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Medicinal plants are an important source of therapeutic compounds used in the treatment of many diseases since ancient times. Interestingly, they form associations with numerous microorganisms developing as endophytes or symbionts in different parts of the plants. Within the soil, arbuscular mycorrhizal fungi (AMF) are the most prevalent symbiotic microorganisms forming associations with more than 70% of vascular plants. In the last decade, a number of studies have reported the positive effects of AMF on improving the production and accumulation of important active compounds in medicinal plants.In this work, we reviewed the literature on the effects of AMF on the production of secondary metabolites in medicinal plants. The major findings are as follows: AMF impact the production of secondary metabolites either directly by increasing plant biomass or indirectly by stimulating secondary metabolite biosynthetic pathways. The magnitude of the impact differs depending on the plant genotype, the AMF strain, and the environmental context (e.g., light, time of harvesting). Different methods of cultivation are used for the production of secondary metabolites by medicinal plants (e.g., greenhouse, aeroponics, hydroponics, in vitro and hairy root cultures) which also are compatible with AMF. In conclusion, the inoculation of medicinal plants with AMF is a real avenue for increasing the quantity and quality of secondary metabolites of pharmacological, medical, and cosmetic interest.

Diabetes mellitus, a chronic metabolic disease, often leads to numerous chronic complications, significantly contributing to global morbidity and mortality rates. High glucose levels trigger epigenetic modifications linked to pathophysiological processes like inflammation, immunity, oxidative stress, mitochondrial dysfunction, senescence and various kinds of cell death. Despite glycemic control, transient hyperglycemia can persistently harm organs, tissues, and cells, a latent effect termed \"metabolic memory\" that contributes to chronic diabetic complications. Understanding metabolic memory's mechanisms could offer a new approach to mitigating these complications. However, key molecules and networks underlying metabolic memory remain incompletely understood. This review traces the history of metabolic memory research, highlights its key features, discusses recent molecules involved in its mechanisms, and summarizes confirmed and potential therapeutic compounds. Additionally, we outline in vitro and in vivo models of metabolic memory. We hope this work will inform future research on metabolic memory's regulatory mechanisms and facilitate the development of effective therapeutic compounds to prevent diabetic complications.

In the specialized nursing setting, nurses are susceptible to developing negative mental health issues. Such conditions among nurses can potentially result in unfavorable medical outcomes. Consequently, this study aims to explore the role of social support in regulating between sleep and mental health in nurses. A cross-sectional study was carried out in September 2022 on 1219 nurses in Quanzhou. The study comprised general demographic information and utilized various questionnaires, namely the Social Support Rate Scale (SSRS), Pittsburgh Sleep Quality Index Questionnaire (PSQI), Generalized Anxiety Disorder Questionnaire (GAD-7), and Patient Health Questionnaire-9 (PHQ-9). The data analysis was performed using t-tests, ANOVAs, Pearsons correlations and hierarchical regression analyses in SPSS software. Results show that significant associations of sleep quality and social support with anxiety and depression. Simple slope analysis shows that under low levels of social support, sleep quality has a positive impact on anxiety(β = 0.598) and depression(β = 0.851), and the impact is significant. Under high levels of social support, sleep quality also has a positive impact on anxiety(β = 0.462) and depression(β = 0.578), but the impact is smaller. This indicates that as the level of social support increases, the positive predictive effect of sleep quality on anxiety and depression gradually diminishes. Social support has the potential to alter the impact of sleep quality on anxiety and depression. Therefore, healthcare policymakers need to focus on enhancing the level of social support and mitigating the impact of poor sleep on anxiety and depression.

