Alzheimer's disease (AD) is marked by cognitive decline and retinal degeneration. This study aimed to explore the potential of dietary chub mackerel (Scomber colias), rich in docosahexaenoic acid (DHA) and vitamin B12, and quinoa, as a source of vitamin B9, to prevent or delay these effects in a 5XFAD mouse model of AD. Thirty-two five-week-old male mice were divided into four groups: control, 10% chub mackerel, 5% quinoa, and 10% chub mackerel plus 5% quinoa, over 28 weeks. After 28 weeks, behavioural tests confirmed that none of the tested diets induced confounding effects related to anxiety-like behaviour or motor impairment. The diet combining chub mackerel and quinoa improved selected memory-associated outcomes and protected retinal integrity (p < 0.05), particularly within the neural layers. This diet also improved the brain n-3/n-6 PUFA ratio, primarily by reducing n-6 PUFA levels rather than by a significant increase in DHA. These benefits likely result from the complementary effects of key nutrients, including DHA and vitamins B9 and B12. The preservation of retinal thickness observed with the combined diet supports the use of retinal layer assessment as a potential non-invasive readout of AD-associated neurodegeneration. These findings indicate that combining chub mackerel and quinoa may help mitigate selected neurodegenerative and retinal alterations in the 5XFAD model, positioning them as promising components of a dietary strategy to support neuroprotection and retinal health during AD-related decline.

The correlation between Alzheimer's disease (AD) and reduced neuronal docosahexaenoic acid (DHA, 22:6n-3) levels suggests that dietary strategies aimed at enhancing brain DHA could slow disease progression and ameliorate symptoms. Given the liver's central role in lipid metabolism, this study evaluated the impact of diets enriched in DHA (via chub mackerel, Scomber colias) and quinoa (Chenopodium quinoa) on the hepatic lipid profile and DHA accumulation in an AD mouse model. Thirty-two 5xFAD transgenic mice were assigned to four dietary groups: Control (standard AIN-93 M diet), Chub mackerel (CM; AIN-93 M + 10% chub mackerel), Quinoa (Q; AIN-93 M + 5% quinoa), and Chub mackerel + Quinoa (CM + Q; AIN-93 M + 10% chub mackerel + 5% quinoa). Although total lipid content remained similar across groups, the mice fed with Q diet had the highest hepatic triacylglycerols (TAG; 37.5 ± 6.9% of total lipids) when compared to CM and CM + Q groups (25.7 ± 2.0% and 29.0 ± 2.7%, respectively). The CM + Q group showed the most elevated hepatic n-3 polyunsaturated fatty acids (n-3 PUFA; 16.3 ± 2.8%) and DHA (12.2 ± 2.8%). DHA enrichment was observed only in TAG and free fatty acids from CM (7.5 ± 3.6% and 2.9 ± 1.2%, respectively) and CM + Q (8.2 ± 2.1% and 3.0 ± 1.0%, respectively). These findings indicate that combining quinoa with chub mackerel significantly enhances hepatic DHA accumulation and modulates lipid metabolism, presenting a promising dietary approach for managing AD-associated lipid dysregulation.

Pancreatic cancer is one of the most lethal and challenging malignancies. Its severity is primarily linked to the constitutively activated mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway. Aquaporins (AQPs) are frequently overexpressed in pancreatic cancer, playing crucial roles in cell signaling, and consequently promoting cell migration, proliferation, and invasion. Here, we investigate the transcriptomics of key players in epithelial-mesenchymal transition (EMT) and the MAPK/ERK signaling pathway in pancreatic cancer tissues, correlating them with tumor AQP expression to highlight their potential as diagnostic or prognostic tools. The transcriptomics analysis was conducted in 24 paired pancreatic tumors and adjacent healthy tissues, and analyses were performed considering the patients' age and gender, as well as tumor invasiveness and aggressiveness. Our results revealed strong positive Pearson correlation coefficients between AQP3 and c-Jun, and between AQP5 and CDH1/EGFR in pancreatic tumors but not in healthy tissues, with posterior in vitro confirmation in pancreatic cancer BxPC3 cells, suggesting a shift in the regulatory mechanisms of gene expression that certainly affect the physiology of the tissue, influencing cancer initiation and progression. This study underscores the interplay between AQPs and cancer signaling pathways, opening new avenues for defining novel clinical biomarkers and improving the early detection of pancreatic cancer.

