Additional file 1: Figure S1. of IL-17A is implicated in lipopolysaccharide-induced neuroinflammation and cognitive impairment in aged rats via microglial activation

The specificity of IL-17A antibody to IL-17. The antibodies were incubated with blocking peptide (BL) 10, 20, and 40 μg/μl, respectively, before injection. TNF-α protein expression in the hippocampus was determined by ELISA. The data are presented as the mean ± s.e.m. (n = 3). **P < 0.01 versus control group, ## P < 0.01 versus LPS treatment group, &&P < 0.01 versus LPS treatment group, ^^P < 0.01 versus LPS + anti-IL-17A group. Figure S2. The full gels of western blots. (DOCX 910 kb

Platinum Nanoparticle-Deposited Ti₃C₂T_<i>x</i> MXene for Hydrogen Evolution Reaction

Nobel metal Pt composites show high catalytic activity for hydrogen evolution reaction (HER) but limited in application by high Pt contents and therefore the cost. Herein, a series of Pt nanoparticle (NP)-deposited 2D Ti3C2Tx MXenes were prepared by an atomic layer deposition (ALD) method with relatively low Pt contents (0.98–3.10 wt %) and showed excellent HER catalytic activity and stability. The electrochemical results indicated that the prepared catalysts showed the optimal HER activity as the ALD deposition cycle reached 40, with an overpotential of 67.8 mV approaching that of the commercial Pt/C catalyst (64.2 mV). The excellent behavior was attributed to the homogeneous dispersion of the Pt NPs and the good conductivity of the 2D Ti3C2Tx MXene supports

Magma hybridization and crust-mantle interaction revealed by mineralogical and geochemical footprints: a case study from the South Qilian Accretionary Belt at the northern Tibetan Plateau

The relationship between mafic magmatic enclaves (MMEs) and host granitoids is ongoing debate due to their significant roles in understanding deep magmatisms and geodynamic processes. This paper reports on Early Palaeozoic granitoids and associated MMEs from the Delingha pluton in the South Qilian Accretionary Belt (NW China) to constrain their petrogenesis and draw implications. The MMEs, occurring as ellipsoidal to rounded shapes, are andesitic and have the same crystallization age (~445 Ma) and mineral assemblage as the host granitoids. However, minor isotopic differences between them and compositional and textural disequilibria on minerals (e.g. plagioclase and amphibole) do not support a cumulate origin that the MMEs were formed at earlier stage of the same magmatic system, but forcefully reflect magma hybridization processes between mafic and felsic magmas, during which the hybridized magma was broken up into discrete enclaves by convective motion in the host felsic magma. Accordingly, the primitive compositions of the MMEs likely originated from metasomatized mantle wedge source, while mantle-derived melt underplated and partially melted the lower continental crust to form the host rocks with a certain mantle contribution. Thus, the Delingha pluton is the product of crust-mantle interaction at an active continental margin subduction setting rather than syn-collisional environment, indicating that subduction of the South Qilian Ocean located between the Central Qilian Block and the Oulongbuluke Block may have lasted till to ~445 Ma.</p

Additional file 1 of Exhausted phenotype of circulating CD8+ T cell subsets in hepatitis B virus carriers

Additional file 1. Table S1. List of antibodies used in the study. Table S2. List of primer sequences used for RT–PCR. Table S3. Correlations between the subsets of exhausted Tfc/Tc17 cells and the serum level of HbsAg. Figure S1. Gating strategy in CD8+ T cell subsets. A: gating strategy to detect inhibitory receptors expressed in CD8+ T cell subsets; B: gating strategy to detect effector cytokines expressed in CD8+ T cell subsets. Figure S2. Additional data of CD8+ T cells in HCs and HBV carriers. A: multiple inhibitory receptor expression on CD8+ T cells in HCs and HBV carriers; B: correlations between the frequencies of PD+ or TIM3+ Tfc/Tc17 cells and the serum level of TNF-α; C: correlations between the frequencies of PD+ or TIM3+ Tfc/Tc17 cells and the serum level of IFN-γ; D-E: the production of effector cytokines in Tc/Tfc subsets in HCs (n = 15) and HBV carriers (n = 15); E: the production of cytokines in the Tc subset in HBV carriers. HCs: healthy controls, HBV: hepatitis B virus, Tfc: follicular cytotoxic T cells (CXCR5+FOXP3-), Tc: cytotoxic T cells (CXCR5-FOXP3-); data are presented as the means ± SEs; *P < 0.01, **P < 0.01

Data_Sheet_1_Impact of Coinfection With SARS-CoV-2 and Influenza on Disease Severity: A Systematic Review and Meta-Analysis.docx

Background: Although coinfection with influenza in COVID-19 patients has drawn considerable attention, it is still not completely understood whether simultaneously infected with these two viruses influences disease severity. We therefore aimed to estimate the impact of coinfected with SARS-CoV-2 and influenza on the disease outcomes compared with the single infection of SARS-CoV-2.Materials and Methods: We searched the PubMed, Web of Science, Embase, Cochrane Library, China National Knowledge Infrastructure Database (CNKI) to identify relevant articles up to July 9, 2021. Studies that assessed the effect of SARS-CoV-2 and influenza coinfection on disease outcomes or those with sufficient data to calculate risk factors were included. Risk effects were pooled using fixed or random effects model.Results: We ultimately identified 12 studies with 9,498 patients to evaluate the risk effects of SARS-CoV-2 and influenza coinfection on disease severity. Results indicated that coinfection was not significantly associated with mortality (OR = 0.85, 95%CI: 0.51, 1.43; p = 0.55, I2 = 76.00%). However, mortality was found significantly decreased in the studies from China (OR = 0.51, 95%CI: 0.39, 0.68; I2 = 26.50%), while significantly increased outside China (OR = 1.56, 95%CI: 1.12, 2.19; I2 = 1.00%). Moreover, a lower risk for critical outcomes was detected among coinfection patients (OR = 0.64, 95%CI: 0.43, 0.97; p = 0.04, I2 = 0.00%). Additionally, coinfection patients presented different laboratory indexes compared with the single SARS-CoV-2 infection, including lymphocyte counts and APTT.Conclusion: Our study revealed that coinfection with SARS-CoV-2 and influenza had no effect on overall mortality. However, risk for critical outcomes was lower in coinfection patients and different associations were detected in the studies from different regions and specific laboratory indexes. Further studies on influenza strains and the order of infection were warranted. Systematic testing for influenza coinfection in COVID-19 patients and influenza vaccination should be recommended.</p

