Miracle-dz/UniFAR-FTUs huggingface dataset:
Pengaruh Kualitas Kehidupan Kerja terhadap Kinerja Karyawan dengan Kepuasan Kerja sebagai Variabel Intervening

Decreased levels of employee performance of sales in the last year, among 1.1 % on a special performance and employee absenteeism rate target of 1% is not achievable indicate satisfaction and quality of life of employees can affect employee performance. The problem in this research is there any influence of the quality of work life , job satisfaction on employee performance. The population in this study were all employees of Honda Semarang Center Setiabudi 521 people with a sample of 84 people using the formula Slovin. Methods of data collection using questionnaires, methods of analysis, test instrument (validity and reliability test), descriptive analysis of the percentage, the classic assumption test, multiple regression analysis and path analysis. The results showed that the variable quality of worklife positive effect on job satisfaction; the variable quality of working life has positive influence on employee performance; variable job satisfaction has positive influence on employee performance; and the variable quality of working life through the indirect effect of job satisfaction on employee performance. Suggestions for the company in improving the performance of employees in order to pay attention to aspects of quality of work life and job satisfaction of employees proved influential on employee performance.
A Binding Site for the Kringle II Domain of Prothrombin in the Apple 1 Domain of Factor XI*

Previously we defined binding sites for high molecular weight kininogen (HK) and thrombin in the Apple 1 (A1) domain of factor XI (FXI). Since prothrombin (and Ca2+) can bind FXI and can substitute for HK (and Zn2+) as a cofactor for FXI binding to platelets, we have attempted to identify a prothrombin-binding site in FXI. The recombinant A1 domain (rA1, Glu1–Ser90) inhibited the saturable, specific and reversible binding of prothrombin to FXI, whereas neither the rA2 domain (Ser90–Ala181), rA3 domain (Ala181–Val271), nor rA4 domain (Phe272–Glu361) inhibited prothrombin binding to FXI. Kinetic binding studies using surface plasmon resonance showed binding of FXI (K d ∼71 nm) and the rA1 domain (K d ∼239 nm) but not rA2, rA3, or rA4 to immobilized prothrombin. Reciprocal binding studies revealed that synthetic peptides (encompassing residues Ala45–Ser86) containing both HK- and thrombin-binding sites, inhibit 125I-rA1 (Glu1–Ser90) binding to prothrombin,125I-prothrombin binding to FXI, and125I-prothrombin fragment 2 (Ser156–Arg271) binding to FXI. However, homologous prekallikrein-derived peptides (encompassing Pro45–Gly86) did not inhibit FXI rA1 binding to prothrombin. The peptides Ala45–Arg54, Phe56–Val71, and Asp72–Ser86, derived from sequences of the A1 domain of FXI, acted synergistically to inhibit 125I-rA1 binding to prothrombin. Mutant rA1 peptides (V64A and I77A), which did not inhibit FXI binding to HK, retained full capacity to inhibit rA1 domain binding to prothrombin, and mutant rA1 peptides Ala45–Ala54 (D51A) and Val59–Arg70 (E66A), which did not inhibit FXI binding to thrombin, retained full capacity to inhibit rA1 domain binding to prothrombin. Thus, these experiments demonstrate that a prothrombin binding site exists in the A1 domain of FXI spanning residues Ala45–Ser86 that is contiguous with but separate and distinct from the HK- and thrombin-binding sites and that this interaction occurs through the kringle II domain of prothrombin.
Transiently evoked otoacoustic emissions as a prognostic indicator in idiopathic sudden hearing loss

Idiopathic sudden sensorineural hearing loss (ISHL) remains a controversial topic. So far, there are no proven objective auditory factors to establish prognosis. Otoacoustic emissions reflect the functional integrity of the outer hair cells. The aim of this study was to assess the presence of transiently evoked otoacoustic emissions (TEOAEs) in the early stages of ISHL cases as a prognostic indicator. Thirty patients hospitalized for ISHL were included in the study. All patients underwent pure-tone audiometry (PTA) and TEOAE recordings on the admission day and at least three measures on the subsequent eight days. The audiometric threshold improvement at each frequency was correlated with the TEOAE parameters on each measure. Finally, the presence of TEOAEs on early examination was correlated with PTA threshold improvement. Twenty-three out of 30 patients experienced hearing recovery. Fourteen of the recovered patients had recordable TEOAEs or acceptable TEOAE peak amplitudes in some frequency bands on the first two measures, despite having audiometric thresholds greater than 40 dB HL. It thus seems that TEOAEs might serve as a clinical tool for prediction of recovery in ISHL cases.
Localized interleukin-10 gene transfer induces apoptosis of alloreactive T cells via FAS/FASL pathway, improves function, and prolongs survival of cardiac allograft

