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Today, food safety and quality are some of the main concerns of consumer and health agencies around the world. Our current lifestyle and market globalization have led to an increase in the number of people affected by food poisoning. Foodborne illness and food poisoning have different origins (bacteria, virus, parasites, mold, contaminants, etc.), and some cases of food poisoning can be traced back to chemical and natural toxins. One of the toxins targeted by the Food and Drug Administration (FDA) and European Food Safety Authority (EFSA) is the biogenic amine histamine. Biogenic amines (BAs) in food constitute a potential public health concern due to their physiological and toxicological effects. The consumption of foods containing high concentrations of biogenic amines has been associated with health hazards. In recent years there has been an increase in the number of food poisoning cases associated with BAs in food, mainly in relation to histamines in fish. We need to gain a better understanding of the origin of foodborne disease and how to control it if we expect to keep people from getting ill. Biogenic amines are found in varying concentrations in a wide range of foods (fish, cheese, meat, wine, beer, vegetables, etc.), and BA formation is influenced by different factors associated with the raw material making up food products, microorganisms, processing, and conservation conditions. Moreover, BAs are thermostable. Biogenic amines also play an important role as indicators of food quality and/or acceptability. Hence, BAs need to be controlled in order to ensure high levels of food quality and safety. All of these aspects will be addressed in this review.

Sensory analysis examines the properties (texture, flavor, taste, appearance, smell, etc [...]

This review summarises the main sensory methods (traditional techniques and the most recent ones) together with consumer research as a key part in the development of new products, particularly meat products. Different types of sensory analyses (analytical and affective), from conventional methods (Quantitative Descriptive Analysis) to new rapid sensory techniques (Check All That Apply, Napping, Flash Profile, Temporal Dominance of Sensations, etc.) have been used as crucial techniques in new product development to assess the quality and marketable feasibility of the novel products. Moreover, an important part of these new developments is analysing consumer attitudes, behaviours, and emotions, in order to understand the complex consumer–product interaction. In addition to implicit and explicit methodologies to measure consumers’ emotions, the analysis of physiological responses can also provide information of the emotional state a food product can generate. Virtual reality is being used as an instrument to take sensory analysis out of traditional booths and configure conditions that are more realistic. This review will help to better understand these techniques and to facilitate the choice of the most appropriate at the time of its application at the different stages of the new product development, particularly on meat products.

Multiple myeloma (MM) is a hematological malignancy characterized by frequent chromosome abnormalities. However, the molecular basis for this genome instability remains unknown. Since both impaired and hyperactive double strand break (DSB) repair pathways can result in DNA rearrangements, we investigated the functionality of DSB repair in MM cells. Repair kinetics of ionizing-radiation (IR)-induced DSBs was similar in MM and normal control lymphoblastoid cell lines, as revealed by the comet assay. However, four out of seven MM cell lines analyzed exhibited a subset of persistent DSBs, marked by γ-H2AX and Rad51 foci that elicited a prolonged G2/M DNA damage checkpoint activation and hypersensitivity to IR, especially in the presence of checkpoint inhibitors. An analysis of the proteins involved in DSB repair in MM cells revealed upregulation of DNA-PKcs, Artemis and XRCC4, that participate in non-homologous end joining (NHEJ), and Rad51, involved in homologous recombination (HR). Accordingly, activity of both NHEJ and HR were elevated in MM cells compared to controls, as determined by in vivo functional assays. Interestingly, levels of proteins involved in a highly mutagenic, translocation-promoting, alternative NHEJ subpathway (Alt-NHEJ) were also increased in all MM cell lines, with the Alt-NHEJ protein DNA ligase IIIα, also overexpressed in several plasma cell samples isolated from MM patients. Overactivation of the Alt-NHEJ pathway was revealed in MM cells by larger deletions and higher sequence microhomology at repair junctions, which were reduced by chemical inhibition of the pathway. Taken together, our results uncover a deregulated DSB repair in MM that might underlie the characteristic genome instability of the disease, and could be therapeutically exploited.

This paper studies the changes that occur in free amino acid and biogenic amine contents of raw meats (beef, pork, lamb, chicken and turkey) during storage (2 °C, 10 days). The meat cuts samples were harvested from a retail outlet (without getting information on the animals involved) as the following: Beef leg (four muscles), pork leg (five muscles), lamb leg (seven muscles), turkey leg (four muscles), and chicken breast (one muscle). Meat composition varied according to meat types. In general, pH, microbiology counts, biogenic amine (BA), and free amino acid (FAA) contents were also affected by meat types and storage time (p < 0.05). Chicken and turkey presented the highest levels (p < 0.05) of FAAs. Total free amino acids (TFAA) were higher (p < 0.05) in white meats than in red ones. The behavior pattern, of the total free amino acids precursors (TFAAP) of Bas, was saw-toothed, mainly in chicken and turkey meat during storage, which limits their use as quality indexes. Spermidine and spermine contents were initially different among the meats. Putrescine was the most prevalent BA (p < 0.05) irrespective of species. In general, chicken and turkey contained the highest (p < 0.05) levels of BAs, and TFAAP of BAs. In terms of the biogenic amine index (BAI), the quality of chicken was the worst while beef meat was the only sample whose quality remained acceptable through the study. This BAI seems to be more suitable as a quality index for white meat freshness than for red meat, especially for beef.

