Seminal quality, testicle and epididymis morphology of bulls fed a diet containing gossypol

The objective was to evaluate the effect of intake of free gossypol on sperm quality and morphology of the testicles and epididymis of Nelore bulls. Twelve bulls were fed diets containing 3.3g of free gossypol/bull/day (cottonseed) (Group 1, n = 6) and a diet free of gossypol (Group 2, n = 6), respectively. Semen samples were collected in the beginning and end of the experiment which lasted 73 days. In the end of the study the testes and epididymis of bulls were removed to study the effect of free gossypol on histological characteristics. The average consumption of 3.3g of free gossypol/bull/day (mean 7.1mg of free gossypol/kg/day) reduced motility and sperm concentration and increased the percentage of major and total sperm defects, as well as the animals showing testes with seminiferous tubules of smaller thickness, fewer layers of spermatogenic lineage cells, smaller epididymal epithelium thickness and smaller number of sperm within the epididymal ducts, compared to animals with a diet free of gossypol (Group 2). The consumption of 3.3g of free gossypol/bull/day led to changes in morphology and morphometry of the testes and epididymis and reduced sperm quality of bulls.Objetivou-se avaliar o efeito da ingestão de gossipol livre sobre a qualidade espermática e a morfologia dos testículos e dos epidídimos de touros da raça Nelore. Doze touros receberam dieta contendo 3,3g de gossipol livre/touro/dia (caroço de algodão) (Grupo 1, n=6) e dieta isenta de gossipol (Grupo 2, n=6), respectivamente. Foram realizadas coletas de sêmen no início e no final do experimento, que teve duração de 73 dias. Ao final do estudo, foram retirados os testículos e os epidídimos dos touros para se estudar o efeito do gossipol livre sobre as características histológicas. O consumo médio de 3,3g de gossipol livre/touro/dia (média 7,1mg de gossipol livre/kg/dia) reduziu a motilidade e a concentração espermática e aumentou a porcentagem de defeitos espermáticos maiores e totais. Além disso, os animais apresentaram testículos com túbulos seminíferos de menor espessura de parede, menor número de camadas de células espermatogênicas, menor espessura do epitélio epididimário e menor número de espermatozoide no interior dos ductos epidídimários, em relação aos animais com dieta isenta de gossipol (Grupo 2). O consumo de 3,3g de gossipol livre/touro/dia acarretou alterações na morfologia e na morfometria dos testículos e dos epidídimos e reduziu a qualidade espermática dos touros.Universidade de Cuiabá Faculdade de Medicina VeterináriaUFMS Faculdade de Medicina Veterinária e ZootecniaEpamigUniversidade Federal do Mato GrossoUNIFESP-EPMUNIFESP, EPMSciEL

RICORS2040 : The need for collaborative research in chronic kidney disease

Chronic kidney disease (CKD) is a silent and poorly known killer. The current concept of CKD is relatively young and uptake by the public, physicians and health authorities is not widespread. Physicians still confuse CKD with chronic kidney insufficiency or failure. For the wider public and health authorities, CKD evokes kidney replacement therapy (KRT). In Spain, the prevalence of KRT is 0.13%. Thus health authorities may consider CKD a non-issue: very few persons eventually need KRT and, for those in whom kidneys fail, the problem is 'solved' by dialysis or kidney transplantation. However, KRT is the tip of the iceberg in the burden of CKD. The main burden of CKD is accelerated ageing and premature death. The cut-off points for kidney function and kidney damage indexes that define CKD also mark an increased risk for all-cause premature death. CKD is the most prevalent risk factor for lethal coronavirus disease 2019 (COVID-19) and the factor that most increases the risk of death in COVID-19, after old age. Men and women undergoing KRT still have an annual mortality that is 10- to 100-fold higher than similar-age peers, and life expectancy is shortened by ~40 years for young persons on dialysis and by 15 years for young persons with a functioning kidney graft. CKD is expected to become the fifth greatest global cause of death by 2040 and the second greatest cause of death in Spain before the end of the century, a time when one in four Spaniards will have CKD. However, by 2022, CKD will become the only top-15 global predicted cause of death that is not supported by a dedicated well-funded Centres for Biomedical Research (CIBER) network structure in Spain. Realizing the underestimation of the CKD burden of disease by health authorities, the Decade of the Kidney initiative for 2020-2030 was launched by the American Association of Kidney Patients and the European Kidney Health Alliance. Leading Spanish kidney researchers grouped in the kidney collaborative research network Red de Investigación Renal have now applied for the Redes de Investigación Cooperativa Orientadas a Resultados en Salud (RICORS) call for collaborative research in Spain with the support of the Spanish Society of Nephrology, Federación Nacional de Asociaciones para la Lucha Contra las Enfermedades del Riñón and ONT: RICORS2040 aims to prevent the dire predictions for the global 2040 burden of CKD from becoming true

Lung adenocarcinoma promotion by air pollutants

A complete understanding of how exposure to environmental substances promotes cancer formation is lacking. More than 70 years ago, tumorigenesis was proposed to occur in a two-step process: an initiating step that induces mutations in healthy cells, followed by a promoter step that triggers cancer development1. Here we propose that environmental particulate matter measuring ≤2.5 μm (PM2.5), known to be associated with lung cancer risk, promotes lung cancer by acting on cells that harbour pre-existing oncogenic mutations in healthy lung tissue. Focusing on EGFR-driven lung cancer, which is more common in never-smokers or light smokers, we found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases in four within-country cohorts. Functional mouse models revealed that air pollutants cause an influx of macrophages into the lung and release of interleukin-1β. This process results in a progenitor-like cell state within EGFR mutant lung alveolar type II epithelial cells that fuels tumorigenesis. Ultradeep mutational profiling of histologically normal lung tissue from 295 individuals across 3 clinical cohorts revealed oncogenic EGFR and KRAS driver mutations in 18% and 53% of healthy tissue samples, respectively. These findings collectively support a tumour-promoting role for PM2.5 air pollutants and provide impetus for public health policy initiatives to address air pollution to reduce disease burden