We hypothesized that localized IL-10 gene transfer can induce alloreactive T cell apoptosis and tested this hypothesis with liposome-mediated ex vivo intracoronary IL-10 gene transfer using a functional heterotopic allograft heart transplant model in rabbits. Localized IL-10 overexpression prolonged cardiac allograft survival over three folds. In parallel with the time-course of IL-10 overexpression, the percentage of apoptotic CD3+ cells among total CD3+ cells was significantly increased in the gene therapy group (36.5±3.9%) compared with that in the control group (6.2±2.6%, P <0.01) on postoperative day (POD) 3–6, and it was further increased (45.8±5.7%) on POD7–10. Apoptotic CD4+ and CD8+ cells were also significantly increased in the gene group (P <0.01). In contrast, the percentage of apoptotic myocytes significantly decreased from 10.1±0.8% in the control group to 3.5±0.4% in the gene group on POD7–10 (P <0.01). This reduction was inversely correlated with the increase in the percentages of apoptotic CD4+ and CD8+ cells (P <0.01). The percentage of caspase-3 positive myocytes was significantly reduced, although percentages of caspase-3 positive CD4+ and CD8+ cells were markedly increased in the gene group (P <0.01). Moreover, about 60–80% of apoptotic T lymphocytes expressed Fas in the gene group compared with less than 10% in the control group (P <0.01). These results suggest that localized IL-10 gene transfer induces alloreactive T cell apoptosis via the Fas/FasL pathway that may contribute to the alleviated acute rejection, improved cardiac function, and prolonged survival in the IL-10 gene-treated cardiac allografts.
Dexamethasone Inhibits Transforming Growth Factor-β Receptor (TβR) Messenger RNA Expression in Hamster Preantral Follicles: Possible Association with NF-YA1

Abstract To evaluate the site(s) and mechanism(s) of glucocorticoid-inhibition of transforming growth factor (TGF) β receptor (TβR) mRNA expression in ovarian cells, steady-state levels of TβR mRNA in hamster preantral follicles exposed to FSH or estradiol with or without dexamethasone were determined by reverse transcription polymerase chain reaction and Southern hybridization. The effect of dexamethasone on follicular DNA and steroid synthesis and the expression of NF-Y and Sp3 were also investigated. Dexamethasone differentially inhibited FSH- or estradiol-induced expression of TβR mRNA in preantral follicles at all stages. Dexamethasone also strongly inhibited FSH-induced but not TGFβ2-induced follicular DNA synthesis, and the inhibition was completely reversed by TGFβ2. However, TGFβ2 markedly attenuated FSH + dexamethasone-stimulated progesterone and FSH-induced follicular estradiol synthesis. Both FSH and estradiol upregulated NF-YA expression, but the effect was significantly attenuated by dexamethasone. Our results suggest that suppression of NF-YA levels is one of the mechanisms whereby dexamethasone reduces hormone-induced TβRI and TβRII mRNA levels in hamster preantral follicles. Dexamethasone potentiates the effect of FSH on granulosa cell steroidogenesis, whereas TGFβ counteracts the effect. These data indicate that glucocorticoid and TGFβ may form an important regulatory loop to modulate FSH regulation of preantral follicular growth and differentiation.
Learning Process Based On Character Education In Natural School In Semarang City

