Erectile dysfunction and cardiovascular disease

W ostatnich latach szczególną uwagę przywiązuje się do współwystępowania zaburzeń erekcji (ED) i schorzeń układu sercowo-naczyniowego. Wiele czynników ryzyka jest wspólnych dla ED i chorób związanych z miażdżycą. Postrzeganie zaburzeń erekcji jako wczesnej manifestacji miażdżycy wydaje się uzasadnione i podkreśla konieczność uwzględnienia pytań o ocenę jakości życia seksualnego w badaniu podmiotowym. Z kolei stwierdzenie ED u mężczyzny bez rozpoznanej wcześniej choroby sercowo-naczyniowej obliguje lekarza do szczegółowej kalkulacji całkowitego ryzyka sercowo-naczyniowego. Profilaktyka wystąpienia cukrzycy i otyłości, niepalenie tytoniu oraz skuteczna terapia dyslipidemii, zaburzeń gospodarki węglowodanowej i nadciśnienia tętniczego mogą pomóc w zachowaniu sprawności seksualnej. Odpowiednia dawka wysiłku fizycznego w znamienny sposób przyczynia się do poprawy sprawności seksualnej, a w szczególności ograniczenia zaburzeń erekcji. Część leków kardiologicznych może również negatywnie wpływać na jakość erekcji. Inhibitory PDE-5 są lekiem pierwszego wyboru w leczeniu zaburzeń erekcji zarówno u pacjentów ze schorzeniami układu sercowo-naczyniowego jak i bez nich. Celem artykułu jest przedstawienie aktualnych poglądów dotyczących wpływu chorób układu krążenia na zaburzenia erekcjiIn recent years a special attention is paid to the co–occurrence of erectile dysfunction and cardiovascular disease.Many risk factors for ED is shared with diseases associated with atherosclerosis. The perception of ED as an earlyindicator of atherosclerosis appears to be justified and emphasizes the importance of questions to assess the qualityof sexual life in a physician examination. The declaration of ED in men with no previous diagnosis of cardiovasculardisease obliges the doctor to a detailed calculation of the total cardiovascular risk. Prevention of diabetes, obesity,not smoking, effective treatment of dyslipidemia, glucose intolerance, and hypertension can help maintain sexualperformance. The appropriate dose of physical activity significally improves sexual performance. Some cardiacdrugs can also negatively affect the quality of erections. PDE-5 inhibitors are the drugs of the first choice in thetreatment erectile dysfunction in both patients with and without cardiovascular disease. The purpose of this articleis to present the current views on the impact of cardiovascular disease on erectile dysfunction

Downstream and Intermediate Interactions of Synovial Sarcoma-Associated Fusion Oncoproteins and Their Implication for Targeted Therapy

Synovial sarcoma (SS), an aggressive type of soft tissue tumor, occurs mostly in adolescents and young adults. The origin and molecular mechanism of the development of SS remain only partially known. Over 90% of SS cases are characterized by the t(X;18)(p11.2;q11.2) translocation, which results mainly in the formation of SS18-SSX1 or SS18-SSX2 fusion genes. In recent years, several reports describing direct and indirect interactions of SS18-SSX1/SSX2 oncoproteins have been published. These reports suggest that the fusion proteins particularly affect the cell growth, cell proliferation, TP53 pathway, and chromatin remodeling mechanisms, contributing to SS oncogenesis. Additional research efforts are required to fully explore the protein-protein interactions of SS18-SSX oncoproteins and the pathways that are regulated by these partnerships for the development of effective targeted therapy

SDH-deficient gastrointestinal stromal tumours

Gastrointestinal stromal tumours (GIST) comprise a heterogeneous group of the most common mesenchymal neoplasms of the gastrointestinal tract. The majority of GIST are induced by activating, mutually exclusive mutations of two genes – KIT and PDGFRA (platelet-derived growth factor receptor-alpha). However, approximately 10–15% of GISTs lack oncogenic KIT or PDGFRA mutations and these tumours are often called “wild type” (WT) GISTs. The SDH-deficient GISTs form a distinctive subset of tumours accounting for 20–40% of KIT/PDGFRA WT GIST, which results from the loss of function mutations in the genes encoding the SDH enzyme complex. The true frequency of SDH-deficient GISTs was reported to be approximately 7.4 to 7.7%. These tumours usually occur in the stomach (most commonly in the antrum) and have a spectrum of beha­viour from indolent to progressive. In most cases the molecular mechanism behind the SDH-deficient GISTs is connected to germline mutations. SDHA germline mutations occur in approximately 30% of the SDH-deficient GIST, those in SDHB, SDHC, and SDHD appear in 20–30% of patients. The SDH-mutated GISTs do not respond well to the commonly used targeted therapy, with no objective tumour response to imatinib. Taking into account the biological features of SDH-deficient GIST, new therapies of potential in­terest comprise PI3K/AKT/mTOR inhibitors, heat-shock protein inhibitors, HIF1-α targeting agents, epigenetic modifiers and demethylating agents. However, further research is necessary in these fields

