Miracle-dz/UniFAR-FTUs huggingface dataset:
A Framework to Mitigate Debugging Difficulty on Agent Migration

A mobile agent is an autonomous software module that can work on different computers and migrate among these computers. The characteristics of a mobile agent, migration and interaction, are helpful to implement distributed systems. In the real world, however, a mobile agent is not widely used because its migration makes debugging distributed systems difficult. Therefore, in this paper, we discuss problems in debugging a mobile agent system and propose a framework that includes a search, a single-step execution, and a reproduction function to help programmers debug a mobile agent system. Results from our experiments on debugging test applications show that our framework is helpful to support programmers and help them to debug. This reduces the number of keystrokes by 41% and number of clicks by 24%.
The two domain hypothesis of limb prepattern and its relevance to congenital limb anomalies

Functional annotation of mutations that cause human limb anomalies is enabled by basic developmental studies. In this study, we focus on the prepatterning stage of limb development and discuss a recent model that proposes anterior and posterior domains of the early limb bud generate two halves of the future skeleton. By comparing phenotypes in humans with those in model organisms, we evaluate whether this prepatterning concept helps to annotate human disease alleles. WIREs Dev Biol 2017, 6:e270. doi: 10.1002/wdev.270
Latency in listeriosis: a review and assessment.

much more appropriately made relating to human disease than disease of animals, but it is not entirely inappropriate with reference to animals. Geographic and cultural implications play a major role in interpreting the "importance" of infectious and non-infectious disease. Regardless of the relevancy of this concept, there is a reawakening to the importance and basic implications of the infectious diseases. For example, with all our knowledge about the pathogenesis and transmission cycles of salmonellosis, problems with the disease seem to compound as technology and society advance. The new problems in salmonellosis, or perhaps staphylococcosis, are the result of man-induced changes in the environment. We cannot make such statements
Altered endothelial function in asymptomatic male adolescents with type 1 diabetes.

OBJECTIVE While adult men and women with diabetes experience similar rates of cardiovascular disease, early microvascular complications show significant gender differences during adolescence. The goal of this study was to determine whether a gender contrast in a preclinical stage of atherosclerosis, or endothelial dysfunction, is present in pediatric diabetic patients. METHODS Reactive hyperemia-peripheral arterial tonometry (RH-PAT), a noninvasive method to assess endothelial dysfunction, was used. Measurements were performed at rest and after hyperemia in 20 diabetic subjects and 20 age- and gender-matched nondiabetics, aged 12-16 years. Confounding risk factors for endothelial dysfunction, including smoking, obesity, and hypertension, were excluded. RESULTS RH-PAT was lower for male diabetic subjects vs. controls (n = 12, 1.60 +/- 0.32 vs. 1.92 +/- 0.28, P < .001). RH-PAT was similar in female diabetic patients vs. controls. Male and females with type 1 diabetes subjects had equivalent metabolic control (HbA1C 7.48 +/- 1.0 vs. 7.51 +/- 0.9) and lipid profiles. No difference was observed in age, HbA1C, and diabetes duration, between male and female diabetic subjects. However, diabetic female patients had a greater body mass index (24.2 +/- 2.5 vs. 20.6 +/- 2.0, P = .003) and were more mature in pubertal status as compared with diabetic male patients. CONCLUSION Endothelial dysfunction was present in adolescent male diabetic subjects as measured using RH-PAT. Considering that endothelial dysfunction is reversible, early detection of this process may have therapeutic and prognostic implications in this young age group.
The Role of Media Literacy in Shaping Adolescents' Understanding of and Responses to Sexual Portrayals in Mass Media

This study was a theory-based, pretest–posttest quasi-experiment conducted in the field (N = 922) to determine whether and how a media literacy curriculum addressing sexual portrayals in the media would influence adolescents' decision-making processes regarding sex. Results of the evaluation, based on the Message Interpretation Process Model, indicated that participants who received media literacy training better understood that media influence teens' decision making about sex and were more likely to report that sexual depictions in the media are inaccurate and glamorized. In addition, participants who received media literacy lessons were more likely than were control group participants to believe that other teens practice abstinence and reported a greater ability to resist peer pressure. An interaction effect existed between gender and condition on attitudes toward abstinence, suggesting that the lessons helped girls and boys in somewhat different ways. Overall, the results indicated that media literacy strengthened key aspects of participants' logic-oriented decision-making process.
PD-L1 promoter methylation mediates the resistance response to anti-PD-1 therapy in NSCLC patients with EGFR-TKI resistance

