Fish Oil Derivatives in Hypertriglyceridemia: Mechanism and Cardiovascular Prevention: What Do Studies Say?

Hypertriglyceridemia is a type of dyslipidemia characterized by high triglyceride levels in the blood and increases the risk of cardiovascular disease. Conventional management includes antilipidemic medications such as statins, lowering LDL and triglyceride levels as well as raising HDL levels. However, the treatment may be stratified using omega-3 fatty acid supplements such as eicosatetraenoic acid (EPA) and docosahexaenoic acid (DHA), aka fish oil derivatives. Studies have shown that fish oil supplements reduce the risk of cardiovascular diseases; however, the underlying mechanism and the extent of reduction in CVD need more clarification. Our paper aims to review the clinical trials and observational studies in the current literature, investigating the use of fish oil and its benefits on the cardiovascular system as well as the proposed underlying mechanism.

[Autophagy Markers Induced by Influenza Virus and MUC1 Expressions in Cancer-Derived Cell Lines]. / Kanser Kökenli Hücre Dizilerinde Influenza Virüsünün Indükledigi Otofaji Belirteçleri ile MUC1 Ekspresyonu Arasindaki Iliskinin Arastirilmasi.

Influenza virus-induced autophagy is often accompanied by apoptosis and results in cell death in virus-infected cells. It is well known that autophagy is modulated by the mTOR/PI3K/Akt pathway, which plays an important role in the response to the presence of energy sources and external stimuli. This pathway is modulated by mucin 1 (MUC1), which has extracellular and intracellular components and plays an important role in metastasis and chemotherapeutic resistance. In this study, it was aimed to investigate the expression of MUC1 after the inoculation of influenza viruses into the cancer-derived cell cultures and, accordingly, the changes in autophagy markers such as mTOR and LC3B. In this study, MCF-7, HeLa and A-549 cell lines were used which have adenocarcinoma origin. To control the growth of influenza virus in these cells, the MDCK cell line was also inoculated. Centrifuge-enhanced shell-vial cell culture method was used in all experiments. Influenza A (H1N1) pdm09 strain was inoculated into these cell lines then the expressions of viral nucleic acid and cycle threshold (Ct) of MUC1, mTOR, LC3B associated genes were investigated by quantitative real-time reverse transcriptase polymerase chain reaction (qRTPCR) method in the samples taken from the supernatants of all cells at the end of the 48-hour incubation period. To investigate whether these markers were present in cells, after all cells were permeabilized with paraformaldehyde, cell-coated infected coverslips were stained with fluorescent labeled monoclonal antibodies developed against MUC1, mTOR, LC3B and influenza virus antigens. In the examination of fluorescence microscopy, all of the cell cultures (MCF-7, He-La and A-549) infected with influenza virus yielded positive results in terms of LC3B, mTOR and MUC1 monoclonal antibody staining, whereas all of the non-infected cells were found negative. Cycle threshold values of MUC1, LC3B and mTOR associated genes were found to be lower in A-549 cell line inoculated with influenza virus. Although protein expression was demonstrated in MCF-7 and He-La cell lines, similar changes were not detected in the 1/Ct values of genes in the autophagy pathway. The Ct value of the MUC1 gene was found to be higher only in the MCF-7 cell line after inoculation. In conclusion, it was observed that the specific expression pattern for influenza virus-induced autophagy was formed only in the A-549 cell line among the adenocarcinoma cells. It was thought that this relationship could constitute a dataset in further research on lung adenocarcinoma. However, in future studies, the determination of the expression of these genes at the protein level by using further tests will provide better comparison of the results.

Premature Myocardial Infarction: A Rising Threat.

Myocardial infarction mostly presents with atypical signs and symptoms and has different risk factors in young individuals compared to older individuals. These risk factors are often preventable, therefore recognizing them and taking precautions can save these patients from suffering myocardial infarction. Scarcity of studies and lack of guidelines for assessment and management of young MI patients, make it more challenging for these individuals to get accurate medical care, even though MI in this age group is on the rise. Traditional risk factors, such as smoking, hyperlipidemia, hypertension, male sex, obesity, and family history of premature cardiovascular disease, contribute to the risk of myocardial infarction at a young age, but additional non-traditional risk factors, such as substance abuse, thrombophilia, coronary anomalies, immune disease, allergic reactions, and psychological stressors, uniquely contribute to the risk profile of young individuals. This review is aimed to discuss and guide the risk factor assessment for the development of myocardial infarction in young individuals based on current evidence and our >20-year of experience in Young Myocardial Infarction Clinic.

Case report: Therapy adherence, MTTP variants, and course of atheroma in two patients with HoFH on low-dose, long-term lomitapide therapy.

Background: Homozygous familial hypercholesterolemia (HoFH) is a rare and devastating genetic condition characterized by extremely elevated levels of low-density lipoprotein cholesterol (LDL-C) leading to an increased risk of premature atherosclerosis. Patients with Homozygous familial hypercholesterolemia mostly present with mutations in LDLR; however, herein, we present two cases with concomitant microsomal triglyceride transfer protein mutations, who showed different clinical courses and treatment adherence on long-term therapy with the new MTTP inhibitor lomitapide. Objectives: We aimed to present the possibility of preventing the progression of atherosclerotic burden with effective and safe LDL-C reduction in patients with Homozygous familial hypercholesterolemia on low-dose lomitapide therapy and emphasize the role of treatment adherence in therapy success. Methods: We present two patients with phenotypically Homozygous familial hypercholesterolemia, a compound heterozygous woman and a simple homozygous man, both with LDLR and additional MTTP mutations, who were treated with the MTTP-inhibiting agent lomitapide, with different treatment compliances. The role of impulsivity was investigated through Barratt Impulsivity Scale 11, and the extent of the atherosclerotic burden was followed up using coronary artery calcium scoring, echocardiographic and sonographic findings, and, eventually, through a strict follow-up of laboratory parameters. The patients were on lomitapide for 8 and 5 years, respectively, with no adverse effects. Conclusion: When accompanied by good adherence to therapy, low-dose lomitapide on top of standard lipid-lowering therapy with decreased frequency of lipid apheresis prevented the progression of atherosclerotic burden. Non-compliance might occur due to patient impulsivity and non-adherence to a low-fat diet.