Alzheimer’s disease (AD) is marked by cognitive decline, and also by retinal degeneration. Having in mind that docosahexaenoic acid (DHA, 22:6n − 3) is a safe, low-cost, and pivotal fatty acid for brain health and sustained cognitive function, this study exploits environmentally friendly non-fish sources as potential dietary supplements enriched with DHA to prevent or reverse AD. Forty 5xFAD transgenic male mice, aged five weeks old, were randomly distributed by five body weight-matched dietary groups (with eight animals each) and fed isocaloric diets based on the AIN-93M standard formulation for rodents for 6 months. Except for the control feed (without supplementation), each diet contained a modified lipidic fraction supplemented with 2% of the following: (1) linseed oil (LSO, rich in alpha-linolenic acid (ALA, 18:3n − 3)); (2) cod liver oil (fish oil, FO, rich in both DHA and eicosapentaenoic acid (EPA, 20:5n − 3)); (3) Schizochytrium sp. microalga oil (Schizo, with 40% of DHA); and (4) commercial DHASCO (DHASCO, with 70% of DHA). The aim of this study was to measure retinal neural layer thickness, calculate ganglion cell layer (GCL) density, and assess retinal injury by means of immunohistochemical staining for β-amyloid plaques deposition, TAU protein levels, and IBA1, as hallmark features of AD progression, in order to elucidate the effects of different dietary DHA treatments in Alzheimer’s retinas. Although no statistical differences were observed across retinal layer thicknesses depending on the diet (p > 0.05), there was a consistent pattern for slightly increased retinal thickness in 5xFAD mice fed fish oil relative to the others for the measurement of total layers, in general and for the inner segment/outer segment layer, the outer nuclear layer, the outer plexiform layer, the inner nuclear layer, and the inner plexiform layer, in particular. The ganglion cell layer (GCL) density was increased in 5xFAD mice fed the DHASCO oil diet relative to the control (p < 0.05), suggesting a benefit of DHA supplementation on the number of viable ganglion cells. No positive staining was observed for β-amyloid plaques deposition or the neuroinflammatory marker, IBA1, corroborating previous findings in human AD retinas. Conversely, the internal retinal layers showed intense TAU immunostaining. Immnunostained TAU area was significantly reduced in 5xFAD mice fed a fish oil diet compared to control (p < 0.05), although the number of TAU-positive cells did not differ across diets (p > 0.05). The retinal protected integrity derived from the benefits of DHA supplementation found, either from fish oil or DHASCO oil, underscores the potential of retinal biomarkers as non-invasive indicators of cognitive decline and overall brain health, opening new avenues for investigating AD pathophysiology in the retina.

Alzheimer’s disease (AD) is the most common cause of dementia, and no cure is currently available. The β-amyloid cascade of AD and neurofibrillary tangles are the basis of the current understanding of AD pathogenesis, driving drug investigation and other discoveries. Up until now, no AD models have entirely validated the β-amyloid cascade hypothesis. AD models must be capable of recapitulating the critical events of this pathology, including β-amyloid plaques and neurofibrillary tangles. The development of plaques is probably derived from the amyloid precursor protein (APP) and presenilin 1 (PS1) familial Alzheimer’s disease (FAD) mutations, while the tangle-like pathology is determined by tau mutations. Transgenic mouse models struggle to replicate the entire spectrum of AD, particularly neuronal death stemming from β-amyloid and tau pathologies. Furthermore, the success of these transgenic mice often relies on the overexpression of APP transgenes enclosing FAD-associated mutations at levels beyond physiological. Ultimate species-specific discrepancies in genome and protein composition between the human and the mouse may hinder the accurate recapitulation of AD pathological events in mouse models. Although none of the AD models fully mirrors human pathology, these experimental in vivo animal models have provided valuable insights into β-amyloid toxicity and the overall pathophysiological basis of AD. Therefore, these experimental models have been widely used in the preclinical evaluation of therapeutic strategies and have played a pivotal role in the development of immunotherapies for AD. In this review, we sum up the main transgenic mouse models used for AD research, whether they are APP mutation-based mice, APP plus presenilin mutation-based mice, or tau mutation-based mice. The specific characteristics of each mouse model and the significance of their use for AD research, focusing on their current advantages and disadvantages, as well as on the progress made and the forthcoming challenges in replicating this neurodegenerative disease, are also highlighted.

