Using Fe biofortification strategies to reduce both Ni concentration and oral bioavailability for rice with high Ni.

Due to naturally high Ni or soil Ni contamination, high Ni concentrations are reported in rice, raising a need to reduce rice Ni exposure risk. Here, reduction in rice Ni concentration and Ni oral bioavailability with rice Fe biofortification and dietary Fe supplementation was assessed using rice cultivation and mouse bioassays. Results showed that for rice grown in a high geogenic Ni soil, increases in rice Fe concentration from ∼10.0 to ∼30.0 µg g-1 with foliar EDTA-FeNa application led to decreases in Ni concentration from ∼4.0 to ∼1.0 µg g-1 due to inhibited Ni transport from shoot to grains via down-regulated Fe transporters. When fed to mice, Fe-biofortified rice was significantly (p < 0.01) lower in Ni oral bioavailability (59.9 ± 11.9% vs. 77.8 ± 15.1%; 42.4 ± 9.81% vs. 70.4 ± 6.81%). Dietary amendment of exogenous Fe supplements to two Ni-contaminated rice samples at 10-40 µg Fe g-1 also significantly (p < 0.05) reduced Ni RBA from 91.7% to 61.0-69.5% and from 77.4% to 29.2-55.2% due to down-regulation of duodenal Fe transporter expression. Results suggest that the Fe-based strategies not only reduced rice Ni concentration but also lowered rice Ni oral bioavailability, playing dual roles in reducing rice-Ni exposure.

Development of a Point-of-Care Test Based on Selenium Nanoparticles for Heart-Type Fatty Acid-Binding Proteins in Human Plasma and Blood.

Purpose: A rapid, convenient, cost-effective in-home test method for identifying heart-type fatty acid-binding protein (H-FABP) in plasma and blood by a lateral-flow immunoassay (LFIA) based on selenium nanoparticles (SeNPs) was developed. Methods: SeNPs were synthesized by using L-ascorbic acid to reduce seleninic acid at room temperature and conjugated with an anti-H-FABP monoclonal antibody. The limit of detection, specificity, and stability were measured, and clinical samples were analyzed. Results: The SeNPs were spherical with a diameter of 39.48 ± 3.72 nm and were conjugated successfully with an anti-H-FABP antibody, resulting in a total diameter of 46.52 ± 2.95 nm. The kit was designed for the determination of H-FABP in plasma specimens and whole blood specimens. The limit of detection was 1 ng/mL in plasma and blood, and the results could be determined within 10 min. No cross-reaction occurred with cardiac troponin I, creatine kinase-MB or myoglobin. The kits were stored at 40 °C for up to 30 days without significant loss of activity. The sensitivity was determined to be 100%, the specificity 96.67%, and the overall coincidence rate 97.83%. Conclusion: This SeNP assay kit can conveniently, rapidly, and sensitively detect H-FABP in plasma or blood with a readout of a simple color change visible to the naked eye with no special device, and can be used as an auxiliary means for the early screening of AMI. Clinical Trial Registration: Plasma and blood samples were used under approval from the Experimental Animal Ethics committee of the Joint National Laboratory for Antibody Drug Engineering, Henan University. The clinical trial registration number was HUSOM-2019-047.

Neuronal loss without amyloid-ß deposits in the thalamus and hippocampus in the late period after middle cerebral artery occlusion in cynomolgus monkeys.

