rac1 and Cdc42 activation and their downstream effectors. Finally, in contrast to other Rho GTPases, RhoJ exhibits a highly EC-restricted expression pattern in several different tissues, including the brain, heart, lung, and liver.
Iron chelation with deferasirox in adult and pediatric patients with thalassemia major: efficacy and safety during 5 years' follow-up
Authors: Cappellini M. Domenica , Bejaoui Mohamed , Agaoglu Leyla , Canatan Duran , Capra Marcello , Cohen Alan , Drelichman Guillermo , Economou Marina , Fattoum Slaheddine , Kattamis Antonis , Kilinc Yurdanur , Perrotta Silverio , Piga Antonio , Porter John B. , Griffel Louis , Dong Victor , Clark Joan , Aydinok Yesim 
Published: June 2011

AbstractPatients with β-thalassemia require lifelong iron chelation therapy from early childhood to prevent complications associated with transfusional iron overload. To evaluate long-term efficacy and safety of once-daily oral iron chelation with deferasirox, patients aged ≥ 2 years who completed a 1-year, phase 3, randomized trial entered a 4-year extension study, either continuing on deferasirox (deferasirox cohort) or switching from deferoxamine to deferasirox (crossover cohort). Of 555 patients who received ≥ 1 deferasirox dose, 66.8% completed the study; 43 patients (7.7%) discontinued because of adverse events. In patients with ≥ 4 years' deferasirox exposure who had liver biopsy, mean liver iron concentration significantly decreased by 7.8 ± 11.2 mg Fe/g dry weight (dw; n = 103; P < .001) and 3.1 ± 7.9 mg Fe/g dw (n = 68; P < .001) in the deferasirox and crossover cohorts, respectively. Median serum ferritin significantly decreased by 706 ng/mL (n = 196; P < .001) and 371 ng/mL (n = 147; P < .001), respectively, after ≥ 4 years' exposure. Investigator-assessed, drug-related adverse events, including increased blood creatinine (11.2%), abdominal pain (9.0%), and nausea (7.4%), were generally mild to moderate, transient, and reduced in frequency over time. No adverse effect was observed on pediatric growth or adolescent sexual development. This first prospective study of long-term deferasirox use in pediatric and adult patients with β-thalassemia suggests treatment for ≤ 5 years is generally well tolerated and effectively reduces iron burden. This trial was registered at www.clinicaltrials.gov as #NCT00171210.
Neurexophilin 1 suppresses the proliferation of hematopoietic progenitor cells
Authors: Kinzfogl John , Hangoc Giao , Broxmeyer Hal E. 
Published: June 2011

AbstractNeurexin I α (NRXN1α) and Dystroglycan (DAG1) are membrane receptors which serve as mutual ligands in the neuronal system. Neurexophilins (NXPHs) bind NRXN1α. NRXN1α was expressed in primitive populations in human CB (huCB) and murine BM (muBM). DAG1 is ubiquitously expressed in hematopoietic tissue; however, osteoblasts appear to be sites of very high expression within muBM. High concentrations of NXPH were found in huCB plasma and murine lineage-positive splenocytes. We evaluated effects of these molecules on huCB and muBM hematopoietic progenitor cells (HPCs) and HSCs. At both a single and population cell level in vitro, we found that NXPH1 was a potent inhibitor of HPC proliferation acting through NRXN1α an effect down-modulated by DAG1. Injection of recombinant NXPH1 in vivo resulted in myelo- and lymphosuppression in the BM, with absolute numbers and cycling status of functional and phenotypically defined HPCs dose- and time-dependently decreased. Competitive HSC transplantations showed no change in the long-term repopulating activity of HSCs from mice exposed to recombinant NXPH1. These results demonstrate the presence and function of a regulated signaling axis in hematopoiesis centered on NRXN1α and its modulation by DAG1 and NXPH1.
Modeling the evolution of ETV6-RUNX1–induced B-cell precursor acute lymphoblastic leukemia in mice
Authors: van der Weyden Louise , Giotopoulos George , Rust Alistair G. , Matheson Louise S. , van Delft Frederik W. , Kong Jun , Corcoran Anne E. , Greaves Mel F. , Mullighan Charles G. , Huntly Brian J. , Adams David J. 
Published: June 2011