Dexmedetomidine inhibits inflammatory reaction in the hippocampus of septic rats by suppressing NF-κB pathway

<div><p>Dexmedetomidine (DEX) is known to provide neuroprotective effect in the central nervous system. However, the detailed mechanism remains far more elusive. This study was designed to investigate the relevant mechanisms of DEX's neuroprotective effect. Sprague–Dawley (SD) rats were injected with dexmedetomidine and/or Lipopolysaccharide (LPS) intraperitoneally, and inflammatory cytokines in serum and in the hippocampus were measured by enzyme linked immunosorbent assay (ELISA). NF-κB in the brain tissue extracts was analyzed with western-blot. Then, we investigated whether NF-κB inhibitor prevents the elevation of inflammatory cytokines in rats injected with LPS. Our results indicated that compared with the control group, the rats exposed to LPS showed significant cognitive dysfunction. When compared to controls, the levels of TNF-α and IL-6 in the serum and hippocampus homogenate were increased in rats treated with LPS. DEX pretreatment inhibited the rats' TNF-α, IL-6 and NF-κB levels induced by LPS. In response to LPS, PDTC pretreatment restrains the production of proinflammatory cytokines (TNF-α and IL-6). Rats treated with PDTC and DEX alongside LPS exhibited less TNF-α and IL-6 than the LPS treated group. In combination, PDTC and DEX showed addictive effects. Our data suggest that DEX exerts a neuroprotective effect through NF-κB in part after LPS-induced cognitive dysfunction.</p></div

Rats pretreated with DEX showed a decrease in p-NF-κB and NF-κB expression.

<p>Western blotting showed that high dose of DEX reduced p-NF-κB and NF-κB protein levels in the hippocampus. (**P<0.01 versus control group; ^# P<0.05 versus LPS group).</p

DEX improved LPS induced memory impairment.

<p>The Y-maze test was performed to observe the cognitive function of rats. (A) Rats were injected with DEX 1h prior to LPS injection, Then Y-maze test was performed to assess the rats' memory function 1d after LPS-injection. LPS significantly impaired the cognitive function of rats, DEX at concentration of 5 and 50μg/kg alone did not influence cognitive function of rats. (B) DEX at concentration of 50 μg/kg prior to LPS hindered the cognitive dysfunction, however, DEX at concentration of 500μg/kg alone significantly impaired cognitive function.</p

LPS induced TNF-α and IL-6 increased in rats' serum and hippocampus homogenate.

<p>Rats pretreated with DEX showed a decrease in TNF-α and IL-6 level. (A,B,C,D) ELISA showed that high dose of DEX reduced TNF-α and IL-6 protein levels in serum and hippocampus homogenate. (**P<0.01 versus control group, ^##P<0.01 and ^#P<0.05 versus control group; data represent the mean ± SEM for at least three separate experiments).</p

Data_Sheet_1_Global Burden and Trends of Norovirus-Associated Diseases From 1990 to 2019: An Observational Trend Study.ZIP

IntroductionAs an important pathogen causing diarrheal diseases, the burden and change in the death rate of norovirus-associated diseases (NADs) globally are still unknown.MethodsBased on global disease burden data from 1990 to 2019, we analyzed the age-standardized death rate (ASDR) of NADs by age, region, country, and Socio-Demographic Index (SDI) level. The discrete Poisson model was applied in the analysis of NADs' spatiotemporal aggregation, the Joinpoint regression model to analyze the trend of death burden of NADs over 30 years, and a generalized linear model to identify the risk factors for the death rate from NADs.ResultsThe ASDR of NADs significantly decreased by a factor of approximately 2.7 times, from 5.02 (95% CI: 1.1, 11.34) in 1990 to 1.86 (95% CI: 0.36, 4.16) in 2019 [average annual percent change (AAPC) = −3.43, 95% CI: −3.56, −3.29]. The death burden of NADs in 2019 was still highest in African regions despite a great decline in recent decades. However, the ASDR in high SDI countries presented an uptrend [0.12 (95% CI: 0.03, 0.26) in 1990 and 0.24 (95% CI: 0.03, 0.53) in 2019, AAPC = 2.52, 95% CI: 2.02–3.03], mainly observed in the elderly over 70 years old. Compared to children under 5 years old, the 2019 death rate of elderly individuals over 80 years old was much higher in high SDI countries. The generalized linear model showed that factors of the number of physicians (RR = 0.67), the proportions of children under 14 years old (RR = 1.21), elderly individuals over 65 years old (RR = 1.13), educational level (RR = 1.03) and urbanization proportion (RR = 1.01) influenced the ASDR of NADs.ConclusionsThe death burden of NADs has remained high in developing regions over the last three decades and has increased among the elderly in countries with high SDI levels, even though the global trend in NAD-associated deaths has decreased significantly in the past three decades. More effective public health policies against NADs need to be implemented in high SDI regions and for the elderly.</p