Conflicting evidence exists regarding whether focal cerebral infarction contributes to cerebral amyloid-ß (Aß) deposition, as observed in Alzheimer's disease. In this study, we aimed to evaluate the presence of Aß deposits in the ipsilateral thalamus and hippocampus 12 months post-stroke in non-human primates, whose brains are structurally and functionally similar to that of humans. Four young male cynomolgus monkeys were subjected to unilateral permanent middle cerebral artery occlusion (MCAO), and another four sham-operated monkeys served as controls. All monkeys underwent magnetic resonance imaging examination on post-operative day 7 to assess the location and size of the infarction. The numbers of neurons, astrocytes, microglia and the Aß load in the non-affected thalamus and hippocampus ipsilaterally remote from infarct foci were examined immunohistochemically at sacrifice 12 months after operation. Thioflavin S and Congo Red stainings were used to identify amyloid deposits. Multiple Aß antibodies recognizing both the N-terminal and C-terminal epitopes of Aß peptides were used to avoid antibody cross-reactivity. Aß levels in cerebrospinal fluid (CSF) and plasma were examined using enzyme-linked immunosorbent assay. The initial infarct was restricted to the left temporal, parietal, insular cortex and the subcortical white matter, while the thalamus and hippocampus remained intact. Of note, there were fewer neurons and more glia in the ipsilateral thalamus and hippocampus in the MCAO group at 12 months post-stroke compared to the control group (all P < 0.05). However, there was no sign of extracellular Aß plaques in the thalamus or hippocampus. No statistically significant difference was found in CSF or plasma levels of Aß40 , Aß42 or the Aß40 /Aß42 ratio between the two groups (P > 0.05). These results suggest that significant secondary neuronal loss and reactive gliosis occur in the non-affected thalamus and hippocampus without Aß deposits in the late period after MCAO in non-human primates.

Qualitative analysis of flavors and fragrances added to tea by using GC-MS.

A precise identification method was developed to identify the flavors and fragrances added to tea matrix artificially using gas chromatography with mass spectrometry and gas chromatography with quadrupole time-of-flight mass spectrometry. The proposed method was based on the corresponding "three-column retention indices, two exact mass numbers, one mass spectrum matching degree" database of 40 kinds of common flavors and fragrances. The intraday and the interday relative standard deviation of the retention indices were less than 0.048 and 0.093%, respectively. The accuracy of exact mass was between 0.15 and 6.22 ppm. And the validation of the created database was performed by analyzing the tea samples. Thus, the proposed method is suitable for the precise identification of the flavors and fragrances added to tea matrix artificially without standard substances as a reference.

2-Cl-MGV-1 Ameliorates Apoptosis in the Thalamus and Hippocampus and Cognitive Deficits After Cortical Infarct in Rats.

BACKGROUND AND PURPOSE: Focal cortical infarction causes neuronal apoptosis in the ipsilateral nonischemic thalamus and hippocampus, which is potentially associated with poststroke cognitive deficits. TSPO (translocator protein) is critical in regulating mitochondrial apoptosis pathways. We examined the effects of the novel TSPO ligand 2-(2-chlorophenyl) quinazolin-4-yl dimethylcarbamate (2-Cl-MGV-1) on poststroke cognitive deficits, neuronal mitochondrial apoptosis, and secondary damage in the ipsilateral thalamus and hippocampus after cortical infarction. METHODS: One hundred fourteen hypertensive rats underwent successful distal middle cerebral artery occlusion (n=76) or sham procedures (n=38). 2-Cl-MGV-1 or dimethyl sulfoxide as vehicle was administrated 2 hours after distal middle cerebral artery occlusion and then for 6 or 13 days (n=19 per group). Spatial learning and memory were tested using the Morris water maze. Secondary degeneration and mitochondrial apoptosis in the thalamus and hippocampus were assessed using Nissl staining, immunohistochemistry, terminal deoxynucleotidyl transferase dUTP nick end labeling, JC-1 staining, and immunoblotting 7 and 14 days after surgery. RESULTS: Infarct volumes did not significantly differ between the vehicle and 2-Cl-MGV-1 groups. There were more neurons and fewer glia in the ipsilateral thalamus and hippocampus in the vehicle groups than in the sham-operated group 7 and 14 days post-distal middle cerebral artery occlusion. 2-Cl-MGV-1 significantly ameliorated spatial cognitive impairment and decreased neuronal death and glial activation when compared with vehicle treatment (P<0.05). The collapse of mitochondrial transmembrane potential and cytoplasmic release of apoptosis-inducing factors and cytochrome c was prevented within the thalamus. Caspase cleavage and the numbers of terminal deoxynucleotidyl transferase dUTP nick end labeling+ or Nissl atrophic cells were reduced within the thalamus and hippocampus. This was accompanied by upregulation of B-cell lymphoma 2 and downregulation of Bax (P<0.05). CONCLUSIONS: 2-Cl-MGV-1 reduces neuronal apoptosis via mitochondrial-dependent pathways and attenuates secondary damage in the nonischemic thalamus and hippocampus, potentially contributing to ameliorated cognitive deficits after cortical infarction.