One route of human exposure to environmental chemicals is oral uptake. This is primarily true for chemicals that may leach from food packaging materials, such as bisphenols and phthalate esters. Upon ingestion, these compounds are transported along the intestinal tract, from where they can be taken up into the blood stream or distributed to mucosal sites. At mucosal sites, mucosal immune cells and in the blood stream peripheral immune cells may be exposed to these chemicals potentially modulating immune cell functions. In the present study, we investigated the impact of three common bisphenols and two phthalate esters on mucosal-associated invariant T (MAIT) cells in vitro, a frequent immune cell type in the intestinal mucosae and peripheral blood of humans. All compounds were non-cytotoxic at the chosen concentrations. MAIT cell activation was only slightly affected as seen by flow cytometric analysis. Phthalate esters did not affect MAIT cell gene expression, while bisphenol-exposure induced significant changes. Transcriptional changes occurred in ∼ 25 % of genes for BPA, ∼ 22 % for BPF and ∼ 8 % for BPS. All bisphenols down-modulated expression of CCND2, CCL20, GZMB and IRF4, indicating an effect on MAIT cell effector function. Further, BPA and BPF showed a high overlap in modulated genes involved in cellular stress response, activation signaling and effector function suggesting that BPF may not be safe substitute for BPA.

In Southeast Asia, the rhizome of Etlingera pavieana is commonly consumed and parts of the rhizomes have been used as a medicine for the treatment of several disorders. Its pharmacological effects have previously been reported. However, its potential toxicity has not been described. This study aimed to evaluate in vivo toxicity of E. pavieana rhizome extract (EPE) in Sprague Dawley rats. Acute toxicity testing of EPE at a single dose of 2,000 mg/kg produced no toxic effects in female rats after 14 days of treatment. Subchronic toxicity testing showed that all doses of EPE (500, 1,000, and 2,000 mg/kg/day) produced no sign of toxicity during 90 days of treatment. All biochemical and hematological values were within normal ranges. There were no significant histopathological differences in the internal organs among the tested groups. Therefore, the no-observed-adverse-effect level of EPE was 2,000 mg/kg/day in both male and female rats, thereby confirming the safety of EPE for use in traditional medicines.

Maternal obesity may compromise the micronutrient status of the offspring. Vitamin A (VA) is an essential micronutrient during neonatal development. Its active metabolite, retinoic acid (RA), is a key regulator of VA homeostasis, which also regulates adipose tissue (AT) development in obese adults. However, its role on VA status and AT metabolism in neonates was unknown and it was determined in the present study. Pregnant Sprague-Dawley rats were randomised to a normal fat diet (NFD) or a high fat diet (HFD). From postnatal day 5 (P5) to P20, half of the HFD pups received oral RA every 3 d (HFDRA group). NFD pups and the remaining HFD pups (HFD group) received placebo. Six hours after dosing on P8, P14 and P20, n 4 pups per group were euthanised for different measures. It was found that total retinol concentration in neonatal liver and lung was significantly lower in the HFD group than the NFD group, while the concentrations were significantly increased in the HFDRA group. The HFD group exhibited significantly higher body weight (BW) gain, AT mass, serum leptin and adiponectin, and gene expression of these adipokines in white adipose tissue compared with the NFD group; these measures were significantly reduced in the HFDRA group. BAT UCP2 and UCP3 gene expression were significantly higher in pups receiving RA. In conclusion, repeated RA treatment during the suckling period improved the tissue VA status of neonates exposed to maternal obesity. RA also exerted a regulatory effect on neonatal obesity development by reducing BW gain and adiposity and modulating AT metabolism.

The aim of this study is to assess the antioxidative profile and related pharmacological potentialities of the ethanolic extract of Amischotolype mollissima leaves, traditionally used in treating pain, injury, malarial fever, epilepsy and hyperacidity, followed by a computational approach for the analysis of bioactive compounds identified by GC-MS. In GC-MS analysis, the extract yielded ten compounds, with 4,6-di-t-butyl-2-alpha-methyl benzyl phenol having the highest amount. In vitro investigation of the antioxidative properties of the plant was conducted with 2,2-diphenyl-1-picryl hydrazyl (DPPH) radical and hydrogen peroxide scavenging assays. The amounts of secondary metabolites phenolics, flavonoids, and tannins were measured at 142 mg GAE/g, 534 mg QE/g, and 110 mg GAE/g, respectively. An acute toxicity study was carried out on mice, which revealed no toxicity up to the dosage of 4000 mg/kg bw. For the dosages of extract at 250 and 500 mg/kg bw, the writhing response test induced by acetic acid exhibited a statistically significant (p < 0.05) analgesic effect in mice. The oral glucose tolerance test (OGTT) and alpha-glucosidase enzyme inhibitory activity assay were used to examine the antihyperglycemic potential, in which the extract reduced the blood glucose level to 6.22 mmol/l and 3.82 mmol/l, at dosages of 250 and 500 mg/kg bw, respectively at 60 min in OGTT even though no activity was observed in the α-glucosidase enzyme inhibitory assay. In an antibacterial assay, the extract\'s minimum inhibitory concentration (MIC) against E. coli, P. aeruginosa, and S. aureus was determined to be 8, 16, and 8 µg/ml, respectively. This study shows that the usage of A. mollissima leaves in folklore medication is justified.

