Rosa Zaragozá

Anatomical knowledge is fundamental to the training of students enrolled in health sciences degree programs. Although the use of images is common in anatomy teaching, it remains unclear whether progressive autonomous exposure to cadaveric images improves student performance in assessments based on cadaveric material. The aim of this study was to evaluate the effectiveness of high‐quality cadaveric images for teaching visceral anatomy to first‐year medical students at the University of Valencia, focusing on their impact on cadaver‐based practical performance. High‐quality images of dissections from the head, neck, and thoracic regions were obtained and made available to students for self‐directed study and self‐assessment in preparation for the practical examination in the dissection room. A cross‐sectional comparative study was conducted in which two theoretical groups of students had access to the images ( n = 180), while two additional groups served as controls ( n = 182). A second analysis was also performed within the intervention groups using online quizzes to evaluate knowledge acquisition, together with a survey assessing student satisfaction with the learning materials. Results showed a significant improvement in online quizzes and practical exam questions with images' aid, indicating enhanced knowledge acquisition. Furthermore, students with access to the images achieved significantly higher scores in the practical examination than those in the control groups. These findings suggest that structured digital resources that support independent learning can improve knowledge acquisition and performance in cadaver‐based assessments. Such resources may be particularly valuable in contexts where access to cadaveric material or teaching time is limited. image

Reduced lactation after forced weaning induces a tumor-promoting environment in the mammary gland, triggering key regulatory nodes common to both post-lactation involution and breast cancer, including calpains and miRs. We investigated how lactation duration modulates these nodes using two murine models: short lactation (forced weaning) and prolonged lactation (spontaneous-weaning). Additionally, the role of inflammation in calpain regulation was assessed in forced-weaned NOS-2 knockout mice. Morphological and molecular analysis in mammary tissue included histochemical staining, qPCR, enzymatic activity, Western blot and miRNA-seq. Mammary gland involution after prolonged lactation resulted in milder inflammation, reduced cell death and tissue remodeling, and lower collagen deposition compared to short lactation. The expression, activity and function of calpain-2 was found to be more sensitive to the model of lactation and inflammatory environment compared to calpain-1. Even after full regression (28 days postpartum), prolonged lactation maintained lower calpain-2 levels and higher expression of tumor suppressors miR-10b and miR-143/145. These persistent molecular differences suggest spontaneous weaning as the optimal model for healthy mammary gland regression, whereas forced weaning sustains alterations in calpain-2 and regulatory miRs that may increase post-partum breast cancer risk. The potential long-term influence of lactation duration on breast cancer development warrants further consideration in both clinical and public health contexts.

The lungs play a vital role in maintaining homeostasis by facilitating gas exchange and serving as a structural and immune barrier. External factors, including nutrition, lifestyle, and environmental exposures, profoundly influence normal lung function and contribute to the development, progression, and prognosis of various respiratory diseases. Deficiencies in key micronutrients, such as vitamins A, D, and C, as well as omega-3 fatty acids, can impair the integrity of the epithelial lining, compromising the lungs’ defense mechanisms and increasing susceptibility to injury and disease. Obesity and physical inactivity further disrupt respiratory function by inducing structural changes in the chest wall and promoting a pro-inflammatory state. Environmental pollutants further worsen oxidative damage and activate inflammatory pathways. Addressing these modifiable factors through interventions such as dietary optimization, physical activity programs, and strategies to reduce environmental exposure offers promising avenues for preserving lung function and preventing disease progression. This review examines the molecular pathways through which nutrition, lifestyle, and environmental influences impact lung homeostasis.

Traditional human anatomy teaching relies on face-to-face models, although new methodologies based on virtual platforms can enhance autonomous learning. However, the specific type of online tools preferred by the students remains unclear. This study compared student engagement with two teaching tools: (1) online unidirectional lessons and (2) an interactive Instagram profile, @eldeanato. Both tools incorporated new anatomical illustrations and detailed dissection photographs. The Instagram profile included questionnaires via the Instagram stories quiz sticker. Students’ satisfaction was assessed by means of online surveys. Engagement with each of the interventions was evaluated using objective measures of web analytics: percentages of interaction with the questionnaires on Instagram and adding Google Analytics tools to the online lessons’ website code. Student satisfaction with both types of material was high, but the participative material had much higher engagement scores. The Instagram profile allowed continuous participation, with increasing followers and interaction levels. Our results show the importance of objective engagement measurements to evaluate the success of innovative teaching interventions. In order to increase student adherence, teaching interventions should be participative and integrated with popular social networks, like Instagram, even though this is a field that could be seen as estranged from academic teaching.

