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Waterlogging has negative effects on crop yield. Physiological and transcriptome data of two peanut cultivars [Zhongkaihua 1 (ZKH 1) and Huayu 39 (HY 39)] were studied under normal water supply and waterlogging stress for 5 or 10 days at the flowering stage. The results showed that the main stem height, the number of lateral branches, lateral branch length, and the stem diameter increased under waterlogging stress, followed by an increase in dry matter accumulation, which was correlated with the increase in the soil and plant analysis development (SPAD) and net photosynthetic rate (Pn) and the upregulation of genes related to porphyrin and chlorophyll metabolism and photosynthesis. However, the imbalance of the source-sink relationship under waterlogging was the main cause of yield loss, and waterlogging caused an increase in the sucrose and soluble sugar contents and a decrease in the starch content; it also decreased the activities of sucrose synthetase (SS) and sucrose phosphate synthetase (SPS), which may be due to the changes in the expression of genes related to starch and sucrose metabolism. However, the imbalance of the source-sink relationship led to the accumulation of photosynthate in the stems and leaves, which resulted in the decrease of the ratio of pod dry weight to total dry weight (PDW/TDW) and yield. Compared with ZKH 1, the PDW of HY 39 decreased more probably because more photosynthate accumulated in the stem and leaves of HY 39 and could not be effectively transported to the pod.What causes variation in species abundance for a given site remains a central question in community ecology. Foundational to trait-based ecology is the expectation that functional traits determine species abundance. However, the relative success of using functional traits to predict relative abundance is questionable. One reason is that the diversity in plant function is greater than that characterized by the few most commonly and easily measurable traits. Here, we measured 10 functional traits and the stem density of 101 woody plant species in a 200,000 m2 permanent, mature, subtropical forest plot (high precipitation and high nitrogen, but generally light- and phosphorus-limited) in southern China to determine how well relative species abundance could be predicted by functional traits. We found that (1) leaf phosphorus content, specific leaf area, maximum CO2 assimilation rate, maximum stomata conductance, and stem hydraulic conductivity were significantly and negatively associated with species abundance, (2) the ratio of leaf nitrogen content to leaf phosphorus content (NP) and wood density were significantly positively correlated with species abundance; (3) neither leaf nitrogen content nor leaf turgor loss point were related to species abundance; (4) a combination of NP and maximum stomata conductance accounted for 44% of the variation in species' abundances. Taken together, our findings suggested that the combination of these functional traits are powerful predictors of species abundance. Species with a resource-conservative strategy that invest more in their tissues are dominant in the mature, subtropical, evergreen forest.[This corrects the article DOI 10.3389/fimmu.2020.585731.].Human genetic control is thought to affect a considerable part of the outcome of infection with Mycobacterium tuberculosis (Mtb). Most of us deal with the pathogen by containment (associated with clinical "latency") or sterilization, but tragically millions each year do not. After decades of studies on host genetic susceptibility to Mtb infection, genetic variation has been discovered to play a role in tuberculous immunoreactivity and tuberculosis (TB) disease. Genes encoding pattern recognition receptors (PRRs) enable a consistent, molecularly direct interaction between humans and Mtb which suggests the potential for co-evolution. In this review, we explore the roles ascribed to PRRs during Mtb infection and ask whether such a longstanding and intimate interface between our immune system and this pathogen plays a critical role in determining the outcome of Mtb infection. The scientific evidence to date suggests that PRR variation is clearly implicated in altered immunity to Mtb but has a more subtle role in limiting the pathogen and pathogenesis. In contrast to 'effectors' like IFN-γ, IL-12, Nitric Oxide and TNF that are critical for Mtb control, 'sensors' like PRRs are less critical for the outcome of Mtb infection. This is potentially due to redundancy of the numerous PRRs in the innate arsenal, such that Mtb rarely goes unnoticed. Genetic association studies investigating PRRs during Mtb infection should therefore be designed to investigate endophenotypes of infection - such as immunological or clinical variation - rather than just TB disease, if we hope to understand the molecular interface between innate immunity and Mtb.Passive antibody therapy has been used to treat outbreaks of viral disease, including the ongoing pandemic of severe respiratory acute respiratory syndrome (SARS) coronavirus 2 (SARS-CoV-2) or COVID-19. However, the real benefits of the procedure are unclear. We infused a concentrated solution of neutralizing anti-SARS-CoV-2 antibodies obtained from a convalescent donor with a single session of double filtration plasmapheresis (DFPP) into a 56-year-old woman with long history of unremitting, severe COVID-19. She was unable to establish an adequate antiviral immune response because of previous chemotherapy, including the infusion of the anti-CD20 monoclonal antibody rituximab, administered to treat a diffuse large B-cell lymphoma. mTOR inhibitor review The disease promptly recovered despite evidence of no endogenous anti-SARS-CoV-2 antibody production. The observation that passive antibody therapy might prove particularly effective in immunodepressed COVID-19 patients requires evaluation in prospective randomized controlled trial.Post-transcriptional regulation is involved in the regulation of many inflammatory genes. Zinc finger protein 36 (ZFP36) family proteins are RNA-binding proteins involved in messenger RNA (mRNA) metabolism pathways. The ZFP36 family is composed of ZFP36 (also known as tristetraprolin, TTP), ZFP36L1, ZFP36L2, and ZFP36L3 (only in rodents). The ZFP36 family proteins contain two tandemly repeated CCCH-type zinc-finger motifs, bind to adenine uridine-rich elements in the 3'-untranslated regions (3' UTR) of specific mRNA, and lead to target mRNA decay. Although the ZFP36 family members are structurally similar, they are known to play distinct functions and regulate different target mRNAs, probably due to their cell-type-specific expression patterns. For instance, ZFP36 has been well-known to function as an anti-inflammatory modulator in murine models of systemic inflammatory diseases by down-regulating the production of various pro-inflammatory cytokines, including TNF-α. Meanwhile, ZFP36L1 is required for the maintenance of the marginal-zone B cell compartment.

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