Alzheimer’s disease (AD) is the most common form of dementia, affecting over 50 million people globally. Since 1906, efforts to understand this neurodegenerative disease and to develop effective treatments have continued to this day. Recognizing docosahexaenoic acid (DHA, 22:6n-3) as a safe, inexpensive and vital nutrient for brain health and cognitive protection due to its key role in brain development and function, this study explores novel, sustainable non-fish sources as potential dietary supplements to prevent or mitigate AD, within a blue biotechnology framework. Forty 5×FAD male mice, five weeks old, were allocated to five body weight-matched dietary groups (n = 8) and fed isocaloric diets based on AIN-93M standard chow for 6 months. Each diet, except the control feed (non-supplemented group), enclosed a modified lipid fraction supplemented with 2% of the following: (1) linseed oil (LSO, rich in alpha-linolenic acid (ALA,18:3n-3)); (2) cod liver oil (fish oil, FO, rich in both DHA and eicosapentaenoic acid (EPA, 20:5n-3)); (3) Schizochytrium sp. microalga oil (Schizo) with 40% of DHA; and (4) commercial DHASCO oil (DHASCO) with 70% of DHA. The different diets did not affect (p > 0.05) growth performance criteria (e.g., final body weight, daily feed intake, and body weight gain) suggesting no effect on the overall caloric balance or mice growth, but n-3 long-chain polyunsaturated-fatty acid (n-3 LCPUFA) supplementation significantly reduced total cholesterol (p < 0.001) and total lipids (p < 0.001). No systemic inflammation was detected in 5×FAD mice. In parallel, a beneficial modulation of lipid metabolism by DHA-enriched diets was observed, with polyunsaturated fatty acid incorporation, particularly DHA, across key metabolic tissues, such as the liver (p < 0.001) and the brain (p < 0.001). No behavioural variations were detected using an open-field test after 6 months of diet (p > 0.05). While mice fed a standard diet or LSO diet showed cognitive deficit, the incorporation of FO, Schizo or DHASCO oils into dietary routine showed promising protective effects on the working memory (p < 0.05) and the last two diets also on the recognition memory (p < 0.05) Increased neuronal count (p < 0.05), reflecting neuronal survival, was clearly observed with the fish oil diet. In turn, the number of TAU-positive cells (p < 0.05) was reduced in the Schizo diet, while β-amyloid deposition (p < 0.01) and the neuroinflammatory marker, IBA1 (p < 0.05), were decreased across all DHA-enriched diets. These promising findings open new avenues for further studies focused on the protective effects of DHA derived from sustainable and underexploited Schizochytrium sp. microalga in the prevention of AD.

The impact of 15% dietary inclusion of Spirulina (Arthrospira platensis) in broiler chickens was explored, focusing on blood cellular components, systemic metabolites and hepatic lipid and mineral composition. From days 14 to 35 of age, 120 broiler chickens were divided and allocated into four dietary treatments: a standard corn and soybean meal-based diet (control), a 15% Spirulina diet, a 15% extruded Spirulina diet, and a 15% Spirulina diet super-dosed with an enzyme blend (0.20% porcine pancreatin plus 0.01% lysozyme). The haematological analysis revealed no significant deviations (p > 0.05) in blood cell counts across treatments, suggesting that high Spirulina inclusion maintains haematological balance. The systemic metabolic assessment indicated an enhanced antioxidant capacity in birds on Spirulina diets (p < 0.001), pointing toward a potential reduction in oxidative stress. However, the study noted a detrimental impact on growth performance metrics, such as final body weight and feed conversion ratio (both p < 0.001), in the Spirulina-fed treatments, with the super-dosed enzyme blend supplementation failing to alleviate these effects but with extrusion mitigating them. Regarding hepatic composition, birds on extruded Spirulina and enzyme-supplemented diets showed a notable increase in n-3 fatty acids (EPA, DPA, DHA) (p < 0.001), leading to an improved n-6/n-3 PUFA ratio (p < 0.001). Despite this positive shift, a reduction in total hepatic lipids (p = 0.003) was observed without a significant change in cholesterol levels. Our findings underscore the need for further exploration into the optimal inclusion levels, processing methods and potential enzymatic enhancements of Spirulina in broiler diets. Ultimately, this research aims to strike a balance between promoting health benefits and maintaining optimal growth performance in poultry nutrition.

