Nutrition screening tools used to identify malnutrition risk in hospitalized patients: a systematic review and meta-analysis protocol

Background: Malnutrition is a clinical problem with a high prevalence in hospitalized adult patients. Many nutritional screening tools have been developed but there is no consensus on which 1 is more useful. The purpose of this review protocol is to provide an overview of which nutritional screening tool is most valid to identify malnutritional risk in hospitalized adult patients and to analyze the sensitivity and specificity of the different tools. Methods: The protocol of this systematic review and meta-analysis was registered on the INPLASY website (https://inplasy.com/inplasy-2020-9-0028/) and INPLASY registration number is INPLASY202090028. We will perform a systematic literature search of main databases: PubMed, EMBASE, CINAHL and Web of Science and the Cochrane database. Also, grey literature will be search. Peer-reviewed studies published in English, Portuguese or Spanish language will be selected. Screening of titles, abstract and full text will be assessed for eligibility by 2 independent blinded reviewers and any discrepancies will be resolved via consensus. After screening the studies, a meta-analysis will be conducted, if it is possible. Results: Results from this systematic review will help health professionals to identify malnutrition in hospitalized patients and to make decisions to prevent or treat it as well as provide new clues to researchers. Conclusion: Our systematic review will provide aknowledge about the most valid malnutrition risk screening tool in hospitalized adult patients

Lipid (per) oxidation in mitochondria:an emerging target in the ageing process?

Lipids are essential for physiological processes such as maintaining membrane integrity, providing a source of energy and acting as signalling molecules to control processes including cell proliferation, metabolism, inflammation and apoptosis. Disruption of lipid homeostasis can promote pathological changes that contribute towards biological ageing and age-related diseases. Several age-related diseases have been associated with altered lipid metabolism and an elevation in highly damaging lipid peroxidation products; the latter has been ascribed, at least in part, to mitochondrial dysfunction and elevated ROS formation. In addition, senescent cells, which are known to contribute significantly to age-related pathologies, are also associated with impaired mitochondrial function and changes in lipid metabolism. Therapeutic targeting of dysfunctional mitochondrial and pathological lipid metabolism is an emerging strategy for alleviating their negative impact during ageing and the progression to age-related diseases. Such therapies could include the use of drugs that prevent mitochondrial uncoupling, inhibit inflammatory lipid synthesis, modulate lipid transport or storage, reduce mitochondrial oxidative stress and eliminate senescent cells from tissues. In this review, we provide an overview of lipid structure and function, with emphasis on mitochondrial lipids and their potential for therapeutic targeting during ageing and age-related disease

Impact of CPAP therapy on health-related quality of life in elderly patients with apnoea–hypopnea syndrome: a systematic review of randomised clinical trials.

Obstructive sleep apnoea (OSA) is a chronic pathology characterised by the presence of repetitive upper airway obstruction during the sleep, the prevalence of which increases with the age [1], and for which continuous positive airway pressure (CPAP) is the treatment of choice [2–4]. However, there have been few studies on diagnosis and management of OSA in elderly people. A qualitative systematic review of randomised clinical trials (RCTs) was conducted to evaluate the impact of CPAP therapy on health-related quality of life (HRQL) in OSA patients (aged >65 years), diagnosed by polysomnography or polygraphy and treated with CPAP for at least 3 months (>4 h·day−1). Studies whose primary outcome did not assess HRQL were excluded. Interventions were categorised according to whether or not they included CPAP treatment. The primary outcome was HRQL based on validated generic or specific questionnaires.post-print106 K

The-383A > C TNFRI polymorphism is associated with soluble levels and clinical activity in rheumatoid arthritis

Tumor necrosis factor-? (TNF-?) plays a central role in inflammation, and it has been directly implicated in the pathogenesis of rheumatoid arthritis (RA). TNF-? activity is mediated through TNFRI and TNFRII cell surface receptors, which act as physiological attenuators of TNF-? activity. We recruited 190 RA patients and 190 healthy subjects (HS) in order to associate the - 383A>C TNFRI polymorphism with sTNFRI levels and DAS28 score in RA. In results, sTNFRI levels were higher in RA patients than HS (P = 0.04). The - 383A>C TNFRI polymorphism did not show significant differences in both studied groups. However, in the RA group the sTNFRI levels were significantly elevated (P = 0.004) in A/A genotype carriers. In addition, the A/A genotype carriers had the higher DAS28 score than A/C genotype (P = 0.02). These data suggest that - 383A>C TNFRI polymorphism is not a susceptibility marker in RA, whereas the increased levels of sTNFRI could reflect the clinical activity in RA patients. � Springer-Verlag 2009

The -383A>C TNFRI polymorphism is associated with soluble levels and clinical activity in rheumatoid arthritis.

Tumor necrosis factor-alpha (TNF-alpha) plays a central role in inflammation, and it has been directly implicated in the pathogenesis of rheumatoid arthritis (RA). TNF-alpha activity is mediated through TNFRI and TNFRII cell surface receptors, which act as physiological attenuators of TNF-alpha activity. We recruited 190 RA patients and 190 healthy subjects (HS) in order to associate the -383A>C TNFRI polymorphism with sTNFRI levels and DAS28 score in RA. In results, sTNFRI levels were higher in RA patients than HS (P = 0.04). The -383A>C TNFRI polymorphism did not show significant differences in both studied groups. However, in the RA group the sTNFRI levels were significantly elevated (P = 0.004) in A/A genotype carriers. In addition, the A/A genotype carriers had the higher DAS28 score than A/C genotype (P = 0.02). These data suggest that -383A>C TNFRI polymorphism is not a susceptibility marker in RA, whereas the increased levels of sTNFRI could reflect the clinical activity in RA patients