Nitric Oxide in the Management of Respiratory Consequences in COVID-19: A Scoping Review of a Different Treatment Approach.

The severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) virus causing COVID-19 significantly affects the respiratory functions of infected individuals by massively disrupting the pulmonary oxygenation and activating the synthesis of proinflammatory cytokines, inducing severe oxidative stress, enhanced vascular permeability, and endothelial dysfunction which have rendered researchers and clinicians to depend on prophylactic treatment due to the unavailability of proper disease management approaches. Previous studies have indicated that nitric oxide (NO) application appears to be significant concerning the antiviral activities, antioxidant, and anti-inflammatory properties in relieving disease-related symptoms. To identify, explore, and map the literature on the role of nitric oxide in the management of respiratory consequences in COVID-19 through this scoping review, Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed during the search to answer the focal question: "What are the potential uses of nitric oxide in the management of respiratory failure in COVID-19?" Administering exogenous NO in the form of inhaled gas or stimulating the system to produce NO appears to be a suitable option to manage COVID-19-induced pneumonia and respiratory illness. This treatment modality seems to attenuate respiratory distress among patients suffering from severe infections or patients with comorbidities. Exogenous NO at different doses effectively reduces systemic hyperinflammation and oxidative stress, improves arterial oxygenation, and restores pulmonary alveolar cellular integrity to prevent the lungs and other organs from further damage. This therapy could pave the way for better management of COVID-19 before the onset of disease-related complications.

Does periodontitis influence the risk of COVID-19? A scoping review.

OBJECTIVE: Research has shown that the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) significantly influences the oral microbiome to expedite systemic diseases by invading harmful oral pathogens near and distant organs. To identify, explore, and map the possible mechanisms underlying periodontitis in severe coronavirus disease 2019 (COVID-19) cases. MATERIAL AND METHODS: Relevant articles published from December 2019 to February 2022 were identified and screened using keywords and inclusion criteria from various databases. RESULTS: This review sheds light on multiple pathways of periodontitis, the spread of periodontal infection and microbial metabolites to the lungs, and the dysregulated immune system with elevated cytokines, reactive oxygen species generation, nuclear DNA damage, and senescence, which have the potential to promote stronger viral attachment to host cells and the onset of COVID-19 manifestation with increased severity and risk of mortality. In addition, the cytokine connection to SARS-CoV-2, T-cell responses against periodontitis, its connection with COVID-19, the role of host factors, and periodontal therapy have been discussed. CONCLUSIONS: The relationship between COVID-19 and periodontitis needs further investigation along with the development of alternative therapies to prevent periodontitis for better management and control of COVID-19.

Association of TOR1A and GCH1 Polymorphisms with Isolated Dystonia in India.

Isolated dystonia is a common movement disorder often caused by genetic mutations, although it is predominantly sporadic in nature. Common variants of dystonia-related genes were reported to be risk factors for idiopathic isolated dystonia. In this study, we aimed to analyse the roles of previously reported GTP cyclohydrolase (GCH1) and Torsin family 1 member A (TOR1A) polymorphisms in an Indian isolated dystonia case-control group. A total of 292 sporadic isolated dystonia patients and 316 control individuals were genotyped for single-nucleotide polymorphisms (SNPs) of GCH1 (rs3759664:G > A, rs12147422:A > G and rs10483639:C > G) and TOR1A (rs13300897:G > A, rs1801968:G > C, rs1182:G > T and rs3842225:G > Δ) using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and confirmed by direct Sanger sequencing. The statistical significance of allelic, genotypic and haplotypic associations of all of the SNPs were evaluated using the two-tailed Fisher exact test. The minor allele (A) of rs3759664 is significantly associated with isolated limb dystonia as a risk factor (p = 0.005). The minor allele (C) of rs1801968 is strongly associated with isolated dystonia (p < 0.0001) and most of its subtypes. The major allele of rs3842225 (G) may act as a significant risk factor for Writer's cramp (p = 0.03). Four different haplogroups comprising of either rs1182 or rs3842225 or in combination with rs1801968 and rs13300897 were found to be significantly associated with isolated dystonia. No other allelic, genotypic or haplotypic association was found to be significant with isolated dystonia cohort or its endophenotype stratified groups. Our study suggests that TOR1A common variants have a significant role in isolated dystonia pathogenesis in the Indian population, whereas SNPs in the GCH1 gene may have a limited role.

Dopamine ß Hydroxylase (DBH) is a potential modifier gene associated with Parkinson's disease in Eastern India.

BACKGROUND: Parkinson's disease (PD) is the debilitating movement disorder, distinguished by dopaminergic and norepinephrinergic neurodegeneration. Apart from candidate gene mutations, several modifier loci have been reported to be associated with the disease manifestation. The Dopamine ß-Hydroxylase (DBH) maintains cellular dopamine content and regulates dopamine turn over in neurons. Genetic polymorphisms of DBH are associated with PD and are found to alter plasma DBH activity in patients compared to healthy controls. Therefore, DBH activity in plasma could be a potential and easily detectable biomarkers for alteration of dopaminergic neuronal function in PD. METHODS: Plasma DBH activity has been assessed among PD cases and age-matched controls to identify correlation with PD. To elucidate the role of DBH polymorphisms in Eastern Indian PD patients, three SNPs (rs1611115, rs1108580 and rs129882) were selected and screened by PCR-RFLP and DNA sequencing analysis. RESULTS: The T-allele of rs129882 was more prevalent among patients than controls posing risk (p-value = 0.02, OR = 1.404, 95% CI = 1.047-1.883) towards PD. The dual-Luciferase assay in SHSY5Y cell line revealed that the T-allele of rs129882 increases Luciferase signal (p = 0.0269). However, the rs1611115 and rs1108580 did not show association with PD; plasma DBH activity was not significantly different between patients and controls (p-value > 0.05). Haplotypes constructed with three SNPs showed that the CAT haplotype to pose risk, TAC haplotype to provide protection against early disease onset and CGT being protective against non-motor symptoms. CONCLUSION: These data suggest that DBH might influence the susceptibility of PD.