Alzheimer’s disease (AD), the leading cause of dementia, presents a significant global health challenge with no known cure to date. Central to our understanding of AD pathogenesis is the β-amyloid cascade hypothesis, which underlies drug research and discovery efforts. Despite extensive studies, no animal models of AD have completely validated this hypothesis. Effective AD models are essential for accurately replicating key pathological features of the disease, notably the formation of β-amyloid plaques and neurofibrillary tangles. These pathological markers are primarily driven by mutations in the amyloid precursor protein (APP) and presenilin 1 (PS1) genes in familial AD (FAD) and by tau protein mutations for the tangle pathology. Transgenic mice models have been instrumental in AD research, heavily relying on the overexpression of mutated APP genes to simulate disease conditions. However, these models do not entirely replicate the human condition of AD. This review aims to provide a comprehensive evaluation of the historical and ongoing research efforts in AD, particularly through the use of transgenic mice models. It is focused on the benefits gathered from these transgenic mice models in understanding β-amyloid toxicity and the broader biological underpinnings of AD. Additionally, the review critically assesses the application of these models in the preclinical testing of new therapeutic interventions, highlighting the gap between animal models and human clinical realities. This analysis underscores the need for refinement in AD research methodologies to bridge this gap and enhance the translational value of preclinical studies.

The 5xFAD transgenic mouse model widely used in Alzheimer’s disease (AD) research recapitulates many AD-related phenotypes with a relatively early onset and aggressive age-dependent progression. Besides developing amyloid peptide deposits alongside neuroinflammation by the age of 2 months, as well as exhibiting neuronal decline by the age of 4 months that intensifies by the age of 9 months, these mice manifest a broad spectrum of behavioural impairments. In this review, we present the extensive repertoire of behavioural dysfunctions in 5xFAD mice, organised into four categories: motor skills, sensory function, learning and memory abilities, and neuropsychiatric-like symptoms. The motor problems, associated with agility and reflex movements, as well as balance and coordination, and skeletal muscle function, typically arise by the time mice reach 9 months of age. The sensory function (such as taste, smell, hearing, and vision) starts to deteriorate when amyloid peptide buildups and neuroinflammation spread into related anatomical structures. The cognitive functions, encompassing learning and memory abilities, such as visual recognition, associative, spatial working, reference learning, and memory show signs of decline from 4 to 6 months of age. Concerning neuropsychiatric-like symptoms, comprising apathy, anxiety and depression, and the willingness for exploratory behaviour, it is believed that motivational changes emerge by approximately 6 months of age. Unfortunately, numerous studies from different laboratories are often contradictory on the conclusions drawn and the identification of onset age, making preclinical studies in rodent models not easily translatable to humans. This variability is likely due to a range of factors associated with animals themselves, housing and husbandry conditions, and experimental settings. In the forthcoming studies, greater clarity in experimental details when conducting behavioural testing in 5xFAD transgenic mice could minimise the inconsistencies and could ensure the reliability and the reproducibility of the results.

