Pengaruh Night And Shift Works (NSWs) Terhadap Kondisi Fisik, Psikologis, Dan Beban Kerja

Bekerja pada malam hari dapat menimbulkan suatu permasalahan yang berkaitan dengan kesehatan badan dan daya kerja, apabila kondisi ini berlangsung terus menerus maka dapat berakibat antara lain kelelahan fisik, peningkatan denyut jantung, menurunnya kemampuan mental. Penelitian ini dilakukan di Rumah Sakit RK Charitas Palembang. Sampel yang diambil dalam penelitian ini adalah 60 orang perawat wanita yang bekerja dengan sistem kerja bergilir pada Paviliun Lukas dan Yoseph Rumah Sakit RK Charitas Palembang. Pengumpulan data dilakukan dengan penyebaran kuesioner untuk mengetahui kondisi fisik dan psikologis yang dikeluhkan oleh perawat. Pengukuran denyut jantung dilakukan untuk mengetahui beban kerja yang dirasakan oleh perawat. Pengukuran denyut jantung dilakukan sebelum dan sesudah bekerja pada setiap shift kerja. Data pengukuran denyut jantung kemudian dianalisis dengan t-paired test . Hasil analisis data berdasarkan pengujian hipotesis diketahui bahwa t hitung > t tabel sehingga H0 ditolak, artinya ada pengaruh night and shift works terhadap beban kerja perawat. Data keluhan fisik dan psikologis diolah dengan menggunakan analysis of variance (anova). Data pengukuran kondisi fisik menunjukkan F hitung > F tabel (32.77 > 3.00) sehingga H0 ditolak, artinya ada pengaruh night and shift works terhadap gangguan fisik perawat. Data pengukuran kondisi psikologis menunjukkan F hitung > F tabel (16.87 > 3.00) sehingga H0 ditolak, artinya ada pengaruh night and shift works terhadap gangguan psikologis perawat. Rotasi kerja yang digunakan di Rumah Sakit RK Charitas saat ini yaitu continental rota (2 kali pagi, 2 kali siang, 3 kali malam). Rotasi kerja yang sebaiknya digunakan untuk mengurangi kondisi fisik, psikologis dan beban kerja perawat adalah metropolitan rota (2 kali pagi, 2 kali siang, 2 kali malam)

Sterilization of granulomas is common in both active and latent tuberculosis despite extensive within-host variability in bacterial killing

Over 30% of the world’s population is infected with Mycobacterium tuberculosis (Mtb), yet only ~5–10% will develop clinical disease1. Despite considerable effort, we understand little about what distinguishes individuals who progress to active tuberculosis (TB) from those who remain latent for decades. The variable course of disease is recapitulated in cynomolgus macaques infected with Mtb2. Active disease in macaques is defined by clinical, microbiologic and immunologic signs and occurs in ~45% of animals, while the remaining are clinically asymptomatic2,3. Here, we use barcoded Mtb isolates and quantitative measures of culturable and cumulative bacterial burden to show that most lesions are likely founded by a single bacterium and reach similar maximum burdens. Despite common origins, the fate of individual lesions varies substantially within the same host. Strikingly, in active disease, the host sterilizes some lesions even while others progress. Our data suggest that lesional heterogeneity arises, in part, through differential killing of bacteria after the onset of adaptive immunity. Thus, individual lesions follow diverse and overlapping trajectories, suggesting critical responses occur at a lesional level to ultimately determine the clinical outcome of infection. Defining the local factors that dictate outcome will be important in developing effective interventions to prevent active TB

X. couchianus and X. hellerii genome models provide genomic variation insight among Xiphophorus species

4 inter-chromosomal rearrangement events between X. hellerii and X. maculatus. (XLSX 40 kb

Surgical Intensive Care Unit Optimal Mobilisation Score (SOMS) trial: a protocol for an international, multicentre, randomised controlled trial focused on goal-directed early mobilisation of surgical ICU patients

