Explore the vast range of titles available.

This review summarizes the current understanding of how brevetoxins, produced by Karenia brevis during harmful algal blooms, impact sea turtle health. Sea turtles may be exposed to brevetoxins through ingestion, inhalation, maternal transfer, and potentially absorption through the skin. Brevetoxins bind to voltage-gated sodium channels in the central nervous system, disrupting cellular function and inducing neurological symptoms in affected sea turtles. Moreover, the current evidence suggests a broader and longer-term impact on sea turtle health beyond what is seen during stranding events. Diagnosis relies on the detection of brevetoxins in tissues and plasma from stranded turtles. The current treatment of choice, intravenous lipid emulsion therapy, may rapidly reduce symptoms and brevetoxin concentrations, improving survival rates. Monitoring, prevention, and control strategies for harmful algal blooms are discussed. However, as the frequency and severity of blooms are expected to increase due to climate change and increased environmental pollution, continued research is needed to better understand the sublethal effects of brevetoxins on sea turtles and the impact on hatchlings, as well as the pharmacokinetic mechanisms underlying brevetoxicosis. Moreover, research into the optimization of treatments may help to protect endangered sea turtle populations in the face of this growing threat.

Unusual ocular abnormalities were documented in 3 wild eastern screech owls (Megascops asio) presented to a wildlife rehabilitation hospital after vehicular strike-induced trauma to the head. All 3 had anterior uveitis and free air bubbles in the anterior chamber, but none of the cases had any discernable corneal damage, either grossly or with fluorescein stain technique. Perforation of the globe at the level of the scleral ossicle was considered a possible cause. All 3 cases recovered with standard treatment for anterior uveitis, and the free air was absorbed within 10–14 days and did not appear to cause any lingering complications. The owls were later released back into the wild after demonstrating the ability to navigate obstacles in a flight cage and capture live prey.

Compensatory growth (CG) is accelerated growth that occurs when food availability increases after food restriction. This rapid growth may be associated with sublethal consequences. In this study, we investigated the effects of food restriction and subsequent realimentation and CG on bone structure in juvenile green turtles (Chelonia mydas). Turtles were fed ad libitum food for 12 weeks (AL), restricted food for 12 weeks (R), or restricted food for 5 weeks followed by ad libitum food for 7 weeks (R-AL). R-AL turtles demonstrated partial CG via enhanced food conversion efficiency (FCE) upon realimentation. After the 12th week, gross morphology (GM), microarchitecture, and mineralization of the right humerus of each turtle were analyzed. Many GM measurements (including proximal and maximal bone lengths, bone widths, and shaft thickness), most measurements of bone microarchitecture (excluding cortical and trabecular thickness and trabecular separation), and all mineralization measurements were labile in response to intake. We examined the possibility that changes in nutrient allocation to bone structure during realimentation facilitated CG in previously food-restricted turtles. Restoration of bone lengths was prioritized over restoration of bone widths during CG. Furthermore, restoration of trabecular number, connectivity density, and bone volume fraction was prioritized over restoration of cortical bone volume fraction. Finally, diaphyseal bone mineralization was partially restored, whereas no restoration of epiphyseal bone mineralization occurred during CG. Shifts in nutrient allocation away from certain bone attributes during food restriction that were not rectified when food availability increased probably provided an energy surplus that enhanced the conversion of food to growth and thus powered the CG response. Our study revealed how resource allocation to various bone attributes is prioritized as nutritional conditions change during development. These “priority rules” may have detrimental consequences later in life, indicating that conservation of green turtle foraging grounds should be given high priority.

Urtica dioica (UD), commonly known as “stinging nettle”, is a herbaceous flowering plant that is a widely used agent in traditional medicine worldwide. Several formulations of UD leaf extract have been reported to exhibit anti-inflammatory and antioxidant properties, with anticancer potential. The current study investigated the possible anticancer properties of nettle tea, prepared from Urtica dioica leaves, on acute myeloid leukemia (AML) cell lines, and deciphered the underlying molecular mechanisms. Treatment of AML cell lines (U-937 and KG-1) with UD aqueous leaf extract resulted in a dose- and time-dependent inhibition of proliferation, an increase in apoptotic hallmarks such as phosphatidylserine flipping to the outer membrane leaflet, and DNA fragmentation as revealed by cell-death ELISA and cell-cycle analysis assays. Apoptosis induction in U937 cells involves alterations in the expression of Bax and Bcl-2 upon exposure to nettle tea. Furthermore, the chemical composition of UD aqueous extract indicated the presence of multiple chemical agents, such as flavonoids and phenolics, mainly patuletin, m/p-hydroxybenzoic acid, and caffeic acid, among others, to which the pro-apoptotic and anti-tumor effects may be attributed.

Similar to tumor-initiating cells (TICs), minimal residual disease (MRD) is capable of reinitiating tumors and causing recurrence. However, the molecular characteristics of solid tumor MRD cells and drivers of their survival have remained elusive. Here we performed dense multiregion transcriptomics analysis of paired biopsies from 17 ovarian cancer patients before and after chemotherapy. We reveal that while MRD cells share important molecular signatures with TICs, they are also characterized by an adipocyte-like gene expression signature and a portion of them had undergone epithelial-mesenchymal transition (EMT). In a cell culture MRD model, MRD-mimic cells showed the same phenotype and were dependent on fatty acid oxidation (FAO) for survival and resistance to cytotoxic agents. These findings identify EMT and FAO as attractive targets to eradicate MRD in ovarian cancer and make a compelling case for the further testing of FAO inhibitors in treating MRD.

In epithelial ovarian cancer (EOC), carboplatin/cisplatin-induced chemoresistance is a major hurdle to successful treatment. Aerobic glycolysis is a common characteristic of cancer. However, the role of glycolytic metabolism in chemoresistance and its impact on clinical outcomes in EOC are not clear. Here, we show a functional interaction between the key glycolytic enzyme hexokinase II (HKII) and activated P-p53 (Ser15) in the regulation of bioenergetics and chemosensitivity. Using translational approaches with proximity ligation assessment in cancer cells and human EOC tumor sections, we showed that nuclear HKII–P-p53 (Ser15) interaction is increased after chemotherapy, and functions as a determinant of chemoresponsiveness as a prognostic biomarker. We also demonstrated that p53 is required for the intracellular nuclear HKII trafficking in the control of glycolysis in EOC, associated with chemosensitivity. Mechanistically, cisplatin-induced P-p53 (Ser15) recruits HKII and apoptosis-inducing factor (AIF) in chemosensitive EOC cells, enabling their translocation from the mitochondria to the nucleus, eliciting AIF-induced apoptosis. Conversely, in p53-defective chemoresistant EOC cells, HKII and AIF are strongly bound in the mitochondria and, therefore, apoptosis is suppressed. Collectively, our findings implicate nuclear HKII–P-p53(Ser15) interaction in chemosensitivity and could provide an effective clinical strategy as a promising biomarker during platinum-based therapy.