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Aim: The study aims to investigate the association between type 2 diabetes and adipokines, particularly resistin and adiponectin, in insulin resistance. It also explores the potential of the resistin to adiponectin ratio as an indicator for these conditions Methods: This research involved 198 participants, including 100 patients with type 2 diabetes and 98 controls. It focused on measuring various biochemical parameters like HbA1c, fasting plasma glucose, lipid profiles (low-density lipoprotein, oxidized low-density lipoprotein, triglyceride, total cholesterol), and adipokines (resistin and adiponectin). The study utilized the Homeostasis Model Assessment of Insulin Resistance and Triglyceride-Glucose index to evaluate insulin resistance. Results: Type 2 diabetic patients exhibited higher levels of HbA1c, fasting plasma glucose, lipid profiles, and resistin, but lower adiponectin levels compared to controls. Adiponectin showed a negative correlation with insulin resistance, while resistin demonstrated a positive correlation. Both adipokines significantly related to atherogenic markers, with adiponectin offering protection against atherosclerosis and resistin augmenting it. Conclusion: The findings underscore the complex roles of resistin and adiponectin in the pathophysiology of type 2 diabetes, insulin resistance. The resistin to adiponectin ratio could be a useful biomarker for insulin resistance. These insights suggest potential therapeutic strategies for treating diabetes and preventing its complications. [ABSTRACT FROM AUTHOR]

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Aim: This study aimed to assess the anti-inflammatory activity and potential mechanisms of essential oil of Tamarix aphylla (EOTA). Methods: The essential oils were extracted from the plant’s aerial parts using hydrodistillation and analyzed through gas chromatography and mass spectrometry (GC/MS). The essential oils were assessed for their anti-inflammatory effects using well-established inflammation models, namely carrageenan-induced paw edema and peritonitis. To evaluate the antioxidant activity of the essential oil, measurements were taken for nitric oxide radical-scavenging activity and lipid peroxidation. Results: The predominant components of the EOTA were 6,10,14-Trimethyl-2-pentadecanone (20.2%), β-Ionone (20.1%), Dodecanoic acid (12.2%), and trans-β-Caryophyllene (10%.1). The study found that EOTA significantly reduced edema, peritonitis, myeloperoxidase activity, and NOx-peritoneal lavage concentration induced by carrageenan. Additionally, the essential oil exhibited significant inhibition of nitric oxide radical production triggered by sodium nitroprusside. Furthermore, EOTA demonstrated the ability to prevent lipid peroxidation induced by Fe+2- or Fe+2 plus H2O2. Conclusion: The findings suggest that EOTA possesses anti-inflammatory activity, potentially linked to its antioxidant capacity. [ABSTRACT FROM AUTHOR]

The aims of this study were to evaluate the anti-inflammatory activity and the possible anti-inflammatory mechanisms of Anastatica hierochuntica essential oil (EOAH). The essential oils were obtained by hydrodistillation of the aerial parts of the plant, and analyzed using gas chromatography and mass spectrometry (GC/MS). Their anti-inflammatory activity was evaluated using classical model of inflammation (carrageenan-induced paw edema and peritonitis). Nitric oxide radical-scavenging activity and lipid peroxidation were determined to assess the antioxidant activity of the essential oil. The EOAH mainly comprised Cuminaldehyde (33.8%), trans-β-Caryophyllene (32.5%), and Linalool (8.2%). EOAH significantly reduced edema, peritonitis, myeloperoxidase activity, and NOx-peritoneal lavage concentration induced by carrageenan. In addition, nitric oxide radical generated from sodium nitroprusside was significantly inhibited by the essential oil. Furthermore, EOAH was able to prevent Fe+2- or Fe+2 plus H2O2-induced lipid peroxidation. In conclusion, the EOAH exerts anti-inflammatory activity that could be related to its antioxidant capacity. [ABSTRACT FROM AUTHOR]