The p53 pathway is inactivated in the majority of human cancers. Although this perturbation frequently occurs through the mutation or deletion of p53 itself, there are other mechanisms that can attenuate the pathway and contribute to tumorigenesis. For example, overexpression of important p53 negative regulators, such as murine double minute 2 (MDM2) or murine double minute 4 (MDM4), epigenetic deregulation, or even alterations in TP53 mRNA splicing. In this work, we will review the different mechanisms of p53 pathway inhibition in cancer with special focus on multiple myeloma (MM), the second most common hematological malignancy, with low incidence of p53 mutations/deletions but growing evidence of indirect p53 pathway deregulation. Translational implications for MM and cancer prognosis and treatment are also reviewed.

The DNA damage response (DDR), a set of signaling pathways for DNA damage detection and repair, maintains genomic stability when cells are exposed to endogenous or exogenous DNA-damaging agents. Alterations in these pathways are strongly associated with cancer development, including ovarian cancer (OC), the most lethal gynecologic malignancy. In OC, failures in the DDR have been related not only to the onset but also to progression and chemoresistance. It is known that approximately half of the most frequent subtype, high-grade serous carcinoma (HGSC), exhibit defects in DNA double-strand break (DSB) repair by homologous recombination (HR), and current evidence indicates that probably all HGSCs harbor a defect in at least one DDR pathway. These defects are not restricted to HGSCs; mutations in ARID1A, which are present in 30% of endometrioid OCs and 50% of clear cell (CC) carcinomas, have also been found to confer deficiencies in DNA repair. Moreover, DDR alterations have been described in a variable percentage of the different OC subtypes. Here, we overview the main DNA repair pathways involved in the maintenance of genome stability and their deregulation in OC. We also recapitulate the preclinical and clinical data supporting the potential of targeting the DDR to fight the disease.

Inherited mutations in BRCA1 are among the primary causes of hereditary breast and ovarian cancer (HBOC). Genetic testing has identified numerous pathogenic and benign mutations in BRCA1 , but also thousands of variants of uncertain significance (VUS) with unclear functional consequences. Accurate cancer risk prediction for carriers of these VUS requires functional assays to assess their pathogenicity. In this study, we analyzed 16 BRCA1 VUS detected at the Hereditary Cancer Genetic Counseling Laboratory in Salamanca, Spain, with the goal of providing additional data to guide their reclassification. Since homologous recombination (HR) is the primary tumor-suppressive function of BRCA1 , we employed two complementary HR repair assays to evaluate HR efficiency. The first, an already established assay, uses a HeLa-DR cell line harboring an HR reporter cassette and involves silencing endogenous BRCA1 followed by complementation with the VUS under study. The second, developed in this work, is also based in complementation assays that restore the green fluorescence protein (GFP) gene, and employs a breast cancer cell line with a similar HR reporter system (HCC1937-HR) that lacks BRCA1 expression, allowing direct complementation. Both assays consistently identified five VUS (p.V11G, p.H888Y, p.G1201S, p.Q1395R, and p.F1734L) as pathogenic due to significantly reduced HR efficiency, whereas the remaining 11 VUS were benign in terms of HR function. Notably, two pathogenic variants (p.H888Y, p.G1201S) were located outside the known functional domains of BRCA1. The five HR-deficient variants were further evaluated for their sensitivity to ionizing radiation, which confirmed the deleterious impact on DNA repair for variants p.V11G, p.H888Y, p.G1201S and p.F1734L. Sensitivity to the PARP inhibitor olaparib revealed hypersensitivity only in cells expressing p.V11G and p.F1734L, suggesting variant-specific mechanistic effects with potential therapeutic relevance. In conclusion, recombination-based functional assays complemented with sensitivity assays are effective tools for assessing the pathogenicity of BRCA1 VUS and can provide valuable information to support clinical decision-making. We propose that these assays can be completed within a timeframe compatible with clinical needs, offering critical insights for genetic counseling and personalized treatment strategies.

Ethanol consumption triggers oxidative stress by generating reactive oxygen species (ROS) through its metabolites. This process leads to steatosis and liver inflammation, which are critical for the development of alcoholic liver disease (ALD). Autophagy is a regulated dynamic process that sequesters damaged and excess cytoplasmic organelles for lysosomal degradation and may counteract the harmful effects of ROS-induced oxidative stress. These effects include hepatotoxicity, mitochondrial damage, steatosis, endoplasmic reticulum stress, inflammation, and iron overload. In liver diseases, particularly ALD, macroautophagy has been implicated as a protective mechanism in hepatocytes, although it does not appear to play the same role in stellate cells. Beyond the liver, autophagy may also mitigate the harmful effects of alcohol on other organs, thereby providing an additional layer of protection against ALD. This protective potential is further supported by studies showing that drugs that interact with autophagy, such as rapamycin, can prevent ALD development in animal models. This systematic review presents a comprehensive analysis of the literature, focusing on the role of autophagy in oxidative stress regulation, its involvement in organ–organ crosstalk relevant to ALD, and the potential of autophagy-targeting therapeutic strategies.