Access to public sports infrastructure in Poland as a preventive factor for cardiovascular diseases

Introduction: Cardiovascular diseases (CVDs) are a significant health concern globally, including in Poland. Physical activity has been identified as a crucial preventive factor for CVDs, and access to public sports infrastructure plays a vital role in promoting physical activity. However, the relationship between access to such infrastructure and its impact on cardiovascular health outcomes in Poland remains understudied. Aim of the study: This study aims to investigate the impact of access to public sports infrastructure on the prevalence of cardiovascular diseases and mortality rates in Poland. Materials and methods: Publicly available data were obtained regarding sports facilities, population structure, hospitalizations, and deaths. Results: There is a moderate negative correlation (r = -0.3096; p < 0.001) between hospitalization rates for cardiovascular diseases and the stadiums and playing fields available in the studied countries. The correlation between cardiovascular hospitalizations and indoor and outdoor arenas and gyms was also negative, but its effect was moderately weak (r = -0.2068, p < 0.001; r = -0.2597, p < 0.001, respectively). The average hospitalization rate for cardiovascular diseases in subjects over 65 years of age (M = 12117.24) was significantly higher compared to the group of all subjects (M = 3082.18) and subjects under 65 years of age (M = 1260.96). There is a negative correlation between the death rate and the availability of selected sports facilities, with a moderately weak effect for all sports infrastructure subgroups (r = -0.215 - -0.233). Conclusion: The effect of accessibility to public sport infrastructure on CVDs prevalence and related deaths is moderate to weak. The studied positive effect particularly affects people under 65 years of age. Further studies of other sport-connected predictors may be beneficial

Access to public sports infrastructure in Poland as a preventive factor for cardiovascular diseases

Introduction: Cardiovascular diseases (CVDs) are a significant health concern globally, including in Poland. Physical activity has been identified as a crucial preventive factor for CVDs, and access to public sports infrastructure plays a vital role in promoting physical activity. However, the relationship between access to such infrastructure and its impact on cardiovascular health outcomes in Poland remains understudied. Aim of the study: This study aims to investigate the impact of access to public sports infrastructure on the prevalence of cardiovascular diseases and mortality rates in Poland. Materials and methods: Publicly available data were obtained regarding sports facilities, population structure, hospitalizations, and deaths. Results: There is a moderate negative correlation (r = -0.3096; p < 0.001) between hospitalization rates for cardiovascular diseases and the stadiums and playing fields available in the studied countries. The correlation between cardiovascular hospitalizations and indoor and outdoor arenas and gyms was also negative, but its effect was moderately weak (r = -0.2068, p < 0.001; r = -0.2597, p < 0.001, respectively). The average hospitalization rate for cardiovascular diseases in subjects over 65 years of age (M = 12117.24) was significantly higher compared to the group of all subjects (M = 3082.18) and subjects under 65 years of age (M = 1260.96). There is a negative correlation between the death rate and the availability of selected sports facilities, with a moderately weak effect for all sports infrastructure subgroups (r = -0.215 - -0.233). Conclusion: The effect of accessibility to public sport infrastructure on CVDs prevalence and related deaths is moderate to weak. The studied positive effect particularly affects people under 65 years of age. Further studies of other sport-connected predictors may be beneficial

Innovations in the systemic treatment of medullary thyroid cancer with kinase inhibitors

Introduction: Medullary thyroid carcinoma is a primary thyroid neoplasm originating from thyroid C cells. It can be familial or sporadic. The familial form is associated with multiple endocrine neoplasia (MEN) syndrome types 2A and 2B and is caused by a mutation in the RET gene, which encodes a tyrosine kinase receptor. Treatment of medullary thyroid cancer is mainly based on surgical resection of the thyroid gland, usually a total thyroidectomy. It can be followed-up by a chemotherapy, which has limited efficacy. Hence, there is a growing interest in new molecular therapies, such as tyrosine kinase inhibitors, which include vandetanib, cabozantinib, selpercatinib, pralsetinib, sorafenib and lenvatinib. Objective: The review and presentation of the current state of knowledge on the systemic treatment of medullary thyroid cancer with kinase inhibitors. Material and methods: Literature review based on available sources from PubMed database and Google Scholar. Conclusions: Though systemic treatment options for medullary thyroid cancer continue to improve, patients with advanced neoplasms still have limited therapeutic options. Hence, further development of targeted treatment with kinase inhibitors, particularly those selective for the RET receptor is crucial. Molecular studies of mutations and signaling pathways involved in the oncopathogenesis of medullary thyroid cancer could contribute to the discovery of new therapeutic mechanisms, and drugs that target them, could potentially further improve disease progression-free survival (PFS) and overall survival (OS)

Particulate matter – a cancerous threat to our health?

