We present results of an experimental study, in which benthic foraminiferal faunas have been kept under strongly hypoxic conditions. Sixteen short sediment cores from a 35m deep site in the Adriatic Sea were incubated for a maximum of 69days. Some of the cores were air-bubbled and remained well oxygenated throughout the experiment. The other cores were bubbled with nitrogen; the overlying waters of these cores became strongly hypoxic, whereas the sediment remained virtually without oxygen. Live foraminifera have been inventoried with the CellTracker Green method. Our results show that all dominant taxa survive strongly hypoxic conditions. Nouria polymorphinoides and Nonionella turgida show a clear tendency to move to the sediment surface in the nitrogen-bubbled cores, whereas Bulimina spp. and Eggerella scabra do not show such a migrational response. We suggest that this is a response to the concentration of nutritional resources at the sediment-water interface.
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http://dx.doi.org/10.1016/j.marpolbul.2009.08.015 | DOI Listing |
PLoS One
January 2025
School of Clinical Medicine, Guizhou Medical University, Guiyang, China.
Legg-Calvé-Perthes disease (LCPD) involves femoral head osteonecrosis caused by disrupted blood supply, leading to joint deformity and early osteoarthritis. This study investigates the role of miRNA-223-5p in regulating hypoxia-induced apoptosis and enhancing osteogenesis in bone marrow mesenchymal stem cells (BMSCs). Utilizing a juvenile New Zealand white rabbit model of LCPD established through femoral neck ligation, we transfected BMSCs with miR-223-5p mimics, inhibitors, and controls, followed by hypoxic exposure.
View Article and Find Full Text PDFJ Biomed Mater Res B Appl Biomater
February 2025
Bioassays and Cellular Dynamics Lab, Department of Chemical and Biological Sciences, Institute of Biosciences, UNESP: São Paulo State University, São Paulo, Brazil.
Calcium phosphates, notably monetite, are valued biomaterials for bone applications owing to their osteogenic properties and rapid uptake by bone cells. This study investigates the enhancement of these properties through Cobalt doping, which is known to induce hypoxia and promote bone cell differentiation. Heat treatments at 700°C, 900°C, and 1050°C are applied to both monetite and Cobalt-doped monetite, facilitating the development of purer, more crystalline phases with varied particle sizes and optimized cellular responses.
View Article and Find Full Text PDFNephrology (Carlton)
February 2025
Department of Quality Management, Tianjin Blood Center, Tianjin, China.
Aim: To study the effect and elucidate the underlying mechanisms of VDAC1-ΔC on autophagy in renal tubular epithelial cells injured by hypoxia/reoxygenation.
Methods: C57/BL6 mice were randomly divided into groups: sham operation group, IRI 1d group and IRI 2d group. The inner canthal blood of mice was collected to detect the levels of serum creatinine and urea nitrogen and kidney tissues were sampled, and sections were stained with Periodic acid-Schiff for morphological evaluation.
Int Ophthalmol
January 2025
Department of Ophthalmology, Xingtai People's Hospital, Xingtai, 054001, Hebei, China.
Background: Retinopathy of prematurity (ROP) is a major cause of childhood blindness worldwide, highlighted by retinal neovascularization. Ubiquitin is present throughout the retina. The deubiquitinating enzyme ubiquitin-specific protease 39 (USP39) has been reported to be involved in angiogenesis.
View Article and Find Full Text PDFNeuromolecular Med
January 2025
Biochemistry and Molecular Biology Laboratory, Department of Zoology, Institute of Science, Banaras Hindu University, Varanasi, 221 005, India.
Hypoxia is a significant stressor, and stabilized hypoxia-inducible factor-1α (HIF-1α) regulates the expression of numerous genes, leading to various biochemical, molecular, physiological and genomic changes. The body's oxygen-sensing system activates gene expression to protect brain tissues from hypoxia. Gamma-aminobutyric acid, an inhibitory neurotransmitter, regulates brain excitability during hypoxia through the activation of HIF-1 α.
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