Penyesuaian Diri Pegawai Dalam Menghadapi Perubahan Organisasi

Pemberian pelimpahan kewenangan walikota kepada camat berimplikasi terhadap kehidupan kerja para pegawai kecamatan untuk mengimplementasikan tugastugas kerja yang belum pernah dilakukan sebelumnya. Penelitian ini bertujuan untuk mendeskripsikan penyesuaian diri pegawai kecamatan dalam menghadapi pelimpahan kewenangan walikota kepada camat di wilayah Kota Yogyakarta. Wawancara mendalam dilakukan dengan melibatkan 3 responden laki-laki dan 1 responden perempuan yang terbagi di 3 wilayah kecamatan. Karakteristik responden dalam penelitian ini antara lain: Individu yang bekerja sebagai pegawai kecamatan dan berada dibawah kendali kepemimpinan organisasi Pemerintahan Kota Yogyakarta, pegawai yang menjadi objek perubahan organisasi atau mereka yang mengalami penyesuaian diri akibat perubahan yang terjadi dalam organisasi, bersedia untuk berpartisipasi dalam proses wawancara dan memberikan komitmen untuk inform concern hingga penelitian berakhir. Analisis dan interpretasi dalam penelitian ini dilakukan dengan cara: 1) Memahami pernyataan penting, 2) Membuat makna pernyataan, 3) Membuat intisari pernyataan, 4) Menggambarkan secara mendalam fenomena yang diteliti. Verifikasi penelitian menggunakan intersubjective validity dan external audits. Pengembangan strategi penyesuaian diri (coping strategy) dilakukan oleh responden dengan banyak belajar, banyak bertanya, aktif komunikasi, optimalisasi peran SDM dan masyarakat, merubah sudut pandang. Bentuk penyesuaian diri pegawai yang dilakukan adalah dengan bekerja sesuai aturan, memunculkan sisi religius, terlibat aktif dalam perencanaan, belajar aktif, dan mengembangkan karakter pembelajar. Disimpulkan bahwa perubahan organisasi selalu membawa dampak psikologis dan memunculkan karakteristik lingkungan yang baru baik relasi kerja maupun tugas dan tanggung jawab. Bentuk penyesuaian diri pegawai pun akan berbeda, tergantung pada tuntutan dan lingkungan kerja yang selalu dimaknai sebagai cara menyesuaikan diri dalam lingkungan kerja. Memaknai penyesuaian diri akan membawa dampak pada kualitas kehidupan kerja pegawai (quality of work life)

Konsumen dan Pandemi Covid-19 (Studi Tentang Perlindungan Hukum di Kedai Makanan Karesidenan Surakarta)

The COVID-19 pandemic has had economic, social, and political implications not only for big countries but for almost all countries in the world. It seems that there is not a single country that is not affected by the current COVID-19 pandemic. Indonesia is one of the most affected countries, especially on the economic side. Indonesia, which is dominated by hawker food entrepreneurs, needs to pay special attention to this sector in order to survive and to provide socialization about health procedures in a restaurant. Therefore, this study aims to analyze how safety and health procedures are when visiting and buying snacks at a shop in Solo. In addition to analyzing safety and health procedures in a restaurant, this article also tries to analyze the impact of the COVID-19 pandemic on the existence of street food entrepreneurs in Solo and how to find solutions to survive in the COVID-19 pandemic situation

Perceived discrimination and health-related quality of life among Arabs and Jews in Israel: A population-based survey

