bluuebunny/crossref_metadata_2025_split huggingface dataset:
Systematic review and meta-analysis of laparoscopic and open gastrectomy for advanced gastric cancer
Authors: Chen Ke , Xu Xiao-Wu , Mou Yi-Ping , Pan Yu , Zhou Yu-Cheng , Zhang Ren-Chao , Wu Di 
Published: August 2013

Abstract

Background
The use of laparoscopic gastrectomy (LG) in advanced gastric cancer (AGC) remains a controversial topic, mainly because of doubts about its oncologic validity. This study is a systematic review and meta-analysis of the available evidence.

Methods
A comprehensive search was performed until June 2013 to identify comparative studies evaluating survival rates, recurrence rates, surgical outcomes and complications. Pooled risk ratios (RR) and weighted mean differences (WMD) with 95% confidence intervals (CI) were calculated using the random effects model. Data synthesis and statistical analysis were carried out using RevMan 5.1 software.

Results
Fifteen trials were involved in this analysis. Compared to open gastrectomy (OG), LG involved a longer operating time (WMD = 48.67 min, 95% CI 34.09 to 63.26, P < 0.001); less blood loss (WMD = −139.01 ml, 95% CI −174.57 to −103.44, P < 0.001); earlier time to flatus (WMD = −0.79 days, 95% CI −1.14 to −0.44, P < 0.001); shorter hospital stay (WMD = −3.11 days, 95% CI −4.13 to −2.09, P < 0.001); and a decrease in complications (RR = 0.74, 95% CI 0.61 to 0.90, P = 0.003). There was no significant difference in the number of harvested lymph nodes, margin distance, mortality, cancer recurrence rate and long-term survival rate between the AGC patients treated with LG or OG (P > 0.05).

Conclusions
Despite a longer operation, LG is a safe technical alternative to OG for AGC with a lower complication rate and enhanced postoperative recovery. Moreover, there were similar outcomes between both approaches in terms of cancer recurrence and the long-term survival rate. Because of the limitation of this study, methodologically high-quality studies are needed for further evaluation.
Uniform SiGe/Si quantum well nanorod and nanodot arrays fabricated using nanosphere lithography
Authors: Chang Hung-Tai , Wu Bo-Lun , Cheng Shao-Liang , Lee Tu , Lee Sheng-Wei 
Published: August 2013

AbstractThis study fabricates the optically active uniform SiGe/Si multiple quantum well (MQW) nanorod and nanodot arrays from the Si0.4Ge0.6/Si MQWs using nanosphere lithography (NSL) combined with the reactive ion etching (RIE) process. Compared to the as-grown sample, we observe an obvious blueshift in photoluminescence (PL) spectra for the SiGe/Si MQW nanorod and nanodot arrays, which can be attributed to the transition of PL emission from the upper multiple quantum dot-like SiGe layers to the lower MQWs. A possible mechanism associated with carrier localization is also proposed for the PL enhancement. In addition, the SiGe/Si MQW nanorod arrays are shown to exhibit excellent antireflective characteristics over a wide wavelength range. These results indicate that SiGe/Si MQW nanorod arrays fabricated using NSL combined with RIE would be potentially useful as an optoelectronic material operating in the telecommunication range.
Screening for duplications, deletions and a common intronic mutation detects 35% of second mutations in patients with USH2A monoallelic mutations on Sanger sequencing
Authors: Steele-Stallard Heather B , Le Quesne Stabej Polona , Lenassi Eva , Luxon Linda M , Claustres Mireille , Roux Anne-Francoise , Webster Andrew R , Bitner-Glindzicz Maria 
Published: August 2013

Abstract

Background
Usher Syndrome is the leading cause of inherited deaf-blindness. It is divided into three subtypes, of which the most common is Usher type 2, and the USH2A gene accounts for 75-80% of cases. Despite recent sequencing strategies, in our cohort a significant proportion of individuals with Usher type 2 have just one heterozygous disease-causing mutation in USH2A, or no convincing disease-causing mutations across nine Usher genes. The purpose of this study was to improve the molecular diagnosis in these families by screening USH2A for duplications, heterozygous deletions and a common pathogenic deep intronic variant USH2A: c.7595-2144A>G.

Methods
Forty-nine Usher type 2 or atypical Usher families who had missing mutations (mono-allelic USH2A or no mutations following Sanger sequencing of nine Usher genes) were screened for duplications/deletions using the USH2A SALSA MLPA reagent kit (MRC-Holland). Identification of USH2A: c.7595-2144A>G was achieved by Sanger sequencing. Mutations were confirmed by a combination of reverse transcription PCR using RNA extracted from nasal epithelial cells or fibroblasts, and by array comparative genomic hybridisation with sequencing across the genomic breakpoints.