Substantial evidence suggests that regular tree nut consumption does not lead to changes in body weight (BW). However, these studies used a variety of dietary substitution instructions which may confound the interpretation of prior BW outcomes. The purpose of the present study was to examine the impact of daily pecan consumption, with or without isocaloric substitution instructions, on BW and composition. This was an 8-week randomised, controlled trial with three treatments: a nut-free control group (n 32) and two pecan groups. ADD (n 30) consumed pecans (68 g/d) as part of a free-living diet, and SUB (n 31) substituted the pecans (68 g/d) for isocaloric foods from their habitual diet. BW and total body fat percentage (BF) were measured, and theoretical changes in these outcomes if pecans were consumed without compensation were determined. BW increased in all groups across the intervention, and there was a trend (P = 0⋅09) for an increase in ADD (1⋅1 ± 0⋅2 kg) and SUB (0⋅9 ± 0⋅3 kg) compared to control (0⋅3 ± 0⋅2 kg). In addition, there was increased BF in SUB (1⋅0 ± 0⋅3 %; P = 0⋅005) but not ADD (0⋅1 ± 0⋅2 %) or control (-0⋅2 ± 0⋅3 %) There was a large difference in the actual v. theoretical change in BW regardless of pecan treatment (actual: 1⋅1 ± 0⋅2 and 0⋅9 ± 0⋅3 v. theoretical: 3⋅3 ± 0⋅0 and 3⋅2 ± 0⋅0 kg in ADD and SUB, respectively; P < 0⋅001). Furthermore, there was a difference in actual v. theoretical change in BF in ADD (0⋅1 ± 0⋅2 v. 1⋅2 ± 0⋅1 %; P = 0⋅002) but not SUB or control. In conclusion, daily pecan consumption for 8 weeks did not result in significant weight gain, regardless of dietary substitution instructions.

A ninety-day oral toxicity study of saponified Capsicum annum fruit extract with 50% (w/w) capsanthin (SCFE-50 C) was performed by oral gavage administration to male and female Sprague-Dawley (SD) rats at doses of 0, 500, 1000 and 2000 mg/kg BW/day for a period of ninety consecutive days. To assess the reversal of toxicity, the treatment phase was followed with a twenty-eight-day recovery period. The treatment with SCFE-50 C in both male and female SD rats showed no mortality, and no treatment-related toxicologically significant changes were observed in any groups. No significant differences between treated and control groups were found in feed consumption, body weight gain, individual organ weights, ocular examination, clinical chemistry or blood biochemistry. The necroscopy and histopathology examination did not reveal any clinically significant changes in male and female rats from the 2000 mg/kg BW/day group. According to this study, the no observable adverse effect level (NOAEL) for saponified Capsicum annum fruit extract with 50% (w/w) capsanthin (SCFE-50 C) administered by oral gavage for 90-days is > 2000 mg/kg BW/day in SD rats.

