Uncertainty shocks and monetary policy: evidence from the troika of China’s economy

Growth in China’s economy is driven by the troika: consumption, investment and export. This paper examines the effect of uncertain events such as the global financial crisis in 2008, and the COVID-19 pandemic on the troika. Based on the construction of a new uncertainty index of China’s economy, the relationship between uncertainty and growth in the troika is examined by using a TVP-VAR model. Results show that fluctuations in the uncertainty index during the COVID-19 epidemic had the greatest negative impact on consumption and investment at a magnitude of 0.27, notably greater than that during the period of the global financial crisis. The negative impact on export reached 0.73, smaller than that during the global financial crisis. Against a backdrop of the novel coronavirus epidemic, it is also found that expansionary monetary policies can have a relatively large impact on investment and export, reaching 1.75 and 1.57 respectively, while short-term impact on consumption is relatively weak, averaging at 0.51

Anthrax Toxin Uptake by Primary Immune Cells as Determined with a Lethal Factor-β-Lactamase Fusion Protein

BACKGROUND:To initiate infection, Bacillus anthracis needs to overcome the host innate immune system. Anthrax toxin, a major virulence factor of B. anthracis, impairs both the innate and adaptive immune systems and is important in the establishment of anthrax infections. METHODOLOGY/PRINCIPAL FINDINGS:To measure the ability of anthrax toxin to target immune cells, studies were performed using a fusion of the anthrax toxin lethal factor (LF) N-terminal domain (LFn, aa 1-254) with beta-lactamase (LFnBLA). This protein reports on the ability of the anthrax toxin protective antigen (PA) to mediate LF delivery into cells. Primary immune cells prepared from mouse spleens were used in conjunction with flow cytometry to assess cleavage and resulting FRET disruption of a fluorescent beta-lactamase substrate, CCF2/AM. In spleen cell suspensions, the macrophages, dendritic cells, and B cells showed about 75% FRET disruption of CCF2/AM due to cleavage by the PA-delivered LFnBLA. LFnBLA delivery into CD4+ and CD8+ T cells was lower, with 40% FRET disruption. When the analyses were done on purified samples of individual cell types, similar results were obtained, with T cells again having lower LFnBLA delivery than macrophages, dendritic cells, and B cells. Relative expression levels of the toxin receptors CMG2 and TEM8 on these cells were determined by real-time PCR. Expression of CMG2 was about 1.5-fold higher in CD8+ cells than in CD4+ and B cells, and 2.5-fold higher than in macrophages. CONCLUSIONS/SIGNIFICANCE:Anthrax toxin entry and activity differs among immune cells. Macrophages, dendritic cells, and B cells displayed higher LFnBLA activity than CD4+ and CD8+ T cells in both spleen cell suspension and the purified samples of individual cell types. Expression of anthrax toxin receptor CMG2 is higher in CD4+ and CD8+ T cells, which is not correlated to the intracellular LFnBLA activity

Selenium deficiency impairs host innate immune response and induces susceptibility to Listeria monocytogenes infection

<p>Abstract</p> <p>Background</p> <p>Susceptibility or resistance to infection with <it>Listeria monocytogenes </it>correlates with Selenium (Se) deficiency in response to infection.</p> <p>Results</p> <p>Se-deficient mouse models of listeriosis were used to study the innate immune response during the course of <it>L. monocytogenes </it>infection. Blood samples from mouse models were used for Se status. The concentration of MDA, SOD, GPx and CAT in blood has revealed that lower Se level exist in Se-deficient mice. Intestine, mesenteric lymph node, liver, spleen and brain from each mouse were to study the bacterial burden in organs. The analysis of cell types of spleen from Se-deficient mice revealed that the ability of the host to elicit a rapid recruitment and activation of systemic innate immune response to infection was to a certain extent compromised under conditions of Se deficiency. The cytokine levels in the serum and cytokine expression levels in the livers from Se-deficient mice revealed that the innate immune response of Se-deficient mice was impaired throughout the course of infection. These results suggest that innate immune response is altered by Se deficiency after infection with <it>L. monocytogenes</it>.</p> <p>Conclusion</p> <p>In conclusion, induced susceptibility of host resistance is associated with an impaired innate immune response following infection with <it>L. monocytogenes </it>in C57BL/6 Se-deficient mice.</p

Predictive values of PD‑L1 expression for survival outcomes in patients with cervical cancer: a systematic review and meta-analysis

Objectives: Cervical cancer is one of the most common cancers in women worldwide. Although mortality has declined over the past 30 years in high-income areas, it remains a problem in several countries. Given that the prognosis of patients with recurrent or metastatic disease is poor, it is necessary to identify valuable predictive indicators to estimate survival outcomes in patients with cervical cancer.Material and methods: We searched electronic databases such as PubMed, Web of Science, Embase, Ovid MEDLINE, and the Cochrane Central Register of Controlled Trials, and investigated the relationship between Programmed death-ligand 1(PD-L1) expression and prognosis. Chi squared tests and I2 were utilized to assess study heterogeneity, and publication bias was estimated using Begg’s funnel plot and Egger linear regression test.Results: Thirteen eligible studies with 1422 patients were included. Generally, high PD-L1 expression was conclusively associated with poor overall survival (OS) (HR: 1.31; 95% CI 1.03–1.66, p = 0.025). However, PD-L1 expression demonstrated no association with progression-free survival (HR: 0.93; 0.73–1.19, p = 0.57). High PD-L1 expression with a sample size over 100 indicated a shorter OS (HR: 1.51; 95% CI 1.13–2.01). High expression of PD-L1 in Asians represented a lower OS (HR: 1.52; 1.14–2.03). Overexpression of PD-L1 in tumor cells (HR: 1.57; 1.29–2.10) and tumor-infiltrating immune cells (HR: 1.75; 1.02-2.99) predicted poor OS. High PD-L1 expression (HR: 4.04; 2.58–6.31) showed a lower effect on OS with a cut-off value of 5%.Conclusions: Our results indicate that high PD-L1 expression could be a valuable biomarker for predicting clinical outcomes in patients with cervical cancer

