The Impact of a Very-Low-Calorie Ketogenic Diet on Monocyte Subsets of Patients with Obesity: A Pilot Study.

Obesity is closely linked to chronic low-grade inflammation and the development of cardio-metabolic comorbidities. Monocyte subsets, which are crucial in immune responses, have been reported to be altered in individuals with obesity, potentially exacerbating inflammation. Although very-low-calorie ketogenic diets (VLCKDs) are recognized for their efficacy in promoting weight loss and improving metabolic health, their impact on circulating monocyte subsets remains poorly understood.

A Novel Homozygous Mutation Causes Ovarian Dysgenesis and Primary Amenorrhea.

Context: Despite a growing number of studies, the genetic etiology in many cases of ovarian dysgenesis is incompletely understood.

Objectives: This work aimed to study the genetic etiology causing absence of spontaneous pubertal development, hypergonadotropic hypogonadism, and primary amenorrhea in 2 sisters.

Methods: Whole-exome sequencing was performed on DNA extracted from peripheral lymphocytes of 2 Palestinian sisters born to consanguineous parents.

A Ketogenic Diet Followed by Gradual Carbohydrate Reintroduction Restores Menstrual Cycles in Women with Polycystic Ovary Syndrome with Oligomenorrhea Independent of Body Weight Loss: Results from a Single-Center, One-Arm, Pilot Study.

: Polycystic ovary syndrome (PCOS) is a common endocrine disorder in women of fertile age. Some studies suggest that a ketogenic diet (KD) may have a role in treating PCOS. We aimed to demonstrate the long-term effectiveness of a KD in PCOS.

PARP1 Characterization as a Potential Biomarker for p190+ Acute Lymphoblastic Leukemia.

Detection of t(9;22), and consequent fusion, is still a marker of worse prognosis for acute lymphoblastic leukemia (ALL), with resistance to tyrosine-kinase inhibitor therapy being a major obstacle in the clinical practice for this subset of patients. In this study, we investigated the effectiveness of targeting poly-ADP-ribose polymerase (PARP) in a model of p190+ ALL, the most common isoform to afflict ALL patients, and demonstrated the use of experimental PARP inhibitor (PARPi), AZD2461, as a therapeutic option with cytotoxic capabilities similar to that of imatinib, the current gold standard in medical care. We characterized cytostatic profiles, induced cell death, and biomarker expression modulation utilizing cell models, also providing a comprehensive genome-wide analysis through an aCGH of the model used, and further validated PARP1 differential expression in samples of ALL p190+ patients from local healthcare institutions, as well as in larger cohorts of online and readily available datasets.