ObjectiveTo determine the impact of sodium-dependent glucose type 2 cotransporter inhibitors on the renal function in acute heart failure.MethodsIn a single-centre, controlled, randomised study, patients were prescribed dapagliflozin in addition to standard therapy, or were in receipt of standard therapy. The prespecified outcome was renal function deterioration; the secondary outcomes were the development of resistance to diuretics, weight loss, death during hospitalisation and the rehospitalisation or death for any reason within 30 days following discharge.Results102 patients were included (73.4±11.7 years, 57.8% men). The average left ventricular ejection fraction was 44.9%±14.7%, the average N-terminal prohormone of brain natriuretic peptide (NT-proBNP) was 4706 (1757; 11 244) pg/mL, the average estimated glomerular filtration rate (eGFR) was 51.6±19.5 mL/min. eGFR decreased 48 hours after randomisation in the dapagliflozin group (−4.2 (−11.03; 2.28) mL/min vs 0.3 (−6; 6) mL/min; p=0.04) but did not differ between the groups on discharge (54.71±19.18 mL/min and 58.92±24.65 mL/min; p=0.36). The incidence of worsening renal function did not differ (34.4% vs 15.2%; p=0.07). In the dapagliflozin group, there was less tendency to increase the dose of loop diuretics (14% vs 30%; p=0.048), lower average doses of loop diuretics (78.46±38.95 mg/day vs 102.82±31.26 mg/day; p=0.001) and more significant weight loss (4100 (2950; 5750) g vs 3000 (1380; 4650) g; p=0.02). In-hospital mortality was 7.8% (4(8%) in the dapagliflozin and 4 (7.7%) in the control group (p=0.95). The number of deaths within 30 days following discharge in the dapagliflozin group and in the control group was 9 (19%) and 12 (25%), p=0.55; the number of rehospitalisations was 14 (29%) and 17 (35%), respectively (p=0.51).ConclusionThe use of dapagliflozin was associated with a more pronounced weight loss and less need to increase diuretic therapy without significant deterioration of the renal function. Dapagliflozin did not improve the in-hospital and 30-day prognosis after discharge.Trial registration numberN04778787.
The primary objective of this clinical study was to evaluate the effect of a dietary multivitamin, multimineral and phytonutrient (VMP) supplement on blood nutrient status and biomarkers of heart health risk in a Russian population. One hundred twenty healthy adults (40–70 years) were recruited for a 56-day (eight-week) randomized, double blind, placebo controlled study with parallel design. Subjects were divided into two groups and received either a VMP or a placebo (PLA) supplement. Blood nutrient levels of β-carotene, α-tocopherol, vitamin C, B6, B12, red blood cell (RBC) folate, Zinc and Selenium were measured at baseline and on Days 28 and 56, and quercetin was measured at baseline and on Day 56. Blood biomarkers of heart health, i.e. homocysteine (Hcy), high-sensitivity C-reactive protein (hs-CRP), oxidized LDL (ox-LDL), gamma-glutamyl transferase (GGT), uric acid and blood lipid profile, were measured at baseline and Day 56. Dietary VMP supplementation for 56 days significantly increased circulating levels of quercetin, vitamin C, RBC folate and partially prevented the decline in vitamin B6 and B12 status. Both serum Hcy and GGT were significantly reduced (−3.97 ± 10.09 µmol/L; −1.68 ± 14.53 U/L, respectively) after VMP supplementation compared to baseline. Dietary VMP supplementation improved the nutrient status and reduced biomarkers of heart health risk in a Russian population.