<p>Abstract</p> <p>Background</p> <p>Studies have shown that perceived discrimination may be associated with impaired health. The aim of this study was to assess the levels of perceived discrimination on the basis of origin and ethnicity and measure the association with health in three population groups in Israel: non-immigrant Jews, immigrants from the former Soviet Union, and Arabs.</p> <p>Methods</p> <p>A cross sectional random telephone survey was performed in 2006 covering 1,004 Israelis aged 35-65; of these, 404 were non-immigrant Jews, 200 were immigrants from the former Soviet Union and 400 were Arabs, the final number for regression analysis was 952. Respondents were asked about their perceived experiences with discrimination in seven different areas. Quality of life, both physical and mental were measured by the Short Form 12.</p> <p>Results</p> <p>Perceived discrimination on the basis of origin was highest among immigrants. About 30% of immigrants and 20% of Arabs reported feeling discriminated against in areas such as education and employment. After adjusting for socioeconomic variables, discrimination was associated with poor physical health among non-immigrant Jews (OR = 0.42, CI = 0.19, 0.91) and immigrants (OR = 0.51, CI = 0.27, 0.94), but not among Arabs. Poor mental health was significantly associated with discrimination only among non-immigrant Jews (OR = 0.42, CI = 0.18, 0.96).</p> <p>Conclusions</p> <p>Perceived discrimination seemed high in both minority populations in Israel (Arabs and immigrants) and needs to be addressed as such. However, discrimination was associated with physical health only among Jews (non-immigrants and immigrants), and not among Arabs. These results may be due to measurement artifacts or may be a true phenomenon, further research is needed to ascertain the results.</p

In Vivo Imaging Reveals Distinct Inflammatory Activity of CNS Microglia versus PNS Macrophages in a Mouse Model for ALS

Mutations in the enzyme superoxide dismutase-1 (SOD1) cause hereditary variants of the fatal motor neuronal disease Amyotrophic lateral sclerosis (ALS). Pathophysiology of the disease is non-cell-autonomous: neurotoxicity is derived not only from mutant motor neurons but also from mutant neighbouring non-neuronal cells. In vivo imaging by two-photon laser-scanning microscopy was used to compare the role of microglia/macrophage-related neuroinflammation in the CNS and PNS using ALS-linked transgenic SOD1G93A mice. These mice contained labeled projection neurons and labeled microglia/macrophages. In the affected lateral spinal cord (in contrast to non-affected dorsal columns), different phases of microglia-mediated inflammation were observed: highly reactive microglial cells in preclinical stages (in 60-day-old mice the reaction to axonal transection was ∼180% of control) and morphologically transformed microglia that have lost their function of tissue surveillance and injury-directed response in clinical stages (reaction to axonal transection was lower than 50% of control). Furthermore, unlike CNS microglia, macrophages of the PNS lack any substantial morphological reaction while preclinical degeneration of peripheral motor axons and neuromuscular junctions was observed. We present in vivo evidence for a different inflammatory activity of microglia and macrophages: an aberrant neuroinflammatory response of microglia in the CNS and an apparently mainly neurodegenerative process in the PNS

The need for multidisciplinarity in specialist training to optimize future patient care

Harmonious interactions between radiation, medical, interventional and surgical oncologists, as well as other members of multidisciplinary teams, are essential for the optimization of patient care in oncology. This multidisciplinary approach is particularly important in the current landscape, in which standard-of-care approaches to cancer treatment are evolving towards highly targeted treatments, precise image guidance and personalized cancer therapy. Herein, we highlight the importance of multidisciplinarity and interdisciplinarity at all levels of clinical oncology training. Potential deficits in the current career development pathways and suggested strategies to broaden clinical training and research are presented, with specific emphasis on the merits of trainee involvement in functional multidisciplinary teams. Finally, the importance of training in multidisciplinary research is discussed, with the expectation that this awareness will yield the most fertile ground for future discoveries. Our key message is for cancer professionals to fulfil their duty in ensuring that trainees appreciate the importance of multidisciplinary research and practice

Different Human Copper-Zinc Superoxide Dismutase Mutants, SOD1G93A and SOD1H46R, Exert Distinct Harmful Effects on Gross Phenotype in Mice