The anti-PD-1/PD-L1 therapy has been demonstrated effective and safe for advanced NSCLC patients, especially for EGFR-TKIs (epidermal growth factor receptor - tyrosine kinase inhibitors) resistant NSCLC (non-small cell lung cancer) patients with EGFR mutations. However, whether the anti-PD-1/PD-L1 therapy also promotes drug resistance as EGFR-TKIs treatment remains unclear. Thus, we conducted the present study to investigate the effects of anti-PD-1 therapy on the expression of PD-L1, which is one important factor mediates the efficacy of anti-PD-1 therapy. To address the expression dynamics of PD-L1 after anti-PD-1 therapy, we first divided the patients into three groups according to the EGFR mutation status (wild type, L858R and T790M mutation). The PD-L1 was highly expressed in the NSCLC tissues than the corresponding normal tissues. After cancer recurrence, the PD-L1 was further up-regulated in patients treated with chemotherapy or EGFR-TKI therapy but decreased in the patients with anti-PD1 therapy. Promoter methylation analysis showed that the secondary NSCLC after cancer recurrence with anti-PD1 therapy had much higher promoter methylation level than the primary cancer tissue or normal tissues. In the mice model, the anti-PD-1 therapy could induce PD-L1 promoter methylation irrespective of EGFR mutation status. Combining DNA hypomethylating agent azacytidine with anti-PD-1 therapy could significantly further reduce the tumor size when comparing with the anti-PD-1 therapy alone. Our results demonstrated that the anti-PD-1 therapy might promote drug resistance through PD-L1 promoter methylation and down-regulation. And combining DNA hypomethylating agent azacytidine with anti-PD-1 therapy might be a promising approach to overcome the resistance.
Clinical Outcomes of Patients With Gastrointestinal Malignancies Participating in Phase I Clinical Trials

Objectives: Early-phase clinical trials play a pivotal role in drug development. However, limited data are available on outcomes of gastrointestinal (GI) cancer patients enrolled in phase I clinical trials. Here, we evaluated the characteristics associated with survival in GI cancer patients participating in phase I clinical trials and attempted to validate previously established prognostic models. Materials and Methods: All consecutive patients with advanced GI tumors who participated in phase I clinical trials at our institution from January 2007 to December 2013 and received at least 1 dose of the study drug were included. Cox regression models were used to estimate multivariable-adjusted hazard ratio (HR) and 95% confidence interval. Results: In 243 study patients (median age, 62 y [range, 26 to 82 y]; 55% male), treatment included chemotherapy only (14%), targeted therapy (41%), chemotherapy+targeted therapy (42%), and others (2%) for the following disease types: pancreatic (42%), colorectal (34%), gastroesophageal (10%), hepatobiliary (13%), and others (2%). Response rate was 4%, with 38% achieving stable disease and 42% having progressive disease. Median survival was 5.8 months (range, 0.2 to 52.4 mo). Our multivariable Cox regression analyses included the following as predictors of survival: Eastern Cooperative Oncology Group performance score ≥1 (HR=1.76), prior systemic therapies ≥2 (HR=1.63), lactate dehydrogenase >618 IU/L (HR=1.85), sodium >135 mmol/L (HR=0.46), and white blood count >6×109/L (HR=1.5). Our data set was consistent with previous prognostic scores. Conclusions: This is the largest study to assess clinical outcomes in this patient population. Phase I trials provide clinical benefit to patients with advanced GI malignancies and should be recommended as a treatment option in appropriate patients.
Killer Cell Lectin-Like Receptor G1 Deficiency Significantly Enhances Survival after Mycobacterium tuberculosis Infection

