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This paper aims to investigate the effect of L-citrulline supplementation on blood pressure (BP) in middle-aged and elderly populations.

Three electronic databases, namely, Google Scholar, PubMed and Scopus, were searched from 1990 to November 2020. Random effects model analysis was applied for quantitative data synthesis, and 6 trials with 150 participants were identified and included in the analysis.

Results showed an overall non-significant effect of L-citrulline supplementation on both systolic BP (SBP) and diastolic BP (DBP) in middle-aged and elderly participants. However, stratified analysis indicated a significant reduction in SBP (SMD: −0.41, 95% CI: −0.84, 0.02; p = 0.06, heterogeneity p = 0.41; I2 = 10%) but not in DBP (SMD:−0.15, 95% CI: −0.57, 0.28; p = 0.51, heterogeneity p = 0.60; I2 = 0%), following longer-term (= 8 weeks) supplementation of L-citrulline. Additionally, higher doses of L-citrulline (= 6 grams) showed a marginally significant reduction in DBP (SMD: −0.38, 95% CI: −0.78, 0.02; p = 0.06, heterogeneity p = 0.50; I2 = 0%).

In conclusion, a higher dosage and longer duration of supplementation with L-citrulline may have potential BP lowering effects in populations at an increased risk of hypertension

The purpose of this paper is to present modelling and mathematical studies of neuronal NO‐synthase and discuss the case for nitric oxide (NO) versus nitroso‐arginine (NA) theory.

Introduces recent studies, NO studied models and the experimental model before considering the diffusion‐reaction model. Enzymatic kinetics and an analysis of systems and the NA diffusion equations in mice cortex are given. Numerical results are featured.

Based on these studies, both a bio‐mathematical and physiological conclusions are given. The way to protect the brain was to inhibit the NO‐synthase of the neurons during a stroke.

The paper is of value, particularly as stroke is the second leading cause of mortality worldwide and the most common cause of dementia in western countries. In Europe, each year, over 1,200,000 people experience a stroke.

Advanced glycation end products (AGEs) are continuously formed in the body during normal metabolism and ageing through a non‐enzymatic glycosylation reaction between proteins and carbohydrates, known as the Maillard's reaction. Many AGEs are capable of forming cross‐links between proteins and most of them have fluorescent properties. Production of AGEs is markedly increased in diabetes mellitus where they play a pathological role. The aim of the present study is to investigate the possible inhibitory effects of urea, metformin and ascorbic acid on in vitro formation of fluorescent AGE products by comparing their inhibitory capacity with a well‐known AGEs inhibitor, aminoguanidine.

Experiments were carried out using bovine serum albumin and D (+) glucose to produce glycated bovine serum albumin, a fluorescent AGE. Fluorometer analysis was then performed to measure AGEs production and fluorescent intensity was compared between glycated samples with and without the inhibitors.

Aminoguanidine which is known to form guanidine‐carbonyl adduct, reversing the glycation process. was found to inhibit AGEs formation by 57 per cent. Although urea and metformin inhibits glycation by the same route, it was the most effective inhibitor among all four inhibiting agents used. Ascorbic acid, an antioxidant, also inhibits fluorescent AGEs by 52 per cent. It was also a good cross‐link inhibitor. Urea showed an inhibitory effect of 27 per cent. It is suggested that urea formed in the body might be a possible natural protector of AGEs formation. Finally, metformin, an antidiabetic drug inhibits AGEs production by only 12 per cent. It is known to rather increase peripheral sensitivity to insulin and lower blood‐glucose level.

The paper shows that aminoguanidine is the most efficient inhibitor and ascorbic acid supplementation could prove useful in diabetic patients to remove reactive species generated in the Maillard's reaction.

The purpose of this paper is to study the adsorption properties of a proven traditional medicine of West Africa origin, Alstonia boonei with an attempt to evaluate its application in the corrosion protection of mild steel in 5 M H₂SO₄ and 5 M HCl.

Phytochemical screening and Fourier transform infrared spectroscopy analysis were used to characterize the methanolic extract of the plant. Gravimetry, gasometry and electrochemical techniques were used in the corrosion inhibition studies of the extract and computational studies were used to describe the electronic and adsorption properties of eugenol, the most abundant phytochemical in Alstonia boonei.

The extract acted as a mixed-type inhibitor in both acidic solutions, with improved inhibition efficiency achieved with increasing concentration. While the efficiency increased with temperature for the HCl system, it decreased for the H₂SO₄ system. The mechanism of adsorption proposed for Alstonia boonei was chemisorption in the HCl system and physisorption in the H₂SO₄ system, and the adsorptions obeyed Langmuir isotherm at low temperatures. Computational parameters showed that eugenol, being a representative of Alstonia boonei, possesses excellent adsorption properties and has the potential to compete with other established plant-based corrosion inhibitors.

As opposed to pure compounds with distinctive corrosion effects, plant extracts are generally composed of a myriad of phytoconstituents that competitively promote or inhibit the corrosion process and their net effect is evident as inhibition efficiencies. This is, therefore, the main research limitation associated with the corrosion inhibition study of Alstonia boonei.

Being very rich in antioxidant properties by its proven curative and preventive effects for diseases, the interest was stimulated towards the attractive results that abound from its corrosion protection of metals via its anti-oxidation route.