Amyotrophic lateral sclerosis (ALS) is a heterogeneous group of fatal neurodegenerative diseases characterized by a selective loss of motor neurons in the brain and spinal cord. Creation of transgenic mice expressing mutant Cu/Zn superoxide dismutase (SOD1), as ALS models, has made an enormous impact on progress of the ALS studies. Recently, it has been recognized that genetic background and gender affect many physiological and pathological phenotypes. However, no systematic studies focusing on such effects using ALS models other than SOD1G93A mice have been conducted. To clarify the effects of genetic background and gender on gross phenotypes among different ALS models, we here conducted a comparative analysis of growth curves and lifespans using congenic lines of SOD1G93A and SOD1H46R mice on two different genetic backgrounds; C57BL/6N (B6) and FVB/N (FVB). Copy number of the transgene and their expression between SOD1G93A and SOD1H46R lines were comparable. B6 congenic mutant SOD1 transgenic lines irrespective of their mutation and gender differences lived longer than corresponding FVB lines. Notably, the G93A mutation caused severer disease phenotypes than did the H46R mutation, where SOD1G93A mice, particularly on a FVB background, showed more extensive body weight loss and earlier death. Gender effect on survival also solely emerged in FVB congenic SOD1G93A mice. Conversely, consistent with our previous study using B6 lines, lack of Als2, a murine homolog for the recessive juvenile ALS causative gene, in FVB congenic SOD1H46R, but not SOD1G93A, mice resulted in an earlier death, implying a genetic background-independent but mutation-dependent phenotypic modification. These results indicate that SOD1G93A- and SOD1H46R-mediated toxicity and their associated pathogenic pathways are not identical. Further, distinctive injurious effects resulted from different SOD1 mutations, which are associated with genetic background and/or gender, suggests the presence of several genetic modifiers of disease expression in the mouse genome

Identification of Novel Pathogenicity Loci in Clostridium perfringens Strains That Cause Avian Necrotic Enteritis

Type A Clostridium perfringens causes poultry necrotic enteritis (NE), an enteric disease of considerable economic importance, yet can also exist as a member of the normal intestinal microbiota. A recently discovered pore-forming toxin, NetB, is associated with pathogenesis in most, but not all, NE isolates. This finding suggested that NE-causing strains may possess other virulence gene(s) not present in commensal type A isolates. We used high-throughput sequencing (HTS) technologies to generate draft genome sequences of seven unrelated C. perfringens poultry NE isolates and one isolate from a healthy bird, and identified additional novel NE-associated genes by comparison with nine publicly available reference genomes. Thirty-one open reading frames (ORFs) were unique to all NE strains and formed the basis for three highly conserved NE-associated loci that we designated NELoc-1 (42 kb), NELoc-2 (11.2 kb) and NELoc-3 (5.6 kb). The largest locus, NELoc-1, consisted of netB and 36 additional genes, including those predicted to encode two leukocidins, an internalin-like protein and a ricin-domain protein. Pulsed-field gel electrophoresis (PFGE) and Southern blotting revealed that the NE strains each carried 2 to 5 large plasmids, and that NELoc-1 and -3 were localized on distinct plasmids of sizes ∼85 and ∼70 kb, respectively. Sequencing of the regions flanking these loci revealed similarity to previously characterized conjugative plasmids of C. perfringens. These results provide significant insight into the pathogenetic basis of poultry NE and are the first to demonstrate that netB resides in a large, plasmid-encoded locus. Our findings strongly suggest that poultry NE is caused by several novel virulence factors, whose genes are clustered on discrete pathogenicity loci, some of which are plasmid-borne

Superoxide Dismutase 1 and tgSOD1G93A Mouse Spinal Cord Seed Fibrils, Suggesting a Propagative Cell Death Mechanism in Amyotrophic Lateral Sclerosis