AbstractThe t(12;21) translocation that generates the ETV6-RUNX1 (TEL-AML1) fusion gene, is the most common chromosomal rearrangement in childhood cancer and is exclusively associated with B-cell precursor acute lymphoblastic leukemia (BCP-ALL). The translocation arises in utero and is necessary but insufficient for the development of leukemia. Single-nucleotide polymorphism array analysis of ETV6-RUNX1 patient samples has identified multiple additional genetic alterations; however, the role of these lesions in leukemogenesis remains undetermined. Moreover, murine models of ETV6-RUNX1 ALL that faithfully recapitulate the human disease are lacking. To identify novel genes that cooperate with ETV6-RUNX1 in leukemogenesis, we generated a mouse model that uses the endogenous Etv6 locus to coexpress the Etv6-RUNX1 fusion and Sleeping Beauty transposase. An insertional mutagenesis screen was performed by intercrossing these mice with those carrying a Sleeping Beauty transposon array. In contrast to previous models, a substantial proportion (20%) of the offspring developed BCP-ALL. Isolation of the transposon insertion sites identified genes known to be associated with BCP-ALL, including Ebf1 and Epor, in addition to other novel candidates. This is the first mouse model of ETV6-RUNX1 to develop BCP-ALL and provides important insight into the cooperating genetic alterations in ETV6-RUNX1 leukemia.
Reprogramming of EBV-immortalized B-lymphocyte cell lines into induced pluripotent stem cells
Authors: Choi Su Mi , Liu Hua , Chaudhari Pooja , Kim Yonghak , Cheng Linzhao , Feng Jian , Sharkis Saul , Ye Zhaohui , Jang Yoon-Young 
Published: June 2011

AbstractEBV-immortalized B lymphocyte cell lines have been widely banked for studying a variety of diseases, including rare genetic disorders. These cell lines represent an important resource for disease modeling with the induced pluripotent stem cell (iPSC) technology. Here we report the generation of iPSCs from EBV-immortalized B-cell lines derived from multiple inherited disease patients via a nonviral method. The reprogramming method for the EBV cell lines involves a distinct protocol compared with that of patient fibroblasts. The B-cell line–derived iPSCs expressed pluripotency markers, retained the inherited mutation and the parental V(D)J rearrangement profile, and differentiated into all 3 germ layer cell types. There was no integration of the reprogramming-related transgenes or the EBV-associated genes in these iPSCs. The ability to reprogram the widely banked patient B-cell lines will offer an unprecedented opportunity to generate human disease models and provide novel drug therapies.
MiR-204 regulates cardiomyocyte autophagy induced by ischemia-reperfusion through LC3-II
Authors: Xiao Jian , Zhu Xiaoyan , He Bin , Zhang Yufeng , Kang Bo , Wang Zhinong , Ni Xin 
Published: June 2011

Abstract

Background
Autophagy plays a significant role in myocardial ischemia-reperfusion (IR) injury. So it is important to inhibit autophagy to protect cardiomyocytes besides anti-apoptosis. MiRNA has been demonstrated to protect cardiomyocytes against apoptosis during IR, while whether it has anti-autophagy effect has not been known. The aim of this study was to investigate whether miR-204 regulated autophagy by regulating LC3-II protein, which is the marker of autophagosome during myocardial IR injury.

Methods
Adult SD rats were randomized to Control and IR groups. IR group was treated with 30 min ischemia by ligating the left anterior descending coronary artery, followed by 2 h reperfusion by loosing the ligation. The expression of miR-204 was measured by RT-PCR, and LC3 protein was measured by western-blot.

Results
We found that IR induced cardiomyocytes autophagy, together with down-regulation of miR-204 and up-regulation of LC3-II protein. And, we have found that LC3-II protein was regulated by miR-204, using the method of transferring miR-204 mimic or AMO-204 into the cardiomyocytes, before.

Conclusions
These studies provided evidence that miR-204 played an important role in regulating autophagy through LC3-IIprotein during IR.
Concurrent analysis of choice and control in childbirth
Authors: Snowden Austyn , Martin Colin , Jomeen Julie , Martin Caroline Hollins 
Published: June 2011

Abstract

Background
This paper reports original research on choice and control in childbirth. Eight women were interviewed as part of a wider investigation into locus of control in women with pre-labour rupture of membranes at term (PROM) [1].

Methods
The following study uses concurrent analysis to sample and analyse narrative aspects of relevant literature along with these interviews in order to synthesise a generalisable analysis of the pertinent issues. The original PROM study had found that women experienced a higher degree of control in hospital, a finding that appeared at odds with contemporary notions of choice. However, this paper contextualises this finding by presenting narratives that lucidly subscribe to the dominant discourse of hospital as the safest place to give birth, under the premise of assuring a live healthy baby irrespective of their management type.

Results
This complex narrative is composed of the following themes: 'perceiving risk', 'being prepared', 'reflecting on experience', maintaining control' and relinquishing control'. These themes are constructed within and around the medical, foetocentric, risk averse cultural context. Primary data are presented throughout to show the origins and interconnected nature of these themes.

Conclusions
Within this context it is clear that there is a highly valued role for competent health professionals that respect, understand and are capable of facilitating genuine choice for women.