Search

Additional file 2: Supplementary Table 2. Risk of bias assessment of individual studies using the QUIPS tool.

Supplemental material, sj-docx-1-ini-10.1177_17534259211053634 for Circulating innate lymphoid cell subtypes and altered cytokine profiles following an atherogenic high-fat diet by Vuyolwethu Mxinwa, Phiwayinkosi V. Dludla, Tawanda M. Nyambuya and Bongani B. Nkambule in Innate Immunity

Oxidative stress is a key pathological feature implicated in both acute and chronic liver diseases, including drug-induced liver injury (DILI). The latter describes hepatic injury arising as a direct toxic effect of administered drugs or their metabolites. Although still underreported, DILI remains a significant cause of liver failure, especially in developed nations. Currently, it is understood that mitochondrial-generated oxidative stress and abnormalities in phase I/II metabolism, leading to glutathione (GSH) suppression, drive the onset of DILI. N-Acetyl cysteine (NAC) has attracted a lot of interest as a therapeutic agent against DILI because of its strong antioxidant properties, especially in relation to enhancing endogenous GSH content to counteract oxidative stress. Thus, in addition to updating information on the pathophysiological mechanisms implicated in oxidative-induced hepatic injury, the current review critically discusses clinical evidence on the protective effects of NAC against DILI, including the reduction of patient mortality. Besides injury caused by paracetamol, NAC can also improve liver function in relation to other forms of liver injury such as those induced by excessive alcohol intake. The implicated therapeutic mechanisms of NAC extend from enhancing hepatic GSH levels to reducing biomarkers of paracetamol toxicity such as keratin-18 and circulating caspase-cleaved cytokeratin-18. However, there is still lack of evidence confirming the benefits of using NAC in combination with other therapies in patients with DILI.

Supplemental material, sj-docx-1-ini-10.1177_17534259211053634 for Circulating innate lymphoid cell subtypes and altered cytokine profiles following an atherogenic high-fat diet by Vuyolwethu Mxinwa, Phiwayinkosi V. Dludla, Tawanda M. Nyambuya and Bongani B. Nkambule in Innate Immunity

Background: The impact of vitamin K in ameliorating diabetes-associated complications, especially those linked with platelet activation and coagulation remains unclear. The current study aims to systematically explore and discuss the available evidence on the impact of vitamin K on the diabetes-cardiovascular disease (CVD)-associated complications. Methods: A systematic review of studies published on the MEDLINE (PubMed), EMBASE, and Google Scholar electronic database will be conducted. The review will include studies published from inception until May 25, 2020, reporting on the effect of vitamin K on CVD-related markers, especially coagulation factors and platelet activation in type 2 diabetes mellitus. Before the full-text screening, all studies will be screened by title, abstract, and keywords. The Downs and Black checklist will be used to assess the quality of the studies. Additionally, the Cochrane collaboration tool will also be used to evaluate the risk of bias across the included studies. Kappa Cohen's calculator will be used to assess the level of agreement between the authors. Discussions: This systematic review will not require ethical approval, and the results will be distributed through conference and peer-reviewed publications. Our results will assist current and future research scientists on the potential use of vitamin K as a protective therapy against CVD-related complications. Systematic review registration: This protocol is registered on the International Prospective Register of Systematic Reviews (PROSPERO) registration number: CRD42020151667.

Additional file 1: Table S1. Search strategy used on the EBSCOHOST search engine. Table S2. Publication bias analysis. Figure S1. Analysis of publication bias. The funnel plots were visually inspected for publication bias in the included studies.

Additional file 1: Table 1S. PUBMED search strategy. Search Strategy run on 13 November 2019. Table 2S. Sensitivity analysis of studies included in meta-analysis reporting on the levels NK cell in T2D adult patients compared to healthy controls. Table 3S. Risk of bias assessment.