ABSTRACT The expression of T cell differentiation markers is known to increase during Mycobacterium tuberculosis infection, and yet the biological role of such markers remains unclear. We examined the requirement of the T cell differentiation marker killer cell lectin-like receptor G1 (KLRG1) during M. tuberculosis infection using mice deficient in KLRG1. KLRG1−/− mice had a significant survival extension after M. tuberculosis infection compared to wild-type controls, and maintained a significantly lower level of pulmonary M. tuberculosis throughout chronic infection. Improved control of M. tuberculosis infection was associated with an increased number of activated pulmonary CD4+ T cells capable of secreting gamma interferon (IFN-γ). Our report is the first to show an in vivo impact of KLRG1 on disease control.
Rac2-Deficient Murine Macrophages Have Selective Defects in Superoxide Production and Phagocytosis of Opsonized Particles1

The Rho family GTPase Rac is a crucial participant in numerous cellular functions and acts as a molecular switch for signal transduction. Mice deficient in hemopoietic-specific Rac2 exhibited agonist-specific defects in neutrophil functions including chemoattractant-stimulated filamentous actin polymerization and chemotaxis, and superoxide production elicited by phorbol ester, fMLP, or IgG-coated particles, despite expression of the highly homologous Rac1 isoform. In this study, functional responses of Rac2-null murine macrophages were characterized to examine whether Rac2 also has nonredundant functions in this phagocytic lineage. In contrast to murine neutrophils, in which Rac1 and Rac2 are present in similar amounts, Rac1 was ∼4-fold more abundant than Rac2 in both bone marrow-derived and peritoneal exudate macrophages, and macrophage Rac1 levels were unchanged by the absence of Rac2. Accumulation of exudate macrophages during peritoneal inflammation was reduced in rac2−/− mice. FcγR-mediated phagocytosis of IgG-coated SRBC was also significantly decreased in Rac2-null macrophages, as was NADPH oxidase activity in response to phorbol ester or FcγR stimulation. However, phagocytosis and oxidant production stimulated by serum-opsonized zymosan was normal in rac2−/− macrophages. Macrophage morphology was also similar in wild-type and Rac2-null cells, as was actin polymerization induced by FcγR-mediated phagocytosis or M-CSF. Hence, Rac2-null macrophages have selective defects paralleling many of the observed functional defects in Rac2-null neutrophils. These results provide genetic evidence that although Rac2 is a relatively minor isoform in murine macrophages, it plays a nonoverlapping role with Rac1 to regulate host defense functions in this phagocyte lineage.
Forecasting-Aided State Estimation—Part I: Panorama

The art of estimating future values of a random process, based upon previously observed or estimated values, is usually known as a priori estimation, prediction, or forecasting. Power system state estimation process can be enhanced if state/measurement forecasts are incorporated into it. Important research efforts have been made in this direction bringing a fresh perspective to the state estimation problem. This paper (Part I) presents a comprehensive survey of forecasting-aided state estimators. It gathers up-covering a period of three decades-research results on the main benefits achieved by state estimators with forecasting capability regarding: data redundancy, innovation analysis, observability, filtering, bad data, and network configuration and parameter error processing. Aspects of modeling, forecasting techniques, and computational effort are also addressed. The second of this two-paper series presents the results of the implementation of a forecasting-aided state estimator in the energy management system of the LIGHT Services of Electricity, a company which provides electric energy to Rio de Janeiro, Brazil.
Improving the outcome of pregnancy in essential thrombocythaemia: The role of aspirin

Duley L, Meher S, Abalos E. 2006. Management of pre-eclampsia. British Medical Journal 332:463–468. Fynn J, Venyo AK. 2004. Renal cell carcinoma presenting as hypertension in pregnancy. Journal of Obstetrics and Gynaecology 24:821–822. Guven S, Guvendag Guven ES, Islamoglu E et al. 2004. Successful management of chromophobe type renal cell carcinoma in pregnancy. Australian and New Zealand Journal of Obstetrics and Gynaecology 44:362–363. Monga M, Benson GS, Parisi VM. 1995. Renal cell carcinoma presenting as hemolytic anemia in pregnancy. American Journal of Perinatology 12:84–86. Umeoka S, Koyama T, Togashi K et al. 2004. Vascular dilatation in the pelvis: identification with CT and MR imaging. Radiographics 24:193–208. Usta IM, Chammas M, Khalil AM. 1998. Renal cell carcinoma with hypercalcemia complicating a pregnancy: case report and review of the literature. European Journal of Gynaecological Oncology 19:584–587. Walker JL, Knight EL. 1986. Renal cell carcinoma in pregnancy. Cancer 58:2343–2347.
Effects of membrane potential and tension on prestin, the outer hair cell lateral membrane motor protein

