PENGARUH PERENCANAAN SUMBER DAYA MANUSIA, PEMBAGIAN KERJA DAN KARAKTERISTIK PEKERJAAN TERHADAP KINERJA KARYAWAN PADA PT. TABUNGAN ASURANSI PENSIUN (PT. TASPEN) PERSERO KCU BANDUNG

ABSTRAK Penelitian ini bertujuan untuk mengetahui dan menganalisis pengaruh perencanaan sumber daya manusia, pembagian kerja dan karakteristik pekerjaan terhadap kinerja karyawan. Metode penelitian yang digunakan adalah deskriptif dan verifikatif dengan jumlah populasi 44 responden. Penelitian ini menggunakan pendekatan kuantitatif, data dikumpulkan dengan teknik kuesioner. Metode analisis data yang digunakan adalah analisis regresi linier berganda, analisis korelasi berganda, dan analisis koefisien determinasi. Hasil penelitian menunjukkan bahwa perencanaan sumber daya manusia, pembagian kerja dan karakteristik pekerjaan secara simultan dan parsial berpengaruh positif dan signifikan terhadap kinerja karyawan. Perencanaan sumber daya manusia, pembagian kerja dan karakteristik pekerjaan memberikan pengaruh terhadap kinerja karyawan yaitu sebesar 65,61%. Perencanaan sumber daya manusia berpengaruh sebesar 23,3%, pengaruh pembagian kerja berpengaruh sebesar 22,2%, sedangkan karakteristik pekerjaan berpengaruh sebesar 20,0% dan sisanya 34,5% dipengaruhi oleh variabel lain. Kata Kunci: Perencanaan Sumber Daya Manusia, Pembagian Kerja, Karakteristik Pekerjaan, Kinerja Karyawa

Evaluation of the online management course from the perspective of former students

Objective To evaluate the online course from the perspective of e-learners as well as the relation between variables. Method A quantitative, descriptive and exploratory study. Results After three years, the satisfaction rates in the three listed categories presented an average rate higher than 75%. The coefficients indicated a high consistency of the questionnaire. Considering the overall rates in the three years period, the Instructor Performance category presented the highest rate. Strong associations between Self-Assessment and Instructor Performance, Self-Evaluation and Program of the Course and Instructor performance and Program of the course were identified. There was no association between the three categories mentioned with any other variables existing in the study. Conclusion E-learners expressed satisfaction with the course that means favored the interaction and the promotion of collective knowledge in nursing management. Also aspects need to be improved, especially the training of the instructor to mediate discussions and encourage student involvement throughout the course.info:eu-repo/semantics/publishedVersio

Inferring stabilizing mutations from protein phylogenies : application to influenza hemagglutinin

One selection pressure shaping sequence evolution is the requirement that a protein fold with sufficient stability to perform its biological functions. We present a conceptual framework that explains how this requirement causes the probability that a particular amino acid mutation is fixed during evolution to depend on its effect on protein stability. We mathematically formalize this framework to develop a Bayesian approach for inferring the stability effects of individual mutations from homologous protein sequences of known phylogeny. This approach is able to predict published experimentally measured mutational stability effects (ΔΔG values) with an accuracy that exceeds both a state-of-the-art physicochemical modeling program and the sequence-based consensus approach. As a further test, we use our phylogenetic inference approach to predict stabilizing mutations to influenza hemagglutinin. We introduce these mutations into a temperature-sensitive influenza virus with a defect in its hemagglutinin gene and experimentally demonstrate that some of the mutations allow the virus to grow at higher temperatures. Our work therefore describes a powerful new approach for predicting stabilizing mutations that can be successfully applied even to large, complex proteins such as hemagglutinin. This approach also makes a mathematical link between phylogenetics and experimentally measurable protein properties, potentially paving the way for more accurate analyses of molecular evolution

Rac1 and Rac3 isoform activation is involved in the invasive and metastatic phenotype of human breast cancer cells

