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The application of deep learning is fast developing in climate prediction, in which El Niño–Southern Oscillation (ENSO), as the most dominant disaster-causing climate event, is a key target. Previous studies have shown that deep learning methods possess a certain level of superiority in predicting ENSO indices. The present study develops a deep learning model for predicting the spatial pattern of sea surface temperature anomalies (SSTAs) in the equatorial Pacific by training a convolutional neural network (CNN) model with historical simulations from CMIP6 models. Compared with dynamical models, the CNN model has higher skill in predicting the SSTAs in the equatorial western-central Pacific, but not in the eastern Pacific. The CNN model can successfully capture the small-scale precursors in the initial SSTAs for the development of central Pacific ENSO to distinguish the spatial mode up to a lead time of seven months. A fusion model combining the predictions of the CNN model and the dynamical models achieves higher skill than each of them for both central and eastern Pacific ENSO.

Ferulic acid (FA), a prevalent dietary phytochemical, has many pharmacological effects, including anti-oxidation and anti-inflammation effects, and has been widely used in the pharmaceutical, food, and cosmetics industries. Many studies have shown that FA can significantly downregulate the expression of reactive oxygen species and activate nuclear factor erythroid-2-related factor-2/heme oxygenase-1 signaling, exerting anti-oxidative effects. The anti-inflammatory effect of FA is mainly related to the p38 mitogen-activated protein kinase and nuclear factor-kappaB signaling pathways. FA has demonstrated potential clinical applications in the treatment of pulmonary diseases. The transforming growth factor-β1/small mothers against decapentaplegic 3 signaling pathway can be blocked by FA, thereby alleviating pulmonary fibrosis. Moreover, in the context of asthma, the T helper cell 1/2 imbalance is restored by FA. Furthermore, FA ameliorates acute lung injury by inhibiting nuclear factor-kappaB and mitogen-activated protein kinase pathways via toll-like receptor 4, consequently decreasing the expression of downstream inflammatory mediators. Additionally, there is a moderate neuraminidase inhibitory activity showing a tendency to reduce the interleukin-8 level in response to influenza virus infections. Although the application of FA has broad prospects, more preclinical mechanism-based research should be carried out to test these applications in clinical settings. This review not only covers the literature on the pharmacological effects and mechanisms of FA, but also discusses the therapeutic role and toxicology of FA in several pulmonary diseases.

In this report, high-brightness green carbon dots were successfully prepared using 3,5-diaminobenzoic acid as the sole precursor and synthesized in one step using a solvothermal strategy. Under the excitation of 365 nm ultraviolet light, the quantum yield of carbon dots is as high as 53.8%. Experiments revealed that the carbon dots are highly carbonized and the surface is rich in amino and carboxyl groups. The synthesized carbon dots have good water solubility, and are resistant to ions and temperature. The fluorescence intensity of CDs is sensitive to pH changes and is linearly correlated with the pH in the near-neutral range (pH = 6.0 to 9.0). Our experiments showed that carbon dots were sensitive and accurate fluorescent probes for measuring the pH value of drinking water, which could provide an effective method for measuring the pH value of water in the future.

Transcranial magnetic stimulation (TMS) is a noninvasive procedure that uses magnetic fields to stimulate neurons in the brain and has been widely applied in the field of clinical neuromodulation. However, traditional TMS has limitations in terms of focality and stimulation depth, making it unable to achieve precise modulation of deep brain regions. As the stimulation depth increases, the focal area expands, potentially stimulating nontarget regions and causing negative side effects. Moreover, strongly induced electric fields can lead to adverse effects such as seizures. Temporal interference transcranial magnetic stimulation (TI-TMS) is a novel noninvasive neuromodulation technique that has considerable potential for reducing the focal area and increasing the stimulation depth. To study the mechanisms and effects of TI-TMS, this research first established a TI-TMS simulation platform based on a five-layer spherical model. This paper designed a double curved-elliptical coil structure, increasing the stimulation depth of the TI-TMS to 5.02 cm while reducing the focal area to 18.61 cm 2 . Finally, a TI-TMS system was developed, with a focus on the design and development of the insulated-gate bipolar transistor (IGBT) driving circuit and the coil capacitor resonance part. The current amplitude and frequency in the coils were measured to validate the system’s effectiveness. This study confirmed that TI-TMS can effectively stimulate deep brain regions and provide new insights for the application of TMS in the rehabilitation of neurological diseases.