Results
Eight mutations were identified in 23 Usher type 2 families (35%) with one previously identified heterozygous disease-causing mutation in USH2A. These consisted of five heterozygous deletions, one duplication, and two heterozygous instances of the pathogenic variant USH2A: c.7595-2144A>G. No variants were found in the 15 Usher type 2 families with no previously identified disease-causing mutations. In 11 atypical families, none of whom had any previously identified convincing disease-causing mutations, the mutation USH2A: c.7595-2144A>G was identified in a heterozygous state in one family. All five deletions and the heterozygous duplication we report here are novel. This is the first time that a duplication in USH2A has been reported as a cause of Usher syndrome.

Conclusions
We found that 8 of 23 (35%) of ‘missing’ mutations in Usher type 2 probands with only a single heterozygous USH2A mutation detected with Sanger sequencing could be attributed to deletions, duplications or a pathogenic deep intronic variant. Future mutation detection strategies and genetic counselling will need to take into account the prevalence of these types of mutations in order to provide a more comprehensive diagnostic service.
COBRApy: COnstraints-Based Reconstruction and Analysis for Python
Authors: Ebrahim Ali , Lerman Joshua A , Palsson Bernhard O , Hyduke Daniel R 
Published: August 2013

Abstract

Background
COnstraint-Based Reconstruction and Analysis (COBRA) methods are widely used for genome-scale modeling of metabolic networks in both prokaryotes and eukaryotes. Due to the successes with metabolism, there is an increasing effort to apply COBRA methods to reconstruct and analyze integrated models of cellular processes. The COBRA Toolbox for MATLAB is a leading software package for genome-scale analysis of metabolism; however, it was not designed to elegantly capture the complexity inherent in integrated biological networks and lacks an integration framework for the multiomics data used in systems biology. The openCOBRA Project is a community effort to promote constraints-based research through the distribution of freely available software.

Results
Here, we describe COBRA for Python (COBRApy), a Python package that provides support for basic COBRA methods. COBRApy is designed in an object-oriented fashion that facilitates the representation of the complex biological processes of metabolism and gene expression. COBRApy does not require MATLAB to function; however, it includes an interface to the COBRA Toolbox for MATLAB to facilitate use of legacy codes. For improved performance, COBRApy includes parallel processing support for computationally intensive processes.

Conclusion
COBRApy is an object-oriented framework designed to meet the computational challenges associated with the next generation of stoichiometric constraint-based models and high-density omics data sets.

Availability

http://opencobra.sourceforge.net/
Relationship between foot function and medial knee joint loading in people with medial compartment knee osteoarthritis
Authors: Levinger Pazit , Menz Hylton B , Morrow Adam D , Bartlett John R , Feller Julian A , Bergman Neil R 
Published: August 2013

AbstractBackgroundDynamic joint loading, particularly the external knee adduction moment (KAM), is an important surrogate measure for the medio‐lateral distribution of force across the knee joint in people with knee osteoarthritis (OA). Foot motion may alter the load on the medial tibiofemoral joint and hence affect the KAM. Therefore, this study aimed to investigate the relationship between tibia, rearfoot and forefoot motion in the frontal and transverse planes and the KAM in people with medial compartment knee OA.MethodMotion of the knee, tibia, rearfoot and forefoot and knee moments were evaluated in 32 patients with clinically and radiographically‐confirmed OA, predominantly in the medial compartment. Pearson's correlation coefficient was used to investigate the association between peak values of tibia, rearfoot and forefoot motion in the frontal and transverse planes and 1st peak KAM, 2nd peak KAM, and the knee adduction angular impulse (KAAI).ResultsLateral tilt of the tibia was significantly associated with increased 1st peak KAM (r = 0.60, p < 0.001), 2nd peak KAM (r = 0.67, p = 0.001) and KAAI (r = 0.82, p = 0.001). Increased peak rearfoot eversion was significantly correlated with decreased 2nd peak KAM (r = 0.59, p < 0.001) and KAAI (r = 0.50, p = 0.004). Decreased rearfoot internal rotation was significantly associated with increased 2nd peak KAM (r = −0.44, p = 0.01) and KAAI (r = −0.38, p = 0.02), while decreased rearfoot internal rotation relative to the tibia was significantly associated with increased 2nd peak KAM (r = 0.43, p = 0.01). Significant negative correlations were found between peak forefoot eversion relative to the rearfoot and 2nd peak KAM (r = −0.53, p = 0.002) and KAAI (r = −0.51, p = 0.003) and between peak forefoot inversion and 2nd peak KAM (r = −0.54, p = 0.001) and KAAI (r = −0.48, p = 0.005).ConclusionIncreased rearfoot eversion, rearfoot internal rotation and forefoot inversion are associated with reduced knee adduction moments during the stance phase of gait, suggesting that medial knee joint loading is reduced in people with OA who walk with greater foot pronation. These findings have implications for the design of load‐modifying interventions in people with knee OA.
The Sex Chromosome Trisomy mouse model of XXY and XYY: metabolism and motor performance
Authors: Chen Xuqi , Williams-Burris Shayna M , McClusky Rebecca , Ngun Tuck C , Ghahramani Negar , Barseghyan Hayk , Reue Karen , Vilain Eric , Arnold Arthur P 
Published: August 2013

