Excess sodium consumption contributes to arterial dysfunction in humans. The C57BL/6 strain of mice have been used to identify mechanisms by which arterial dysfunction occurs after excess sodium consumption. However, there are concerns that C57BL/6 mice have strain-specific resistance to high-sodium (HS) diet-induced hypertension. To address this concern, we performed a meta-analysis to determine if excess sodium consumption in C57BL/6 mice induces arterial dysfunction. Databases were searched for HS vs. standard diet studies that measured arterial function (i.e., systolic blood pressure [BP], endothelium-dependent dilation [EDD], and central arterial stiffness) in C57BL/6 mice. A total of 39 studies were included, demonstrating that HS condition resulted in higher systolic BP than control mice with a mean difference of 9.8 mmHg (95% CI [5.6, 14], P<0.001). Subgroup analysis indicated that the systolic BP was higher in HS compared to the control condition when measured during night compared to daytime with telemetry (P<0.001). We also identified that the difference in systolic BP between HS and control was ~2.5-fold higher when administered through drinking water than through food (P<0.001). A total of 12 studies were included, demonstrating that HS condition resulted in lower EDD than control with a weighted mean difference of -12.0% (95% CI [-20.0, -4.1], P=0.003). It should be noted that there was considerable variability across studies with more than half of the studies showing no effect of HS condition on systolic BP and EDD. In summary, excess sodium consumption elevates systolic BP and impairs EDD in C57BL/6 mice.

This article provides comprehensive data on degradation performance and microbial dynamics derived from a set of 24 lab-scale batch anaerobic digesters involving various types of inhibitors and the addition of zeolite as a support material. In the first series of 12 digesters, three inhibitors were investigated at the following concentrations: 20 g/L of sodium chloride, 400 mg/L of erythromycin, and 5 mg/L of S-metolachlor. Each inhibitor was tested in triplicate, along with a control condition without inhibition. A parallel series was set up identically, except that 15 g/L of zeolite was introduced into each digester to mitigate the inhibition and promote the degradation process. The provided data comprises information regarding the experimental setup, monitoring measurements that assess the degradation performance (production, composition, and apparent isotopic factor of biogas, pH, dissolved inorganic and organic carbon and volatile fatty acids concentrations), microbial samples information, and 16S rRNA gene sequencing data that decipher changes in microbial structure. This datapaper is associated with research article [1] and presents both the sequencing data and the associated physicochemical data in a structured table format. The sequencing data were generated using the Ion Torrent PGM sequencer and have been deposited in the European Nucleotide Archive (ENA) database at EMBL-EBI under accession number PRJEB65129 (https://www.ebi.ac.uk/ena/browser/view/PRJEB65129), with sample accession numbers ranging from ERS16257742 to ERS16257691 [2]. The data serves as a valuable resource for comparisons with data from other studies on lab-scale batch anaerobic digesters, particularly those utilizing zeolite as a support material or involving inhibition caused by similar types of inhibitors (salts, antibiotics, or pesticides).

Frozen surimi sol incline to protein oxidation, but the quality control strategies based on oxidation remain limited. Hence, the antioxidant and cryoprotective effects of γ-polyglutamic acid (γ-PGA) on freeze-thawed salt-dissolved myofibrillar protein (MP) sol were investigated. Results showed that γ-PGA could effectively regulate protein oxidation of MP sol during freeze-thawing with lower carbonyl contents and less oxidative cross-linking. Meanwhile, γ-PGA primely maintained sol protein structures, showing reduction of 15.28% of salt soluble protein contents at γ-PGA addition of 0.04% under unoxidized condition. Additionally, compared to the control group without oxidation treatment, cooking loss of heat-induced gel with 0.04% γ-PGA decreased by 47.19%, while gel strength obviously increased by 57.22% respectively. Overall, moderate γ-PGA addition (0.04%) could inhibit protein oxidation of sol, further improving frozen stability of sol through hydrogen bonds and hydrophobic interaction, but excessive γ-PGA was adverse to sol quality due to severe cross-linking between γ-PGA and MP.

Cardiovascular diseases account for almost 18 million deaths annually, the most of all non-communicable diseases. The reduction of dietary salt consumption is a modifiable risk factor. The WHO recommends a daily sodium intake of <2000 mg but average consumption exceeds this in many countries globally. Strategies proposed to aid effective salt reduction policy include product reformulation, front of pack labelling, behavioural change campaigns and establishing a low-sodium-supportive environment. Yet, salt for household and processed food use is, in countries wholly or partially adopting a universal salt iodisation policy, the principal vehicle for population-wide iodine fortification. With salt reduction policies in place, there is concern that iodine deficiency disorders may re-emerge. Recognising the urgency to tackle the rising prevalence of NCDs yet not risk the re-emergence and detrimental effect of inadequate iodine intakes, this review lays out the feasibility of integrating both salt reduction and salt iodine fortification strategies. Reducing the burden of health risks associated with an excessive sodium intake or inadequate iodine through population-tailored, cost-effective strategies involving salt is both feasible and achievable, and represents an opportunity to improve outcomes in public health.