Structured lipids (SLs) offer a promising avenue for designing novel formulations enriched in n-3 long-chain polyunsaturated fatty acids (LCPUFAs) with potential health benefits. Triacylglycerols (TAGs), the most common fats in the human diet, are both non-toxic and chemically stable. The metabolic efficiency and digestibility of TAGs are significantly influenced by the position of fatty acids (FAs) within the glycerol backbone, with FAs at the sn-2 position being readily absorbed. Over the past two decades, advancements in SL research have led to the development of modified TAGs, achieved either through chemical or enzymatic processes, resulting in SLs. The ideal structure of SLs involves medium-chain FAs at the sn-1,3 positions and long-chain n-3 LCPUFAs at the sn-2 position of the glycerol backbone, conferring specific physicochemical and nutritional attributes. These tailored SL formulations find wide-ranging applications in the food and nutraceutical industries, showing promise for dietary support in promoting health and mitigating various diseases. In particular, SLs can be harnessed as functional oils to augment TAG metabolism, thereby impeding the development of fatty liver, countering the onset of obesity, and preventing atherosclerosis and age-related chronic diseases. In scrutinising prevailing research trajectories, this review endeavours to provide an in-depth analysis of the multifaceted advantages and repercussions associated with the synthesis of SLs. It elucidates their burgeoning potential in enhancing health and well-being across a range of demographic cohorts. Specifically, the implications of SL utilisation are discussed in the context of healthcare environments and early childhood developmental support.

Ulva lactuca is a seaweed with antinutritional cell wall for monogastrics. Carbohydrate-Active enZymes (CAZymes) supplementation can potentially cause its disruption. This study evaluates four diets: Ctrl-control diet; UL-control + 7% U. lactuca (wild caught, powdered form); ULR-UL + 0.005% Rovabio® Excel AP; ULU-UL + 0.01% ulvan lyase on piglets' haematologic and serologic profiles, hepatic lipids and minerals. White blood cells and lymphocytes reached the highest values in piglets fed UL compared to control, and to control and ULR; respectively (P < 0.05). IgG levels were boosted by seaweed incorporation compared to control (P = 0.015). The glycaemic homeostasis was assured by the seaweed inclusion. Dietary seaweed decreased serum lipids (P < 0.001), with the exception of ULU, due to HDL-cholesterol increase (P < 0.001). Cortisol was decreased in ULR and ULU (P < 0.001). No systemic inflammation was observed (P > 0.05). While hepatic n-3 PUFA increased in piglets fed with seaweed diets due to increment of beneficial 22:5n-3 and 22:6n-3 fatty acids (P < 0.05), the opposite occurred for n-6 PUFA, PUFA/SFA and n-6/n-3 ratios (P < 0.05). Hepatic pigments were unchanged (P > 0.05). ULR reduced α-tocopherol levels (P = 0.036) and increased serum potassium levels (P < 0.001) compared to control. Seaweed contributed to overcome piglets' weaning stress, with some benefits of including CAZyme supplementation.

The most well-characterized hereditary form of gastric cancer is hereditary diffuse gastric cancer (HDGC), an autosomal dominant syndrome characterized by an increased risk of diffuse gastric and lobular breast cancer. HDGC is predominantly caused by germline pathogenic variants in the CDH1 gene, and more rarely in the CTNNA1 gene. Furthermore, the International Gastric Cancer Linkage Consortium (IGCLC) guidelines do not clarify whether or not mixed gastric cancer (with a diffuse component) should be considered in the HDGC genetic testing criteria. We aimed to evaluate the contribution of CTNNA1 and CTNND1 germline variants to HDGC. Additionally, we also intended to compare the frequencies of CDH1 and CTNNA1 (and eventually CTNND1) germline variants between patients with diffuse and mixed gastric carcinomas to evaluate if genetic testing for these genes should or should not be considered in patients with the latter. We analyzed the CDH1 gene in 67 cases affected with early-onset/familial mixed gastric carcinomas and the CTNNA1 and CTNND1 genes in 208 cases with diffuse or mixed gastric cancer who had tested negative for CDH1 pathogenic germline variants. A deleterious CTNNA1 germline variant was found in 0.7% (1/141) of diffuse gastric cancer patients meeting the 2020 IGCLC criteria, as compared to the rate of 2.8% of CDH1 deleterious variants found by us in this setting. No deleterious variants were found in CTNND1, but six variants of uncertain significance were identified in this gene. We did not find any pathogenic CDH1, CTNNA1 or CTNND1 variant in index patients with early-onset/familial mixed gastric cancer, so there is no evidence that supports including this tumor type in the testing criteria for germline variants in these genes. The role of the CTNND1 gene in inherited gastric cancer predisposition is still unclear.