Introduction: Immobilisation in the intensive care unit (ICU) leads to muscle weakness and is associated with increased costs and long-term functional disability. Previous studies showed early mobilisation of medical ICU patients improves clinical outcomes. The Surgical ICU Optimal Mobilisation Score (SOMS) trial aims to test whether a budget-neutral intervention to facilitate goal-directed early mobilisation in the surgical ICU improves participant mobilisation and associated clinical outcomes. Methods and analysis The SOMS trial is an international, multicentre, randomised clinical study being conducted in the USA and Europe. We are targeting 200 patients. The primary outcome is average daily SOMS level and key secondary outcomes are ICU length of stay until discharge readiness and ‘mini’ modified Functional Independence Measure (mmFIM) at hospital discharge. Additional secondary outcomes include quality of life assessed at 3 months after hospital discharge and global muscle strength at ICU discharge. Exploratory outcomes will include: ventilator-free days, ICU and hospital length of stay and 3-month mortality. We will explore genetic influences on the effectiveness of early mobilisation and centre-specific effects of early mobilisation on outcomes. Ethics and dissemination Following Institutional Review Board (IRB) approval in three institutions, we started study recruitment and plan to expand to additional centres in Germany and Italy. Safety monitoring will be the domain of the Data and Safety Monitoring Board (DSMB). The SOMS trial will also explore the feasibility of a transcontinental study on early mobilisation in the surgical ICU. Results: The results of this study, along with those of ancillary studies, will be made available in the form of manuscripts and presentations at national and international meetings. Registration This study has been registered at clinicaltrials.gov (NCT01363102)

Common Variants in 40 Genes Assessed for Diabetes Incidence and Response to Metformin and Lifestyle Intervention in the Diabetes Prevention Program

OBJECTIVE: Genome-wide association studies have begun to elucidate the genetic architecture of type 2 diabetes. We examined whether single nucleotide polymorphisms (SNPs) identified through targeted complementary approaches affect diabetes incidence in the at-risk population of the Diabetes Prevention Program (DPP) and whether they influence a response to preventive interventions. RESEARCH DESIGN AND METHODS: We selected SNPs identified by prior genome-wide association studies for type 2 diabetes and related traits, or capturing common variation in 40 candidate genes previously associated with type 2 diabetes, implicated in monogenic diabetes, encoding type 2 diabetes drug targets or drug-metabolizing/transporting enzymes, or involved in relevant physiological processes. We analyzed 1,590 SNPs for association with incident diabetes and their interaction with response to metformin or lifestyle interventions in 2,994 DPP participants. We controlled for multiple hypothesis testing by assessing false discovery rates. RESULTS: We replicated the association of variants in the metformin transporter gene $SLC47A1$ with metformin response and detected nominal interactions in the AMP kinase (AMPK) gene $STK11$, the AMPK subunit genes $PRKAA1$ and $PRKAA2$, and a missense SNP in $SLC22A1$, which encodes another metformin transporter. The most significant association with diabetes incidence occurred in the AMPK subunit gene $PRKAG2$ (hazard ratio 1.24, 95% CI 1.09–1.40, P = 7 × 10$^{−4}$). Overall, there were nominal associations with diabetes incidence at 85 SNPs and nominal interactions with the metformin and lifestyle interventions at 91 and 69 mostly nonoverlapping SNPs, respectively. The lowest $P$ values were consistent with experiment-wide 33% false discovery rates. CONCLUSIONS: We have identified potential genetic determinants of metformin response. These results merit confirmation in independent samples

Therapeutic strategies to modulate gut microbial health: Approaches for sarcopenia management