Albendazole (ABZ) is a highly effective yet poorly water-soluble antiparasitic drug known to form salts (ABZ-FMA, ABZ-DTA, and ABZ-HCl) with fumaric acid (FMA), D-tartaric acid (DTA), and hydrochloric acid (HCl). This research utilized a range of analytical techniques, including Fourier transform infrared spectroscopy (FT-IR), nuclear magnetic resonance hydrogen spectroscopy (1H NMR), powder X-ray diffraction (PXRD), dynamic vapor sorption (DVS), thermogravimetric analysis (TGA), differential scanning calorimetry (DSC), and scanning electron microscopy (SEM), to validate and characterize the solid-state properties of these drug salts. This study also assessed the solubility and intrinsic dissolution rate (IDR) of these salts under different pH conditions compared to the active pharmaceutical ingredient (API) and conducted stability studies. Moreover, the in vivo pharmacokinetic performance of ABZ salt was evaluated. The results of this study reveal that the new solid form of ABZ is primarily associated with amino acid esters and benzimidazole groups, forming intermolecular interactions. All three ABZ salts significantly improved the solubility and dissolution rate of ABZ, with ABZ-HCl demonstrating the optimal performance. Importantly, the drug salt exhibited robust physical stability when exposed to adverse conditions, including strong light irradiation (4500 ± 500 lux), high humidity (92.5 ± 5% relative humidity), elevated temperatures (50 ± 2 °C), and accelerated test conditions (40 °C/75 ± 5% relative humidity). Lastly, the in vivo pharmacokinetic analysis demonstrated that ABZ salt led to a substantial increase in AUC(0-24) and Cmax compared to ABZ. This elevation in solubility in aqueous solvents signifies that ABZ salt exhibits characteristics that can enhance oral bioavailability and pharmacokinetics. These findings provide potential solutions for the development of more effective and innovative drug formulations.

Recent evidence suggests that necroptosis may contribute to the development of kidney injury. Renalase is a novel secretory protein that exerts potent prosurvival and anti-inflammatory effects. We hypothesized that renalase could protect the kidney from salt-induced injury by modulating necroptosis. High salt and renalase treatments were administered to Dahl salt-sensitive (SS) rats, renalase knockout (KO) mice, and HK-2 cells. Furthermore, a cohort of 514 eligible participants was utilized to investigate the association between single nucleotide polymorphisms (SNPs) in the genes RIPK1, RIPK3, and MLKL, and the risk of subclinical renal damage (SRD) over 14 years. A high-salt diet significantly increased the expression of key components of necroptosis, namely RIPK1, RIPK3, and MLKL, as well as the release of inflammatory factors in SS rats. Treatment with recombinant renalase reduced both necroptosis and inflammation. In renalase KO mice, salt-induced kidney injury was more severe than in wild-type mice, but supplementation with renalase attenuated the kidney injury. In vitro experiments with HK-2 cells revealed high salt increased necroptosis and inflammation. Renalase exhibited a dose-dependent decrease in salt-induced necroptosis, and this cytoprotective effect was negated by the knockdown of PMCA4b, which is the receptor of renalase. Furthermore, the cohort study showed that SNP rs3736724 in RIPK1 and rs11640974 in MLKL were significantly associated with the risk of SRD over 14 years. Our analysis shows that necroptosis plays a significant role in the development of salt-induced kidney injury and that renalase confers its cytoprotective effects by inhibiting necroptosis and inflammation.