Poultry meat and pork, the two most consumed types of meat worldwide, are currently facing major challenges regarding feeding sustainability, use of antibiotics, and meat quality. This chapter addresses the current and promising applications of microalgae to mitigate all of the aforementioned aspects. Microalgae are studied as a natural marine resource for a number of economically relevant applications, including monogastric feeding. Although microalgae composition is diverse, they all display similar levels of macronutrients in relation to conventional feedstuffs and are enriched in beneficial n-3 long-chain polyunsaturated (LC-PUFA) and antioxidants. Research performed so far has shown that the inclusion of microalgae in feed could improve animals’ growth and meat quality in both poultry and pigs. On the negative side, it is well known that microalgae are largely indigestible by monogastrics, and thus, their utilization by the feed industry has been limited to supplement applications. Thus, the development of novel technologies to improve microalgae nutrient utilization is also described here. Among these novel technologies is the use of feed enzymes, mainly carbohydrases and peptidases, which represents a promising cost-effective strategy for cell disruption in order to disclose the extra nutritional value of microalgae for monogastrics feeding. In addition, the cost-effective cultivation of microalgae is also a key challenge in the near future mainly directed to reduce its production costs. In conclusion, the incorporation of microalgae in monogastric diets is defying but also very promising for livestock production desired to be more efficient, competitive, and environmentally sustainable.

Pathology InternationalVolume 74, Issue 1 p. 48-50 LETTER TO THE EDITOR The enigmatic occurrence of Pacinian corpuscles in the prostate gland: Report of a case with pericorpuscular and intracorpuscular growth of prostatic acinar adenocarcinoma João Lobo, João Lobo orcid.org/0000-0001-6829-1391 Department of Pathology, Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal Cancer Biology and Epigenetics Group, IPO Porto Research Center (GEBC CI-IPOP), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal Department of Pathology and Molecular Immunology, ICBAS—School of Medicine and Biomedical Sciences, University of Porto, Porto, PortugalSearch for more papers by this authorPaula Lopes, Paula Lopes Department of Pathology, Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, PortugalSearch for more papers by this authorRui Henrique, Rui Henrique orcid.org/0000-0003-3171-4666 Department of Pathology, Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal Cancer Biology and Epigenetics Group, IPO Porto Research Center (GEBC CI-IPOP), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal Department of Pathology and Molecular Immunology, ICBAS—School of Medicine and Biomedical Sciences, University of Porto, Porto, PortugalSearch for more papers by this authorÂngelo Rodrigues, Ângelo Rodrigues Department of Pathology, Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal Cancer Biology and Epigenetics Group, IPO Porto Research Center (GEBC CI-IPOP), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal Department of Pathology and Molecular Immunology, ICBAS—School of Medicine and Biomedical Sciences, University of Porto, Porto, PortugalSearch for more papers by this author João Lobo, João Lobo orcid.org/0000-0001-6829-1391 Department of Pathology, Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal Cancer Biology and Epigenetics Group, IPO Porto Research Center (GEBC CI-IPOP), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal Department of Pathology and Molecular Immunology, ICBAS—School of Medicine and Biomedical Sciences, University of Porto, Porto, PortugalSearch for more papers by this authorPaula Lopes, Paula Lopes Department of Pathology, Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, PortugalSearch for more papers by this authorRui Henrique, Rui Henrique orcid.org/0000-0003-3171-4666 Department of Pathology, Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal Cancer Biology and Epigenetics Group, IPO Porto Research Center (GEBC CI-IPOP), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal Department of Pathology and Molecular Immunology, ICBAS—School of Medicine and Biomedical Sciences, University of Porto, Porto, PortugalSearch for more papers by this authorÂngelo Rodrigues, Ângelo Rodrigues Department of Pathology, Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal Cancer Biology and Epigenetics Group, IPO Porto Research Center (GEBC CI-IPOP), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal Department of Pathology and Molecular Immunology, ICBAS—School of Medicine and Biomedical Sciences, University of Porto, Porto, PortugalSearch for more papers by this author First published: 05 December 2023 https://doi.org/10.1111/pin.13392Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Supporting Information Additional Supporting Information may be found in the online version of this article at the publisher's website. Filename Description pin13392-sup-0001-Supplementary_Information.docx16.6 KB Supporting information. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article. REFERENCES 1Feito J, García-Suárez O, García-Piqueras J, García-Mesa Y, Pérez-Sánchez A, Suazo I, et al. The development of human digital meissner's and pacinian corpuscles. Ann Anat. 2018; 219: 8–24. 10.1016/j.aanat.2018.05.001 CASPubMedWeb of Science®Google Scholar 2de Souza MF, Athanazio DA. Intraprostatic pacinian corpuscle does exist! Pathology. 2022; 54: 479–480. 10.1016/j.pathol.2021.06.126 PubMedWeb of Science®Google Scholar 3Medlicott SA, Larsen ET, Gao Y, Trpkov K. Pacinian corpuscle in the prostate: fact-not fiction! Hum PatholCase Rep. 2019; 15: 71–72. 10.1016/j.ehpc.2018.12.001 Google Scholar 4Pai SA. Ectopic pacinian corpuscle in the prostate. Int J Surg Pathol. 2017; 25: 609–610. 10.1177/1066896917705200 PubMedWeb of Science®Google Scholar 5Feito J, Esteban R, García-Martínez ML, García-Alonso FJ, Rodríguez-Martín R, Rivas-Marcos MB, et al. Pacinian corpuscles as a diagnostic clue of ledderhose disease—a case report and mapping of pacinian corpuscles of the sole. Diagnostics. 2022; 12: 1705. 10.3390/diagnostics12071705 PubMedWeb of Science®Google Scholar Volume74, Issue1January 2024Pages 48-50 ReferencesRelatedInformation