INTRODUCTION: The metastatic progression of cancer is a direct result of the disregulation of numerous cellular signaling pathways, including those associated with adhesion, migration, and invasion. Members of the Rac family of small GTPases are known to act as regulators of actin cytoskeletal structures and strongly influence the cellular processes of integrin-mediated adhesion and migration. Even though hyperactivated Rac proteins have been shown to influence metastatic processes, these proteins have never been directly linked to metastatic progression. METHODS: To investigate a role for Rac and Cdc42 in metastatic breast cancer cell invasion and migration, relative endogenous Rac or Cdc42 activity was determined in a panel of metastatic variants of the MDA-MB-435 metastatic human breast cancer cell line using a p21-binding domain-PAK pull down assay. To investigate the migratory and invasive potential of the Rac isoforms in human breast cancer, namely Rac1 and the subsequently cloned Rac3, we stably expressed either dominant active Rac1 or dominant active Rac3 into the least metastatic cell variant. Dominant negative Rac1 or dominant negative Rac3 were stably expressed in the most metastatic cell variant. Cell lines expressing mutant Rac1 or Rac3 were analyzed using in vitro adhesion, migration and invasion assays. RESULTS: We show that increased activation of Rac proteins directly correlates with increasing metastatic potential in a panel of cell variants derived from a single metastatic breast cancer cell line (MDA-MB-435). The same correlation could not be found with activated Cdc42. Expression of a dominant active Rac1 or a dominant active Rac3 resulted in a more invasive and motile phenotype. Moreover, expression of either dominant negative Rac1 or dominant negative Rac3 into the most metastatic cell variant resulted in decreased invasive and motile properties. CONCLUSION: This study correlates endogenous Rac activity with high metastatic potential and implicates Rac in the regulation of cell migration and invasion in metastatic breast cancer cells. Taken together, these results suggest a role for both the Rac1 and Rac3 GTPases in human breast cancer progression

Prognostic value of tissue-type plasminogen activator (tPA) and its complex with the type-1 inhibitor (PAI-1) in breast cancer

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The Protein Phosphatase 7 Regulates Phytochrome Signaling in Arabidopsis

The psi2 mutant of Arabidopsis displays amplification of the responses controlled by the red/far red light photoreceptors phytochrome A (phyA) and phytochrome B (phyB) but no apparent defect in blue light perception. We found that loss-of-function alleles of the protein phosphatase 7 (AtPP7) are responsible for the light hypersensitivity in psi2 demonstrating that AtPP7 controls the levels of phytochrome signaling. Plants expressing reduced levels of AtPP7 mRNA display reduced blue-light induced cryptochrome signaling but no noticeable deficiency in phytochrome signaling. Our genetic analysis suggests that phytochrome signaling is enhanced in the AtPP7 loss of function alleles, including in blue light, which masks the reduced cryptochrome signaling. AtPP7 has been found to interact both in yeast and in planta assays with nucleotide-diphosphate kinase 2 (NDPK2), a positive regulator of phytochrome signals. Analysis of ndpk2-psi2 double mutants suggests that NDPK2 plays a critical role in the AtPP7 regulation of the phytochrome pathway and identifies NDPK2 as an upstream element involved in the modulation of the salicylic acid (SA)-dependent defense pathway by light. Thus, cryptochrome- and phytochrome-specific light signals synchronously control their relative contribution to the regulation of plant development. Interestingly, PP7 and NDPK are also components of animal light signaling systems

No association between the common calcium-sensing receptor polymorphism rs1801725 and irritable bowel syndrome

Background The calcium-sensing receptor (CaSR) is a calcium (Ca2+) sensitive G protein-coupled receptor implicated in various biological processes. In particular, it regulates Ca2+/Mg2+- homeostasis and senses interstitial Ca2+ levels and thereby controls downstream signalling cascades. Due to its expression in the gut epithelium, the enteric nervous system and smooth muscles and its key function in regulation and coordination of muscular contraction and secretion, it represents an excellent candidate gene to be investigated in the pathophysiology of irritable bowel syndrome (IBS). Disturbed CaSR structure and function may impact gastrointestinal regulation of muscular contraction, neuronal excitation and secretion and consequently contribute to symptoms seen in IBS, such as disordered defecation as well as disturbed gut motility and visceral sensitivity. Methods We have therefore genotyped the functional CASR SNP rs1801725 in three case control samples from the UK, Belgium and the USA. Results Genotype frequencies showed no association in the three genotyped case–control samples, neither with IBS nor with IBS subtypes. Conclusions Although we could not associate the SNP to any of the established bowel symptom based IBS subtypes we cannot rule out association to altered Ca2+ levels and disturbed secretion and gut motility which were unfortunately not assessed in the patients genotyped. This underlines the necessity of a more detailed phenotyping of IBS patients and control individuals in future studies