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Peptide transfection systems are poised to become a flexible and efficient platform incorporating new chemistries, functionalities, and improved DNA cargos to usher in a new era of gene therapy.Tendinopathies represent half of all musculoskeletal injuries worldwide. Inflammatory events contribute to both tendon healing and to tendinopathy conditions but the cellular triggers leading to one or the other are unknown. In previous studies, we showed that magnetic field actuation modulates human tendon cells (hTDCs) behavior in pro-inflammatory environments, and that magnetic responsive membranes could positively influence inflammation responses in a rat ectopic model. Herein, we propose to investigate the potential synergistic action of the magnetic responsive membranes, made of a polymer blend of starch with polycaprolactone incorporating magnetic nanoparticles (magSPCL), and the actuation of pulsed electromagnetic field (PEMF) 5 Hz, 4mT of intensity and 50% of duty cycle, in IL-1β-treated-hTDCs, and in the immunomodulatory response of macrophages. It was found that the expression of pro-inflammatory (TNFα, IL-6, IL-8, COX-2) and ECM remodeling (MMP-1,-2,-3) markers tend to decrease in cells cultured oreviously reported that magnetic fields modulate the response of human tendon cells (hTDCs) conditioned to pro-inflammatory environments (IL-1β-treated-hTDCs), and that magnetic responsive membranes positively influence immune responses. In the present work, we combined pulsed electromagnetic field (PEMF) and magnetic responsive membranes to guide the inflammatory profile of IL-1β-treated-hTDCs and of macrophages. The results showed that the synergistic action of PEMF and magnetic membranes supports the applicability of magnetically actuated systems to regulate inflammatory events and stimulate tendon regeneration.

Retinol and β-carotene have been reported to be involved in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). However, clinical studies are limited. The aim of this study was to investigate the relationship between serum the ratio of β-carotene to retinol (SC/SR) and hepatic steatosis in NAFLD diagnosed by ultrasonography.

The participants were 606 Japanese adults who were enrolled in a health survey. Clinical profile, dietary nutrition intake, blood biochemistry, serum retinol, and carotenoids were analyzed. NAFLD was defined as fatty liver on ultrasonography in the absence of other causes of steatosis.

Women had higher daily intake of α- and β-carotene, although there were no differences in daily retinol and carotenoid intake between participants with or without NAFLD in both men and women. Women had a higher SC/SR ratio than men regardless of the presence or absence of NAFLD, and the SC/SR ratio in women decreased with exacerbation of hepatic steatosis, whereas the SC/SR ratio in men did not change despite exacerbation of hepatic steatosis. After adjusting for confounding factors, the likelihood of NAFLD among participants in the highest quartile of SC/SR ratio decreased by two-thirds compared with participants in the lowest quartile (adjusted odds ratio, 0.64; 95% confidence interval, 0.21-1.92; P=0.041). The SC/SR ratio was positively correlated with serum high-density lipoprotein cholesterol level, and negatively correlated with serum triacylglycerol level.

The SC/SR ratio was lower in NAFLD with sex differences, and was associated with the severity of hepatic steatosis and lipid profile. Future studies are needed to expand on these findings.

The SC/SR ratio was lower in NAFLD with sex differences, and was associated with the severity of hepatic steatosis and lipid profile. Future studies are needed to expand on these findings.

Children with autism spectrum disorders (ASD) have lower serum vitamin D and higher serotonin and interleukin (IL)-6 levels compared with healthy children. The aim of this study was to evaluate the effect of vitamin D on core symptoms and serum levels of serotonin and IL-6 in these children.

This parallel randomized double-blind, placebo-controlled trial was conducted with 43 children with ASD (7 girls and 36 boys; 8.91 ± 2.87 y of age). Children were randomly allocated to receive either vitamin D drop (300 IU/kg up to a maximum of 6000 IU daily) or placebo for 15 wk. Serum levels of 25-hydroxyvitamin (OH)D, IL-6, and serotonin were measured at baseline and at the end of the trial. Also, the severity of autism and the social and individual maturity of the children were measured by the Childhood Autism Rating Scale (CARS), the Autism Treatment Assessment Checklist (ATEC), and Aberrant Behavior Checklist-Community (ABC-C) questionnaires before and after intervention. Randomization and allocation to groups were done using computer-generated numbers.

More than 86% of patients had vitamin D deficiency at the beginning of the study. Serum levels of 25(OH)D increased significantly in the vitamin D group (P=0.001). The clinical symptoms of autism measured by CARS and ATEC scales were alleviated significantly (P=0.021 and P=0.020, respectively); however, the serum levels of serotonin and IL-6 and the scale of ABC-C remained without a significant change.

These findings suggest that vitamin D supplementation may improve ASD symptoms; however, more studies with longer duration are indispensable to confirm our results.

These findings suggest that vitamin D supplementation may improve ASD symptoms; however, more studies with longer duration are indispensable to confirm our results.Histamine or scombrotoxin fish poisoning is caused by ingestion of bacterially produced histamine in fish. Histamine-producing bacteria generally contain the histidine decarboxylase gene (hdc). However, some strains of Photobacterium phosphoreum are known to produce significant levels of histamine, although the hdc gene in these strains has not been recognized. The objective of this study was to investigate a previously unidentified mechanism of histamine production by P. phosphoreum. We identified a protein with histidine decarboxylase (HDC) activity comparable to activity of the pyridoxal-5-phosphate (PLP) dependent HDC from P. kishitanii and M. selleckchem morganii. The newly identified protein (HDC2) in P. phosphoreum and P. kishitanii strains, was approximately 2× longer than the HDC protein from other Gram-negative bacteria and had 12% similarity to previously identified HDCs. In addition, the hdc2 gene cluster in P. phosphoreum was identical to the hdc gene cluster in P. kishitanii. HDC2 had optimal activity at 20-35 °C, at pH 4, and was not affected by 0-8% NaCl concentrations.

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