GMC collisions as triggers of star formation – VIII. The core mass function

Compression in giant molecular cloud (GMC) collisions is a promising mechanism to trigger the formation of massive star clusters and OB associations. We simulate colliding and non-colliding magnetized GMCs and examine the properties of pre-stellar cores, selected from projected mass surface density maps, including after synthetic ALMA observations. We then examine core properties, including mass, size, density, velocity, velocity dispersion, temperature, and magnetic field strength. After 4 Myr, ∼1000 cores have formed in the GMC collision, and the high-mass end of the core mass function (CMF) can be fit by a power-law dN/dlogM ∝ M-α with α ≃ 0.7, i.e. relatively top heavy compared to a Salpeter mass function. Depending on how cores are identified, a break in the power law can appear around a few 710 M☉. The non-colliding GMCs form fewer cores with a CMF with α ≃ 0.8–1.2, i.e. closer to the Salpeter index. We compare the properties of these CMFs to those of several observed samples of cores. Considering other properties, cores formed from colliding clouds are typically warmer, have more disturbed internal kinematics, and are more likely to be gravitational unbound, than cores formed from non-colliding GMCs. The dynamical state of the protocluster of cores formed in the GMC–GMC collision is intrinsically subvirial but can appear to be supervirial if the total mass measurement is affected by observations that miss mass on large scales or at low densities

Estimation of Agricultural Groundwater Usage by Well Pumping Efficiency and Electric Consumption

Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchive

Deuterium Chemodynamics of Massive Pre-Stellar Cores

High levels of deuterium fractionation of $\rm N_2H^+$ (i.e., $\rm D_{frac}^{N_2H^+} \gtrsim 0.1$) are often observed in pre-stellar cores (PSCs) and detection of $\rm N_2D^+$ is a promising method to identify elusive massive PSCs. However, the physical and chemical conditions required to reach such high levels of deuteration are still uncertain, as is the diagnostic utility of $\rm N_2H^+$ and $\rm N_2D^+$ observations of PSCs. We perform 3D magnetohydrodynamics simulations of a massive, turbulent, magnetised PSC, coupled with a sophisticated deuteration astrochemical network. Although the core has some magnetic/turbulent support, it collapses under gravity in about one freefall time, which marks the end of the simulations. Our fiducial model achieves relatively low $\rm D_{frac}^{N_2H^+} \sim 0.002$ during this time. We then investigate effects of initial ortho-para ratio of $\rm H_2$ ($\rm OPR^{H_2}$), temperature, cosmic ray (CR) ionization rate, CO and N-species depletion factors and prior PSC chemical evolution. We find that high CR ionization rates and high depletion factors allow the simulated $\rm D_{frac}^{N_2H^+}$ and absolute abundances to match observational values within one freefall time. For $\rm OPR^{H_2}$, while a lower initial value helps the growth of $\rm D_{frac}^{N_2H^+}$, the spatial structure of deuteration is too widespread compared to observed systems. For an example model with elevated CR ionization rates and significant heavy element depletion, we then study the kinematic and dynamic properties of the core as traced by its $\rm N_2D^+$ emission. The core, undergoing quite rapid collapse, exhibits disturbed kinematics in its average velocity map. Still, because of magnetic support, the core often appears kinematically sub-virial based on its $\rm N_2D^+$ velocity dispersion.Comment: 25 pages, 20 figures, 2 tables, accepted for publication in MNRAS, comments welcom

Interplay between Cell Migration and Neurite Outgrowth Determines SH2B1β-Enhanced Neurite Regeneration of Differentiated PC12 Cells

The regulation of neurite outgrowth is crucial in developing strategies to promote neurite regeneration after nerve injury and in degenerative diseases. In this study, we demonstrate that overexpression of an adaptor/scaffolding protein SH2B1β promotes neurite re-growth of differentiated PC12 cells, an established neuronal model, using wound healing (scraping) assays. Cell migration and the subsequent remodeling are crucial determinants during neurite regeneration. We provide evidence suggesting that overexpressing SH2B1β enhances protein kinase C (PKC)-dependent cell migration and phosphatidylinositol 3-kinase (PI3K)-AKT-, mitogen activated protein kinase (MAPK)/extracellular signal-regulated protein kinase (ERK) kinase (MEK)-ERK-dependent neurite re-growth. Our results further reveal a cross-talk between pathways involving PKC and ERK1/2 in regulating neurite re-growth and cell migration. We conclude that temporal regulation of cell migration and neurite outgrowth by SH2B1β contributes to the enhanced regeneration of differentiated PC12 cells

