Birthrates and delay times of Type Ia supernovae

Type Ia supernovae (SNe Ia) play an important role in diverse areas of astrophysics, from the chemical evolution of galaxies to observational cosmology. However, the nature of the progenitors of SNe Ia is still unclear. In this paper, according to a detailed binary population synthesis study, we obtained SN Ia birthrates and delay times from different progenitor models, and compared them with observations. We find that the Galactic SN Ia birthrate from the double-degenerate (DD) model is close to those inferred from observations, while the birthrate from the single-degenerate (SD) model accounts for only about 1/2-2/3 of the observations. If a single starburst is assumed, the distribution of the delay times of SNe Ia from the SD model is a weak bimodality, where the WD + He channel contributes to the SNe Ia with delay times shorter than 100Myr, and the WD + MS and WD + RG channels to those with age longer than 1Gyr.Comment: 11 pages, 2 figures, accepted by Science in China Series G (Dec.30, 2009

Higher fibrinogen and neutrophil-to-lymphocyte ratio are associated with the early poor response to intravenous thrombolysis in acute ischemic stroke

BackgroundInflammation and platelet activation play pivotal roles in acute ischemic stroke (AIS) pathogenesis. Early response to thrombolysis is a vital indicator for the long-term prognosis of AIS. However, the correlation between fibrinogen or the neutrophil-to-lymphocyte ratio (NLR) and the early response to intravenous thrombolysis in patients with AIS remains unclear.MethodsAIS patients undergoing intravenous thrombolysis were enrolled between January 2018 and May 2023. Blood cell counts were sampled before thrombolysis. A good response was defined as a National Institutes of Health Stroke Scale (NIHSS) score decreased ≥4 or complete recovery 24 h after thrombolysis treatment. A poor response was defined as any increase in the NIHSS score or a decrease in the NIHSS score <4 at the 24 h after thrombolysis treatment compared with that at admission. Logistic regression analysis was performed to explore the relationship of the fibrinogen level and NLR with a poor thrombolysis response. Receiver operating characteristic (ROC) analysis was used to assess the ability of the fibrinogen level and NLR to discriminate poor responders.ResultsAmong 700 recruited patients, 268 (38.29%) were diagnosed with a good response, and 432 (61.71%) were diagnosed with a poor response to intravenous thrombolysis. A binary logistic regression model indicated that an elevated fibrinogen level (odds ratio [OR], 1.693; 95% confidence interval [CI] 1.325–2.122, P < 0.001) and NLR (OR, 1.253; 95% CI, 1.210–2.005, P = 0.001) were independent factors for a poor response. The area under the curve (AUC) values for the fibrinogen level, NLR and fibrinogen level combined with the NLR for a poor response were 0.708, 0.605, and 0.728, respectively.ConclusionsOur research indicates that the levels of fibrinogen and NLR at admission can be used as a prognostic factor to predict early poor response to intravenous thrombolysis

The impact of human EGFR kinase domain mutations on lung tumorigenesis and in vivo sensitivity to EGFR-targeted therapies

SummaryTo understand the role of human epidermal growth factor receptor (hEGFR) kinase domain mutations in lung tumorigenesis and response to EGFR-targeted therapies, we generated bitransgenic mice with inducible expression in type II pneumocytes of two common hEGFR mutants seen in human lung cancer. Both bitransgenic lines developed lung adenocarcinoma after sustained hEGFR mutant expression, confirming their oncogenic potential. Maintenance of these lung tumors was dependent on continued expression of the EGFR mutants. Treatment with small molecule inhibitors (erlotinib or HKI-272) as well as prolonged treatment with a humanized anti-hEGFR antibody (cetuximab) led to dramatic tumor regression. These data suggest that persistent EGFR signaling is required for tumor maintenance in human lung adenocarcinomas expressing EGFR mutants

5-hydroxymethylcytosine is dynamically regulated during forebrain organoid development and aberrantly altered in Alzheimer’s disease

5-hydroxymethylcytosine (5hmC) undergoes dynamic changes during mammalian brain development, and its dysregulation is associated with Alzheimer's disease (AD). The dynamics of 5hmC during early human brain development and how they contribute to AD pathologies remain largely unexplored. We generate 5hmC and transcriptome profiles encompassing several developmental time points of healthy forebrain organoids and organoids derived from several familial AD patients. Stage-specific differentially hydroxymethylated regions demonstrate an acquisition or depletion of 5hmC modifications across developmental stages. Additionally, genes concomitantly increasing or decreasing in 5hmC and gene expression are enriched in neurobiological or early developmental processes, respectively. Importantly, our AD organoids corroborate cellular and molecular phenotypes previously observed in human AD brains. 5hmC is significantly altered in developmentally programmed 5hmC intragenic regions in defined fetal histone marks and enhancers in AD organoids. These data suggest a highly coordinated molecular system that may be dysregulated in these early developing AD organoids