Background: Lipopolysaccharide (LPS), an effective stimulator of the immune system, has been widely applied in an experimental pig model for human sepsis. Aquaporins (AQPs), a family of small integral membrane proteins responsible for facilitating water fluxes through the cell membrane, offer potential promising drug targets for sepsis treatment due to their role in water balance and inflammation. Methods: In order to investigate the potential effect of a dietary amino acid mixture supplementation on LPS-challenged weaned piglets, a total of 30, 28-day-old, males were randomly allocated to 1 of 3 dietary treatments for a 5-week period, with 10 animals in each: diet 1 was a control (CTL) treatment; diet 2 was LPS treatment, where the piglets were intraperitoneally administered LPS (at 25 µg/kg body weight); diet 3 was LPS + cocktail treatment, where the piglets were intraperitoneally administered LPS and fed a diet supplemented with a mixture of arginine, branched-chain amino acids (BCAA, leucine, valine, and isoleucine), and cystine. Key organs that control sepsis were collected and processed by real time quantitative PCR (RT-qPCR) for the AQPs and cytokines transcriptional profiles. Results: Minor variations were detected for AQPs and inflammatory markers mRNA levels, upon the dependence of LPS or the amino acid cocktail suggesting the piglets’ immune recovery. Using a discriminant analysis tool, we report for the first time, a tissue-specific variation in AQPs and cytokines transcriptional profiles that clearly distinguish the small intestine and the kidney from the liver and the spleen. Conclusions: This study provides a novel insight into the gene expression signature of AQPs and cytokines in the functional physiology of each organ in piglets.

Seaweeds, such as Laminaria digitata , are a sustainable alternative to conventional feedstuffs for weaned piglet diets, improving their health and mitigating environmental impacts. L. digitata has a complex cell wall that can be difficult for monogastrics to digest. However, carbohydrate-active enzymes (CAZymes) such as Rovabio ® Excel AP and alginate lyase can help break down these polysaccharides and render intracellular nutrients more accessible. This study aimed to evaluate the impact of 10% L. digitata feed inclusion and CAZyme supplementation on piglet blood cells, serum metabolites, liver lipid and mineral profiles. Forty weaned piglets were randomly assigned to one of four diets (n = 10 each): a control diet, 10% L. digitata (LA), 10% L. digitata + 0.005% Rovabio ® Excel AP (LAR), and 10% L. digitata + 0.01% alginate lyase (LAL). After two weeks of trial, animals were slaughtered and liver and blood serum samples taken for analysis. The results showed that the LA and LAL diets increased blood lymphocytes, IgG and IgM, and decreased serum lipids, improving both cellular and humoral immune response and cardiovascular health. Dietary CAZymes reversed the anti-inflammatory and hematopoietic effects. Additionally, cortisol levels were reduced with seaweed inclusion compared to the control diet (P < 0.001). In the liver, total n-3 PUFA and n-6/n-3 ratio were increased and decreased, respectively, due to eicosapentaenoic acid and α-linolenic acid accumulation (P < 0.001). However, total liver mineral content was incorporated to a lesser extent with the combined seaweed and enzyme diets (P < 0.001), potentially indicating a negative effect on mineral bioavailability. Overall, results suggest that a 10% L. digitata inclusion can effectively improve piglet health by reducing stress during weaning, without the need for dietary CAZymes.

