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Background: Mitochondrial genes are involved in tumor metabolism in ovarian cancer (OC) and affect immune cell infiltration and treatment responses.

Aim: To predict prognosis and immunotherapy response in patients diagnosed with OC using mitochondrial genes and neural networks.

Methods: Prognosis, immunotherapy efficacy, and next-generation sequencing data of patients with OC were downloaded from The Cancer Genome Atlas and Gene Expression Omnibus.

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ATP synthase dysregulation has been implicated in many diseases, including cancer and neurodegenerative diseases. Whilst ATP synthase-targeting compounds have been reported, most are large or polar compounds and lack appropriate properties for a CNS drug. We designed, synthesised, and evaluated a novel series of ATP synthase targeting compounds, resulting in a 1,3,4-oxadiazin-5-one scaffold with improved physiochemical properties.

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Avian parasites can be pathogenic to their vertebrate hosts. Although cases of anaemia are frequently reported in parasitized birds, the potential damage caused by the parasite during the exoerythrocytic reproduction phase remains poorly investigated. Here, we report 2 individuals of red-legged seriemas () infected with 2 different lineages of , one of them exhibiting potential malarial-compatible tissue lesions in the spleen, liver, brain and lungs, alongside molecular confirmation of parasite presence in the spleen.

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Modelling the human Coenzyme Q deficiency in Drosophila melanogaster.

Free Radic Biol Med

January 2025

Centro Andaluz de Biología del Desarrollo, Universidad Pablo de Olavide-CSIC-JA, Sevilla, Spain; CIBERER, U729, Instituto de Salud Carlos III, Madrid, Spain. Electronic address:

The interference of the expression of each of the genes involved in the synthesis of coenzyme Q (CoQ) in Drosophila melanogaster can help to understand the pathophysiology of CoQ-dependent mitochondrial diseases in humans. We have knocked-down all genes involved in the CoQ biosynthesis pathway at different temperatures to induce depletion of CoQ at different levels throughout the body and in a tissue-specific manner. The efficiency of the knockdowns was quantified by Q-RTPCR and determination of CoQ levels by HPLC-UV+ECD.

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One hallmark of cancer is the upregulation and dependency on glucose metabolism to fuel macromolecule biosynthesis and rapid proliferation. Despite significant pre-clinical effort to exploit this pathway, additional mechanistic insights are necessary to prioritize the diversity of metabolic adaptations upon acute loss of glucose metabolism. Here, we investigated a potent small molecule inhibitor to Class I glucose transporters, KL-11743, using glycolytic leukemia cell lines and patient-based model systems.

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