AbstractBackgroundKlinefelter syndrome (KS), caused by XXY karyotype, is characterized by low testosterone, infertility, cognitive deficits, and increased prevalence of health problems including obesity and diabetes. It has been difficult to separate direct genetic effects from hormonal effects in human studies or in mouse models of KS because low testosterone levels are confounded with sex chromosome complement.MethodsIn this study, we present the Sex Chromosome Trisomy (SCT) mouse model that produces XXY, XYY, XY, and XX mice in the same litters, each genotype with either testes or ovaries. The independence of sex chromosome complement and gonadal type allows for improved recognition of sex chromosome effects that are not dependent on levels of gonadal hormones. All mice were gonadectomized and treated with testosterone for 3 weeks. Body weight, body composition, and motor function were measured.ResultsBefore hormonal manipulation, XXY mice of both sexes had significantly greater body weight and relative fat mass compared to XY mice. After gonadectomy and testosterone replacement, XXY mice (both sexes) still had significantly greater body weight and relative fat mass, but less relative lean mass compared to XY mice. Liver, gonadal fat pad, and inguinal fat pad weights were also higher in XXY mice, independent of gonadal sex. In several of these measures, XX mice also differed from XY mice, and gonadal males and females differed significantly on almost every metabolic measure. The sex chromosome effects (except for testis size) were also seen in gonadally female mice before and after ovariectomy and testosterone treatment, indicating that they do not reflect group differences in levels of testicular secretions. XYY mice were similar to XY mice on body weight and metabolic variables but performed worse on motor tasks compared to other groups.ConclusionsWe find that the new SCT mouse model for XXY and XYY recapitulates features found in humans with these aneuploidies. We illustrate that this model has significant promise for unveiling the role of genetic effects compared to hormonal effects in these syndromes, because many phenotypes are different in XXY vs. XY gonadal female mice which have never been exposed to testicular secretions.
Psychotropic drug prescribing in an Australian specialist child and adolescent eating disorder service: a retrospective study
Authors: Moore Julia K , Watson Hunna J , Harper Emily , McCormack Julie , Nguyen Thinh 
Published: August 2013

Abstract

Background
To describe the rates, indications, and adverse effects of psychotropic drug prescription in a specialist tertiary hospital child and adolescent eating disorder service.

Methods
Retrospective case note study of all active eating disorder patients (N = 115) over the period of treatment from referral to time of study (M = 2 years), covering patient demographics, clinical characteristics, drug prescriptions, indications, and adverse effects.

Results
Psychotropic drugs were prescribed in 45% of cases, most commonly antidepressants (41%), followed by anxiolytics (29%) and antipsychotics (22%), with 8% initiated before referral to the specialist eating disorder program. Common indications were depressed mood, agitation, anxiety, and insomnia. Patient clinical severity and complexity was associated with prescribing. Adverse effects, mostly minor, were recorded in 23% of antidepressant prescriptions, 39% of antipsychotic prescriptions, and 13% of anxiolytic prescriptions. Second generation antipsychotic prescription was associated with subsequent new onset binge eating, in this preliminary observational study. Self-harm by overdose of psychotropics occurred in 11% of patients prescribed medication.

