FAKTOR-FAKTOR YANG MEMPENGARUHI MOTIVASI KERJA PERAWAT DALAM PENDOKUMENTASIAN ASUHAN KEPERAWATAN DI PUSKESMAS RAWAT INAP (PUSKESMAS SIKUMANA DAN PASIR PANJANG).

Motivasi adalah perasaan atau pikiran yang mendorong seseorang untuk melakukan pekerjaan atau menjalankan kekuasaan, terutama dalam berperilaku. Hal ini termasuk faktor yang menyebabkan, menyalurkan, dan mempertahankan tingkalakuh manusia dalam arah tekat tertentu. Tujuan umum untuk mengetahui faktor-faktor yang mempengaruhi pengaruh motivasi perawat dalam pendokumentasian asuhan keperawatan di Puskesmas rawat Inap se-Kota Kupang. Jenis penilitian ini adalah deskriptif, dimana penelitian yang digunakan untuk mengdeskripsikan dan menjawab persoalan-persoalan suatu fenomena atau peristiwa yang terjadi saat ini. Berdasarkan hasil penelitian yang dilakukan terhadap 25 responden menunjukan bahwa responden yang memiliki motivasi internal dikatakan tinggi 21 responden (84%) dan sebanyak 4 responden (16%) dikatakan rendah. Untukfaktor eksternal, berdasarkan hasil penelitian yang dilakukan terhadap 25 responden menunjukan bahwa responden yang memiliki motivasi tinggi sebesar 14 orang (56%) dan rendah 11 orang (44%). Saran bagi pihak puskesmas khususnya ruang rawat nginap, diharapkan supervisi dilakukan lebih optimal dan teratur pada perawat di ruang rawat inap Puskesmas Sikumana dan Pasir Panjang agar lebih meningkatkan motivasi eksternal perawat dalam melakukan dokumentasi asuhan keperawatan di Puskesmas Sikumana dan Pasir Panjang Kota Kupang

Genome-Wide Mapping of Yeast Histone Chaperone Anti-Silencing Function 1 Reveals Its Role in Condensin Binding with Chromatin

Genome-wide participation and importance of the histone chaperone Asf1 (Anti-Silencing Function 1) in diverse DNA transactions like replication, repair, heterochromatic silencing and transcription are well documented. Yet its genome-wide targets have not been reported. Using ChIP-seq method, we found that yeast Asf1 associates with 590 unique targets including centromeres, telomeres and condensin-binding sites. It is found selectively on highly transcribed regions, which include replication fork pause sites. Asf1 preferentially associates with the genes transcribed by RNA polymerase (pol) III where its presence affects RNA production and replication-independent histone exchange. On pol II-transcribed genes, a negative correlation is found between Asf1 and nucleosome occupancy. It is not enriched on most of the reported sites of histone exchange or on the genes, which are misregulated in the asf1Δ cells. Interestingly, chromosome-wide distributions of Asf1 and one of the condensin subunits, Brn1 show a nearly identical pattern. Moreover, Brn1 shows reduced occupancy at various condensin-binding sites in asf1Δ cells. These results along with high association of Asf1 with heterochromatic centromeres and telomeres ascribe novel roles to Asf1 in condensin loading and chromatin dynamics

The N-terminus of Stag1 is required to repress the 2C program by maintaining rRNA expression and nucleolar integrity

Our understanding of how STAG proteins contribute to cell identity and disease have largely been studied from the perspective of chromosome topology and protein-coding gene expression. Here, we show that STAG1 is the dominant paralog in mouse embryonic stem cells (mESCs) and is required for pluripotency. mESCs express a wide diversity of naturally occurring Stag1 isoforms, resulting in complex regulation of both the levels of STAG paralogs and the proportion of their unique terminal ends. Skewing the balance of these isoforms impacts cell identity. We define a novel role for STAG1, in particular its N-terminus, in regulating repeat expression, nucleolar integrity, and repression of the two-cell (2C) state to maintain mESC identity. Our results move beyond protein-coding gene regulation via chromatin loops to new roles for STAG1 in nucleolar structure and function, and offer fresh perspectives on how STAG proteins, known to be cancer targets, contribute to cell identity and disease

