Hair Selenium of Residents in Keshan Disease Endemic and Non-endemic Regions in China.

Few nationwide investigations on hair selenium (Se) and Keshan disease (KD) have been conducted. KD is closely associated with Se deficiency. Hair Se is an important biomarker for selenium nutrition. This research aimed to provide evidence for assessment of KD prevention, control, and elimination at the molecular level from the etiological perspective of selenium nutrition. The hair Se of the residents living in the KD endemic and non-endemic areas were determined through atomic fluorescence spectrometer. The median of the hair Se levels of the inhabitants living in KD endemic counties was significantly lower than that in KD non-endemic counties (0.34 vs 0.39 mg/kg, U = -10.03, P < 0.0001). The proportion of Se-deficient or Se-marginal residents in KD endemic counties was significantly higher than that in KD non-endemic counties (56.9% vs 36.6%, U = -9.57, P < 0.0001). The medians of the hair Se levels in KD endemic provinces of Shannxi, Heilongjiang, and Gansu were the lowest (0.35mg/kg), and in the category of Se-marginal status. The hair Se level featured a positive Spearman correlation with per capita disposable income (rs = 0.20, P < 0.0001). In conclusion, the median of the hair Se contents of residents living in KD endemic counties was significantly lower than that in KD non-endemic counties. The hair Se contents of nearly 57% of inhabitants living in KD endemic regions were in Se-deficient or Se-marginal status. The KD endemic provinces of Shannxi, Heilongjiang, and Gansu should be given high priority in KD prevention and control.

Sodium selenite inhibits cervical cancer growth via ROS mediated AMPK/FOXO3a /GADD45a axis.

Selenium is a trace element that has been shown to inhibit the growth of various cancer cell types. However, its role in cervical cancer and its underlying mechanisms remains largely unknown. Herein, we explored the anti-cervical cancer effect of selenium and its potential mechanisms through xenograft and in vitro experiments. HeLa cell xenografts in female nude mice showed tumor growth retardation, with no obvious liver and kidney toxicity, after being intraperitoneally injected with 3 mg/kg sodium selenite (SS) for 14 days. Compared to the control group, selenium levels in the tumor tissue increased significantly after SS treatment. In vitro experiments, SS inhibited the viability of HeLa and SiHa cells, blocked the cell cycle at the S phase, and enhanced apoptosis. RNA-sequencing, Kyoto encyclopedia of genes and genomes pathway analysis showed that forkhead box protein O (FOXO) was a key regulatory signaling pathway for SS to exhibit anticancer effects. Gene Ontology analysis filtered multiple terms associated with apoptosis, anti-proliferation, and cell cycle arrest. Further research revealed that SS increased intracellular reactive oxygen species (ROS) and impaired mitochondrial function, which activated adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) via phosphorylation at Thr172, resulting in activation of FOXO3a and its downstream growth arrest and DNA damage-inducible alpha (GADD45a). In summary, SS exhibited anti-cervical cancer effects, and their mechanisms may be that SS is involved in inducing cell cycle arrest and potentiating cell apoptosis caused by ROS-dependent activation of the AMPK/FOXO3a/GADD45a axis.

Field Evaluation of an Automated Pollen Sensor.

Background: Seasonal pollen is a common cause of allergic respiratory disease. In the United States, pollen monitoring occurs via manual counting, a method which is both labor-intensive and has a considerable time delay. In this paper, we report the field-testing results of a new, automated, real-time pollen imaging sensor in Atlanta, GA. Methods: We first compared the pollen concentrations measured by an automated real-time pollen sensor (APS-300, Pollen Sense LLC) collocated with a Rotorod M40 sampler in 2020 at an allergy clinic in northwest Atlanta. An internal consistency assessment was then conducted with two collocated APS-300 sensors in downtown Atlanta during the 2021 pollen season. We also investigated the spatial heterogeneity of pollen concentrations using the APS-300 measurements. Results: Overall, the daily pollen concentrations reported by the APS-300 and the Rotorod M40 sampler with manual counting were strongly correlated (r = 0.85) during the peak pollen season. The APS-300 reported fewer tree pollen taxa, resulting in a slight underestimation of total pollen counts. Both the APS-300 and Rotorod M40 reported Quercus (Oak) and Pinus (Pine) as dominant pollen taxa during the peak tree pollen season. Pollen concentrations reported by APS-300 in the summer and fall were less accurate. The daily total and speciated pollen concentrations reported by two collocated APS-300 sensors were highly correlated (r = 0.93-0.99). Pollen concentrations showed substantial spatial and temporal heterogeneity in terms of peak levels at three locations in Atlanta. Conclusions: The APS-300 sensor was able to provide internally consistent, real-time pollen concentrations that are strongly correlated with the current gold-standard measurements during the peak pollen season. When compared with manual counting approaches, the fully automated sensor has the significant advantage of being mobile with the ability to provide real-time pollen data. However, the sensor's weed and grass pollen identification algorithms require further improvement.

Glycine bidirectionally regulates ischemic tolerance via different mechanisms including NR2A-dependent CREB phosphorylation.

The exact effect of glycine pre-treatment on brain ischemic tolerance (IT) remains quite controversial. The objective of this study was to investigate the potential effects of glycine on IT. We used rat models of both in vitro ischemia (oxygen and glucose deprivation) and in vivo ischemia (transient middle cerebral artery occlusion). Low doses of glycine (L-Gly) significantly decreased hippocampal ischemic LTP (i-LTP), infarct volume, and neurological deficit scores which were administered before ischemia was induced in rats, whereas high doses of glycine exerted deteriorative effects under the same condition. These findings suggested that exogenous glycine may induce IT in a dose-dependent manner. Furthermore, L-Gly-dependent neuronal protection was inversed by L689, a selective NMDAR glycine site antagonist both in vitro (abolished i-LTP depression) and in vivo (increased infarct size reduction), but not glycine receptor (GlyR) inhibitor strychnine. Importantly, L-Gly-induced IT was achieved by NR2A-dependent cAMP-response element binding protein phosphorylation. These data imply that glycine pre-treatment may represent a novel strategy for inducing IT based on synaptic NMDAR-dependent neuronal transmission. A model of glycine induced dose-dependent bidirectional regulations in ischemic tolerance. (a) Under low dose of Gly pre-treatment, glycine induces NMDAR potentiation and CREB-dependent neuroprotection through the NMDAR co-agonist binding site. (b) Under high dose of Gly pre-treatment, the excessive glycine in synaptic cleft can activate neighboring extrasynaptic sites and combine to the GlyRs. Then, the deteriorative effects would be triggered after NMDAR endocytosis and synaptic depression. AMPAR, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor; CREB, cAMP response element-binding protein; Gly, glycine; GlyR, glycine receptor; GlyT1, gycine transportor 1; NMDAR, N-methyl-d-aspartate receptor.