Statistical model results suggest that the declining growth rate from autumn to spring is the key to cause El Nino-Southern Oscillation (ENSO) spring persistence barrier (SPB). Using a dynamical approach, we develop the physical mechanisms responsible for ENSO SPB in the framework of recharge oscillator by adding a seasonally varying Bjerknes (BJ) stability index and linking it with ENSO growth rate. By decomposing BJ index, it is indicated that seasonal thermodynamic damping and thermocline positive feedback play an important role in determining the ENSO SPB. We further show that the increasing/decreasing upper-level cloud/low-level cloud and the deepening thermocline from autumn to spring are the main factors to control the SPB of ENSO. Our proposed mechanisms also have useful implications for the understanding of ENSO prediction. (Less)

https://agupubs.onlinelibrary.wiley.com/doi/pdf/10.1029/2019GL085205

Seasonal Cycle of Background in the Tropical Pacific as a Cause of ENSO Spring Persistence Barrier

https://doi.org/10.1016/j.apsb.2022.08.025

Emerging biotechnology applications in natural product and synthetic pharmaceutical analyses

This paper investigates potential factors that control the El Nino–Southern Oscillation (ENSO) Spring Persistence Barrier (SPB) strength in two different ENSO regimes and apply it to explain the ENSO SPB strength modulation after the 21st century. In a damped, noise-driven model, the theoretical solution of SPB strength illustrates that a weaker ENSO growth rate strengthens SPB. In the self-sustained regime, as in the Cane-Zebiak model (chaotic system), the strengthened thermodynamic damping and weakened thermocline positive feedback lead to a more negative ENSO growth rate and, in turn, a stronger SPB. Therefore, in both ENSO regimes, a weaker ENSO growth rate intensifies the SPB. The application of the theory to the real world suggests that a more negative ENSO growth rate, corresponding to a more damped feedback system, is responsible for the stronger SPB in recent decades than in 1980–2000. (Less)

Controls of Spring Persistence Barrier Strength in Different ENSO Regimes and Implications for 21st Century Changes

Neurodegenerative diseases (NDs) affect the West due to the increase in life expectancy. Nervous cells accumulate oxidative damage, which is one of the factors that triggers and accelerates neurodegeneration. However, cells have mechanisms that scavenge reactive oxygen species (ROS) and alleviate oxidative stress (OS). Many of these endogenous antioxidant systems are regulated at the gene expression level by the transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2). In the presence of prooxidant conditions, Nrf2 translocates to the nucleus and induces the transcription of genes containing ARE (antioxidant response element). In recent years, there has been an increase in the study of the Nrf2 pathway and the natural products that positively regulate it to reduce oxidative damage to the nervous system, both in in vitro models with neurons and microglia subjected to stress factors and in vivo models using mainly murine models. Quercetin, curcumin, anthocyanins, tea polyphenols, and other less studied phenolic compounds such as kaempferol, hesperetin, and icariin can also modulate Nrf2 by regulating several Nrf2 upstream activators. Another group of phytochemical compounds that upregulate this pathway are terpenoids, including monoterpenes (aucubin, catapol), diterpenes (ginkgolides), triterpenes (ginsenosides), and carotenoids (astaxanthin, lycopene). This review aims to update the knowledge on the influence of secondary metabolites of health interest on the activation of the Nrf2 pathway and their potential as treatments for NDs.

/pdf/natural-products-as-modulators-of-nrf2-signaling-pathway-in-1ga4ty7u.pdf

Natural Products as Modulators of Nrf2 Signaling Pathway in Neuroprotection

Stochastic reduced models are an important tool in climate systems whose many spatial and temporal scales cannot be fully discretized or underlying physics may not be fully accounted for. O...

/pdf/a-bayesian-approach-to-regional-decadal-predictability-3mc5fxhssi.pdf

A Bayesian Approach to Regional Decadal Predictability: Sparse Parameter Estimation in High-Dimensional Linear Inverse Models of High-Latitude Sea Surface Temperature Variability