Introduction: Particulate matter (PM) as a part of outdoor air pollutants are classified as human carcinogens. They are formed majorly as a result of combustion process by industry, power plants and engines. PM can be divided by the size of their particles into PM2.5 and PM10, where PM2.5 are small enough to penetrate into the alveoli sacs in the lung reaching the bloodstream, whereas PM10 affect mostly oral cavity, nose and the throat. Aim of the study: This study aims to investigate the impact of PM2.5 and PM10 particle concentrations in the EU NUTS 2 subregions on the death rates due to the most common malignant neoplasms. Results: There is a positive moderate correlation (r = 0.421; p &lt; 0.001) between the annual mean concentration of PM2.5 and deaths due to malignant tumors. The strongest correlation was observed for malignant neoplasms of larynx, which is a positive correlation with a strong effect (r = 0.641; p &lt; 0.001); and malignant neoplasm of bladder (r = 0.523; p &lt; 0.001). For PM10, there is a moderately weak positive correlation (r = 0,195; p = 0.008) between the annual average concentration of PM10 and deaths due to malignant tumors. The strongest correlation was observed for malignant neoplasms of larynx, which is a positive correlation with a strong effect (r = 0,551; p &lt; 0.001). Conclusion: The effect of PM impact on the malignant neoplasms is strong to moderate. The most affected neoplasm site are the ones the PMs intake occurs, being in the respiratory system. However other sites, where PMs can accumulate can be impacted as well. Further studies about the population with the highest risk due to the PMs exposure may be beneficial as other non-air quality-connected predictors may be found

Evaluation of the effect of simvastatin on key enzymes of monounsaturated fatty acid synthesis in the cardiac muscle tissue of rats.

Syntaza kwasów tłuszczowych (FAS), elongaza 6 (ELOVL6) oraz stearylo-CoA desaturaza (SCD) katalizują reakcje syntezy jednonienasyconych kwasów tłuszczowych (monounsaturated fatty acid - MUFA). Ekspresja tych enzymów jest najwyższa w tkance wątrobowej, ale wykazano ją również w mięśniu sercowym. Regulowana jest na poziomie transkrypcji z udziałem czynników transkrypcyjnych takich jak PPAR, SREBP oraz LXR. Badania kliniczne, prowadzone na liniach komórkowych oraz z wykorzystaniem modeli zwierzęcych wskazują, że ekspresja genów kodujących FAS, ELOVL6 oraz SCD jest modyfikowana przez inhibitory reduktazy HMG-CoA (statyny), do których należy simwastatyna.Celem pracy było określenie wpływu simwastatyny na poziom mRNA dla FAS, ELOVL6 oraz SCD w mięśniu sercowym szczurów Wistar. Do badań zostały wykorzystane tkanki mięśnia sercowego pozostałe po wcześniejszym eksperymencie. Grupie badanej (ST+S1-6) podawano simwastatynę w dawce 80 mg/kgm.c./dzień, natomiast grupa kontrolna (ST1-5) otrzymywała 0,3% metylocelulozę, rozpuszczalnik dla substancji. Simwastatynę i rozpuszczalnik dla substancji podawano sondą dożołądkową raz dziennie przez 14 dni. Do oceny ekspresji genów dla FAS, ELOVL6 oraz SCD wykorzystano półilościową metodę PCR z odwrotną transkrypcją (RT-PCR).W przeprowadzonych badaniach wykazano, że simwastatyna powoduje istotne statystycznie obniżenie względnego poziomu mRNA dla FAS. Można przypuszczać, że simwastatyna wpływa na aktywność czynników transkrypcyjnych regulujących ekspresję genu dla FAS. Mechanizm ten może obejmować aktywację kinazy AMPK lub/oraz hamowanie syntezy oksysteroli. Nie wykazano wpływu simwastatyny na względny poziom mRNA dla ELOVL6 oraz SCD, co sugeruje, że simwastatyna w użytej dawce nie ma wpływu na syntezę MUFA w mięśniu sercowym szczurów. Konieczne są kolejne badania dotyczące poznania mechanizmu wpływu simwastatyny na czynniki transkrypcyjne regulujące ekspresję genów dla tych enzymów.Fatty acid synthase (FAS), elongase 6 (ELOVL6) and stearyl-CoA desaturase (SCD) catalyze the synthesis of monounsaturated fatty acids (MUFA). The expression of these enzymes is the highest in the liver, but it also occurs in the myocardium. It is regulated mainly at the transcriptional level by transcription factors such as PPAR, SREBP, and LXR. Many studies indicate that the expression of genes encoding FAS, ELOVL6, and SCD is modified by HMG-CoA reductase inhibitors (statins), which include simvastatin.The aim of the study was to determine the effect of simvastatin on Fas, Elovl6, and Scd mRNA levels in the cardiac muscle tissue of Wistar rats. The study group (ST+S1-6) and the control group (ST1-5), for 14 days, have received simvastatin (80mg/kg bw/day) and 0.3% methylcellulose (the vehicle), respectively. Relative levels of Fas, Elovl6, and Scd mRNA in rat’s myocardium were assessed by semi-quantitative reverse transcription–polymerase chain reaction (RT-PCR).It has been found that simvastatin significantly decreases the mRNA level for Fas in rat’s cardiac muscle tissue. It can be hypothesized that simvastatin affects the activity of transcription factors that regulate Fas gene expression. The mechanism may include activation of AMPK and/or oxysterol synthesis suppression. Simvastatin does not influence the mRNA relative level for Elovl6 and Scd, suggesting that simvastatin, at dosage used in this study, does not affect MUFA synthesis in rats’ myocardium. Further studies are necessary to explain the mechanism by which simvastatin influences transcription factors regulating gene expression for these enzymes