Osteoarthritis (OA) is the most common degenerative joint disease and a major cause of pain and disability in adult individuals. The etiology of OA includes joint injury, obesity, aging, and heredity. However, the detailed molecular mechanisms of OA initiation and progression remain poorly understood and, currently, there are no interventions available to restore degraded cartilage or decelerate disease progression. The diathrodial joint is a complicated organ and its function is to bear weight, perform physical activity and exhibit a joint-specific range of motion during movement. During OA development, the entire joint organ is affected, including articular cartilage, subchondral bone, synovial tissue and meniscus. A full understanding of the pathological mechanism of OA development relies on the discovery of the interplaying mechanisms among different OA symptoms, including articular cartilage degradation, osteophyte formation, subchondral sclerosis and synovial hyperplasia, and the signaling pathway(s) controlling these pathological processes.

There is growing evidence that mesenchymal stem cell-derived extracellular vesicles and exosomes can significantly improve the curative effect of oxidative stress-related diseases. Mesenchymal stem cell extracellular vesicles and exosomes (MSC-EVs and MSC-Exos) are rich in bioactive molecules and have many biological regulatory functions. In this review, we describe how MSC-EVs and MSC-Exos reduce the related markers of oxidative stress and inflammation in various systemic diseases, and the molecular mechanism of MSC-EVs and MSC-Exos in treating apoptosis and vascular injury induced by oxidative stress. The results of a large number of experimental studies have shown that both local and systemic administration can effectively inhibit the oxidative stress response in diseases and promote the survival and regeneration of damaged parenchymal cells. The mRNA and miRNAs in MSC-EVs and MSC-Exos are the most important bioactive molecules in disease treatment, which can inhibit the apoptosis, necrosis and oxidative stress of lung, heart, kidney, liver, bone, skin and other cells, and promote their survive and regenerate.

Intestinal fibrosis is induced by excessive myofibroblast proliferation and collagen deposition, which has been regarded as a general pathological feature in inflammatory bowel disease (IBD). Therefore, identifying clinical markers and targets to treat and prevent intestinal fibrosis is urgently needed. The traditional Chinese medicine maggot, commonly known as “wu gu chong”, has been shown to reduce oxidative stress and alleviate inflammation in chronic colitis. This study investigated the mechanisms underlying the effects of maggot extract (ME) on inflammation-associated intestinal fibrosis in TGF-β1-stimulated human intestinal fibroblasts (CCD-18Co cells) and dextran sodium sulphate (DSS)-induced chronic colitis murine model. To assess the severity of inflammation and fibrosis, histological and macroscopic evaluation were carried out. The results showed that ME was a significant inhibitor of body weight loss and colon length shortening in mice with chronic colitis. In addition, ME suppressed the intestinal fibrosis by downregulating TGF-β1/SMADs pathway via upregulation of Nrf2 expression at both protein and mRNA levels. ME markedly increased the expression of Nrf2, thus resulting in a higher level of HO-1. After treatment with Nrf2 inhibitor (ML385) or siRNA-Nrf2 for deactivating Nrf2 pathway, the protective effects of ME were abolished both in vitro and in vivo . Moreover, the histopathological results for the major organs of DSS mice treated with ME showed no signs of clinically important abnormalities. Treatment with ME had no effect on the viability of CCD-18Co cells, suggesting its low in vitro cytotoxicity. Furthermore, ME could mediate intestine health by keeping the balance of the gut microbes through the enhancement of beneficial microbes and suppression of pathogenic microbes. In conclusion, this is the first ever report demonstrating that ME ameliorates inflammation-associated intestinal fibrosis by suppressing TGF-β1/SMAD pathway via upregulation of Nrf2 expression. Our findings highlight the potential of Nrf2 as an effective therapeutic target for alleviating intestinal fibrosis.