Human anatomy teaching has traditionally relied on lecture-based instruction and passive learning through cadaver prosections. However, contemporary educational frameworks demand a more active integration of practical experiences with anatomical knowledge. To maintain educational quality, innovative methods incorporating new technologies are being adopted within health sciences higher education. Such innovations require robust evaluation protocols that extend beyond student satisfaction surveys to accurately assess their effectiveness. This paper explores various strategies for educational innovation in human anatomy performed at the Department of Anatomy and Human Embryology of the Faculty of Medicine at the University of Valencia. The innovative interventions were based on teaching videos on the YouTube platform, an Instagram profile with interactive quizzes on the stories, gamification using the Kahoot! application and collaborative approaches based on movement simulations. Objective measurement tools are presented alongside satisfaction questionnaires in order to improve the evaluation of the success of the interventions. The teaching of human anatomy in health sciences continues to require face-to-face and active guidance of university professors, along with teaching on cadaveric dissections, to help the students visualize the anatomical structures and their functional relationship. In addition, educational innovation interventions are useful complements to promote the integration of anatomical knowledge, motivate students and develop transversal skills required for higher education competences.

Vitamin A deficiency (VAD) induced TGF-β hyperactivation and reduced expression of cell adhesion proteins in the lung, suggesting that the disruption of retinoic acid (RA) signaling leads to epithelial–mesenchymal transition (EMT). To elucidate the role of lung vitamin A status in EMT, several EMT markers and the expression of the proprotein convertase furin, which activates TGF-β, were analyzed in two experimental models. Our in vivo model included control rats, VAD rats, and both control rats and VAD rats, treated with RA. For the in vitro studies, human bronchoalveolar epithelial cells treated with RA were used. Our data show that EMT and furin are induced in VAD rats. Furthermore, furin expression continues to increase much more markedly after treatment of VAD rats with RA. In control rats and cell lines, an acute RA treatment induced a significant increase in furin expression, concomitant with changes in EMT markers. A ChIP assay demonstrated that RA directly regulates furin transcription. These results emphasize the importance of maintaining vitamin A levels within the physiological range since both levels below and above this range can cause adverse effects that, paradoxically, could be similar. The role of furin in EMT is discussed.

Calpain-1 and calpain-2 are calcium-dependent Cys-proteases ubiquitously expressed in mammalian tissues with a processive, rather than degradative activity. They are crucial for physiological mammary gland homeostasis as well as for breast cancer progression. A growing number of evidences indicate that their pleiotropic functions depend on the cell type, tissue and biological context where they are expressed or dysregulated. This review considers these standpoints to cover the paradoxical role of calpain-1 and -2 in the mammary tissue either, under the physiological conditions of the postlactational mammary gland regression or the pathological context of breast cancer. The role of both calpains will be examined and discussed in both conditions, followed by a brief snapshot on the present and future challenges for calpains, the two-gateway proteases towards tissue homeostasis or tumor development.

Background: Limb-girdle muscular dystrophy (LGMD) is a rare neuromuscular disease including a growing and heterogeneous number of subtypes with variable phenotype. Their clinical and histopathological characteristics frequently overlap with other neuromuscular dystrophies. Our goal was to identify, by a non-invasive method, a molecular signature including biochemical and epigenetic parameters with potential value for patient prognosis and stratification. Results: Circulating miRNome was obtained by smallRNA-seq in plasma from LGMD patients (n = 6) and matched-controls (n = 6). Data, validated by qPCR in LGMD samples, were also examined in other common muscular dystrophies: Duchenne (DMD) (n = 5) and facioscapulohumeral muscular dystrophy (FSHD) (n = 4). Additionally, biochemical and clinical parameters were analyzed. miRNome analysis showed that thirteen differentially expressed miRs could separate LGMD vs control group by hierarchical clustering. Most of differentially expressed miRs in LGMD patients were up-regulated (miR-122-5p, miR-122b-3p, miR-6511a-3p, miR-192-5p, miR-574-3p, mir-885-3p, miR-29a-3p, miR-4646-3p, miR-203a-3p and miR-203b-5p) whilst only three of sequenced miRs were significantly down-regulated (miR-19b-3p, miR-7706, miR-323b-3p) when compared to matched controls. Bioinformatic analysis of target genes revealed cell cycle, muscle tissue development, regeneration and senescence as the most affected pathways. Four of these circulating miRs (miR-122-5p, miR-192-5p, miR-19b-3p and miR-323b-3p), together with the myomiR miR-206, were further analysed by qPCR in LGMD, DMD and FSHD. The receiver operating characteristic curves (ROC) revealed high area under the curve (AUC) values for selected miRs in all groups, indicating that these miRs have good sensitivity and specificity to distinguish LGMD, DMD and FSHD patients from healthy controls. miR-122-5p, miR-192-5p and miR-323-3p were differentially expressed compared to matched-controls in all groups but apparently, each type of muscular dystrophy showed a specific pattern of miR expression. Finally, a strong correlation between miRs and biochemical data was only found in LGMD patients: while miR-192-5p and miR-122-5p negatively correlated with CK, miR-192-5p positively correlated with vitamin D3 and ALP. Conclusions: Although limited by the small number of patients included in this study, we propose here a specific combination of circulating miR-122-5p/miR-192-5p/miR-323-3 and biochemical parameters as a potential molecular signature whose clinical value for LGMD patient prognosis and stratification should be further confirmed in a larger cohort of patients.