BACKGROUND: Rapid correction of dysnatremias can result in neurological complications. Therefore, various formulas are available to predict changes in plasma sodium concentration ([Na+]) after treatment, but these have been shown to be inaccurate. This could be explained by sodium acumulation in skin and muscle tissue, which is not explicitly considered in these formulas. We assessed the association between clinical and biochemical factors related to tissue sodium accumulation and the discrepancy between predicted and measured plasma [Na+].
METHODS: We used data from an intensive care unit (ICU) cohort with complete data on sodium, potassium, and water balance. The predicted plasma [Na+] was calculated using the Barsoum-Levine (BL) and the Nguyen-Kurtz (NK) formula. We calculated the discrepancy between predicted and measured plasma sodium and fitted a linear mixed-effect model to investigate its association with factors related to tissue sodium accumulation.
RESULTS: We included 594 ICU days of sixty-three patients in our analysis. The mean plasma [Na+] at baseline was 147±6 mmol/L. The median (IQR) discrepancy between predicted and measured plasma [Na+] was 3.14 mmol/L (1.48, 5.55) and 3.53 mmol/L (1.81, 6.44) for the BL and NK formulas, respectively. For both formulas, estimated total body water (p=0.027), initial plasma [Na+] (p<0.001) and plasma [Na+] change (p<0.001) were associated with the discrepancy between predicted and measured plasma [Na+].
CONCLUSIONS: In this ICU cohort, initial plasma [Na+], total body water, and plasma [Na+] changes, all factors that are related to tissue sodium accumulation, were associated with the inaccurateness of plasma [Na+] prediction.

Intrinsically disordered protein α-synuclein (αS) is implicated in Parkinson\'s disease due to its aberrant aggregation propensity. In a bid to identify the traits of its aggregation, here we computationally simulate the multi-chain association process of αS in aqueous as well as under diverse environmental perturbations. In particular, the aggregation of αS in aqueous and varied environmental condition led to marked concentration differences within protein aggregates, resembling liquid-liquid phase separation (LLPS). Both saline and crowded settings enhanced the LLPS propensity. However, the surface tension of αS droplet responds differently to crowders (entropy-driven) and salt (enthalpy-driven). Conformational analysis reveals that the IDP chains would adopt extended conformations within aggregates and would maintain mutually perpendicular orientations to minimize inter-chain electrostatic repulsions. The droplet stability is found to stem from a diminished intra-chain interactions in the C-terminal regions of αS, fostering inter-chain residue-residue interactions. Intriguingly, a graph theory analysis identifies small-world-like networks within droplets across environmental conditions, suggesting the prevalence of a consensus interaction patterns among the chains. Together these findings suggest a delicate balance between molecular grammar and environment-dependent nuanced aggregation behavior of αS.

The endothelial glycocalyx is closely associated with various physiological and pathophysiological events. Significant modification of the endothelial glycocalyx is an early process in the pathogenesis of cardiovascular disease. High dietary salt and HIV infection damages the endothelial glycocalyx causing endothelial dysfunction and increasing the risk for salt-sensitive hypertension and cardiovascular disease. The two factors, HIV infection and dietary salt are critical independent predictors of hypertension and cardiovascular disease and often synergize to exacerbate and accelerate disease pathogenesis. Salt-sensitive hypertension is more common among people living with HIV and is associated with risk for cardiovascular disease, stroke, heart attack and even death. However, the underlying mechanisms linking endothelial glycocalyx damage to dietary salt and HIV infection are lacking. Yet, both HIV infection/treatment and dietary salt are closely linked to endothelial glycocalyx damage and development of salt-sensitive hypertension. Moreover, the majority of individuals globally, consume more salt than is recommended and the burden of HIV especially in sub-Sahara Africa is disproportionately high. In this review, we have discussed the missing link between high salt and endothelial glycocalyx shedding in the pathogenesis of salt-sensitive hypertension. We have further elaborated the role played by HIV infection and treatment in modifying endothelial glycocalyx integrity to contribute to the development of hypertension and cardiovascular disease.

BACKGROUND: Regarding the importance of the prevention of non-communicable diseases (NCDs) and higher consumption of salt among the Iranian population than the level recommended by the World Health Organization, the aim of this study was to evaluate the accuracy of the salt mentioned in the traffic light labelling of nuts and seeds. Study Design: A cross-sectional study.
METHODS: A total of 53 packaged nuts and seeds, including 7, 8, 9, 9, 10, and 10 samples of pumpkin, pistachios, almond, sunflower, peanut, and watermelon nuts and seeds, respectively, with traffic light labelling, were randomly purchased from several local markets in Isfahan, Iran. The amount of sodium was measured by the inductively coupled plasma-optical emission spectroscopy technique and then multiplied by 2.5 to achieve the amount of salt.
RESULTS: Varying levels of traffic light labeling value accuracy were observed in most of the samples. In the almond, pistachio, peanut, and watermelon groups, the average amount of laboratory value had a statistically significant difference with the label value (P<0.05).
CONCLUSIONS: The results demonstrated that the salt content of 82% of the studied samples had discrepancies with the values stated on the traffic light labelling. The presentation of an accurate amount of salt content is essential for promoting healthy eating habits and enabling individuals to make informed choices about their diet. It is recommended that regulatory authorities should review labelling guidelines and enforce stricter compliance to ensure accurate representation of salt content on packaged foods.