Probing the DNA kink structure induced by the hyperthermophilic chromosomal protein Sac7d

Sac7d, a small, abundant, sequence-general DNA-binding protein from the hyperthermophilic archaeon Sulfolobus acidocaldarius, causes a single-step sharp kink in DNA (∼60°) via the intercalation of both Val26 and Met29. These two amino acids were systematically changed in size to probe their effects on DNA kinking. Eight crystal structures of five Sac7d mutant–DNA complexes have been analyzed. The DNA-binding pattern of the V26A and M29A single mutants is similar to that of the wild-type, whereas the V26A/M29A protein binds DNA without side chain intercalation, resulting in a smaller overall bending (∼50°). The M29F mutant inserts the Phe29 side chain orthogonally to the C2pG3 step without stacking with base pairs, inducing a sharp kink (∼80°). In the V26F/M29F-GCGATCGC complex, Phe26 intercalates deeply into DNA bases by stacking with the G3 base, whereas Phe29 is stacked on the G15 deoxyribose, in a way similar to those used by the TATA box-binding proteins. All mutants have reduced DNA-stabilizing ability, as indicated by their lower T(m) values. The DNA kink patterns caused by different combinations of hydrophobic side chains may be relevant in understanding the manner by which other minor groove-binding proteins interact with DNA

Immunotherapy: rAAV2 expressing interleukin-15 inhibits HeLa cell tumor growth in mice

Human interleukin-15 (hIL15) has anti-tumor activities, but it is not convenient for tumor treatment because of its short half-life. A gene therapy for mouse lung cancer using an adenovirus vector expressing IL15 has been reported. However, adenovirus vector-mediated gene therapy can provoke cellular toxicity and inflammatory reactions. The recombinant adenovirus-associated vector 2 (rAAV2) is safer due to minimal cellular toxicity and immune response. In order to demonstrate that gene therapy can be used safely and successfully for human cancer treatment, the rAAV2 expressing hIL15 gene (rAAV2-hIL15) is applied for human cervical cancer, HeLa cell, in this study. This study successfully demonstrates that rAAV2-hIL15 can express IL15 with bioactivities in vitro and in vivo. In conclusion, our studies show that human cervical cancers are inhibited on animal model with rAAV2-hIL15 treatment and provide a safer and important reference for human cancer gene therapy

Differential Presentations of Arterial Thromboembolic Events Between Venous Thromboembolism and Atrial Fibrillation Patients

Objective: Atrial fibrillation (AF) and venous thromboembolism (VTE) share several risk factors related to arterial thromboembolism. No study has reported the differential contribution to arterial thromboembolic events and mortality between these two conditions in the same population. We therefore assessed the differential arterial thromboembolic events between AF and VTE. Methods: We included AF and VTE national cohorts derived from Taiwan National Health Insurance Research Database between 2001 and 2013. The eligible population was 314,861 patients in the AF cohort and 41,102 patients in the VTE cohort. The primary outcome was arterial thromboembolic events, including ischemic stroke, extracranial arterial thromboembolism (ECATE) and myocardial infarction (MI). Secondary outcomes were all-cause mortality and cardiovascular death. Results: After a 1:1 propensity matching, 32,688 patients in either group were analyzed. The risk of arterial thromboembolic events was lower in the VTE cohort than that in the AF cohort (subdistribution hazard ratio [SHR], 0.60; 95% confidence interval [CI], 0.57–0.62). The risk of ischemic stroke (SHR, 0.44; 95% CI, 0.42–0.46) and MI (SHR, 0.80; 95% CI, 0.72–0.89) were lower in the VTE cohort, while the risk of ECATE (SHR, 1.23; 95% CI, 1.14–1.33; particularly lower extremities) was higher in the VTE cohort. All-cause mortality rate was higher in the VTE cohort (HR, 1.18; 95% CI, 1.15–1.21) while the risk of cardiovascular death was lower in the VTE cohort (HR, 0.96; 95% CI, 0.93–0.995). Conclusions: Patients with AF had higher risks of arterial thromboembolic events compared to patients with VTE, despite having risk factors in common. The VTE cohort had higher risks of all-cause mortality and ECATE, particularly lower extremity events, compared to AF patients. The differential manifestations of thromboembolism sequelae and mortality between AF and VTE patients merit further investigation