Background: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that specifically affects motor neurons and leads to a progressive and ultimately fatal loss of function, resulting in death typically within 3 to 5 years of diagnosis. The disease starts with a focal centre of weakness, such as one limb, and appears to spread to other parts of the body. Mutations in superoxide dismutase 1 (SOD1) are known to cause disease and it is generally accepted they lead to pathology not by loss of enzymatic activity but by gain of some unknown toxic function(s). Although different mutations lead to varying tendencies of SOD1 to aggregate, we suggest abnormal proteins share a common misfolding pathway that leads to the formation of amyloid fibrils.Methodology/Principal Findings: Here we demonstrate that misfolding of superoxide dismutase 1 leads to the formation of amyloid fibrils associated with seeding activity, which can accelerate the formation of new fibrils in an autocatalytic cascade. The time limiting event is nucleation to form a stable protein "seed" before a rapid linear polymerisation results in amyloid fibrils analogous to other protein misfolding disorders. This phenomenon was not confined to fibrils of recombinant protein as here we show, for the first time, that spinal cord homogenates obtained from a transgenic mouse model that overexpresses mutant human superoxide dismutase 1 (the TgSOD1(G93A) mouse) also contain amyloid seeds that accelerate the formation of new fibrils in both wildtype and mutant SOD1 protein in vitro.Conclusions/Significance: These findings provide new insights into ALS disease mechanism and in particular a mechanism that could account for the spread of pathology throughout the nervous system. This model of disease spread, which has analogies to other protein misfolding disorders such as prion disease, also suggests it may be possible to design assays for therapeutics that can inhibit fibril propagation and hence, possibly, disease progression

Stressful situation if CENP-A not front and CENter

The exclusive localization of the histone H3 variant CENP-A to centromeres is essential for accurate chromosome segregation. Ubiquitin-mediated proteolysis helps to ensure that CENP-A does not mislocalize to euchromatin, which can lead to genomic instability. Consistent with this, overexpression of the budding yeast CENP-A(Cse4) is lethal in cells lacking Psh1, the E3 ubiquitin ligase that targets CENP-A(Cse4) for degradation. To identify additional mechanisms that prevent CENP-A(Cse4) misincorporation and lethality, we analyzed the genome-wide mislocalization pattern of overexpressed CENP-A(Cse4) in the presence and absence of Psh1 by chromatin immunoprecipitation followed by high throughput sequencing. We found that ectopic CENP-A(Cse4) is enriched at promoters that contain histone H2A.Z(Htz1) nucleosomes, but that H2A.Z(Htz1) is not required for CENP-A(Cse4) mislocalization. Instead, the INO80 complex, which removes H2A.Z(Htz1) from nucleosomes, promotes the ectopic deposition of CENP-A(Cse4). Transcriptional profiling revealed gene expression changes in the psh1Δ cells overexpressing CENP-A(Cse4). The down-regulated genes are enriched for CENP-A(Cse4) mislocalization to promoters, while the up-regulated genes correlate with those that are also transcriptionally up-regulated in an htz1Δ strain. Together, these data show that regulating centromeric nucleosome localization is not only critical for maintaining centromere function, but also for ensuring accurate promoter function and transcriptional regulation

African-American health: the role of the social environment

Cooper and colleagues have noted that the forces affecting the health of minority populations are the same forces, on a less intensive scale, that affect the health of the overall population. 90 That is, we can view the health of the African-American population as the visible tip of an iceberg. This tip of the iceberg is a function of the average health of the entire population. Thus, an effective strategy must address not only the tip, but also should attack the entire iceberg and reduce the risk that it is creating throughout the population. Similarly, Wallace and Wallace have shown how the mechanisms of hierarchical diffusion, spatial contagion, and network diffusion lead to the spread of health and social problems initially confined in inner cities to suburban areas and smaller cities. 91 That is, because of the economic links typing various communities together, there are mechanisms that will ensure the diffusion of disease and disorder from one area to another. If unaddressed, the problems of stigmatized and marginalized urban populations will have adverse impacts on the health, well-being, and quality of life of the more affluent. Thus, investments that will improve the social conditions of a marginalized population can have long-term positive health and social consequences for the entire society.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/45781/1/11524_2006_Article_BF02345099.pd