The aim of the present study was to examine the neuroprotective effects of a panel of active components of ginseng and to explore their molecular mechanisms of action in two rotenone (Rot)-induced models of Parkinson's disease: An in vitro model using the human neuroblastoma cell line SH-SY5Y and an in vivo model using Drosophila. Ginsenoside Re (Re) was identified as the most potent inhibitor of Rot-induced cytotoxicity in SH-SY5Y cells by Cell Counting kit-8 assay and lactate dehydrogenase release assay. Flow cytometry, Hoechst staining, Rhodamine 123 staining, ATP and cytochrome c release revealed that Re rescue of Rot-induced mitochondrial dysfunction and inhibition of the mitochondrial apoptotic pathway. Western blot analysis demonstrated that Re alleviated Rot-induced oxidative stress by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) anti-oxidant pathway, and these effects were abolished by RNA interference-mediated knockdown of Nrf2. Re enhanced phosphorylation of components of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) and extracellular regulated protein kinase (ERK) pathways, and pharmacological inhibition of these pathways reduced Re-mediated Nrf2 activation and neuroprotection. In the Drosophila model, Immunofluorescence microscopy, reactive oxygen species (ROS), hydrogen peroxide and knockdown analysis revealed that Re reversed Rot-induced motor deficits and dopaminergic neuron loss while concomitantly alleviating Rot-induced oxidative damage. The findings of the present study suggest that Re protects neurons against Rot-induced mitochondrial dysfunction and oxidative damage, at least in part, by inducing Nrf2/heme oxygenase-1 expression and activation of the dual PI3K/AKT and ERK pathways.

/pdf/neuroprotective-effect-of-ginsenoside-re-against-neurotoxin-3gzwmqe1.pdf

Neuroprotective effect of Ginsenoside Re against neurotoxin-induced Parkinson's disease models via induction of Nrf2

We performed parameter estimation in the Zebiak–Cane model for the real-world scenario using the approach of ensemble Kalman filter (EnKF) data assimilation and the observational data of se...

/pdf/parameter-optimization-for-real-world-enso-forecast-in-an-4q8zjfp9f9.pdf

Parameter Optimization for Real-World ENSO Forecast in an Intermediate Coupled Model

The mechanism of the seasonal persistence barrier (SPB) is studied in the framework of an autoregressive (AR) model. In contrast to the seasonal variance, whose minimum is modulated mainly by the minimum growth rate or noise forcing, the SPB is caused primarily by the declining growth rate or increasing noise forcing, instead of the minimum/maximum of the growth rate or noise forcing. In other words, the SPB is caused by the declining signal-to-noise ratio (SNR) rather than the weakest SNR. In a weakly damped system, the phase of the SPB is delayed from that of declining SNR by about a season. The mechanism is further applied to explain the observed SST variability in the tropical and North Pacific. For the tropical Pacific, the spring SPB could be caused by the decreasing growth rate from September to March and weak annual mean damping rate, instead of the minimum growth rate in spring. Over the North Pacific, the increasing noise forcing from March to June may lead to the summer SPB. Our mechanism provides a null hypothesis for understanding the SPB of climate variability.

/pdf/on-the-formation-mechanism-of-the-seasonal-persistence-1fw78o8znj.pdf

On the Formation Mechanism of the Seasonal Persistence Barrier

In an increasingly aged global population, achieving healthy life expectancy through natural and safe drug interventions is highly desirable. Here we show that total ginsenosides (TGGR), the main active components in the traditional Chinese medicine, ginseng, promote longevity across species. In Drosophila, an intriguing effect of TGGR on lifespan was the relatively narrow treatment window to elicit long-term benefits. TGGR administration during early adulthood, and especially during midlife, was sufficient to extend lifespan in both sexes. TGGR did not increase lifespan by reducing food intake or reproductive capacity; rather, TGGR increased the fertility of male Drosophila. TGGR augmented healthspan readouts associated with youth and with healthy aging, such as motility, intestinal barrier integrity, and biorhythm homeostasis. TGGR treatment also improved some types of stress resistance in both sexes, including increased tolerance to starvation and oxidation, and shifting “aged” gene expression patterns toward “healthy” patterns seen in the young. Gene expression, pharmacological and genetic epistatic analyses demonstrated that TGGR effects require normal expression of genes involved in insulin, TOR and MAPK signaling. The positive effects of TGGR on both healthspan and lifespan, coupled with its mechanism of action via evolutionarily conserved signaling pathways, demonstrate it to be a promising anti-aging drug.

https://www.frontiersin.org/articles/10.3389/fnagi.2022.870326/pdf

Yuchu Zhao

Papers

Neuroprotective effect of Ginsenoside Re against neurotoxin-induced Parkinson's disease models via induction of Nrf2

Parameter Optimization for Real-World ENSO Forecast in an Intermediate Coupled Model

On the Formation Mechanism of the Seasonal Persistence Barrier

Studies on the Regulation and Molecular Mechanism of Panax Ginseng Saponins on Senescence and Related Behaviors of Drosophila melanogaster

Ginseng polysaccharide attenuates red blood cells oxidative stress injury by regulating red blood cells glycolysis and liver gluconeogenesis.