Background/Aim: A series of experiments on HeLa cells were conducted to provide new information concerning the anti-cancer properties of jaspine B hydrochloride (JBH). Materials and Methods: HeLa cells treated with 0.5 μmol/l JBH for 24, 48, and 72 h underwent flow cytometric analysis of the cell cycle, and measurement of phosphatidylserine externalization, mitochondrial membrane potential (MMP), casp-3 activation, cleavage of PARP, ceramide levels, aSMase activity, and Bcl-2 release. nSMase activity was measured by a colorimetric assay. Gene expression was determined by qRT-PCR. Immunocytochemistry was performed to detect p21 and p27 expression. Results: JBH-induced apoptosis in HeLa cells associated with externalization of phosphatidylserine, reduced MMP, activation of casp-3, and cleavage of PARP as well as up-regulation of TNF-α, FasL, and casp-8. Significant increase in nSMase activity, ceramide levels, Bcl-2 release (predominantly in the inactive form), and pro-apoptotic nuclear localization of p21 and p27 were also detected. Conclusion: JBH-induced apoptosis in HeLa cells is associated with disrupted sphingolipid homeostasis resulting in increased ceramide levels.Cervical cancer (CC) is the fourth most common type of malignancy and cause of cancer death in women worldwide (1). Even though the incidence and mortality rates have declined in the developed countries over past few decades, CC still remains the most common gynecological cancer (2). Furthermore, women treated for cervical intraepithelial neoplasia are also at increased risk to develop invasive CC (3). Most commonly, the treatment involves combination of surgery, radiotherapy, cisplatin-based chemotherapy and brachytherapy (4). Although, current approaches have improved patient survival, treatment is still associated with significant reduction in quality-of-life. Therefore, the search for new promising anticancer agents with lower toxicity has to continue to increase the efficiency and tolerability of treatment.Natural compounds play an important role in cancer prevention and treatment (5). The marine environment provides a unique reservoir of biologically active substances, which represent a promising source of potential novel anticancer agents. Primitive multicellular sea sponges from the genus Jaspis (family Jaspidae) represent a rich source of structurally novel natural compounds acting as antifungal 2875
1 ФГБУН «ФИЦ питания и биотехнологии», Москва, Россия 2 ФГБОУ ВО "Российский национальный исследовательский медицинский университет имени Н.И. Пирогова", Москва, Россия 3 Городская клиническая больница №1 Департамента здравоохранения г. Москвы, РоссияОбоснование. Изучение молекулярно-генетических маркеров и патогенетических механизмов нейрогормональной активации, а также их значения в формировании сердечной недостаточности при ожирении является актуальной проблемой современной медицины, решение которой позволит осуществлять эффективную профилактику сердечно-сосудистых осложнений, оптимизировать лечение и улучшить прогноз пациентов с ожирением. Цель. Поиск генетических маркеров, предположительно вовлеченных в патогенез вторичной диастолической сердечной недостаточности (ДСН) у больных с ожирением. Методы. Проводилась диагностика методом полимеразной цепной реакции цельной крови 104 больных ожирением, которые были разделены на 2 группы в зависимости от наличия диастолической сердечной недостаточности. Анализировались следующие гены-кандидаты: ген ангиотензиногена AGT (C521T и T704C), ген рецептора ангиотензина II первого типа AGTR1 (A1166C), ген рецептора ангиотензина II второго типа AGTR2 (G1675A), ген альдостеронсинтазы CYP11B2 (C(-344)T). Результаты. Показано, что развитие вторичной ДСН у лиц с ожирением обоих полов ассоциируется с мутацией гена альдостеронсинтазы CYP11B2, а именно с заменой аллеля С в положении -344 на аллель Т и наличием генотипа Т/Т. Относительный риск развития заболевания при генотипе Т/Т повышен в 5,93 раза у мужчин (р=0,008) и в 4,57 раза у женщин (р=0,014). Для мужчин имеет значение мутация гена ангиотензиногена AGT, а именно замена аллеля C в положении 521 на аллель T. При этом относительный риск развития ДСН при генотипе Т/Т повышен в 4,26 раза (р=0,039). Мутации генов рецептора ангиотензина II первого типа AGTR1 (A1166C) и рецептора ангиотензина II второго типа AGTR2 (G1675A) не ассоциированы с развитием ДСН у больных с ожирением. Заключение. Представленные данные могут быть использованы при стратификации риска развития вторичной сердечной недостаточности у лиц с ожирением.КЛЮЧЕВЫЕ СЛОВА: сердечная недостаточность, ожирение, генетические полиморфизмы, ген ангиотензиногена AGT, ген рецептора ангиотензина II первого типа AGTR1, ген рецептора ангиотензина II второго типа AGTR2, ген альдостеронсинтазы CYP11B2. 3 First Graduate Hospital named after NI Pirogov, Moscow, Russia Background: the study of molecular genetic markers and pathogenetic mechanisms of neurohormonal activation, as well as their importance in the formation of heart failure in obesity, is an urgent problem of modern medicine, the solution of which will allow eff ective prevention of cardiovascular complications, optimize treatment and improve the prognosis of obese patients. Aims: search for genetic markers presumably involved in the pathogenesis of secondary diastolic heart failure in patients with obesity. Materials and methods: PCR-diagnostics of whole blood of 104 patients with obesity was carried out, which were divid...
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