The progenitor and central engine of a peculiar GRB 230307A

Recently, a lack of supernova-associated long-duration gamma-ray burst (GRB 230307A) at such a low redshift $z=0.065$, but associated with a possible kilonova emission, has attracted great attention. Its heavy element nucleosynthesis and the characteristic of soft X-ray emission suggests that the central engine of GRB 230307A is magnetar which is originated from a binary compact star merger. The calculated lower value of $\varepsilon \sim 0.05$ suggests that the GRB 230307A seems to be with ambiguous progenitor. The lower value of $f_{\rm eff}=1.23$ implies that the GRB 230307A is not likely to be from the effect of "tip of iceberg". We adopt the magnetar central engine model to fit the observed soft X-ray emission with a varying efficiency and find that the parameters constraints of magnetar fall into a reasonable range, i.e., $B<9.4\times10^{15}$ G and $P<2.5$ ms for $\Gamma_{\rm sat} = 10^3$, and $B<3.6\times10^{15}$ G and $P<1.05$ ms for $\Gamma_{\rm sat} = 10^4$. Whether the progenitor of GBR 230307A is from the mergers of neutron star - white dwarf (NS - WD) or neutron star - neutron star (NS - NS) remains unknown.Comment: 7 pages, 1 table, 4 figures. Accepted for publication in ApJ Letters, 962:L27, 202

A predictive scoring system for proximal junctional kyphosis after posterior internal fixation in elderly patients with chronic osteoporotic vertebral fracture: A single-center diagnostic study

ObjectiveTo establish a predictive scoring system for proximal junctional kyphosis (PJK) after posterior internal fixation in elderly patients with chronic osteoporotic vertebral fracture (COVF).Materials and methodsThe medical records of 88 patients who were diagnosed with COVF and underwent posterior internal fixation in our hospital from January 2013 to December 2017 were retrospectively analyzed. The included patients were divided into two groups according to whether they suffered PJK after surgery, namely, the PJK group (25 cases) and non-PJK group (63 cases). The following clinical characteristics were recorded and analyzed: age, gender, body mass index (BMI), bone mineral density (BMD), smoking history, fracture segment, proximal junction angle, sagittal vertebral axis, pelvic incidence (PI)–lumbar lordosis (LL), pelvic tilt (PT), sacral slope (SS), posterior ligamentous complex (PLC) injury, upper instrumented vertebra, lower instrumented vertebra, and the number of fixed segments. The prevalence of these clinical characteristics in the PJK group was evaluated, and the scoring system was established using logistic regression analysis. The performance of the scoring system was also prospectively validated.ResultsThe predictive scoring system was established based on five clinical characteristics confirmed as significant predictors of PJK, namely, age &gt; 70 years, BMI &gt; 28 kg/m2, BMD &lt; −3.5 SD, preoperative PI-LL &gt; 20°, and PLC injury. PJK showed a significantly higher score than non-PJK (7.80 points vs. 2.83 points, t=9.556, P&lt;0.001), and the optimal cutoff value for the scoring system was 5 points. The sensitivity and specificity of the scoring system for predicting postoperative PJK were 80.00% and 88.89%, respectively, in the derivation set and 75.00% and 80.00% in the validation set.ConclusionThe predictive scoring system was confirmed with satisfactory sensitivity and specificity in predicting PJK after posterior internal fixation in elderly COVF patients. The risk of postoperative PJK in patients with a score of 6–11 is high, while the score of 0–5 is low

Cigarette Smoke Extract Stimulates Rat Pulmonary Artery Smooth Muscle Cell Proliferation via PKC-PDGFB Signaling

Accumulating evidence suggests a direct role for cigarette smoke in pulmonary vascular remodeling, which contributes to the development of pulmonary hypertension. However, the molecular mechanisms underlying this process remain poorly understood. Platelet-derived growth factor (PDGF) is a potential mitogen and chemoattractant implicated in several biological processes, including cell survival, proliferation, and migration. In this study, we investigated the effect of cigarette smoke extract (CSE) on cell proliferation of rat pulmonary artery smooth muscle cells (rPASMCs). We found that stimulation of rPASMCs with CSE significantly increased cell proliferation and promoted cell cycle progression from G1 phase to the S and G2 phases. CSE treatment also significantly upregulated the mRNA and protein levels of PDGFB and PDGFRβ. Our study also revealed that Rottlerin, an inhibitor of PKCδ signaling, prevented CSE-induced cell proliferation, attenuated the increase of S and G2 phase populations induced by CSE treatment, and downregulated PDGFB and PDGFRβ mRNA and protein levels in rPASMCs exposed to CSE. Collectively, our data demonstrated that CSE-induced cell proliferation of rPASMCs involved upregulation of the PKCδ-PDGFB pathway

N′-[1-(4-Amino­phen­yl)ethyl]pyrazine-2-carbohydrazide

The title compound, C13H13N5O, crystallizes with two mol­ecules in the asymmetric unit. The crystal structure is stabilized by intra­molecular N—H⋯N and N—H⋯O hydrogen bonds. The dihedral angles between the pyrazine ring and the 4-aminolphenyl ring are 2.5 (1) and 6.5 (1)° in the two molecules

The Other Press, February 19, 1987

<p>Energy profile (in kcal.mol^-1) of face-on path for Erlotinib bioactivation by the Cpd I model of CYP3A4 and 1A2 in the gas and solvent phases.</p

Salmonella Outer Protein B Suppresses Colitis Development via Protecting Cell From Necroptosis

Salmonella effectors translocated into epithelial cells contribute to the pathogenesis of infection. They mediate epithelial cell invasion and subsequent intracellular replication. However, their functions in vivo have not been well-identified. In this study, we uncovered a role for Salmonella outer protein B (SopB) in modulating necroptosis to facilitate bacteria escape epithelial cell and spread to systemic sites through a Salmonella-induced colitis model. Mice infected with SopB deleted strain ΔsopB displayed increased severity to colitis, reduced mucin expression and increased bacterial translocation. In vitro study, we found there was an increased goblet cell necroptosis following ΔsopB infection. Consistently, mice infected with ΔsopB had a strong upregulation of mixed lineage kinase domain-like (MLKL) phosphorylation. Deletion of MLKL rescued severity of tissue inflammatory, improved mucin2 expression and abolished the increased bacterial translocation in mice infected with ΔsopB. Intriguingly, the expression of sopB in LS174T cells was downregulated. The temporally regulated SopB expression potentially switched the role from epithelial cell invasion to bacterial transmission. Collectively, these results indicated a role for SopB in modulating the onset of necroptosis to increased bacteria pathogenesis and translocated to systemic sites