This study aims to describe the process of learning based on character education in natural schools. This research method is designed with qualitative research. Research subjects are early childhood education teacher in Ar-Ridlo Nature School Semarang City. Data collection by in-depth interview method, observation and documentation. Validity of data with honesty reliability, observational persistence, triangulation of sources and methods, comprehension. Analysis of interactive model data. The results showed that the nature school in Semarang City placed teachers as learning managers with duties ranging from arranging lesson plans, organizing school resources, implementing up to evaluating learning as a form of supervision. Teachers act as motivators, facilitators, mentors, modeling and students as active learning subjects. The character education system in the natural school through integrated learning in the thematic form or the net web of themes (spider web), creating a green learning environment as a science research laboratory, through gardening activities, raising, applying character-based learning as harmonization with the environment Social culture, through habituation and exemplary, inquiry based learning as a scientiest or scientist through the approach of "scientific and multiple intelligence based learning", children are given free space creative and expression in accordance with the field of intelligence of each child. Assessment of learning includes cognitive, affective and psychomotor aspects through test and non-test techniques that teachers do by involving parents.
Fever of unknown origin: 98 cases from Saudi Arabia

Background and Objectives : Fever of unknown origin (FUO) is mainly secondary to infectious, neoplastic or inflammatory diseases. To increase the body of knowledge on this diagnosis in the region, we collected information on all patients admitted to our institution with FUO in a 13-year period. Methods : We conducted a retrospective chart review of all immunocompetent males and females aged 13 years and older admitted between January 1995 and June 2008 who fulfilled the criteria for FUO. Data collection included demographics, laboratory investigations, imaging studies, procedures and discharge diagnoses. For true FUO, we recorded the duration of follow-up and the outcome. Results : The 98 patients who met the criteria included 44 males and 54 females with a mean (SD) age of 41.3 (18.5) years and range of 14 to 85 years. The most frequent diagnostic etiology was infectious in 32 (32.7%). Seventeen (17.3%) patients were undiagnosed or had true FUO. Of 9 patients followed up, 8 recovered and 1 expired. The mean duration of follow-up was 20.6 months (range, 0-168 months). Conclusion : Infectious diseases, especially TB, continue to be the leading etiology of FUO in our area. Our data did not identify any predictor of certain FUO diagnoses except for older age and neoplastic etiology. True FUO patients generally did well. Reporting local experience is important in guiding clinicians about the epidemiologic patterns of FUO in their regions.
Ionizing Radiation Potentiates High-Fat Diet–Induced Insulin Resistance and Reprograms Skeletal Muscle and Adipose Progenitor Cells

Exposure to ionizing radiation increases the risk of chronic metabolic disorders such as insulin resistance and type 2 diabetes later in life. We hypothesized that irradiation reprograms the epigenome of metabolic progenitor cells, which could account for impaired metabolism after cancer treatment. C57Bl/6 mice were treated with a single dose of irradiation and subjected to high-fat diet (HFD). RNA sequencing and reduced representation bisulfite sequencing were used to create transcriptomic and epigenomic profiles of preadipocytes and skeletal muscle satellite cells collected from irradiated mice. Mice subjected to total body irradiation showed alterations in glucose metabolism and, when challenged with HFD, marked hyperinsulinemia. Insulin signaling was chronically disrupted in skeletal muscle and adipose progenitor cells collected from irradiated mice and differentiated in culture. Epigenomic profiling of skeletal muscle and adipose progenitor cells from irradiated animals revealed substantial DNA methylation changes, notably for genes regulating the cell cycle, glucose/lipid metabolism, and expression of epigenetic modifiers. Our results show that total body irradiation alters intracellular signaling and epigenetic pathways regulating cell proliferation and differentiation of skeletal muscle and adipose progenitor cells and provide a possible mechanism by which irradiation used in cancer treatment increases the risk for metabolic disease later in life.
Multimodal transit network design in a hub-and-spoke network framework

ABSTRACT This study focuses on the reconfiguration of bus services in an urban area with a newly constructed rail system. A hub-and-spoke network framework is introduced for the multimodal transit system. The rail services are taken as the backbone, and the bus services (main bus lines and feeder bus lines) are reconfigured to better integrate with rail services forming the core of a Mobility as a Service (MaaS). A cluster-based approach is used for selecting hubs from rail stations. Bus stops are taken as non-hub nodes. Main bus lines are designed based on a heuristic line generation approach and feeder bus lines are developed by solving a travelling salesman problem. A bi-level programming model is proposed to determine frequencies of each mode and addressed by the artificial bee colony algorithm. The effectiveness of the proposed methods is illustrated by numerical examples and applied to the Mandl's benchmark compared with existing studies.
Using franking machine messages to promote health