Sarcopenia is a progressive and generalized loss of skeletal muscle and functions associated with ageing with currently no definitive treatment. Alterations in gut microbial composition have emerged as a significant contributor to the pathophysiology of multiple diseases. Recently, its association with muscle health has pointed to its potential role in mediating sarcopenia. The current review focuses on the association of gut microbiota and mediators of muscle health, connecting the dots between the influence of gut microbiota and their metabolites on biomarkers of sarcopenia. It further delineates the mechanism by which the gut microbiota affects muscle health with progressing age, aiding the formulation of a multi-modal treatment plan involving nutritional supplements and pharmacological interventions along with lifestyle changes compiled in the review. Nutritional supplements containing proteins, vitamin D, omega-3 fatty acids, creatine, curcumin, kefir, and ursolic acid positively impact the gut microbiome. Dietary fibres foster a conducive environment for the growth of beneficial microbes such as Bifidobacterium, Faecalibacterium, Ruminococcus, and Lactobacillus. Probiotics and prebiotics act by protecting against reactive oxygen species (ROS) and inflammatory cytokines. They also increase the production of gut microbiota metabolites like short-chain fatty acids (SCFAs), which aid in improving muscle health. Foods rich in polyphenols are anti-inflammatory and have an antioxidant effect, contributing to a healthier gut. Pharmacological interventions like faecal microbiota transplantation (FMT), non-steroidal anti-inflammatory drugs (NSAIDs), ghrelin mimetics, angiotensin-convertin

Structural and optical properties of CsI thin films: Influence of film thickness and humidity

Structural and optical studies have been performed on the thermally-evaporated "as-deposited" and "humid air aged" CsI thin films. The structural analysis for both "as-deposited" and "humid air aged" films shows a well-oriented peaks position of (110) and (220) lattice planes with a compressive stress in the films. The crystal quality has been investigated through the structural parameters. The increase in peak intensity as well as sharpness with film thickness implies the improvement of crystallinity. The optical absorbance of CsI films has been analyzed in the wavelength range of 190 nm - 900 nm in order to estimate the band gap energy of the films. Slater's model has also been used to explain the degradation of band gap energy with the increase in crystallite size.Comment: Accepted for publication in Physica B: Condensed Matter Journa

Transferability and Fine Mapping of Type 2 Diabetes Loci in African Americans: The Candidate Gene Association Resource Plus Study

Type 2 diabetes (T2D) disproportionally affects African Americans (AfA) but, to date, genetic variants identified from genome-wide association studies (GWAS) are primarily from European and Asian populations. We examined the single nucleotide polymorphism (SNP) and locus transferability of 40 reported T2D loci in six AfA GWAS consisting of 2,806 T2D case subjects with or without end-stage renal disease and 4,265 control subjects from the Candidate Gene Association Resource Plus Study. Our results revealed that seven index SNPs at the TCF7L2, KLF14, KCNQ1, ADCY5, CDKAL1, JAZF1, and GCKR loci were significantly associated with T2D (P < 0.05). The strongest association was observed at TCF7L2 rs7903146 (odds ratio [OR] 1.30; P = 6.86 × 10−8). Locus-wide analysis demonstrated significant associations (Pemp < 0.05) at regional best SNPs in the TCF7L2, KLF14, and HMGA2 loci as well as suggestive signals in KCNQ1 after correction for the effective number of SNPs at each locus. Of these loci, the regional best SNPs were in differential linkage disequilibrium (LD) with the index and adjacent SNPs. Our findings suggest that some loci discovered in prior reports affect T2D susceptibility in AfA with similar effect sizes. The reduced and differential LD pattern in AfA compared with European and Asian populations may facilitate fine mapping of causal variants at loci shared across populations

NPM1 directs PIDDosome-dependent caspase-2 activation in the nucleolus

The PIDDosome (PIDD–RAIDD–caspase-2 complex) is considered to be the primary signaling platform for caspase-2 activation in response to genotoxic stress. Yet studies of PIDD-deficient mice show that caspase-2 activation can proceed in the absence of PIDD. Here we show that DNA damage induces the assembly of at least two distinct activation platforms for caspase-2: a cytoplasmic platform that is RAIDD dependent but PIDD independent, and a nucleolar platform that requires both PIDD and RAIDD. Furthermore, the nucleolar phosphoprotein nucleophosmin (NPM1) acts as a scaffold for PIDD and is essential for PIDDosome assembly in the nucleolus after DNA damage. Inhibition of NPM1 impairs caspase-2 processing, apoptosis, and caspase-2–dependent inhibition of cell growth, demonstrating that the NPM1-dependent nucleolar PIDDosome is a key initiator of the caspase-2 activation cascade. Thus we have identified the nucleolus as a novel site for caspase-2 activation and function