Conclusions
Psychotropic medications were frequently prescribed to adolescent eating disorder patients to treat distressing symptoms. Prospective randomised controlled trials to clarify efficacy and safety are needed. Given the difficulties of conducting clinical trials in this population, services are encouraged to monitor and audit medication safety and efficacy in everyday practice, and to report their findings.
Anthropogenic organic micro-pollutants and pathogens in the urban water cycle: assessment, barriers and risk communication (ASKURIS)
Authors: Jekel Martin , Ruhl Aki Sebastian , Meinel Felix , Zietzschmann Frederik , Lima Stephan Pflugmacher , Baur Nina , Wenzel Melanie , Gnirß Regina , Sperlich Alexander , Dünnbier Uwe , Böckelmann Uta , Hummelt Daniel , van Baar Patricia , Wode Florian , Petersohn Dietmar , Grummt Tamara , Eckhardt Alexander , Schulz Wolfgang , Heermann Alexandra , Reemtsma Thorsten , Seiwert Bettina , Schlittenbauer Linda , Lesjean Boris , Miehe Ulf , Remy Christian , Stapf Michael , Mutz Daniel 
Published: August 2013

Abstract
In urban areas, water often flows along a partially closed water cycle in which treated municipal wastewater is discharged into surface waters which are one source of raw waters used for drinking water supply. A number of organic micro-pollutants (OMP) can be found in different water compartments. In the near future, climatic and demographic changes will probably contribute to an increase of OMP and antibiotic-resistant pathogens in aquatic ecosystems. The occurrence of OMP, possible adverse effects on aquatic organisms and human health and the public perception must be carefully assessed to properly manage and communicate potentially associated risks and to implement appropriate advanced treatment options at the optimum location within the water cycle. Therefore, the interdisciplinary research project ASKURIS focuses on identification and quantification, toxicological assessment and removal of organic micro-pollutants and antibiotic-resistant pathogens in the Berlin water cycle, life cycle-based economic and environmental assessment, public perception and management of potential risks.
Type 2 innate lymphoid cells constitutively express arginase-I in the naïve and inflamed lung
Authors: Bando Jennifer K , Nussbaum Jesse C , Liang Hong-Erh , Locksley Richard M 
Published: August 2013

ABSTRACTArg1 is produced by AAMs and is proposed to have a regulatory role during asthma and allergic inflammation. Here, we use an Arg1 reporter mouse to identify additional cellular sources of the enzyme in the lung. We demonstrate that ILC2s express Arg1 at rest and during infection with the migratory helminth Nippostrongylus brasiliensis. In contrast to AAMs, which express Arg1 following IL-4/IL-13-mediated STAT6 activation, ILC2s constitutively express the enzyme in a STAT6-independent manner. Although ILC2s deficient in the IL-33R subunit T1/ST2 maintain Arg1 expression, IL-33 can regulate total lung Arg1 by expanding the ILC2 population and by activating macrophages indirectly via STAT6. Finally, we find that ILC2 Arg1 does not mediate ILC2 accumulation, ILC2 production of IL-5 and IL-13, or collagen production during N. brasiliensis infection. Thus, ILC2s are a novel source of Arg1 in resting tissue and during allergic inflammation.
Moderate and high amounts of tamoxifen in α-MHC-MerCreMer mice induce a DNA damage response, leading to heart failure and death
Authors: Bersell Kevin , Choudhury Sangita , Mollova Mariya , Polizzotti Brian D. , Ganapathy Balakrishnan , Walsh Stuart , Wadugu Brian , Arab Shima , Kühn Bernhard 
Published: August 2013

Summary
Numerous mouse models have utilized Cre-loxP technology to modify gene expression. Adverse effects of Cre recombinase activity have been reported, including in the heart. However, the mechanisms associated with cardiac Cre toxicity are largely unknown. Here, we show that expression of Cre in cardiomyocytes induces a DNA damage response, resulting in cardiomyocyte apoptosis, cardiac fibrosis and cardiac dysfunction. In an effort to increase the recombination efficiency of a widely used tamoxifen-sensitive Cre transgene under control of the α-myosin-heavy-chain promoter (αMHC-MerCreMer), we observed myocardial dysfunction and decreased survival, which were dependent on the dose of tamoxifen injected. After excluding a Cre-independent contribution by tamoxifen, we found that Cre induced myocardial fibrosis, activation of pro-fibrotic genes and cardiomyocyte apoptosis. Examination of the molecular mechanisms showed activation of DNA damage response signaling and p53 stabilization in the absence of loxP sites, suggesting that Cre induced illegitimate DNA breaks. Cardiomyocyte apoptosis was also induced by expressing Cre using adenoviral transduction, indicating that the effect was not dependent on genomic integration of the transgene. Cre-mediated homologous recombination at loxP sites was dose-dependent and had a ceiling effect at ~80% of cardiomyocytes showing recombination. By titrating the amount of tamoxifen to maximize recombination while minimizing animal lethality, we determined that 30 μg tamoxifen/g body weight/day injected on three consecutive days is, in our lab, the optimal condition for the αMHC-MerCreMer system to induce recombination in the Rosa26-lacZ strain. Our results further highlight the importance of experimental design, including the use of appropriate genetic controls for Cre expression.
Cardiac fibrosis in mice expressing an inducible myocardial-specific Cre driver
Authors: Lexow Jonas , Poggioli Tommaso , Sarathchandra Padmini , Santini Maria Paola , Rosenthal Nadia 
Published: August 2013

