Impact of administration of folic acid on selected indicators of inflammation in patients with primary arterial hypertension.

The results of epidemiological and clinical tests have shown that in patients with primary arterial hypertension, a chronic mild inflammation develops. The purpose of the study was to determine whether administration of folic acid to patients with primary arterial hypertension influences concentrations of indicators of inflammation: hsCRP, sICAM-1 and sVCAM-1. MATERIAL AND METHODS: The examination was carried out in 41 patients with primary arterial hypertension, aged 19-65 (21 men and 20 women), without complications of hypertension and/or coexisting diseases. The examined patients were administered 15 mg of folic acid once a day for 45 days. Before and after administration of folic acid, concentrations of folic acid, homocysteine, hsCRP, sICAM-1 and sVCAM-1 in serum were assessed. Concentrations of folic acid and homocysteine were determined using the immunoenzymatic method (Abbott) on an AxSYM analyzer. The level of C-reactive protein (CRP) was determined with an ultra-sensitive turbidimetric assay on a Dimension analyzer (Siemens). Next, concentrations of adhesion particles sICAM-1 and sVCAM-1 were assessed with the ELISA technique (R&D). RESULTS: After the administration of folic acid in patients with primary arterial hypertension, a significant decrease in median concentrations of homocysteine in blood was observed. Simultaneously, the median hsCRP, ICAM-1 and VCAM-1 concentrations in serum in patients with primary arterial hypertension were significantly reduced. CONSLUSIONS: Administration of folic acid to persons with primary arterial hypertension in a dose of 15 mg/ day for 45 days caused a decrease in the concentration of homocysteine in serum. That could indirectly result in the decrease in concentrations of the indicators of inflammation (hsCRP, ICAM-1 and VCAM-1), as it is apparent from previous studies that hyperhomocysteinemia stimulates the synthesis of CRP and the expression of adhesion molecules.

Risk-based lung cancer screening performance in a universal healthcare setting.

Globally, lung cancer is the leading cause of cancer death. Previous trials demonstrated that low-dose computed tomography lung cancer screening of high-risk individuals can reduce lung cancer mortality by 20% or more. Lung cancer screening has been approved by major guidelines in the United States, and over 4,000 sites offer screening. Adoption of lung screening outside the United States has, until recently, been slow. Between June 2017 and May 2019, the Ontario Lung Cancer Screening Pilot successfully recruited 7,768 individuals at high risk identified by using the PLCOm2012noRace lung cancer risk prediction model. In total, 4,451 participants were successfully screened, retained and provided with high-quality follow-up, including appropriate treatment. In the Ontario Lung Cancer Screening Pilot, the lung cancer detection rate and the proportion of early-stage cancers were 2.4% and 79.2%, respectively; serious harms were infrequent; and sensitivity to detect lung cancers was 95.3% or more. With abnormal scans defined as ones leading to diagnostic investigation, specificity was 95.5% (positive predictive value, 35.1%), and adherence to annual recall and early surveillance scans and clinical investigations were high (>85%). The Ontario Lung Cancer Screening Pilot provides insights into how a risk-based organized lung screening program can be implemented in a large, diverse, populous geographic area within a universal healthcare system.

Proprotein convertase subtilisin/kexin type 9: a new target molecule for gene therapy.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a novel target for controlling plasma levels of low-density lipoprotein cholesterol (LDL-C) and decreasing the risk of cardiovascular diseases. At present it is clear that the major classes of commonly prescribed lipid-lowering medications increase serum PCSK9 levels and fail to protect a significant percentage of patients from cardiovascular events. Therefore development of new LDL-C lowering medications that either do not increase circulating PCSK9 levels or work through inhibition of PCSK9 expression and protease activity is a highly desirable approach to overcome hypercholesterolemia. Since there are several agents which are being evaluated in human preclinical and clinical trials, this review summarizes current therapeutic strategies targeting PCSK9, including specific antibodies, antisense oligonucleotides, small interfering RNAs (siRNAs) and other small-molecule inhibitors.

Highly upregulated expression of CD36 and MSR1 in circulating monocytes of patients with acute coronary syndromes.

Acute Coronary Syndromes (ACS) are a group of disorders caused by the significant reduction of circulation in coronary arteries. The most common reason of the dysfunction is a blood clot formed in place of plaque rupture. The role of scavenger receptors in development and progression of atherosclerosis has been confirmed in many animal experiments, however the knowledge about contribution of the receptors in the development of ACS symptoms in humans still remains insufficient. The aim of this work was to define the expression of two scavenger receptors: CD36 and MSR1 in monocytes of patients with ACS after the onset of symptoms and after the 6 months of treatment. The analysis of CD36 and MSR1 expression was carried out with the use of real-time PCR and flow cytometry. Analyses of lipid and glucose concentration in blood and the level of inflammatory markers in plasma were performed additionally for all ACS patients. All data obtained during the research were analyzed using statistical tests, such as Mann Whitney test, Wilcoxon test, or correlation. In all patients with symptoms of ACS the amount of CD36 and MSR1 mRNA in circulating monocytes, as well as the density of both receptors on the cells surface was significantly higher. Re-analysis of subjects after 6 months of treatment, showed a significant decrease in the CD36 and MSR1 expression in all patients who received atorvastatin. The results of presented studies demonstrate that both investigated receptors are involved in the development and/or progression of ACS.