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Myocardial damage significantly impacts the prognosis of patients with cancer; however, the mechanisms of myocardial damage induced by cancer and its treatment remain unknown. We previously reported that medium-chain fatty acids (MCFAs) improve cancer-induced myocardial damage but did not evaluate the differences in effect according to MCFA type. Therefore, this study investigated the role of inflammatory cytokines in cancer-induced myocardial damage and the effects of three types of MCFAs (caprylic acid [C8], capric acid [C10], and lauric acid [C12]). In a mouse model, the C8 diet showed a greater effect on improving myocardial damage compared with C10 and C12 diets. Myocardial tubes differentiated from H9C2 cardiomyoblasts demonstrated increased mitochondrial oxidative stress, decreased membrane potential and mitochondrial volume, and inhibited myocardial tube differentiation following treatment with high-mobility group box-1 (HMGB1) but not interleukin-6 and tumor necrosis factor-α cytokines. However, HMGB1 treatment combined with C8 improved HMGB1-induced mitochondrial damage, enhanced autophagy, and increased mitochondrial biogenesis and maturation. However, these effects were only partial when combined with beta-hydroxybutyrate, a C8 metabolite. Thus, HMGB1 may play an important role in cancer-related myocardial damage. C8 counteracts HMGB1's effects and improves cancer-related myocardial damage. Further clinical studies are required to investigate the effects of C8. [ABSTRACT FROM AUTHOR]

Nutritional interventions are one focus of sarcopenia treatment. As medium-chain fatty acids (MCFAs) are oxidized in the mitochondria and produce energy through oxidative phosphorylation (OXPHOS), they are key parts of nutritional interventions. We investigated the in vitro effects of three types of MCFA, caprylic acid (C8), capric acid (C10), and lauric acid (C12), in skeletal muscle cells. Compared with C10 and C12, C8 promoted mitophagy through the phosphatase and tensin homolog (PTEN)-induced kinase 1-Parkin pathway and increased the expression of peroxisome proliferator-activated receptor gamma coactivator 1-α and dynamin-related protein 1 to reduce mitochondrial oxidative stress and promote OXPHOS. Furthermore, the expression of myogenic differentiation 1 and myosin heavy chain increased in myotubes, thus promoting muscle differentiation and maturation. These results suggest that C8 improves mitochondrial quality and promotes skeletal muscle maturation; in contrast, C10 and C12 poorly promoted mitochondrial quality control and oxidative stress and suppressed energy production. Future animal experiments are required to establish the usefulness of C8 for nutritional interventions for sarcopenia. [ABSTRACT FROM AUTHOR]

Mini-EUSO is the first mission of the JEM-EUSO program on board the International Space Station. It was launched in 2019 and it is currently located in the Russian section (Zvezda module) of the station and viewing our planet from a nadir-facing UV-transparent window. The instrument is based on the concept of the original JEM-EUSO mission and consists of an optical system employing two Fresnel lenses and a focal surface composed of 36 Multi-Anode Photomultiplier tubes, 64 channels each, for a total of 2304 channels with single photon counting sensitivity and an overall field of view of 44° × 44°. Mini-EUSO can map the night-time Earth in the near UV range (predominantly between 290 nm and 430 nm), with a spatial resolution of about 6.3 km and different temporal resolutions of 2.5 µ, 320 µs and 41 ms. Mini-EUSO observations are extremely important to better assess the potential of a space-based detector in studying Ultra-High Energy Cosmic Rays (UHECRs) such as K-EUSO and POEMMA. In this contribution we focus the attention on UV measurements, the observation of clouds and of certain categories of events that Mini-EUSO triggers with the shortest temporal resolution. We place them in the context of UHECR observations from space, namely the estimation of exposure and sensitivity to Extensive Air Showers.

Mini-EUSO is a wide Field-of-View (FoV, 44°) telescope currently in operation from a nadir-facing UV-transparent window in the Russian Zvezda module on the International Space Station (ISS). It is the first detector of the JEM-EUSO program deployed on the ISS, launched in August 2019. The main goal of Mini-EUSO is to measure the UV emissions from the ground and atmosphere, using an orbital platform. Mini-EUSO is mainly sensitive in the 290–430 nm bandwidth. Light is focused by a system of two Fresnel lenses of 25 cm diameter each on the Photo-Detector-Module (PDM), which consists of an array of 36 Multi-Anode Photomultiplier Tubes (MAPMTs), arranged in blocks of 2 × 2 called Elementary Cells (ECs), for a total of 2304 pixels working in photon counting mode, in three different time resolutions of 2.5 µs (defined as 1 Gate Time Unit, GTU), 320 µs and 40.96 ms operating in parallel. In the longest time scale, the data is continuously acquired to monitor the UV emission of the Earth. It is best suited for the observation of ground sources and therefore has been used for the observational campaigns of the ground-based UV flasher in order to perform an end-to-end calibration of Mini-EUSO. In this contribution, the assembled UV flasher, the operation of the field campaign and the analysis of the obtained data are presented. The result is compared with the overall effi ciency computed from the expectations which takes into account the atmospheric attenuation and the parametrisation of different effects such as the optics effi ciency, the MAPMT detection effi ciency, BG3 filter transmittance and the transparency of the ISS window.

This article discusses a study that examined the effects of cancer on the heart muscle. The study compared tissue samples from elderly patients with and without cancer and found that cancer patients had reduced cellular recycling and increased oxidative stress in the heart muscle. These findings suggest that cancer may contribute to heart dysfunction and aging in the heart muscle. However, the study acknowledges the need for more research to fully understand these mechanisms. [Extracted from the article]

Pancreatic ductal adenocarcinoma (PDAC) is highly malignant, with a 5-year survival rate of less than 10%. Furthermore, the acquisition of anticancer drug resistance makes PDAC treatment difficult. We established MIA-GEM cells, a PDAC cell line resistant to gemcitabine (GEM), a first-line anticancer drug, using the human PDAC cell line—MIA-PaCa-2. Microtubule-associated serine/threonine kinase-4 (MAST4) expression was increased in MIA-GEM cells compared with the parent cell line. Through inhibitor screening, dysregulated AKT signaling was identified in MIA-GEM cells with overexpression of AKT3. MAST4 knockdown effectively suppressed AKT3 overexpression, and both MAST4 and AKT3 translocation into the nucleus, phosphorylating forkhead box O3a (FOXO3) in MIA-GEM cells. Modulating FOXO3 target gene expression in these cells inhibited apoptosis while promoting stemness and proliferation. Notably, nuclear MAST4 demonstrated higher expression in GEM-resistant PDAC cases compared with that in the GEM-sensitive cases. Elevated MAST4 expression correlated with a poorer prognosis in PDAC. Consequently, nuclear MAST4 emerges as a potential marker for GEM resistance and poor prognosis, representing a novel therapeutic target for PDAC. [ABSTRACT FROM AUTHOR]