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Abstract SN 2023ehl, a normal Type Ia supernova with a typical decline rate, was discovered in the galaxy UGC 11555 and offers valuable insights into the explosion mechanisms of white dwarfs. We present a detailed analysis of SN 2023ehl, including spectroscopic and photometric observations. The supernova exhibits high-velocity features in its ejecta, which are crucial for understanding the physical processes during the explosion. We compared the light curves of SN 2023ehl with other well-observed Type Ia supernovae, finding similarities in their evolution. The line strength ratioR(Siii) was calculated to be 0.17 ± 0.04, indicating a higher photospheric temperature compared to other supernovae. The maximum quasi-bolometric luminosity was determined to be 1.52 × 10⁴³erg s⁻¹, and the synthesized⁵⁶Ni mass was estimated at 0.77 ± 0.05M_⊙. The photospheric velocity atB-band maximum light was measured as 10,150 ± 240 km s⁻¹, classifying SN 2023ehl as a normal velocity Type Ia supernova. Our analysis suggests that SN 2023ehl aligns more with both the gravitationally confined detonation, providing a comprehensive view of the diversity and complexity of Type Ia supernovae. 

The female reproductive tract (FRT) is the most common site of infection during HIV transmission to women, but viral remodeling complicates characterization of cells targeted for infection. Here, we report extensive phenotypic analyses of HIV-infected endometrial cells by CyTOF, and use a ‘nearest neighbor’ bioinformatics approach to trace cells to their original pre-infection phenotypes. Like in blood, HIV preferentially targets memory CD4+ T cells in the endometrium, but these cells exhibit unique phenotypes and sustain much higher levels of infection. Genital cell remodeling by HIV includes downregulating TCR complex components and modulating chemokine receptor expression to promote dissemination of infected cells to lymphoid follicles. HIV also upregulates the anti-apoptotic protein BIRC5, which when blocked promotes death of infected endometrial cells. These results suggest that HIV remodels genital T cells to prolong viability and promote viral dissemination and that interfering with these processes might reduce the likelihood of systemic viral spread.