Snakebites have been reported to induce hematological complications. Thrombocytopenia usually occurs secondary to disseminated intravascular coagulation (DIC) and coagulopathy induced by the snake bite. However, thrombocytopenia can develop after the snake bite, even in the absence of significant coagulopathy. We reported the case of a 36-year-old Jordanian male patient who was bitten by Arabian Macrovipera Lebetina Obtusa (Levantine viper), which developed venom-induced severe thrombocytopenia without coagulopathy. A progressive drop in platelet count was observed during his admission. His condition improved after anti-venom therapy, and he was discharged after 4 weeks of treatment for a full recovery. This case supports that snake venom can produce severe thrombocytopenia without significant coagulopathy, which can be treated successfully with anti-venom and the best supportive care. [ABSTRACT FROM AUTHOR]

Aims Cord blood-derived endothelial colony-forming cells (CB-ECFCs) are a defined progenitor population with established roles in vascular homeostasis and angiogenesis, which possess low immunogenicity and high potential for allogeneic therapy and are highly sensitive to regulation by reactive oxygen species (ROS). The aim of this study was to define the precise role of the major ROS-producing enzyme, NOX4 NADPH oxidase, in CB-ECFC vasoreparative function. Methods and results In vitro CB-ECFC migration (scratch-wound assay) and tubulogenesis (tube length, branch number) was enhanced by phorbol 12-myristate 13-acetate (PMA)-induced superoxide in a NOX-dependent manner. CB-ECFCs highly-expressed NOX4, which was further induced by PMA, whilst NOX4 siRNA and plasmid overexpression reduced and potentiated in vitro function, respectively. Increased ROS generation in NOX4-overexpressing CB-ECFCs (DCF fluorescence, flow cytometry) was specifically reduced by superoxide dismutase, highlighting induction of ROS-specific signalling. Laser Doppler imaging of mouse ischaemic hindlimbs at 7 days indicated that NOX4-knockdown CB-ECFCs inhibited blood flow recovery, which was enhanced by NOX4-overexpressing CB-ECFCs. Tissue analysis at 14 days revealed consistent alterations in vascular density (lectin expression) and eNOS protein despite clearance of injected CB-ECFCs, suggesting NOX4-mediated modulation of host tissue. Indeed, proteome array analysis indicated that NOX4-knockdown CB-ECFCs largely suppressed tissue angiogenesis, whilst NOX4-overexpressing CB-ECFCs up-regulated a number of pro-angiogenic factors specifically-linked with eNOS signalling, in parallel with equivalent modulation of NOX-dependent ROS generation, suggesting that CB-ECFC NOX4 signalling may promote host vascular repair. Conclusion Taken together, these findings indicate a key role for NOX4 in CB-ECFCs, thereby highlighting its potential as a target for enhancing their reparative function through therapeutic priming to support creation of a pro-reparative microenvironment and effective post-ischaemic revascularization. [ABSTRACT FROM AUTHOR]

Despite being first described 45 years ago, the existence of a distinct diabetic cardiomyopathy remains controversial. Nonetheless, it is widely accepted that the diabetic heart undergoes characteristic structural and functional changes in the absence of ischaemia and hypertension, which are independently linked to heart failure progression and are likely to underlie enhanced susceptibility to stress. A prominent feature is marked collagen accumulation linked with inflammation and extensive extracellular matrix changes, which appears to be the main factor underlying cardiac stiffness and subclinical diastolic dysfunction, estimated to occur in as many as 75% of optimally controlled diabetics. Whether this characteristic remodelling phenotype is primarily driven by microvascular dysfunction or alterations in cardiomyocyte metabolism remains unclear. Although hyperglycaemia regulates multiple pathways in the diabetic heart, increased reactive oxygen species (ROS) generation is thought to represent a central mechanism underlying associated adverse remodelling. Indeed, experimental and clinical diabetes are linked with oxidative stress which plays a key role in cardiomyopathy, while key processes underlying diabetic cardiac remodelling, such as inflammation, angiogenesis, cardiomyocyte hypertrophy and apoptosis, fibrosis and contractile dysfunction, are redox sensitive. This review will explore the relative contributions of the major ROS sources (dysfunctional nitric oxide synthase, mitochondria, xanthine oxidase, nicotinamide adenine dinucleotide phosphate oxidases) in the diabetic heart and the potential for therapeutic targeting of ROS signalling using novel pharmacological and non-pharmacological approaches to modify specific aspects of the remodelling phenotype in order to prevent and/or delay heart failure development and progression. [ABSTRACT FROM AUTHOR]