The HEX-ACO-18:Developing an age-invariant HEXACO short scale using ant colony optimization

In this study, we developed an age-invariant 18-item short form of the HEXACO Personality Inventory for use in developmental personality research. We combined the item selection procedure ant colony optimization (ACO) and the model estimation approach local structural equation modeling (LSEM). ACO is a metaheuristic algorithm that evaluates items based on the quality of the resulting short scale, thus directly optimizing criteria that can only be estimated with combinations of items, such as model fit and measurement invariance. LSEM allows for model estimation and measurement invariance testing across a continuous age variable by weighting participants, rather than splitting the sample into artificial age groups. Using a HEXACO-100 dataset of N = 6,419 participants ranging from 16 to 90 years of age, we selected a short form optimized for model fit, measurement invariance, facet coverage, and balance of item keying. To achieve scalar measurement invariance and brevity, but maintain construct coverage, we selected 18 items to represent three out of four facets from each HEXACO trait domain. The resulting HEX-ACO-18 short scale showed adequate model fit and scalar measurement invariance across age. Furthermore, the usefulness and versatility of the item and person sampling procedures ACO and LSEM is demonstrated

Exploring EGR-1 as a Master Regulator of Prostate Field Cancerization

Field cancerization denotes the presence of molecular aberrations (genetic, epigenetic, biochemical) in structurally intact cells residing in histologically normal tissues adjacent to tumors. Markers of field cancerization in prostate tissues have the potential to improve the clinical management of this malignancy through their potential to act as indicators of early disease and to serve as molecular targets for early intervention. However, for this, a detailed understanding of the functional pathways underlying field cancerization is necessary. We have recently identified four protein markers of prostate field cancerization, i.e. the key transcription factor early growth response 1 (EGR-1), the lipogenic enzyme fatty acid synthase (FASN), and the secreted growth factors platelet derived growth factor A (PDGF-A) and macrophage inhibitory cytokine 1 (MIC-1). In this study, we provide for the first time a comprehensive association analysis between these factors, especially a potentially regulatory role of EGR-1 for the other factors, using cell models of prostate cancer and expression data in human prostate tissues. Our results indicate a potential discrepancy between research in vitro and observations in situ. More importantly, our detailed tissue expression analyses reveal novel functional pathways of prostate cancerization with a central regulatory role for EGR-1

Molecular Insights into Prostate Field Cancerization: Telomere Length, EGR-­‐1 Expression, and Regulation of MIC-­‐1, PDGF-­‐A, and FAS

The diagnosis of prostate cancer (adenocarcinoma) relies on screening for elevated prostate-specific antigen (PSA) in blood samples and on digital rectal examination (DRE). With high PSA levels and/or abnormal DRE, physicians recommend a biopsy, which often misses the location of the adenocarcinoma and results in false negatives. Previous studies have shown expression of the key transcription factor early growth response 1 (EGR-1), the pro-survival factor macrophage inhibitor cytokine 1 (MIC-1), and the growth stimulatory platelet derived growth factor A (PDGF-A) to be up-regulated in histologically normal tissues 1 centimeter adjacent to prostate adenocarcinomas. We hypothesize that tumors emerge from “field cancerized” tissues, and while such tissues appear normal under gross histological examination, further analysis reveals a molecular history that adds insight into development of oncogenesis. We aim to explore EGR-1, MIC-1, and PDGF-A as essential markers of field cancerization and prostate oncogenesis that may also provide an early detection of premalignant cells by biochemical and molecular biological methods. We present here data from our ongoing investigations into the effect of tissue microenvironmental factors involved in tumorigenesis, for example oxidative stress and telomere-mediated genomic instability in human prostate cancer cell models. We also present data on the regulation of expression of MIC-1 and PDGF-A by EGR-1 using human prostate cancer cell models

PERTANGGUNGJAWABAN PIDANA TERHADAP PELAKU PENCEMARAN LINGKUNGAN SEBAGAI AKIBAT LIMBAH B3 (Studi Kasus Putusan Nomor 1482/Pid.Sus-LH/2021/PT MDN)

