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The Relationship Between Aortic Tissue Sirtuin 1 Levels and Type A Aortic Dissections and Ascending Aortic Aneurysms
No full textINTRODUCTION: Type A aortic dissections are pathologies with high mortality rates. Although ascending aortic aneurysms are typically planned for elective surgery, they are significant conditions in cardiovascular surgery due to their potential to cause type A aortic dissection. This study, which is the first to examine sirtuin 1 (SIRT1) in human ascending aortic tissues, aims to elucidate the relationship between ascending aortic pathologies and the SIRT1 protein. METHODS: A case-control study was conducted using aortic tissues and demographic data from patients who underwent surgery for ascending aortic aneurysm and type A aortic dissection. Coronary artery bypass patients were selected as the control group. The groups were compared in terms of SIRT1 levels. RESULTS: The study included a total of 46 patients (16 in the aneurysm group, 14 in the dissection group, and 16 in the control group). The SIRT1 protein level was the highest in the ascending aortic aneurysm group (214, interquartile range [IQR] 79 - 270), followed by the dissection group (172, IQR 148 - 224), and the lowest in the control group (104, IQR 78 - 123) (P = 0.014). SIRT1 level was found to be low in patients with coronary artery disease (P = 0.001), peripheral artery disease (P = 0.008), and hypertension (P = 0.023). CONCLUSIONS: Type A aortic dissections are associated with elevated SIRT1 levels in the tissue. Systemic atherosclerotic diseases, such as coronary and peripheral artery diseases, are associated with decreased SIRT1 levels. There is also a relationship between hypertension and sirtuin1 levels
Human Papilloma Virüs (HPV) testi Öncesi ve Sonrası Bazı Değişkenler Açısından Kadınların Algılanan Stres Düzeylerinin Değerlendirilmesi
No full textIncreased vein wall thickness in Behçet’s disease: from intravascular mechanical stress to vascular remodelling and venous thrombosis
No full textComparative Investigation of Cytotoxic Effects of Structurally Diverse Small Molecules and In Silico Analysis of 1‐Acetyl‐4‐(4‐Hydroxyphenyl)piperazine
No full textAntibacterial and immuno-oxidative effects of Melittin against Helicobacter pylori: in vitro and in vivo evidence
No full textBackground: Helicobacter pylori (H. pylori) is a common pathogen that causes serious pathologies such as gastritis, ulcers, and gastric cancer. This study evaluates the therapeutic effects of melittin on H. pylori induced gastric injury, oxidative stress, and tissue damage in an in vivo model. Methods and results: Melittin was administered at two doses (10 µg/kg and 40 µg/kg) and outcomes were compared with standard antibiotic therapy. H. pylori infection significantly increased gastric urease activity, the pro-inflammatory cytokine IL-1β, and oxidative stress markers total oxidant status (TOS) and malondialdehyde (MDA); these increases were suppressed by melittin treatment. Melittin also enhanced antioxidant capacity total antioxidant status (TAS) and glutathione (GSH) and supported gastric tissue healing by reducing inflammation and neutrophil activity. Notably, 10 µg/kg melittin led to a ~ 74% reduction in bacterial colony counts and decreased tissue damage. Histopathology confirmed that melittin lowered H. pylori colonization and inflammation scores. Furthermore, the higher dose (40 µg/kg) showed more limited effects on oxidative stress than the lower dose. GSH levels improved with melittin. Conclusions: Melittin demonstrates antibacterial and anti-inflammatory activity against H. pylori associated gastric pathology, with several outcomes favoring the lower dose (10 µg/kg). These findings indicate melittin as a promising therapeutic candidate; however, additional comprehensive studies are needed to support clinical translation
Spermine synthase in Snyder-Robinson syndrome and cancer
No full textSpermine synthase (Sms), a key enzyme in polyamine biosynthesis, catalyzes the conversion of spermidine to spermine using decarboxylated S-adenosylmethionine (dcAdoMet) as an aminopropyl donor. Although Sms is well-characterized in eukaryotes, it is relatively rare in bacteria, where spermine in some species is probably produced by non-specific aminopropyltransferases. In humans, SMS mutations cause Snyder-Robinson syndrome (SRS), an X-linked disorder characterized by intellectual disability, osteoporosis, and neurological dysfunction due to disrupted polyamine homeostasis. Structural studies reveal that Sms functions as a dimer, with its N-terminal domain essential for enzymatic activity. Loss of Sms leads to spermine deficiency, elevated spermidine levels, and metabolic imbalances, contributing to SRS pathology. Therapeutic strategies under investigation include rebalancing spermidine/spermine ratio, polyamine biosynthesis inhibitors (e.g., DFMO), antioxidants and gene therapy using AAV vectors. Conversely, in multiple cancer types, Sms overexpression promotes tumor progression by altering polyamine metabolism, activating oncogenic pathways (e.g., AKT, mTOR), and facilitating immune evasion. Elevated Sms expression correlates with poor prognosis in colorectal, pancreatic, hepatocellular, and head and neck cancers, highlighting its potential as a therapeutic target. However, spermine’s role is context-dependent, exhibiting both pro-tumorigenic and cytotoxic effects. While inhibition of Sms may suppress cancer growth, its deficiency in SRS underscores the delicate balance required in polyamine regulation. Insights from SRS and cancer studies highlight Sms as a critical enzyme in cellular homeostasis, with therapeutic implications for both degenerative and proliferative diseases. Further research is needed to elucidate its complex role and optimize targeted interventions