Mantle cell lymphoma (MCL) is a phenotypically and genetically heterogeneous malignancy in which the genetic alterations determining clinical indications are not fully understood. Here, we performed a comprehensive whole-exome sequencing analysis of 152 primary samples derived from 134 MCL patients, including longitudinal samples from 16 patients and matched RNA-Seq data from 48 samples. We classified MCL into 4 robust clusters (C1-C4). C1 featured mutated immunoglobulin heavy variable (IGHV), CCND1 mutation, amp(11q13), and active B cell receptor (BCR) signaling. C2 was enriched with del(11q)/ATM mutations and upregulation of NF-κB and DNA repair pathways. C3 was characterized by mutations in SP140, NOTCH1, and NSD2, with downregulation of BCR signaling and MYC targets. C4 harbored del(17p)/TP53 mutations, del(13q), and del(9p), and active MYC pathway and hyperproliferation signatures. Patients in these 4 clusters had distinct outcomes (5-year overall survival [OS] rates for C1-C4 were 100%, 56.7%, 48.7%, and 14.2%, respectively). We also inferred the temporal order of genetic events and studied clonal evolution of 16 patients before treatment and at progression/relapse. Eleven of these samples showed drastic clonal evolution that was associated with inferior survival, while the other samples showed modest or no evolution. Our study thus identifies genetic subsets that clinically define this malignancy and delineates clonal evolution patterns and their impact on clinical outcomes.

The water quality index model is a popular tool for evaluating drinking water quality. To overcome low precision and significant errors in the traditional single prediction model, a novel autoregressive integrated moving average (ARIMA)-sparrow search algorithm (SSA)-long short-term memory (LSTM) combination model is proposed to accurately predict residual chlorine, turbidity, and pH in drinking water. First, the ARIMA model is used to extract the linear part of water quality data and output the nonlinear residual. Then, the LSTM model is used to predict the residual, and the SSA is used to find the optimal hyperparameters of the LSTM model, which plays an essential role in reducing the error of the model. To prove the superiority of the model developed, the ARIMA-SSA-LSTM model is compared with SSA-LSTM, whale optimization algorithm-LSTM, PSO-LSTM, ARIMA-LSTM, ARIMA, and LSTM. The results show that the coefficient of determination (R2) of the combination model for residual chlorine, turbidity, and pH are 0.950, 0.990, and 0.998, respectively, which are greater than all comparison models. Therefore, the model is more suitable for the prediction and analysis of water quality data.

Background Rats with hyperandrogen-induced polycystic ovary syndrome (PCOS) have been shown to develop ovarian oxidative stress (OS) and fibrosis. The Sirt1 agonist, resveratrol, can reduce OS through inhibiting p66Shc in other models of OS. Methods We created a rat PCOS model with increased OS levels following treatment with one of the two androgens, dehydroepiandrosterone (DHEA) and dihydrotestosterone (DHT). The PCOS related features were determined by measurement of malondialdehyde (MDA) and superoxide dismutase (SOD) levels or by examining the reactive oxygen species (ROS) levels using the DCF-DA probe. The potential mechanisms by which p66Shc/Sirt1 mediates ovarian fibrosis were explored by western blotting, quantitative reverse transcription-PCR, immunofluorescence staining, and immunohistochemistry. Results Hyperandrogen dramatically augmented OS and activation of fibrotic factors in the ovary. Our data demonstrated that treatment with resveratrol enhanced Sirt1 and decreased ovarian OS as well as inhibited phosphorylation of p66Shc both in vivo and in vitro. The treatment suppressed fibrotic factor activation and improved ovarian morphology. Lentivirus- or siRNA-mediated p66Shc knockdown resulted in a dramatic enhancement of Sirt1 expression, down-regulation of ROS and suppression of fibrotic factors in granulosa cells. Moreover, p66Shc overexpression markedly increased the expression of fibrotic factors. Additionally, silencing Sirt1 induced a dramatic increase in p66Shc and enhanced activation of fibrotic factors. Conclusions p66Shc may be a direct target of Sirt1 for inducing ROS and thus promoting fibrosis. Further exploration of the mechanisms of p66Shc in both fibrosis and OS may provide novel therapeutic strategies that will facilitate the improvement in PCOS symptoms and reproductive functions.