Atomic fountain of laser-cooled Yb atoms for precision measurements

We demonstrate launching of laser-cooled Yb atoms in a cold atomic fountain. Atoms in a collimated thermal beam are first cooled and captured in a magneto-optic trap (MOT) operating on the strongly-allowed ${^1S}_0 \rightarrow {^1P}_1$ transition at 399~nm (blue line). They are then transferred to a MOT on the weakly-allowed ${^1S}_0 \rightarrow {^3P}_1$ transition at 556~nm (green line). Cold atoms from the green MOT are launched against gravity at a velocity of around 2.5~m/s using a pair of green beams. We trap more than $10^7$ atoms in the blue MOT and transfer up to 70\% into the green MOT. The temperature for the odd isotope, $^{171}$Yb, is $\sim$1~mK in the blue MOT, and reduces by a factor of 40 in the green MOT.Comment: 6 pages, 7 figure

Reionization constraints on primordial magnetic fields

We study the impact of the extra density fluctuations induced by primordial magnetic fields on the reionization history in the redshift range: $6 < z < 10$. We perform a comprehensive MCMC physical analysis allowing the variation of parameters related to primordial magnetic fields (strength, $B_0$, and power-spectrum index $n_{\scriptscriptstyle \rm B}$), reionization, and $\Lambda$CDM cosmological model. We find that magnetic field strengths in the range: $B_0 \simeq 0.05{-}0.3$ nG (for nearly scale-free power spectra) can significantly alter the reionization history in the above redshift range and can relieve the tension between the WMAP and quasar absorption spectra data. Our analysis puts upper-limits on the magnetic field strength $B_0 < 0.358, 0.120, 0.059$ nG (95 % c.l.) for $n_{\scriptscriptstyle \rm B} = -2.95, -2.9, -2.85$, respectively. These represent the strongest magnetic field constraints among those available from other cosmological observables.Comment: Accepted for publication in MNRAS; 9 pages, 6 figure

Primordial magnetic field limits from cosmological data

We study limits on a primordial magnetic field arising from cosmological data, including that from big bang nucleosynthesis, cosmic microwave background polarization plane Faraday rotation limits, and large-scale structure formation. We show that the physically-relevant quantity is the value of the effective magnetic field, and limits on it are independent of how the magnetic field was generated.Comment: 7 pages, 6 figure

Is Low Alveolar Type II Cell SOD3 in the Lungs of Elderly Linked to the Observed Severity of COVID-19?

Human lungs single cell RNA sequencing data from healthy donors (elderly and young; GEO accession number GSE122960) were analyzed to isolate and specifically study gene expression in alveolar type II cells. Co-localization of ACE2 and TMPRSS2 enables SARS-CoV 2 to enter the cells. Expression of these genes in the alveolar type II cells of elderly and young patients were comparable and therefore do not seem to be responsible for worse outcomes observed in COVID-19 affected elderly. In cells from the elderly, 263 genes were downregulated and 95 upregulated. SOD3 was identified as the top-ranked gene that was most down-regulated in the elderly. Other redox-active genes that were also downregulated in cells from the elderly included ATF4 and M2TA. ATF4, an ER stress sensor that defends lungs via induction of heme oxygenase 1. The study of downstream factors known to be induced by ATF4, according to Ingenuity Pathway AnalysisTM, identified 24 candidates. Twenty-one of these were significantly downregulated in the cells from the elderly. These downregulated candidates were subjected to enrichment using the Reactome Database identifying that in the elderly, the ability to respond to heme deficiency and the ATF4-dependent ability to respond to endoplasmic reticulum stress is significantly compromised. SOD3-based therapeutic strategies have provided beneficial results in treating lung disorders including fibrosis. The findings of this work propose the hypotheses that lung-specific delivery of SOD3/ATF4 related antioxidants may work in synergy with promising anti-viral drugs such as remdesivir to further improve COVID-19 outcomes in the elderly

miR-146a suppresses cellular immune response during Japanese encephalitis virus JaOArS982 strain infection in human microglial cells

Background: Japanese encephalitis virus (JEV) is the causative agent of Japanese encephalitis which is more prevalent in South and Southeast Asia. JEV is a neurotropic virus which infiltrates into the brain through vascular endothelial cells. JEV infects neurons and microglial cells which causes neuronal damage and inflammation. However, JEV also evades the cellular immune response to survive in host cells. Viruses are known to modulate the expression of microRNAs, which in turn modulate cellular immune response by targeting expression of antiviral genes. The aim of this study is to understand the anti-inflammatory role of miR-146a during JEV infection, which facilitates immune evasion. Methods: Human brain microglial cells (CHME3) were infected by JEV: JaOArS982 and P20778 strain, and expression of miR-146a were analyzed. Overexpression and knockdown studies of miR-146a were done to see the effect on NF-κB pathway and antiviral Jak-STAT pathway. Regulatory role of miR-146a on expression of interferon-stimulated genes was determined by real-time PCR and luciferase assays. Results: JEV infection elevated the expression of miR-146a in JaOArS982 strain which caused downregulation of TRAF6, IRAK1, IRAK2, and STAT1 genes. Exogenous overexpression of miR-146a led to suppression of NF-κB activation and abrogation of Jak-STAT pathway upon JEV infection which led to downregulation of interferon-stimulated genes (IFIT-1 and IFIT-2) and facilitated viral replication. JEV infection initially upregulated cytokine production and activated STAT1 activity but STAT1 levels reduced at later time point, which led to the downregulation of interferon-stimulated genes. Conclusion: Upregulation of miR-146a by JEV JaOArS982 strain leads to suppression of NF-κB activity and disruption of antiviral Jak-STAT signaling which helps the virus to evade the cellular immune response. This effect of JEV infection on miR-146a expression was found to be strain specific