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Type 2 diabetes accounts for a large proportion of cardiovascular disease within the UK. Inflammation is increasingly seen as a core process (even touted as a causative factor) connecting the metabolic syndrome and cardiovascular disease. Inflammatory markers, adhesion molecules, transcription regulators such as PPAR-gamma and NF-kappa B are being recognised as key elements of the underlying pathological process. In particular the links between oxidative stress, metabolic syndrome components and a pro-inflammatory milieu are becoming increasingly recognised.Salicylates have been used extensively for more than a hundred years but remain the subject of much research and scientific debate. Mechanisms of aspirin action, such as effects on endothelial function, oxidative stress, hyperglycaemia, inflammation, and mechanisms of aspirin resistance are being elucidated. With the advent of COX-2 selective inhibitors, the importance of the cyclo-oxygenase (COX-1 & COX-2 enzymes) pathways and the implications of more selective COX manipulation are being re-evaluated. There is no universal consensus on the use and dose of aspirin in diabetes. This review focuses upon the impact that aspirin may have to ameliorate the pathophysiology of diabetes and CVD. [ABSTRACT FROM AUTHOR]

KIF1A-associated neurological diseases (KANDs) are a group of inherited conditions caused by changes in the microtubule (MT) motor protein KIF1A as a result of KIF1A gene mutations. Anterograde transport of membrane organelles is facilitated by the kinesin family protein encoded by the MT-based motor gene KIF1A . Variations in the KIF1A gene, which primarily affect the motor domain, disrupt its ability to transport synaptic vesicles containing synaptophysin and synaptotagmin leading to various neurological pathologies such as hereditary sensory neuropathy, autosomal dominant and recessive forms of spastic paraplegia, and different neurological conditions. These mutations are frequently misdiagnosed because they result from spontaneous, non-inherited genomic alterations. Whole-exome sequencing (WES), a cutting-edge method, assists neurologists in diagnosing the illness and in planning and choosing the best course of action. These conditions are simple to be identified in pediatric and have a life expectancy of 5-7 years. There is presently no permanent treatment for these illnesses, and researchers have not yet discovered a medicine to treat them. Scientists have more hope in gene therapy since it can be used to cure diseases brought on by mutations. In this review article, we discussed some of the experimental gene therapy methods, including gene replacement, gene knockdown, symptomatic gene therapy, and cell suicide gene therapy. It also covered its clinical symptoms, pathogenesis, current diagnostics, therapy, and research advances currently occurring in the field of KAND-related disorders. This review also explained the impact that gene therapy can be designed in this direction and afford the remarkable benefits to the patients and society.

COVID-19 is a serious respiratory infection caused by a beta-coronavirus that is closely linked to SARS. Hypoxemia is a symptom of infection, which is accompanied by acute respiratory distress syndrome (ARDS). Augmenting supplementary oxygen may not always improve oxygen saturation; reversing hypoxemia in COVID-19 necessitates sophisticated means to promote oxygen transfer from alveoli to blood. Inhaled nitric oxide (iNO) has been shown to inhibit the multiplication of the respiratory coronavirus, a property that distinguishes it from other vasodilators. These findings imply that NO may have a crucial role in the therapy of COVID-19, indicating research into optimal methods to restore pulmonary physiology. According to clinical and experimental data, NO is a selective vasodilator proven to restore oxygenation by helping to normalize shunts and ventilation/perfusion mismatches. This study examines the role of NO in COVID-19 in terms of its specific physiological and biochemical properties, as well as the possibility of using inhaled NO as a standard therapy. We have also discussed how NO could be used to prevent and cure COVID-19, in addition to the limitations of NO., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Infectious diseases are defined as a group of diseases caused by any infecting microorganism which are highly potent to severely affect human life. The end can vary from critical infection to mortality. Most infectious diseases are reported with a rapid rate of transmission. Marburg virus disease is a kind of infectious viral disease usually manifested as hemorrhagic fever. The latest reported case of Marburg virus disease confirmed by WHO was on 6th August 2021 in the south-western province of Guinea. Marburg virus disease exhibit similar manifestations to that of infection with the Ebola virus. Though not widely spread to emerge as a pandemic, Marburg virus disease remains a serious threat to human life. This review emphasizes the novel current facts determined through various studies related to Marburg virus infection. From these promising theories, the review tries to put forward the importance of various study conclusions, which are likely to have a major impact on the health sector in the near future., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Objectives: The effect of aspirin upon platelet function is well documented although experimental studies suggest that aspirin may also affect oxidative stress, vascular inflammation, endothelial dysfunction and dysglycaemia. The optimal dose of aspirin for cardiovascular protection in type 2 diabetes is still debated. We examined the effects of different doses of aspirin upon these novel markers of cardiovascular risk and any association between aspirin-mediated changes in these markers., Methodology: Subjects with type 2 diabetes attended for baseline evaluation including BMI, glycaemic and lipid markers, endothelial function (photoplethysmography), insulin resistance (HOMA), inflammation (sVCAM-1 and Hs-CRP) and markers of oxidative stress [total anti-oxidant status (TAOS and FRAP), whole blood total glutathione (GSH) assays]. Subjects then received in random, sequential, blinded fashion aspirin 75 mg day(-1) , aspirin 300 mg day(-1) , aspirin 3.6 g day(-1) or placebo for 2 weeks with a 2-week washout. The above investigations were repeated after each intervention. Aspirin-related changes compared with placebo were analysed using repeated measures ANOVA., Results: Subjects = 17 (M - 12; F - 5), mean age - 57.4 ± 9.1 years (mean ± 1 SD), HbA1c - 63 ± 13 mmol mol(-1) (7.9 ± 1.2%), total cholesterol 4.57 ± 1.01 mmol l(-1) . At baseline TAOS value was 59.3 ± 9.7 μM AEAC (Ascorbate Equivalent Anti-oxidant Concentration), glutathione 302.2 ± 183.3 mmol l(-1) and FRAP 0.86 ± 0.23 mM FeII. None of the aspirin doses had a significant impact upon BMI, blood pressure, lipid parameters, insulin sensitivity (HOMA), FRAP, TAOS, GSH, endothelial function, glycaemic control (fructosamine) or inflammation (sVCAM-1 and HsCRP)., Conclusions: Aspirin exhibited no significant dose-dependent effect on markers of vascular inflammation, oxidative stress, insulin resistance and endothelial function (photoplethysmography) when used in type 2 diabetes over a 2-week period. (, Clinical Trials Registration: NCT00898950, EUDRACT:2004-001418-14)., (© 2013 John Wiley & Sons Ltd.)