Canagliflozin prevents acute kidney Injury in euglycemics rats.

The aim of this study was to investigate the impact of canagliflozin on AKI caused by ischemia-reperfusion injury (IRI) in non-diabetic rats. Male Wistar rats weighing 250-300g were randomized into four groups: SHAM (rats subjected to sham renal ischemia-reperfusion surgery); CANA (canagliflozin by gavage, 200mg/kg, once, daily, 5 days); I/R: rats subjected to I/R- AKI (bilateral renal hilum clamping, 30 minutes); CANA+I/R: I/R rats that received canagliflozin 5 days prior to I/R. Evaluated parameters: renal function (serum creatinine [CrS], inulin clearance [inCl]; renal hemodynamics (mean arterial pressure [MAP], renal blood flow [RBF], renal vascular resistance [RVR]); redox profile (urinary peroxides, lipid peroxidation, urinary nitrate, renal tissue thiols and nuclear factor erythroid 2-related factor 2 [Nrf2] protein expression), western blot for identification of SGLT2 in the kidneys and renal histology.

Mpox in a Patient With a Signal Transducer and Activator of Transcription 1 Gain-of-Function Mutation.

We report a case of mpox in a patient with a signal transducer and activator of transcription 1 gain-of-function mutation. Despite initial improvement with intravenous immune globulin and tecovirimat, severe symptoms developed and the patient died. This underscores the need for immune system optimization and effective virucidal treatments for mpox.

Donor-Derived Ehrlichiosis Caused by Ehrlichia chaffeensis from Living Donor Kidney Transplant.

Tickborne infections are challenging to diagnose, particularly among solid organ transplant recipients. We report a US case of donor-derived ehrlichiosis from a living kidney donation that highlights how screening for living donors may miss tickborne infections. Clinicians should consider the epidemiology of the donor when screening donations and evaluating recipients for donor-derived infection.

Calcium (Ca) fluxes at mitochondria-ER contact sites (MERCS) are a new target of senolysis in therapy-induced senescence (TIS).

Therapy-induced senescence (TIS) alters calcium (Ca²⁺) flux and Mitochondria-ER Contact Sites (MERCS), revealing critical vulnerabilities in senescent cells. In this study, TIS was induced using Doxorubicin and Etoposide, resulting in an increased MERCS contact surface but a significant reduction in ER-mitochondria Ca²⁺ flux. Mechanistically, TIS cells exhibit decreased expression of IP3R isoforms and reduced interaction between type 1 IP3R and VDAC1, impairing Ca²⁺ transfer.

Experience of Biology Degree students in the recognition of tissue alterations in human histopathological samples.

Introduction: The analysis of histological images plays a fundamental role in studying pathological alterations associated with human diseases, especially in the context of practical teaching. However, in the Biology Degree programme there is a lack of practical activities based on the study of human histological preparations.

Material And Methods: A collaboration with an Anatomical Pathology department was established for this project, which aimed to carry out an innovative practice based on the study of human biopsies in the subject of Cell Biology and Cellular Pathology of the Biology Degree programme.