OVER a 12-month period, the Oxfordshire Health Unit experimented with the addition of four different health promotion messages to all franked mail leav ing the unit. Each message was evaluated by enclos ing a return questionnaire in a sample of the mail. More than half the respondents read the messages (before seeing the questionnaire). Of all those who read the messages, 40 per cent said they would take some action as a result. Four out of five people thought the idea a good one. Using the evaluation results — including observed differences between the messages, some guidelines were created on the use of this relatively cost-effective form of health promotion.
Two Consecutive Outbreaks of Stenotrophomonas Maltophilia (Xanthomonas Maltophilia) in an Intensive-care Unit Defined by Restriction Fragment-Length Polymorphism Typing

Abstract Objective: To investigate and control consecutive outbreaks of Stenotrophomonas maltophilia infections in intensive-care–unit (ICU) patients. Design: Epidemiological investigation; restriction fragment-length polymorphism typing by pulsed-field gel electrophoresis (PFGE) of genomic DNA of outbreak strains; institution of infection control measures to limit spread. Setting: The medical-surgical ICU in an 800-bed tertiary-care center in Calgary, Alberta, Canada. Results: S maltophilia was recovered from 14 ICU patients (12 infected, 2 colonized) between February 1993 and February 1994. Ten of the 14 patient isolates and 1 environmental isolate were available for PFGE typing. Patient isolates from 6 of the first 10 patients were identical. Isolates from the next 3 of 4 patients and an isolate recovered from a ventilator being used by a patient not infected with S maltophilia also were identical, but different from the first 6. The ventilator isolate was temporally associated with the latter 4 patients. Conclusion: Molecular typing allowed us to determine that there were two separate consecutive S maltophilia outbreaks rather than a single protracted outbreak. Recovery of S maltophilia from patient ventilators and an in-line suction catheter suggests that the organism may have been spread by cross-contamination from contaminated equipment or from an environmental source.
Deletion of phenylalanine 508 causes attenuated phosphorylation‐dependent activation of CFTR chloride channels

1 In cell‐attached patches stimulated with cAMP agonists, the single‐channel open probability (Po) of the phenylalanine 508‐deleted cystic fibrosis transmembrane conductance regulator (ΔF508‐CFTR) channel, the most common disease‐associated mutation in cystic fibrosis, was abnormally low (a functional defect). To investigate the mechanism for the poor response of ΔF508‐CFTR to cAMP stimulation, we examined, in excised inside‐out patches, protein kinase A (PKA)‐dependent phosphorylation activation and ATP‐dependent gating of wild‐type (WT) and ΔF508‐CFTR channels expressed in NIH3T3 mouse fibroblasts. 2 For WT‐CFTR, the activation time course of CFTR channel current upon addition of PKA and ATP followed a sigmoidal function with time constants that decreased as [PKA] was increased. The curvilinear relationship between [PKA] and the apparent activation rate suggests an incremental phosphorylation‐dependent activation of CFTR at multiple phosphorylation sites. 3 The time course of PKA‐dependent activation of ΔF508‐CFTR channel current also followed a sigmoidal function, but the rate of activation was at least 7‐fold slower than that with WT channels. This result suggests that deletion of phenylalanine 508 causes attenuated PKA‐dependent phosphorylation of the CFTR chloride channel. 4 Once ΔF508‐CFTR channels were maximally activated with PKA, the mutant channel and WT channel had indistinguishable steady‐state Po values, ATP dose‐response relationships and single‐channel kinetics, indicating that ΔF508‐CFTR is not defective in ATP‐dependent gating. 5 By measuring whole‐cell current density, we compared the number of functional channels in WT‐ and ΔF508‐CFTR cell membrane. Our data showed that the estimated channel density for ΔF508‐CFTR was ∼10‐fold lower than that for WT‐CFTR, but the cAMP‐dependent whole‐cell current density differed by ∼200‐fold. We thus conclude that the functional defect (a decrease in Po) of ΔF508‐CFTR is as important as the trafficking defect (a decrease in the number of functional channels in the plasma membrane) in cystic fibrosis pathogenesis.
Meta‐Analysis of Factors Which Influence Delirium Following Cardiac Surgery