Summary
Tamoxifen-inducible Cre-mediated manipulation of animal genomes has achieved wide acceptance over the last decade, with numerous important studies heavily relying on this technique. Recently, a number of groups have reported transient complications of using this protocol in the heart. In the present study we observed a previously unreported focal fibrosis and depressed left-ventricular function in tamoxifen treated αMHC-MerCreMer-positive animals in a Tβ4shRNAflox x αMHC-MerCreMer cross at 6-7 weeks following standard tamoxifen treatment, regardless of the presence of the floxed transgene. The phenotype was reproduced by treating mice from the original αMHC-MerCreMer strain with tamoxifen. In the acute phase after tamoxifen treatment, cell infiltration into the myocardium was accompanied by increased expression of pro-inflammatory cytokines (IL-1β, IL-6, TNFα, IFNγ, Ccl2) and markers of hypertrophy (ANF, BNP, Col3a1). These observations highlight the requirement for including tamoxifen-treated MerCreMer littermate controls to avert misinterpretation of conditional mutant phenotypes. A survey of the field as well as the protocols presented here suggests that controlling the parameters of tamoxifen delivery is important in avoiding the chronic MerCreMer-mediated cardiac phenotype reported here.
Modeling human neurodevelopmental disorders in theXenopustadpole: from mechanisms to therapeutic targets
Authors: Pratt Kara G. , Khakhalin Arseny S. 
Published: August 2013

SummaryThe Xenopus tadpole model offers many advantages for studying molecular, cellular and network mechanisms underlying neurodevelopmental disorders. Essentially every stage of normal neural circuit development, from axon outgrowth and guidance to activity-dependent homeostasis and refinement, has been studied in the frog tadpole, making it an ideal model to determine what happens when any of these stages are compromised. Recently, the tadpole model has been used to explore the mechanisms of epilepsy and autism, and there is mounting evidence to suggest that diseases of the nervous system involve deficits in the most fundamental aspects of nervous system function and development. In this Review, we provide an update on how tadpole models are being used to study three distinct types of neurodevelopmental disorders: diseases caused by exposure to environmental toxicants, epilepsy and seizure disorders, and autism.
Insights from venous oxygen profiles: oxygen utilization and management in diving California sea lions
Authors: McDonald Birgitte I. , Ponganis Paul J. 
Published: August 2013

SUMMARY
The management and depletion of O2 stores underlie the aerobic dive capacities of marine mammals. The California sea lion (Zalophus californianus) presumably optimizes O2 store management during all dives, but approaches its physiological limits during deep dives to greater than 300 m depth. Blood O2 comprises the largest component of total body O2 stores in adult sea lions. Therefore, we investigated venous blood O2 depletion during dives of California sea lions during maternal foraging trips to sea by: (1) recording venous partial pressure of O2 (PO2) profiles during dives, (2) characterizing the O2–hemoglobin (Hb) dissociation curve of sea lion Hb and (3) converting the PO2 profiles into percent Hb saturation (SO2) profiles using the dissociation curve. The O2–Hb dissociation curve was typical of other pinnipeds (P50=28±2 mmHg at pH 7.4). In 43% of dives, initial venous SO2 values were greater than 78% (estimated resting venous SO2), indicative of arterialization of venous blood. Blood O2 was far from depleted during routine shallow dives, with minimum venous SO2 values routinely greater than 50%. However, in deep dives greater than 4 min in duration, venous SO2 reached minimum values below 5% prior to the end of the dive, but then increased during the last 30–60 s of ascent. These deep dive profiles were consistent with transient venous blood O2 depletion followed by partial restoration of venous O2 through pulmonary gas exchange and peripheral blood flow during ascent. These differences in venous O2 profiles between shallow and deep dives of sea lions reflect distinct strategies of O2 store management and suggest that underlying cardiovascular responses will also differ.