1 Under whole‐cell voltage clamp, the effects of initial voltage conditions and membrane tension on gating charge and voltage‐dependent capacitance were studied in human embryonic kidney cells (TSA201 cell line) transiently transfected with the gene encoding the gerbil protein prestin. Conformational changes in this membrane‐bound protein probably provide the molecular basis of the outer hair cell (OHC) voltage‐driven mechanical activity, which spans the audio spectrum. 2 Boltzmann characteristics of the charge movement in transfected cells were similar to those reported for OHCs (amax= 0.99 ± 0.16 pC, z = 0.88 ± 0.02; n= 5, means ±s.e.m.). Unlike that of the adult OHC, the voltage at peak capacitance (apkcm) was very negative (‐74.7 ± 3.8 mV). Linear capacitance in transfected cells was 43.7 ± 13.8 pF and membrane resistance was 458 ± 123 MΩ. 3 Voltage steps from the holding potential preceding the measurement of capacitance‐voltage functions caused a time‐ and voltage‐dependent shift in Vpkcm. For a prepulse to ‐150 mV, from a holding potential of 0 mV, Vpkcm shifted 6.4 mV, and was fitted by a single exponential time constant of 45 ms. A higher resolution analysis of this time course was made by measuring the change in capacitance during a fixed voltage step and indicated a double exponential shift (τ0= 51.6 ms, τ1= 8.5 s) similar to that of the native gerbil OHC. 4 Membrane tension, delivered by increasing pipette pressure, caused a positive shift in Vpkcm. A maximal shift of 7.5 mV was obtained with 2 kPa of pressure. The effect was reversible. 5 Our results show that the sensitivity of prestin to initial voltage and membrane tension, though present, is less than that observed in adult OHCs. It remains possible that some other interacting molecular species within the lateral plasma membrane of the native OHC amplifies the effect of tension and prior voltage on prestin's activity.
Basic functional analysis of six unknown open reading frames from Saccharomyces cerevisiae: four from chromosome VII and two from chromosome XV

Six open reading frames (ORFs) of unknown function from Saccharomyces cerevisiae from the left arms of chromosomes VII and XV were disrupted by the short‐flanking homology method in the diploid strains FY1679 and CENPK2. In each case, the entire ORF, with the exception of the first nucleotide of the start codon, was eliminated and replaced by the kanMX4 cassette. Correct integration of the disrupting marker was checked by colony PCR of the geneticin (G418)‐resistant transformants. Sporulation followed by tetrad dissection of the diploids revealed that none of the ORFs encoded a product essential for the viability of either yeast strain. The neutral effect of these disruptions extended to mating and sporulation, since it was possible to create homozygous diploid disruptants that were capable of sporulation. Basic phenotypic analysis was carried out on all strains by growing them on three different media at three different temperatures and revealed no significant differences between disruptants and the parental strains. A cognate clone and a kanMX4 disruption cassette were created for five of the six ORFs by gap repair with specific long‐flanking homology cassettes. For experimental reasons, the cognate clone and disruption cassette corresponding to the sixth ORF (YGL161w) had to be created by PCR. Copyright © 2002 John Wiley & Sons, Ltd.
RESEARCH: Validation of the Massachusetts General Hospital Antidepressant Treatment History Questionnaire (ATRQ)