Impacts of Duck-Origin Parvovirus Infection on Cherry Valley Ducklings From the Perspective of Gut Microbiota

Duck-origin goose parvovirus (D-GPV) is the causative agent of beak atrophy and dwarfism syndrome (BADS), characterized by growth retardation, skeletal dysplasia, and persistent diarrhea. However, the pathogenic mechanism of D-GPV remains undefined. Here, we first reported the gut microbiome diversity of D-GPV infected Cherry Valley ducks. In the investigation for the influence of D-GPV infection on gut microbiota through a period of infection, we found that D-GPV infection caused gut microbiota dysbiosis by reducing the prevalence of the dominant genera and decreasing microbial diversity. Furthermore, exfoliation of the intestinal epithelium, proliferation of lymphocytes, up-regulated mRNA expression of pro-inflammatory TNF-α, IL-1β, IL-6, IL-17A, and IL-22 and down-regulated mRNA expression of anti-inflammatory IL-10 and IL-4 occurred when D-GPV targeted in cecal epithelium. In addition, the content of short chain fatty acids (SCFAs) in cecal contents was significantly reduced after D-GPV infection. Importantly, the disorder of pro-inflammatory and anti-inflammatory cytokines was associated with the decrease of SCFAs-producing bacteria and the enrichment of opportunistic pathogens. Collectively, the decrease of SCFAs and the enrichment of pathogen-containing gut communities promoted intestinal inflammatory injury. These results may provide a new insight that target the gut microbiota to understand the progression of BADS disease and to research the pathogenic mechanism of D-GPV

Hybrid Space Division Multiple Access and Quasi-Orthogonal Multiple Access for Multi-User Underwater Visible Light Communication

Due to severe inter-beam interference and high cost of conventional full space division multiple access (SDMA)-based multi-user underwater visible light communication (MU-UVLC) systems, partial SDMA has been considered to substantially reduce inter-beam interference and costs by enabling closely located users to share the same light beam. Moreover, non-orthogonal multiple access (NOMA) is generally adopted to multiplex users in the same beam. However, for users with similar channel gains, the use of NOMA may suffer from severe error propagation. To this end, we propose and demonstrate a hybrid SDMA and quasi-orthogonal multiple access (QOMA) scheme for performance enhancement of partial SDMA-based MU-UVLC systems. Simulation and experimental results show that, in two-user UVLC system applying hybrid SDMA/QOMA, the bit error rate (BER) performance of the near user can be substantially improved and a much wider range of effective power allocation ratio can be achieved compared with that using conventional hybrid SDMA/NOMA

Comparison of Ferroptosis-Inhibitory Mechanisms between Ferrostatin-1 and Dietary Stilbenes (Piceatannol and Astringin)

Synthetic arylamines and dietary phytophenolics could inhibit ferroptosis, a recently discovered regulated cell death process. However, no study indicates whether their inhibitory mechanisms are inherently different. Herein, the ferroptosis-inhibitory mechanisms of selected ferrostatin-1 (Fer-1) and two dietary stilbenes (piceatannol and astringin) were compared. Cellular assays suggested that the ferroptosis-inhibitory and electron-transfer potential levels decreased as follows: Fer-1 >> piceatannol > astringin; however, the hydrogen-donating potential had an order different from that observed by the antioxidant experiments and quantum chemistry calculations. Quantum calculations suggested that Fer-1 has a much lower ionization potential than the two stilbenes, and the aromatic N-atoms were surrounded by the largest electron clouds. By comparison, the C4′O-H groups in the two stilbenes exhibited the lowest bond disassociation enthalpies. Finally, the three were found to produce corresponding dimer peaks through ultra-performance liquid chromatography coupled with electrospray ionization quadrupole time-of-flight tandem mass spectrometry analysis. In conclusion, Fer-1 mainly depends on the electron transfer of aromatic N-atoms to construct a redox recycle. However, piceatannol and astringin preferentially donate hydrogen atoms at the 4′-OH position to mediate the conventional antioxidant mechanism that inhibits ferroptosis, and to ultimately form dimers. These results suggest that dietary phytophenols may be safer ferroptosis inhibitors for balancing normal and ferroptotic cells than arylamines with high electron-transfer potential