Oncogene expression from extrachromosomal DNA is driven by copy number amplification and does not require spatial clustering in glioblastoma stem cells

Extrachromosomal DNA (ecDNA) are frequently observed in human cancers and are responsible for high levels of oncogene expression. In glioblastoma (GBM), ecDNA copy number correlates with poor prognosis. It is hypothesized that their copy number, size, and chromatin accessibility facilitate clustering of ecDNA and colocalization with transcriptional hubs, and that this underpins their elevated transcriptional activity. Here, we use super-resolution imaging and quantitative image analysis to evaluate GBM stem cells harbouring distinct ecDNA species (EGFR, CDK4, PDGFRA). We find no evidence that ecDNA routinely cluster with one another or closely interact with transcriptional hubs. Cells with EGFR-containing ecDNA have increased EGFR transcriptional output, but transcription per gene copy is similar in ecDNA compared to the endogenous chromosomal locus. These data suggest that it is the increased copy number of oncogene-harbouring ecDNA that primarily drives high levels of oncogene transcription, rather than specific interactions of ecDNA with each other or with high concentrations of the transcriptional machinery

Yeast H2A.Z, FACT complex and RSC regulate transcription of tRNA gene through differential dynamics of flanking nucleosomes

FACT complex is involved in elongation and ensures fidelity in the initiation step of transcription by RNA polymerase (pol) II. Histone variant H2A.Z is found in nucleosomes at the 5′-end of many genes. We report here H2A.Z-chaperone activity of the yeast FACT complex on the short, nucleosome-free, non-coding, pol III-transcribed yeast tRNA genes. On a prototype gene, yeast SUP4, chromatin remodeler RSC and FACT regulate its transcription through novel mechanisms, wherein the two gene-flanking nucleosomes containing H2A.Z, play different roles. Nhp6, which ensures transcription fidelity and helps load yFACT onto the gene flanking nucleosomes, has inhibitory role. RSC maintains a nucleosome abutting the gene terminator downstream, which results in reduced transcription rate in active state while H2A.Z probably helps RSC in keeping the gene nucleosome-free and serves as stress-sensor. All these factors maintain an epigenetic state which allows the gene to return quickly from repressed to active state and tones down the expression from the active SUP4 gene, required probably to maintain the balance in cellular tRNA pool

LRIG1 is a gatekeeper to exit from quiescence in adult neural stem cells

Adult neural stem cells (NSCs) must tightly regulate quiescence and proliferation. Single-cell analysis has suggested a continuum of cell states as NSCs exit quiescence. Here we capture and characterize in vitro primed quiescent NSCs and identify LRIG1 as an important regulator. We show that BMP-4 signaling induces a dormant non-cycling quiescent state (d-qNSCs), whereas combined BMP-4/FGF-2 signaling induces a distinct primed quiescent state poised for cell cycle re-entry. Primed quiescent NSCs (p-qNSCs) are defined by high levels of LRIG1 and CD9, as well as an interferon response signature, and can efficiently engraft into the adult subventricular zone (SVZ) niche. Genetic disruption of Lrig1 in vivo within the SVZ NSCs leads an enhanced proliferation. Mechanistically, LRIG1 primes quiescent NSCs for cell cycle re-entry and EGFR responsiveness by enabling EGFR protein levels to increase but limiting signaling activation. LRIG1 is therefore an important functional regulator of NSC exit from quiescence

Bias i intergruppinteraktioner i rekryteringsammanhang : med avseende på kön

2017-01-11</p

Replication-independent H3 exchange on pol III-transcribed genes.

<p>(A) and (B) Time-course analysis of histone H3 exchange at different loci in wild-type (A) versus <i>asf1Δ</i> (B) cells is shown. Histone exchange assay by ChIP-qPCR analysis was made to follow the H3 exchange <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0108652#pone.0108652-Jamai1" target="_blank">[34]</a> at various pol III-transcribed genes. Averages of ChIP data for three independent experiments with error bars are shown.</p