UNASSIGNED: Quantitative evaluations of function, volume and mass are fundamental in the diagnostic workup of different cardiovascular diseases and can be exactly determined by CMRI in sinus rhythm. This does not hold true in arrhythmia as CMR is hampered by reconstruction artifacts caused by inconsistent data from multiple heartbeats. Real-time (RT) MRI at high temporal resolution might reduce these problems.
UNASSIGNED: Consecutive patients with atrial fibrillation were prospectively included and underwent RT and conventional CINE CMR in randomized order. 29 patients were studied at 1.5 T and 30 patients at 3 T. At 3 T a group of 20 subjects in sinus rhythm served as controls. RT and CINE image quality was evaluated in different planes and for different wall sections using a Likert scale (from zero to four). Volumetric analysis was performed using two types of software and differences between RT and CINE CMR were evaluated.
UNASSIGNED: In patients with atrial fibrillation RT CMR short axis (SA) resulted in a significantly higher image quality compared to CINE imaging both at 1.5 T and 3 T (1.5 T: mid SA: 3.55 ± 0.5 RT vs 2.6 ± 0.9 CINE, p = 0.0001; 3 T: mid SA: 3.15 ± 0.9 RT vs 2.6 ±1.0 CINE, p = 0.03); This qualitative difference was more marked and significant for the long axis views (2CV and 4CV) at 1.5 T (1.5 T: 2CV: 3.2 ± 0.6 RT vs 2.65 ± 1.1 CINE; p = 0.011; 4CV: 2.9 ± 0.69 RT vs 2.4 ± 0.9 CINE; p = 0.0044). During sinus rhythm CINE images were superior concerning diagnostic quality (3 T mid SA: 3.35 ± 0.45 RT vs 3.8 ± 0.5 CINE, p = 0.008). Quantitative analysis was successful with both software packages and the results showed a good correlation (Pearson correlation between 0.679 and 0.921 for patients). RT CMR resulted in slightly lower functional volumes than CINE CMR (3 T: patients: EDVI 86 ± 29 ml/m2 RT vs 93 29 ml/m2± 29 CINE, Pearson r = 0.902) but similar ejection fractions (3 T: patients: EF 47 ± 16% RT vs 45 ± 13% CINE, Pearson r = 0679; controls: EF 63 ± 6 RT vs 63 ± 3 CINE, Pearson r = 0.695).
UNASSIGNED: RT CMR improves image quality in arrhythmic patients and renders studies more comfortable. Volumetric analysis is feasible with slightly lower values relative to CINE CMR, while ejection fractions are comparable.

This study was conducted to investigate whether or not there are sex differences in canola oil (CAN)-induced adverse events in the rat and to understand the involvement and the role of testosterone in those events, including life-shortening. Stroke-prone spontaneously hypertensive rats (SHRSP) of both sexes were fed a diet containing 10 wt/wt% soybean oil (SOY, control) or CAN as the sole dietary fat. The survival of the males fed the CAN diet was significantly shorter than that of those fed the SOY diet. In contrast, the survival of the females was not affected by CAN. The males fed the CAN diet showed elevated blood pressure, thrombopenia and insulin-tolerance, which are major symptoms of metabolic syndrome, whereas such changes by the CAN diet were not found in the females. Plasma testosterone was significantly lower in animals of both sexes fed the CAN diet than in those fed the SOY diet, but interestingly, the lowered testosterone was accompanied by a marked increase in plasma aldosterone only in the males. These results demonstrate significant sex differences in CAN-toxicity and suggest that those sex differences may be attributable to the increased aldosterone level, which triggers aggravation of the genetic diseases specific to SHRSP, that is, metabolic syndrome-like conditions, but only in the males. The present results also suggest that testosterone may negatively regulate aldosterone production in the physiology of the males, and the inhibition of that negative regulation caused by the CAN diet is one of the possible causes of the adverse events.

Anamorelin (ANA) is approved for treating cancer cachexia (CCX) in Japan. We report the case of a 69-year-old man with stage IVB squamous cell lung cancer complicated by CCX, having a 13.6% weight loss in 6 months. After chemotherapy was initiated, his weight was further reduced. Therefore, we started ANA combined with a treatment approach by a multidisciplinary collaboration, including nutritionists and physical therapists. After initiation of ANA, the body weight, appetite, psoas muscle index, and physical functions rapidly improved during chemotherapy. ANA administration combined with a multidisciplinary collaboration approach can be an effective supportive therapy against CCX during chemotherapy.

Cardiovascular disease remains the leading cause of death globally, and heart failure (HF) represents its terminal stage. Asthma, one of the most common chronic diseases, has been reported to be associated with an increased risk of cardiovascular disease. However, the link between asthma and HF has rarely been studied, and the possible mechanisms by which asthma affects HF are unclear. This study aimed to explore the influence of asthma on HF and the possible mechanisms. We analyzed data from the National Health and Nutrition Examination Survey and found a higher prevalence of HF among asthmatic individuals, and identified an independent association between HF and asthma. Subsequently, we produced mice with concurrent ovalbumin (OVA) sensitization-induced allergic asthma and angiotensin Ⅱ infusion-induced cardiac remodeling to explore the effect of asthma on cardiac remodeling in vivo. The results showed that OVA-induced asthma impaired heart function and aggravated cardiac remodeling in mice. We also found that OVA sensitization increased the expression levels of immunoglobulin E (IgE) in serum and IgE receptor (FcεR1) in the heart, and enhanced the activation of downstream signaling molecules of IgE-FcεR1 in the heart. Importantly, blockage of IgE-FcεR1 using FcεR1-deficient mice or an anti-IgE antibody prevented asthma-induced decline of cardiac function, and alleviated cardiac remodeling. These findings demonstrate the adverse effects of allergic asthma on the heart, and suggest the potential application of anti-IgE therapy in the treatment of asthma complicated with heart conditions.