Pencemaran lingkungan yang disebabkan oleh Limbah B3 (Bahan Berbahaya dan Beracun) menjadi masalah serius di Indonesia, termasuk di Rumah Sakit Umum Berkah Medan. Penelitian ini bertujuan untuk mengkaji pertanggungjawaban pidana terhadap pelaku pencemaran lingkungan akibat Limbah B3, dengan fokus pada studi kasus Putusan Nomor 1482/Pid.Sus-LH/2021/PT MDN. Metode penelitian yang digunakan adalah penelitian normatif dengan data primer berupa Putusan PT Medan, serta data sekunder berupa peraturan-undangan di bidang Lingkungan Hidup, jurnal, dan buku. Analisis data dilakukan secara yuridis kualitatif. Hasil penelitian menunjukkan bahwa pertanggungjawaban Rumah Sakit Umum Berkah Medan berupa hukuman denda sebesar Rp 1 miliar, subsider 3 bulan kurungan.Kemudian dalam kasus limbah B3, PPNS memiliki peran yang sangat penting dalam pencegahan pencemaran lingkungan yang terjadi akibat limbah B3. Dalam hal penegakan hukum lingkungan, PPNS dapat melakukan tindakan seperti penyertaan barang bukti, pemanggilan Saksi, dan pemeriksaan dokumen

The Keck+Magellan Survey for Lyman Limit Absorption I: The Frequency Distribution of Super Lyman Limit Systems

We present the results of a survey for super Lyman limit systems (SLLS; defined to be absorbers with 19.0 <= log(NHI) <= 20.3 cm^-2) from a large sample of high resolution spectra acquired using the Keck and Magellan telescopes. Specifically, we present 47 new SLLS from 113 QSO sightlines. We focus on the neutral hydrogen frequency distribution f(N,X) of the SLLS and its moments, and compare these results with the Lyman-alpha forest and the damped Lyman alpha systems (DLA; absorbers with log(NHI) >= 20.3 cm^-2). We find that that f(N,X) of the SLLS can be reasonably described with a power-law of index alpha = -1.43^{+0.15}_{-0.16} or alpha = -1.19^{+0.20}_{-0.21} depending on whether we set the lower N(HI) bound for the analysis at 10^{19.0} cm^-2 or 10^{19.3}$ cm^-2, respectively. The results indicate a flattening in the slope of f(N,X) between the SLLS and DLA. We find little evidence for redshift evolution in the shape of f(N,X) for the SLLS over the redshift range of the sample 1.68 < z < 4.47 and only tentative evidence for evolution in the zeroth moment of f(N,X), the line density l_lls(X). We introduce the observable distribution function O(N,X) and its moment, which elucidates comparisons of HI absorbers from the Lyman-alpha through to the DLA. We find that a simple three parameter function can fit O(N,X) over the range 17.0 <= log(NHI) <=22.0. We use these results to predict that f(N,X) must show two additional inflections below the SLLS regime to match the observed f(N,X) distribution of the Lyman-alpha forest. Finally, we demonstrate that SLLS contribute a minor fraction (~15%) of the universe's hydrogen atoms and, therefore, an even small fraction of the mass in predominantly neutral gas.Comment: 15 pages, 10 figures, accepted to the Astrophysical Journal. Revision includes updated reference

Stanniocalcin 2 alters PERK signalling and reduces cellular injury during cerulein induced pancreatitis in mice

BACKGROUND: Stanniocalcin 2 (STC2) is a secreted protein activated by (PKR)-like Endoplasmic Reticulum Kinase (PERK) signalling under conditions of ER stress in vitro. Over-expression of STC2 in mice leads to a growth-restricted phenotype; however, the physiological function for STC2 has remained elusive. Given the relationship of STC2 to PERK signalling, the objective of this study was to examine the role of STC2 in PERK signalling in vivo. RESULTS: Since PERK signalling has both physiological and pathological roles in the pancreas, STC2 expression was assessed in mouse pancreata before and after induction of injury using a cerulein-induced pancreatitis (CIP) model. Increased Stc2 expression was identified within four hours of initiating pancreatic injury and correlated to increased activation of PERK signalling. To determine the effect of STC2 over-expression on PERK, mice systemically expressing human STC2 (STC2Tg) were examined. STC2Tg pancreatic tissue exhibited normal pancreatic morphology, but altered activation of PERK signalling, including increases in Activating Transcription Factor (ATF) 4 accumulation and autophagy. Upon induction of pancreatic injury, STC2Tg mice exhibited limited increases in circulating amylase levels and increased maintenance of cellular junctions. CONCLUSIONS: This study links STC2 to the pathological activation of PERK in vivo, and suggests involvement of STC2 in responding to pancreatic acinar cell injury