The aim of this work was to study effects of mild preconditioning hypobaric hypoxia (380 Torr for 2 h, repeated 3 or 6 times spaced at 24 h) on brain NGFI-A immunoreactivity and passive avoidance (PA) behavior in rats exposed to severe hypoxia (160 Torr for 3 h). Severe hypobaric hypoxia produced extensive neuronal loss in hippocampal CA1, while the preceding hypoxic preconditioning had clear protective effect on neuronal viability of vulnerable hippocampal cells. Besides, the hypoxic preconditioning prevented impairment of acquisition and retention of PA caused by severe hypoxia. The six-trial hypobaric preconditioning was more effective in protection against PA learning deficits in severe hypoxia exposed rats than the three-trial preconditioning. The preconditioning up-regulated severe hypoxia-suppressed neocortical and hippocampal expression of NGFI-A, suggesting a possible role for NGFI-A in the neuroprotective mechanisms activated by hypoxic preconditioning.
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http://dx.doi.org/10.1016/j.bbr.2004.11.023 | DOI Listing |
Curr Cancer Drug Targets
January 2025
Division of Pharmacology, Guru Nanak Institute of Pharmaceutical Science and Technology, Kolkata, 700114, India.
Immune checkpoint blockade (ICB) has fundamentally transformed cancer treat-ment by unlocking the potency of CD8+ T cells by targeting the suppression of the CTLA-4 and PD-1/PD-L1 pathways. Nevertheless, ICBs are associated with the risk of severe side effects and resistance in certain patients, driving the search for novel and safer immune check-point modulators. Monoamine Oxidase A (MAO-A) plays an unexpected role in the field of cancer.
View Article and Find Full Text PDFNat Sci Sleep
December 2024
Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, People's Republic of China.
Objective: There is a connection between obstructive sleep apnea (OSA) and coronary microvascular dysfunction (CMD), but the underlying mechanisms remain unclear. This study aims to evaluate the correlation between OSA-related nocturnal hypoxemia parameters and CMD.
Methods: This is an observational, single-center study that included patients who underwent polysomnography and coronary angiography during hospitalization.
Front Vet Sci
December 2024
School of Veterinary Medicine, College of Bio-Resources and Agriculture, Institute of Veterinary Clinical Science, National Taiwan University, Taipei, Taiwan.
Introduction: Hypoxia-inducible factors (HIF) regulate gene transcription, which aids hypoxia adaptation while promoting renal fibrosis. Non-transferrin-bound iron (NTBI) is a catalytic form of iron that can lead to oxidative damage. However, NTBI in cat biofluids has rarely been evaluated.
View Article and Find Full Text PDFCardiovasc Drugs Ther
January 2025
State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, First Affiliated Hospital of Xinjiang Medical University, Clinical Medical Research Institute, Xinjiang Medical University, No. 137 Liyushan South Road, Urumqi, 830054, China.
Purpose: To investigate the protective effect and mechanism of enhanced expression of endogenous macrophage migration inhibitory factor (MIF) on cardiac ischemia-reperfusion (I/R) injury.
Methods: A recombinant double-stranded adeno-associated virus serotype 9 with MIF or green fluorescent protein (GFP) genes (dsAAV9-MIF/GFP) was transduced into mice and neonatal rat ventricular myocytes (NRVMs). The models of cardiac 60 min ischemia and 24 h reperfusion and 12 h hypoxia/12 h reoxygenation (H/R) were established in mice and NRVMs, respectively.
Br J Haematol
January 2025
Laboratoire de Cytologie Clinique et Cytogénétique, LBMR néoplasies myéloprolifératives, CHU CAREMEAU, Nîmes, France.
Hereditary congenital erythrocytosis results from constitutive activation of the hypoxia pathway. This pathway is controlled by regulation of the α isoforms of the hypoxia-inducible factor α/β heterodimer, notably via hydroxylation by prolyl hydroxylase domain 2 (PHD2). Mutations affecting PHD2 are involved in Type 3 erythrocytosis.
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