To buy or not buy food online: The impact of the COVID-19 epidemic on the adoption of e-commerce in China.

Drawing on a recent online survey combined with city-level data, this paper examines the impact of the COVID-19 on consumers' online food purchase behavior in the short term. To address the potential endogeneity issues, we adopt an instrumental variable (IV) strategy, using the distance from the surveyed city to Wuhan as the instrumental variable. We show that our IV method is effective in minimizing potential bias. It is found that the share of confirmed COVID-19 cases increases the possibility of consumers purchasing food online. This is more likely to be the case for young people having a lower perceived risk of online purchases and living in large cities. Despite some limitations, this paper has policy implications for China and other countries that have been influenced by the COVID-19 epidemic. Specifically, government support and regulation should focus on (i) ensuring the safety of food sold on the internet, (ii) protecting the carrier from becoming infected, and (iii) providing financial support to the poor since they may have difficulties in obtaining access to food living in small cities. Moreover, how to help those who are unable to purchase food online because of their technical skills (e.g., the elderly who are not familiar with smart phones or the internet) also deserves more attention for the government and the public

Methylprednisolone alleviates limb damage in rat models with high-pressure injection injuries of lower limbs

Objective To study the intervention effect of methylprednisolone(MP) on high pressure injection injuries(HPII) of lower limbs of rats. Methods Thirty rats were randomly divided into control group, model group (high-pressure injection injury model) and treatment group (tail vein injection of MP 30 mg/kg). After 6 hours, the jet area and limb circulation were observed, blood vessels, nerve and muscle tissues were examined by HE staining microscopy. Liver index was calculated and serum TNF-α, IL-1β and IL-6 were tested by ELISA. Comparison between multiple groups was performed by One-way Anova. Results Compared with the control group, limb circulation , blood vessels, nerves and muscles were significantly damaged.The liver index decreased while the serum content of TNF-α, IL-1β, and IL-6 all increased significantly (P＜0.05). Compared with the model group, the above indicators improved significantly in the treatment group(P＜0.05). Conclusions Injection of MP after high-pressure injection injuries can alleviate limb damage, reduce liver load and improve serum inflammatory markers of injured rats

Inhibiting NLRP3 inflammasome signaling pathway promotes neurological recovery following hypoxic-ischemic brain damage by increasing p97-mediated surface GluA1-containing AMPA receptors

Abstract Background The nucleotide-binding oligomeric domain (NOD)-like receptor protein 3 (NLRP3) inflammasome is believed to be a key mediator of neuroinflammation and subsequent secondary brain injury induced by ischemic stroke. However, the role and underlying mechanism of the NLRP3 inflammasome in neonates with hypoxic-ischemic encephalopathy (HIE) are still unclear. Methods The protein expressions of the NLRP3 inflammasome including NLRP3, cysteinyl aspartate specific proteinase-1 (caspase-1) and interleukin-1β (IL-1β), the α-amino-3-hydroxy-5-methyl-4-isoxazole-propionicacid receptor (AMPAR) subunit, and the ATPase valosin-containing protein (VCP/p97), were determined by Western blotting. The interaction between p97 and AMPA glutamate receptor 1 (GluA1) was determined by co-immunoprecipitation. The histopathological level of hypoxic-ischemic brain damage (HIBD) was determined by triphenyltetrazolium chloride (TTC) staining. Polymerase chain reaction (PCR) and Western blotting were used to confirm the genotype of the knockout mice. Motor functions, including myodynamia and coordination, were evaluated by using grasping and rotarod tests. Hippocampus-dependent spatial cognitive function was measured by using the Morris-water maze (MWM). Results We reported that the NLRP3 inflammasome signaling pathway, such as NLRP3, caspase-1 and IL-1β, was activated in rats with HIBD and oxygen-glucose deprivation (OGD)-treated cultured primary neurons. Further studies showed that the protein level of the AMPAR GluA1 subunit on the hippocampal postsynaptic membrane was significantly decreased in rats with HIBD, and it could be restored to control levels after treatment with the specific caspase-1 inhibitor AC-YVAD-CMK. Similarly, in vitro studies showed that OGD reduced GluA1 protein levels on the plasma membrane in cultured primary neurons, whereas AC-YVAD-CMK treatment restored this reduction. Importantly, we showed that OGD treatment obviously enhanced the interaction between p97 and GluA1, while AC-YVAD-CMK treatment promoted the dissociation of p97 from the GluA1 complex and consequently facilitated the localization of GluA1 on the plasma membrane of cultured primary neurons. Finally, we reported that the deficits in motor function, learning and memory in animals with HIBD, were ameliorated by pharmacological intervention or genetic ablation of caspase-1. Conclusion Inhibiting the NLRP3 inflammasome signaling pathway promotes neurological recovery in animals with HIBD by increasing p97-mediated surface GluA1 expression, thereby providing new insight into HIE therapy

In Glaucoma the Upregulated Truncated TrkC.T1 Receptor Isoform in Glia Causes Increased TNF-α Production, Leading to Retinal Ganglion Cell Death

The authors show a paracrine mechanism by which high IOP causes early upregulation of a truncated neurotrophin receptor, TrkC.T1, in glia. This receptor in turn regulates TNF-α production by retinal glia, causing glaucomatous RGC death. This article provides evidence on the physiological relevance of truncated neurotrophin receptors in disease and potentially validates TrkC.T1 as a novel target for glaucoma therapy