Adult Attachment Styles Associated with Brain Activity in Response to Infant Faces in Nulliparous Women: An Event-Related Potentials Study

Adult attachment style is a key for understanding emotion regulation and feelings of security in human interactions as well as for the construction of the caregiving system. The caregiving system is a group of representations about affiliative behaviors, which is guided by the caregiver’s sensitivity and empathy, and is mature in young adulthood. Appropriate perception and interpretation of infant emotions is a crucial component of the formation of a secure attachment relationship between infant and caregiver. As attachment styles influence the ways in which people perceive emotional information, we examined how different attachment styles associated with brain response to the perception of infant facial expressions in nulliparous females with secure, anxious, and avoidant attachment styles. The event-related potentials of 65 nulliparous females were assessed during a facial recognition task with joy, neutral, and crying infant faces. The results showed that anxiously attached females exhibited larger N170 amplitudes than those with avoidant attachment in response to all infant faces. Regarding the P300 component, securely attached females showed larger amplitudes to all infant faces in comparison with avoidantly attached females. Moreover, anxiously attached females exhibited greater amplitudes than avoidantly attached females to only crying infant faces. In conclusion, the current results provide evidence that attachment style differences are associated with brain responses to the perception of infant faces. Furthermore, these findings further separate the psychological mechanisms underlying the caregiving behavior of those with anxious and avoidant attachment from secure attachment

Role of the SaeRS two-component regulatory system in Staphylococcus epidermidis autolysis and biofilm formation

<p>Abstract</p> <p>Background</p> <p><it>Staphylococcus epidermidis </it>(SE) has emerged as one of the most important causes of nosocomial infections. The SaeRS two-component signal transduction system (TCS) influences virulence and biofilm formation in <it>Staphylococcus aureus</it>. The deletion of <it>saeR </it>in <it>S. epidermidis </it>results in impaired anaerobic growth and decreased nitrate utilization. However, the regulatory function of SaeRS on biofilm formation and autolysis in <it>S. epidermidis </it>remains unclear.</p> <p>Results</p> <p>The <it>saeRS </it>genes of SE1457 were deleted by homologous recombination. The <it>saeRS </it>deletion mutant, SE1457<it>ΔsaeRS</it>, exhibited increased biofilm formation that was disturbed more severely (a 4-fold reduction) by DNase I treatment compared to SE1457 and the complementation strain SE1457<it>saec</it>. Compared to SE1457 and SE1457<it>saec</it>, SE1457<it>ΔsaeRS </it>showed increased Triton X-100-induced autolysis (approximately 3-fold) and decreased cell viability in planktonic/biofilm states; further, SE1457<it>ΔsaeRS </it>also released more extracellular DNA (eDNA) in the biofilms. Correlated with the increased autolysis phenotype, the transcription of autolysis-related genes, such as <it>atlE </it>and <it>aae</it>, was increased in SE1457<it>ΔsaeRS</it>. Whereas the expression of accumulation-associated protein was up-regulated by 1.8-fold in 1457<it>ΔsaeRS</it>, the expression of an N-acetylglucosaminyl transferase enzyme (encoded by <it>icaA</it>) critical for polysaccharide intercellular adhesin (PIA) synthesis was not affected by the deletion of <it>saeRS.</it></p> <p>Conclusions</p> <p>Deletion of <it>saeRS </it>in <it>S. epidermidis </it>resulted in an increase in biofilm-forming ability, which was associated with increased eDNA release and up-regulated Aap expression. The increased eDNA release from SE1457<it>ΔsaeRS </it>was associated with increased bacterial autolysis and decreased bacterial cell viability in the planktonic/biofilm states.</p

Adiponectin Protects Against Cerebral Ischemic Injury Through AdipoR1/AMPK Pathways

Excitotoxicity induced by excessive N-methyl-D-aspartate (NMDA) receptor activation underlies the pathology of ischemic injury. Adiponectin (APN) is an adipocyte-derived protein hormone that modulates a number of metabolic processes. APN exerts a wide range of biological functions in the central nervous system. However, the role of APN and its receptors in cerebral ischemia/reperfusion (I/R)-induced injury and the related mechanisms remain to be clarified. Here, we found that APN and APN receptor agonist AdipoRon (APR) were protective against excitotoxicity induced by oxygen and glucose deprivation/reperfusion (OGD/R) and NMDA in primary neurons. Adiponectin receptor 1 (AdipoR1) knockdown reversed the protection conferred by either APN or APR. Moreover, the protective effects offered by both APN and APR were compromised by compound C, an inhibitor of amp-activated protein kinase (AMPK) phosphorylation. Both APN and APR protected the dissipation of the ΔΨm caused by OGD/R. They also up-regulated the PGC-1α expression, which was reversed by compound C. Furthermore, both APN and APR ameliorated but APN knockout aggravated the infarct volume and neurological deficient induced by transient middle cerebral artery occlusion (tMCAO) in vivo. Taken together, these findings show that APN and APR protect against ischemic injury in vitro and in vivo. The protective mechanism is mainly related to AdipoR1-dependent AMPK phosphorylation and PGC-1α up-regulation