Pancreatic cancer is anticipated to be the second leading cause of cancer-related death by 2030. Aquaporins (AQPs), a family of water channel proteins, have been linked to carcinogenesis. The aim of this study was to determine AQP gene expression in pancreatic cancer tissues and to validate aquaporins as possible diagnosis and/or prognosis genes. The relative gene expression levels of AQP1, AQP3, AQP5, and AQP9 were analyzed using real-time quantitative PCR (RT-qPCR) in 24 paired pancreatic tumors and adjacent healthy tissues according to variables such as age, gender, and tumor invasiveness and aggressiveness. AQPs transcripts were detected in both healthy and tumor tissues. While AQP1 was downregulated in the tumor samples, AQP3 was particularly overexpressed in low-grade invasive tumors. Interestingly, most of the strong positive Pearson correlation coefficients found between AQPs in healthy tissues were lost when analyzing the tumor tissues, suggesting disruption of the coordinated AQP-gene expression in pancreatic cancer.

The implication of high dietary level of Chlorella vulgaris, individually and supplemented with two carbohydrase mixtures, on pigs' health and liver metabolism was assessed in this study. Forty crossbred (Large White × Landrace sows crossed with Pietrain boars) entire male pigs were randomly allocated to the following feeding treatments (n = 10): cereal-soybean meal basal diet (control); basal diet with 5% C. vulgaris; basal diet with 5% C. vulgaris supplemented with 0.005% Rovabio® Excel AP; and basal diet with 5% C. vulgaris supplemented with 0.01% of a preselected four-CAZyme mixture. The trial lasted from 59.1 ± 5.69 kg of initial live weight to 101 ± 1.9 kg of slaughter weight. Data indicate that this high dietary level of C. vulgaris has impact on several blood parameters of finishing pigs. However, the most relevant health outcome observed was a strong immunosuppressive effect promoted by the microalga, which increases pigs' susceptibility to infection diseases. In addition, the dietary incorporation of C. vulgaris reduced the systemic antioxidant capacity of pigs. In turn, the dietary supplementation with the four-CAZyme mixture promoted a clear decrease on some blood parameters compared with the control group. Regarding hepatic lipids, pigs fed C. vulgaris diets, had an increased hepatic content of n-3 PUFA, with a consequent decrease on the n-6/n-3 ratio. In conclusion, the use of C. vulgaris as feed ingredient appears to be safe under controlled experimental conditions. However, it is imperative test it in industrial production systems, with more stressful and less hygienic environments.

Grape by-products could be used in monogastric animals′ nutrition to reduce feeding costs with conventional crops (e.g., maize and soybean meal) and to improve meat quality. The main grape by-products with the largest expression worldwide, particularly in the Mediterranean region, are grape pomace, grape seed, grape seed oil and grape skins. These by-products are rich sources of bioactive polyphenols, dietary fiber and polyunsaturated fatty acids (PUFA), more specifically, the beneficial n-3 PUFA, that could be transferred to pork and poultry meat. The potential biological activities, mainly associated with antimicrobial and antioxidant properties, make them putative candidates as feed supplements and/or ingredients capable of enhancing meat quality traits, such as color, lipid oxidation and shelf life. However, grape by-products face several limitations, namely, the high level of lignified cell wall and tannin content, both antinutritional compounds that limit nutrients absorption. Therefore, it is imperative to improve grape by-products’ bioavailability, taking advantage of enzyme supplementation or pretreatment processes, to use them as feed alternatives contributing to boost a circular agricultural economy. The present review summarizes the current applications and challenges of using grape by-products from the agro-industrial sector in pig and poultry diets aiming at improving meat quality and nutritional value.