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ACUTE HYPERGLYCEMIA INDUCES PODOCYTE APOPTOSIS BY MONOCYTE TNF-α RELEASE, A PROCESS ATTENUATED BY VITAMIN D AND GLP-1 RECEPTOR AGONISTS.
J Steroid Biochem Mol Biol
January 2025
Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA; Department of Medicine, VA Medical Center, St. Louis, MO, USA; Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO, USA. Electronic address:
Targeting optimal glycemic control based on hemoglobin A1c (A1c) values reduces but does not abolish the onset of diabetic kidney disease and its progression to chronic kidney disease (CKD). This suggests that factors other than the average glucose contribute to the residual risk. Vitamin D deficiency and frequent episodes of acute hyperglycemia (AH) are associated with the onset of albuminuria and CKD progression in diabetes.
View Article and Find Full Text PDFChapter 4: DIFFERENTIAL DIAGNOSIS of PRIMARY HYPERPARATHYROIDISM.
Ann Endocrinol (Paris)
January 2025
Service d'Endocrinologie, Diabétologie, Métabolisme, Nutrition; Hôpital Huriez, CHU Lille; Inserm U1190, Institut Génomique Européen pour le Diabète, Université de Lille, F-59000 Lille, France. Electronic address:
The differential diagnosis of primary hyperparathyroidism can be considered clinically, biologically and radiologically. Clinically, primary hyperparathyroidism should be suspected in case of diffuse pain, renal lithiasis, osteoporosis, repeated fracture, cognitive or psychiatric disorder, or disturbance of consciousness. Nevertheless, the differential diagnosis of primary hyperparathyroidism is mainly biological, particularly in atypical forms, which must be differentiated from hypercalcemia with hypocalciuria or non- elevated PTH on the one hand, and from normo-calcemia with elevated PTH, hypophosphatemia or hypercalciuria on the other.
View Article and Find Full Text PDFLow maternal iodine intake and subsequent risk of pharmacologically treated hypertension: A population-based prospective cohort study.
Clin Nutr
January 2025
Department of Food Safety, Centre of Sustainable Diets, Norwegian Institute of Public Health, P.O. Box 222, NO-0213 Oslo, Norway. Electronic address:
Background & Aims: Iodine deficiency is linked to multiple adverse health outcomes, but there is scarce knowledge regarding iodine intake and development of chronic hypertension. We aimed to investigate the prospective association between habitual dietary iodine intake and pharmacologically treated hypertension in mothers up to 10 years after delivery.
Methods: The present study is based on data from an ongoing pregnancy cohort and includes 58,629 women without thyroid dysfunction and hypertension at baseline.
Impact of Fli1 deletion on B cell populations: A focus on age-associated B cells and transcriptional dynamics.
J Dermatol Sci
December 2024
Department of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan; Department of Dermatology, Tohoku University Graduate School of Medicine, Sendai, Japan. Electronic address:
Background: Altered Fli1 expression is associated with various autoimmune diseases, yet its impact on B cells remains unexplored.
Objective: This study investigated the direct effects of Fli1 depletion on B cell populations, focusing on age-associated B cells (ABCs).
Methods: Splenocytes of Fli1 BcKO (Cd19-Cre; Fli1) and Cd19-Cre mice were analyzed flow cytometrically.
Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis.
Cell Rep
January 2025
Department of Basic Medical Sciences, School of Medicine, Xiamen University, Xiamen, Fujian, P.R. China; State Key Laboratory of Cellular Stress Biology, Xiamen University, Xiamen, Fujian, P.R. China. Electronic address:
Menin is a scaffold protein encoded by the Men1 gene, and it interacts with a variety of chromatin regulators to activate or repress cellular processes. The potential importance of menin in immune regulation remains unclear. Here, we report that myeloid deletion of Men1 results in the development of spontaneous pulmonary alveolar proteinosis (PAP).
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