The low rate of response to antidepressants in treatment resistant depression (TRD) justifies studies of next‐step therapies following a treatment failure. In TRD clinical trials, it is important to verify the accurate diagnosis of treatment resistance for all enrolled subjects using a reliable and valid instrument. Self‐rated scales can reduce the impact of investigator bias and reduce the time burden for clinical researchers. The Massachusetts General Hospital (MGH) Antidepressant Treatment Response Questionnaire (ATRQ) is a self‐rated scale used to determine treatment resistance in major depressive disorder (MDD). The ADAPT‐A study is a multi‐center double‐blind, placebo‐controlled study of low‐dose aripiprazole adjunctive to ADT among outpatients with TRD. At the screening assessment, potential subjects completed the MGH ATRQ. The ADAPT‐A medical monitors subsequently performed remote patient interviews and obtained detailed medication histories. The data obtained from the MGH ATRQ and by the medical monitors were compared for congruency. Of the 186 patients enrolled by the local sites, no subjects deemed treatment resistant by the MGH ATRQ were found to be nonresistant by the medical monitors. In 76.3% (n = 142) of the subjects, the number of failed adequate antidepressant trials reported by the MGH ATRQ was concordant with the data collected by medical monitors. In 16.1% (n = 30) of all cases, the medical monitors found a greater number of failed trials; in 7.5% (n = 14) of cases, the medical monitors found fewer failed medication trials. The discrepancy was by more than one medication trial in only 4.0% (n = 7) of cases. We found the MGH ATRQ to be relatively concordant in its assessment of treatment resistance in depression compared with independent clinical researchers. Although the MGH ATRQ tended to underreport the number of unsuccessful treatment trials relative to the clinical interviews, its accuracy in cases it detected was confirmed by raters.
Relevance of sleep neurobiology for cognitive neuroscience and anesthesiology

Although general anesthetics are used for approximately 21 million patients per year in the United States,1 the molecular and cellular mechanisms by which anesthetics produce loss of waking consciousness are poorly understood. The complexity of consciousness and relatively imprecise clinical signs that are used to evaluate the depth of anesthesia are significant limitations for the study of consciousness. Recent advances in sleep neurobiology continue to enhance the understanding of different physiological traits that define altered states of consciousness. The original hypothesis2 that neural networks that evolved to generate sleep are preferentially modulated by anesthetic drugs has been supported by multiple lines of evidence.3–9 These data demonstrate that sleep neurobiology can contribute to understanding the mechanisms by which anesthetics cause loss of consciousness. The goal of this chapter is to selectively review the neurobiology of sleep and wakefulness in relation to anesthesia-induced loss of consciousness.
Effective Treatment of Chronic Plantar Fasciitis with Dorsiflexion Night Splints: A Crossover Prospective Randomized Outcome Study

Chronic plantar fasciitis frustrates patients and treating physicians. Our hypothesis was that use of a dorsiflexion night splint for 1 month would effectively treat patients with recalcitrant plantar fasciitis. A 6-month randomized crossover study included 37 patients with chronic plantar fasciitis. Patients were treated with dorsiflexion night splints for 1 month. Group A wore splints for the 1st month and group B for the 2nd month. No splints were used in either group for the final 4 months of the study. No other medications, stretching, or strengthening exercises were prescribed. Eighty-eight percent of patients who completed the study improved. Eighty percent of the involved feet improved subjectively. Results of the AOFAS Ankle-Hindfoot Rating System 17 and the Mayo Clinical Scoring System 7 demonstrated significant improvement for both groups during the period of splint wear. Improvements were maintained at study completion. Response to splinting did not correlate with foot type, degree of obesity, or the presence of heel spur on radiographs. We believe dorsiflexion splints provide relief from the symptoms of recalcitrant plantar fasciitis in the majority of patients.
Localization, anchoring and translational control of oskar, gurken, bicoid and nanos mRNA during Drosophila oogenesis

mRNA localization, and translation that is regulated spatially and temporally, are key mechanisms in the execution of polarized developmental programs. For over two decades, the Drosophila oocyte has served as a valuable model to study these mechanisms. Genetic and biochemical studies in flies have greatly contributed to the identification and understanding of factors that govern RNA localization and translational control. Embryonic axis formation is mediated through the subcellular localization and precise translational regulation of four key determinant mRNAs during oogenesis encoded by oskar, bicoid, gurken and nanos. In this review we aim to summarize recent insights into the mechanisms governing the asymmetric distribution and translation of these mRNAs.