Abstract Background: The aim of this study is to determine the risk factors of delirium after cardiac surgery. Methods: A systematic literature search of MEDLINE, EMBASE, the Cochrane Library, and Science Citation Index limited to 2008 to 2011 and review of studies was conducted. Eligible studies were of randomized controlled trials or cohort studies, using delirium assessment tool, reporting at least one risk factor associated with delirium, and available to full text. Results: The search identified 106 potentially relevant publications; only 25 met selection criteria. Our systematic review revealed 33 risk factors: 17 predisposing and 16 precipitating factors for delirium after elective cardiac surgery. The most established predisposing risk factors were age, depression, and history of stroke, cognitive impairment, diabetes mellitus, and atrial fibrillation. The most established precipitating risk factors were duration of surgery, prolonged intubation, surgery type, red blood cell transfusion, elevation of inflammatory markers and plasma cortisol level, and postoperative complications. Moreover, sedation with dexmedetomidine may significantly predict the absence of postoperative delirium. Conclusions: Postoperative delirium is related to several risk factors following cardiac surgery. Sedation with dexmedetomidine and fast‐track weaning protocols may decrease the incidence of delirium in cardiac surgical patients. (J Card Surg 2012;27:481‐492)
Spatiotemporal separation of PER and CRY posttranslational regulation in the mammalian circadian clock

Significance Maintaining robust circadian rhythms has been linked to longevity and metabolic health. Because these rhythms are disturbed by factors such as jet lag, shift work, and high-fat diets, there is interest in developing pharmacological control strategies to modulate circadian function. The design of therapeutic strategies is currently limited by the lack of a clear mechanistic understanding of interactions between posttranslational regulators, as efficient control of clock behavior will likely require several simultaneous modulations. Here we show fundamentally different clock responses from the manipulation of two clock regulators previously thought to act via similar mechanisms. Using mathematical modeling, we provide a mechanistic interpretation for the relationship between these two regulators, lending insight into circadian regulation and potential pharmacological control. Posttranslational regulation of clock proteins is an essential part of mammalian circadian rhythms, conferring sensitivity to metabolic state and offering promising targets for pharmacological control. Two such regulators, casein kinase 1 (CKI) and F-box and leucine-rich repeat protein 3 (FBXL3), modulate the stability of closely linked core clock proteins period (PER) and cryptochrome (CRY), respectively. Inhibition of either CKI or FBXL3 leads to longer periods, and their effects are independent despite targeting proteins with similar roles in clock function. A mechanistic understanding of this independence, however, has remained elusive. Our analysis of cellular circadian clock gene reporters further differentiated between the actions of CKI and FBXL3 by revealing opposite amplitude responses from each manipulation. To understand the functional relationship between the CKI-PER and FBXL3-CRY pathways, we generated robust mechanistic predictions by applying a bootstrap uncertainty analysis to multiple mathematical circadian models. Our results indicate that CKI primarily regulates the accumulating phase of the PER-CRY repressive complex by controlling the nuclear import rate, whereas FBXL3 separately regulates the duration of transcriptional repression in the nucleus. Dynamic simulations confirmed that this spatiotemporal separation is able to reproduce the independence of the two regulators in period regulation, as well as their opposite amplitude effect. As a result, this study provides further insight into the molecular clock machinery responsible for maintaining robust circadian rhythms.
Multi-case study of bullying gone digital: the investigation of educators’ perceptions and experiences of cyberbullying in Manitoban schools

This thesis is a qualitative study that examines permanent middle years guidance counselor’s perceptions regarding their experiences in dealing with cyberbullying. This study is based on a cognitive social framework that is related to adolescent development. It draws upon the works of Jean Piaget, Erik Erikson, and Urie Bronfenbrenner. Their work is described below beginning with Piaget’s cognitive development theory, Erikson’s psychosocial development, and Bronfenbrenner’s bioecological model of human development. The researcher investigates educators’ position and obligations in regards to cyberbullying and explores the various ways in which educators deal with cyberbullying issues. The participants of this study are four certified, middle year guidance counselors who have had experiences with cyberbullying. Findings suggests the ways in which educators handle cyberbullying and concludes with recommendations for educators in regard to classroom instruction, roles and responsibilities, and improving awareness in dealing with incidences of cyberbullying that may benefit both educators and students.