Chronic kidney disease as cardiovascular risk factor in routine clinical practice: a position statement by the Council of the European Renal Association

The European Society of Cardiology 2021 guideline on cardiovascular (CV) disease (CVD) prevention in clinical practice has major implications for both CV risk screening and kidney health of interest to primary care physicians, cardiologists, nephrol-ogists, and other professionals involved in CVD prevention. The proposed CVD prevention strategies require as first step the categorization of individuals into those with established atherosclerotic CVD, diabetes, familiar hypercholesterolaemia, or chronic kidney disease (CKD), i.e. conditions that are already associated with a moderate to very-high CVD risk. This places CKD, defined as decreased kidney function or increased albuminuria as a starting step for CVD risk assessment. Thus, for adequate CVD risk assessment, patients with diabetes, familiar hypercholesterolaemia, or CKD should be identified by an initial laboratory assessment that requires not only serum to assess glucose, cholesterol, and creatinine to estimate the glomerular filtration rate, but also urine to assess albuminuria. The addition of albuminuria as an entry-level step in CVD risk assessment should change clinical practice as it differs from the current healthcare situation in which albuminuria is only assessed in persons already considered to be at high risk of CVD. A diagnosis of moderate of severe CKD requires a specific set of interventions to prevent CVD. Further research should address the optimal method for CV risk assessment that includes CKD assessment in the general population, i.e. whether this should remain opportunistic screening or whether systematic screening

Chronic kidney disease as cardiovascular risk factor in routine clinical practice: a position statement by the Council of the European Renal Association

The European Society of Cardiology 2021 guideline on cardiovascular (CV) disease (CVD) prevention in clinical practice has major implications for both CV risk screening and kidney health of interest to primary care physicians, cardiologists, nephrologists, and other professionals involved in CVD prevention. The proposed CVD prevention strategies require as first step the categorization of individuals into those with established atherosclerotic CVD, diabetes, familiar hypercholesterolaemia, or chronic kidney disease (CKD), i.e. conditions that are already associated with a moderate to very-high CVD risk. This places CKD, defined as decreased kidney function or increased albuminuria as a starting step for CVD risk assessment. Thus, for adequate CVD risk assessment, patients with diabetes, familiar hypercholesterolaemia, or CKD should be identified by an initial laboratory assessment that requires not only serum to assess glucose, cholesterol, and creatinine to estimate the glomerular filtration rate, but also urine to assess albuminuria. The addition of albuminuria as an entry-level step in CVD risk assessment should change clinical practice as it differs from the current healthcare situation in which albuminuria is only assessed in persons already considered to be at high risk of CVD. A diagnosis of moderate of severe CKD requires a specific set of interventions to prevent CVD. Further research should address the optimal method for CV risk assessment that includes CKD assessment in the general population, i.e. whether this should remain opportunistic screening or whether systematic screening

Interactions between immunotoxicants and parasite stress: Implications for host health

Many organisms face a wide variety of biotic and abiotic stressors which reduce individual survival, interacting to further reduce fitness. Here we studied the effects of two such interacting stressors: immunotoxicant exposure and parasite infection. We model the dynamics of a within-host infection and the associated immune response of an individual. We consider both the indirect sub-lethal effects on immunosuppression and the direct effects on health and mortality of individuals exposed to toxicants. We demonstrate that sub-lethal exposure to toxicants can promote infection through the suppression of the immune system. This happens through the depletion of the immune response which causes rapid proliferation in parasite load. We predict that the within-host parasite density is maximised by an intermediate toxicant exposure, rather than continuing to increase with toxicant exposure. In addition, high toxicant exposure can alter cellular regulation and cause the breakdown of normal healthy tissue, from which we infer higher mortality risk of the host. We classify this breakdown into three phases of increasing toxicant stress, and demonstrate the range of conditions under which toxicant exposure causes failure at the within-host level. These phases are determined by the relationship between the immunity status, overall cellular health and the level of toxicant exposure. We discuss the implications of our model in the context of individual bee health. Our model provides an assessment of how pesticide stress and infection interact to cause the breakdown of the within-host dynamics of individual bees

Correction to: Textural Quantification and Classification of Drill Cores for Geometallurgy: Moving Toward 3D with X-ray Microcomputed Tomography (μCT)

Correction to: Natural Resources Research https://doi.org/10.1007/s11053-020-09685-5 The original version of the article unfortunately contained an error in Table 9

Investigations of genotoxic activity of antimicrobial/antiviral agent FS-1 in human lymphocytes and tumor cell

A very promising antiviral and antimicrobial agent FS-1 was studied for its ability to induce DNA damage and micronuclei in human tumor cell lines HeLa and Caco-2 at concentrations of 200, 500 and 1000 mg/ml without exogenous metabolic activation. The compound was additionally tested for DNA damaging ability in human lymphocytes at concentrations of 200, 400 and 800 mg/ml. Neither DNA damage nor micronucleus formation was observed after treatment of all types of cells with FS-1. Based on these results, FS-1 can be further studied for its safety to humans for potential application in clinical medicine as an antimicrobial/antiviral drug.Исследовали способность перспективного антивирусного и антибактериального соединения ФС-1 вызывать повреждения ДНК и микроядра в клеточных линиях опухоли человека HeLa и Caco-2 при концентрациях 200, 500 и 1000 мкг/мл без экзогенной метаболической активации. Соединение было дополнительно проверено на ДНК-повреждающую способность в лимфоцитах человека при концентрациях 200, 400 и 800 мкг/мл. Ни повреждения ДНК, ни формирования микроядер не наблюдалось после обработки всех типов клеток ФС-1. На основании этих результатов, ФС-1 может быть далее изучен на предмет безопасности для возможного применения в клинической медицине как антибактериального/противовирусного препарата.Досліджували здатність перспективного противірусного та антибактеріального препарату ФС-1 викликати пошкодження ДНК та мікроядра в клітинних лініях пухлини людини HeLa і Сасо-2 при концентраціях 200, 500 та 1000 мкг/мл без екзогенної метаболічної активації. Препарат був додатково перевірений на ДНК-пошкоджуючу здатність в лімфоцитах людини при концентраціях 200, 400, 800 мкг/мл. Ні пошкодження ДНК, ні формування мікроядер не спостерігалось після обробки всіх типів клітин ФС-1. Базуючись на цих результатах, ФС-1 може далі вивчатись на предмет безпеки для потенційного застосування в клінічній медицині як антибактеріального/противірусного препарату