SDH-deficient gastrointestinal stromal tumours

Gastrointestinal stromal tumours (GIST) comprise a heterogeneous group of the most common mesenchymal neoplasms of the gastrointestinal tract. The majority of GIST are induced by activating, mutually exclusive mutations of two genes – KIT and PDGFRA (platelet-derived growth factor receptor-alpha). However, approximately 10–15% of GISTs lack oncogenic KIT or PDGFRA mutations and these tumours are often called “wild type” (WT) GISTs. The SDH-deficient GISTs form a distinctive subset of tumours accounting for 20–40% of KIT/PDGFRA WT GIST, which results from the loss of function mutations in the genes encoding the SDH enzyme complex. The true frequency of SDH-deficient GISTs was reported to be approximately 7.4 to 7.7%. These tumours usually occur in the stomach (most commonly in the antrum) and have a spectrum of beha­viour from indolent to progressive. In most cases the molecular mechanism behind the SDH-deficient GISTs is connected to germline mutations. SDHA germline mutations occur in approximately 30% of the SDH-deficient GIST, those in SDHB, SDHC, and SDHD appear in 20–30% of patients. The SDH-mutated GISTs do not respond well to the commonly used targeted therapy, with no objective tumour response to imatinib. Taking into account the biological features of SDH-deficient GIST, new therapies of potential in­terest comprise PI3K/AKT/mTOR inhibitors, heat-shock protein inhibitors, HIF1-α targeting agents, epigenetic modifiers and demethylating agents. However, further research is necessary in these fields

POMIAR CZASU MARTWEGO METODĄ DWÓCH ŹRÓDEŁ – OPTYMIZACJA PODZIAŁU CZASU POMIARU

The article presents the analysis of the dead time measurement using two sources for a non-paralyzable detector. It determined the optimum division of count rate measurement time between both source measurement and a single source one. Results of the work can be used to optimize dead time measurement for systems which count photons or particles.W artykule zaprezentowano analizę pomiaru czasu martwego detektora nieparaliżowalnego metodą dwóch źródeł. Wyznaczono optymalny podział czasu pomiaru częstości zliczeń dla pomiaru jednym i dwoma źródłami. Wyniki pracy mogą być wykorzystane do optymalizacji systemów zliczających fotony lub cząstki

Degradation of polylactic acid/polypropylene carbonate films in soil and phosphate buffer and their potential usefulness in agriculture and agrochemistry

Blends of poly(lactic acid) (PLA) with poly(propylene carbonate) (PPC) are currently in the phase of intensive study due to their promising properties and environmentally friendly features. Intensive study and further commercialization of PPC-based polymers or their blends, as usual, will soon face the problem of their waste occurring in the environment, including soil. For this reason, it is worth comprehensively studying the degradation rate of these polymers over a long period of time in soil and, for comparison, in phosphate buffer to understand the difference in this process and evaluate the potential application of such materials toward agrochemical and agricultural purposes. The degradation rate of the samples was generally accompanied by weight loss and a decrease in molecular weight, which was facilitated by the presence of PPC. The incubation of the samples in the aqueous media yielded greater surface erosions compared to the degradation in soil, which was attributed to the leaching of the low molecular degradation species out of the foils. The phytotoxicity study confirmed the no toxic impact of the PPC on tested plants, indicating it as a “green” material, which is crucial information for further, more comprehensive study of this polymer toward any type of sustainable application.Uniwersytet Humanistyczno-Przyrodniczy im. Jana Długosza w Częstochowie, UJD; Ministerstvo Školství, Mládeže a Tělovýchovy, MŠMT; Ministerstwo Edukacji i Nauki, MNiSWDKRVO; Ministry of Science and Higher Education for the Jan Dlugosz University in Czestochow

Is the retinol-binding protein 4 a possible risk factor for cardiovascular diseases in obesity?

Although many preventive and treatment approaches have been proposed, cardiovascular disease (CVD) remains one of the leading causes of deaths worldwide. Current epidemiological data require the specification of new causative factors, as well as the development of improved diagnostic tools to provide better cardiovascular management. Excessive accumulation of adipose tissue among patients suffering from obesity not only constitutes one of the main risk factors of CVD development but also alters adipokines. Increased attention is devoted to bioactive adipokines, which are also produced by the adipose tissue. The retinol-binding protein 4 (RBP4) has been associated with numerous CVDs and is presumably associated with an increased cardiovascular risk. With this in mind, exploring the role of RBP4, particularly among patients with obesity, could be a promising direction and could lead to better CVD prevention and management in this patient group. In our review, we summarized the current knowledge about RBP4 and its association with essential aspects of cardiovascular disease—lipid profile, intima-media thickness, atherosclerotic process, and diet. We also discussed the RBP4 gene polymorphisms essential from a cardiovascular perspective.info:eu-repo/semantics/publishedVersio

TEORIA WZMOCNIENIA JEDNOFOLIOWEGO DETEKTORA Z GAZOWYM POWIELANIEM ELEKTRONÓW

Gain prediction theory of single foil Gas Electron Multiplier detector was developed. Gas electron multiplier (GEM) detector with single foil was developed. Soft X-ray spectra with an energy of 5.9 keV emitted by the isotope Fe-55 were measured. On this basis, the dependence of gain and energy resolution from the detector voltage was determined. The simple theory of gain dependence on various detector parameters was developed. Preliminary results of the study confirmed the potential usefulness of the GEM detector as a substitute for the multiwire proportional chamber.Opracowano teorię wzmocnienia jednofoliowego detektora z gazowym powielaniem elektronów. Opracowano detektor z gazowym powielaniem elektronów z pojedynczą folią. Zmierzono widmo miękkiego promieniowania X, o energii 5,9 keV, emitowanego przez izotop Fe-55. Na tej podstawie wyznaczono zależność wzmocnienia i energetycznej zdolności rozdzielczej od napięcia zasilającego detektor. Opracowano prosta teorią zależności wzmocnienia od różnych parametrów detektora. Wstępne rezultaty badań potwierdzają potencjalną przydatność detektora GEM jako substytutu wielodrutowej komory proporcjonalnej