Endogenous p53 inhibitor TIRR dissociates systemic metabolic health from oncogenic activity.

It is unclear whether metabolic health corresponds to reduced oncogenesis or vice versa. We study Tudor-interacting repair regulator (TIRR), an inhibitor of p53 binding protein 1 (53BP1)-mediated p53 activation, and the physiological consequences of enhancing tumor suppressor activity. Deleting TIRR selectively activates p53, significantly protecting against cancer but leading to a systemic metabolic imbalance in mice.

'Nowhere and no one is safe': spatial analysis of damage to critical civilian infrastructure in the Gaza Strip during the first phase of the Israeli military campaign, 7 October to 22 November 2023.

Background: Since the Hamas attacks in Israel on 7 October 2023, the Israeli military has launched an assault in the Gaza Strip, which included over 12,000 targets struck and over 25,000 tons of incendiary munitions used by 2 November 2023. The objectives of this study include: (1) the descriptive and inferential spatial analysis of damage to critical civilian infrastructure (health, education, and water facilities) across the Gaza Strip during the first phase of the military campaign, defined as 7 October to 22 November 2023 and (2) the analysis of damage clustering around critical civilian infrastructure to explore broader questions about Israel's adherence to International Humanitarian Law (IHL).

Methods: We applied multi-temporal coherent change detection on Copernicus Sentinel 1-A Synthetic Aperture Radar (SAR) imagery to detect signals indicative of damage to the built environment through 22 November 2023.

Clearance of p16Ink4a-positive cells in a mouse transgenic model does not change β-cell mass and has limited effects on their proliferative capacity.

Type 2 diabetes is partly characterized by decreased β-cell mass and function which have been linked to cellular senescence. Despite a low basal proliferative rate of adult β-cells, they can respond to growth stimuli, but this proliferative capacity decreases with age and correlates with increased expression of senescence effector, p16Ink4a. We hypothesized that selective deletion of p16Ink4a-positive cells would enhance the proliferative capacity of the remaining β-cells due to the elimination of the local senescence-associated secretory phenotype (SASP).

Diabetes mellitus correlates with increased biological age as indicated by clinical biomarkers.

Chronological age (CA) is determined by time of birth, whereas biological age (BA) is based on changes on a cellular level and strongly correlates with morbidity, mortality, and longevity. Type 2 diabetes (T2D) associates with increased morbidity and mortality; thus, we hypothesized that BA would be increased and calculated it from biomarkers collected at routine clinical visits. Deidentified data was obtained from three cohorts of patients (20-80 years old)-T2D, type 1 diabetes (T1D), and prediabetes-and compared to gender- and age-matched non-diabetics.