Genetic manipulation of bacteriophage T4 utilizing the CRISPR-Cas13b system.

CRISPR-Cas type II and type V systems are inefficient in modifying bacteriophage T4 genome, due to hypermodification of its DNA. Here, we present a genome editing technique for bacteriophage T4 using the type VI CRISPR-Cas system. Using BzCas13b targeting of T4 phage, we were able to individually delete both T4 glucosyl transferase genes, and .

Concurrent High-Grade Serous Carcinoma with Mucinous Differentiation and Ectopic Complete Molar Pregnancy of the Fallopian Tube: A Case Report.

Objective: We report the first documented case of concurrent ectopic complete hydatidiform mole (CHM) and high-grade serous carcinoma (HGSC) of the fallopian tube, associated with unique histologic features and mutations in the HGSC.

Case Report: The patient presented with pelvic pain and vaginal bleeding. Laboratory examination revealed a positive urine pregnancy test and high serum beta-human chorionic gonadotropin (β-hCG).

Herpes virus entry mediator signaling blockade produces mortality in neonatal sepsis through induced cardiac dysfunction.

Introduction: Sepsis remains a major source of morbidity and mortality in neonates, and characterization of immune regulation in the neonatal septic response remains limited. HVEM is a checkpoint regulator which can both stimulate or inhibit immune responses and demonstrates altered expression after sepsis. We hypothesized that signaling via HVEM would be essential for the neonatal response to sepsis, and that therefore blockade of this pathway would improve survival to septic challenge.

Real-time monitoring of replication errors' fate reveals the origin and dynamics of spontaneous mutations.

The efficiency of replication error repair is a critical factor governing the emergence of mutations. However, it has so far been impossible to study this efficiency at the level of individual cells and to investigate if it varies within isogenic cell populations. In addition, why some errors escape repair remains unknown.