Calpain-2 (CAPN2) is a processing enzyme ubiquitously expressed in mammalian tissues whose pleiotropic functions depend on the role played by its cleaved-products. Nuclear interaction networks, crucial for a number of molecular processes, could be modified by CAPN2 activity. However, CAPN2 functions in cell nucleus are poorly understood. To unveil CAPN2 functions in this compartment, the result of CAPN2-mediated interactions in cell nuclei was studied in breast cancer cell (BCC) lines. CAPN2 abundance was found to be determinant for its nucleolar localization during interphase. Those CAPN2-dependent components of nucleolar proteome, including the actin-severing protein cofilin-1 (CFL1), were identified by proteomic approaches. CAPN2 binding, cleavage and activation of LIM Kinase-1 (LIMK1), followed by CFL1 phosphorylation was studied. Upon CAPN2-depletion, full-length LIMK1 levels increased and CFL1/LIMK1 binding was inhibited. In addition, LIMK1 accumulated at the cell periphery and perinucleolar region and, the mitosis-specific increase of CFL1 phosphorylation and localization was altered, leading to aberrant mitosis and cell multinucleation. These findings uncover a mechanism for the role of CAPN2 during mitosis, unveil the critical role of CAPN2 in the interactions among nuclear components and, identifying LIMK1 as a new CAPN2-target, provide a novel mechanism for LIMK1 activation. CFL1 is crucial for cytoskeleton remodeling and mitosis, but also for the maintenance of nuclear structure, the movement of chromosomes and the modulation of transcription frequently altered in cancer cells. Consequently, the role of CAPN2 in the nuclear compartment might be extended to other actin-associated biological and pathological processes.

The blood-brain-barrier (BBB), present in brain capillaries, constitutes an essential barrier mechanism for normal functioning and development of the brain. The presence of tight junctions between adjacent endothelial cells restricts permeability and movement of molecules between extracellular fluid and plasma. The protein complexes that control cell-cell attachment also polarize cellular membrane, so that it can be divided into luminal (blood-facing) and abluminal (brain) sides, and each solute that enters/leaves the brain must cross both membranes. Several amino acid (AA) transport systems with different distributions on both sides of the BBB have been described. In a broad sense, there are at least five different systems of facilitative transporters and all of them are found in the luminal membrane. Some of these transporters are very specific for a small group of substrates and are located exclusively on the luminal side of the BBB. However, the two major facilitative carriers, system L and system y⁺, are located in both membranes, although asymmetrically. The position of these Na⁺-independent transporters ensures AA availability in the brain and also its bidirectional transport across the endothelial cells. On the other hand, there are several Na⁺-dependent transport systems that transport AAs against its concentration gradient together with the movement of Na⁺ ions. The majority of these active transporters are present exclusively at the abluminal membrane and are responsible for AA efflux from the brain into the endothelial cells. Since they are Na⁺-coupled, the sodium pump Na⁺/K⁺-ATPase is also highly expressed on this abluminal side of the BBB. Once inside the cell, the facilitative transporters located in the luminal membranes mediate export from the endothelial cell to the blood. In summary, the polarized distribution of these transport systems between the luminal and abluminal membranes, and the fact that more than one transporter may carry the same substrate, ensures supply and excretion of AAs in and out of the brain, thereby controlling its homeostasis and proper function.