The folding nucleus (FN) initiates and enables an efficient protein folding pathway. Despite its essential role, the FN has long remained cryptic. Here we directly visualize the tubulin FN consisting of a nonnative, partially assembled Rossmann fold, in the closed chamber of human chaperonin TRiC. Chaperonin TRiC interacts with nonnatively folded secondary structure elements of tubulin, stabilizing the nucleus poised for transition into its first native domain tertiary structure. Through progressive folding into the native state, we observe that the unfolded sequence of tubulin undergoes drastic spatial rearrangement in the TRiC chamber to sample the conformational space, mediated by the highly dynamic CCT tails. The observed presence of individual nonnative secondary structure elements first in the nonnative FN and then around the incrementally folded native domains supports the hypothesis that tubulin folding in TRiC is a hierarchical process of nucleation, condensation and propagation in cooperation with TRiC subunits. Protein folding is crucial for proper cellular function but often requires assistance. Here, researchers visualize how the chaperonin TRiC guides tubulin folding by stabilizing a nonnative folding nucleus, revealing a stepwise, hierarchical process of protein folding inside a confined chamber.

Polycystic Ovary Syndrome (PCOS) is a heterogeneous endocrine disease with high incidences in women of reproductive age. Although miR-185-5p (miR-185) was decreased in PCOS patients, the exact function of miR-185 on PCOS development still requires further investigation. In this study, rat injected with dehydroepiandrosterone (DHEA) was established as a PCOS model. A lentivirus carrying miR-185 was employed to examine its effect on PCOS symptoms. Then we performed the luciferase reporter assay to validate the interactions between miR-185 and vascular endothelial growth factor A (VEGFA). Finally, human ovarian microvascular endothelial cells (HOMECs) were induced by VEGF to explore the role of miR-185 in the angiogenic process. The results showed that miR-185 overexpression improved insulin level alteration and ovarian histological lesion in PCOS rats. We also found that miR-185 reduced the excessive angiogenesis as indicated by alterations of VEGFA, ANGPT1/2, PDGFB/D, α-SMA and CD31 in the ovary of PCOS rats. Luciferase reporter assay identified that VEGFA directly interacted with miR-185, and its expression level was negatively regulated by miR-185. The in vitro results further demonstrated that miR-185-induced suppression of cell proliferation, migration and tube formation was attenuated by VEGF in HOMECs. In summary, this is the first study to show that miR-185 can target VEGFA to inhibit angiogenesis, thus improving the development of PCOS. These findings develop a molecular candidate for PCOS prevention and therapy.

The rapid growth, demand, and production of batteries to meet various emerging applications, such as electric vehicles and energy storage systems, will result in waste and disposal problems in the next few years as these batteries reach end-of-life. Battery reuse and recycling are becoming urgent worldwide priorities to protect the environment and address the increasing need for critical metals. As a review article, this paper reveals the current global battery market and global battery waste status from which the main battery chemistry types and their management, including reuse and recycling status, are discussed. This review then presents details of the challenges, opportunities, and arguments on battery second-life and recycling. The recent research and industrial activities in the battery reuse domain are summarized to provide a landscape picture and valuable insight into battery reuse and recycling for industries, scientific research, and waste management.

The tumor microenvironment (TME) can aid tumor cells in evading surveillance and clearance by immune cells, creating an internal environment conducive to tumor cell growth. Consequently, there is a growing focus on researching anti-tumor immunity through the regulation of immune cells within the TME. Various bioactive compounds in traditional Chinese medicine (TCM) are known to alter the immune balance by modulating the activity of immune cells in the TME. In turn, this enhances the body’s immune response, thus promoting the effective elimination of tumor cells. This study aims to consolidate recent findings on the regulatory effects of bioactive compounds from TCM on immune cells within the TME. The bioactive compounds of TCM regulate the TME by modulating macrophages, dendritic cells, natural killer cells and T lymphocytes and their immune checkpoints. TCM has a long history of having been used in clinical practice in China. Chinese medicine contains various chemical constituents, including alkaloids, polysaccharides, saponins and flavonoids. These components activate various immune cells, thereby improving systemic functions and maintaining overall health. In this review, recent progress in relation to bioactive compounds derived from TCM will be covered, including TCM alkaloids, polysaccharides, saponins and flavonoids. This study provides a basis for further in-depth research and development in the field of anti-tumor immunomodulation using bioactive compounds from TCM.

Aims To analyze expression of members of the Toll-like receptor (TLR)4/myeloid differentiation primary response 88 (MyD88)/nuclear factor (NF)-κB signaling pathway in the heart and liver in a rat model of type 2 diabetes mellitus (T2DM). Our overall goal was to understand the underlying pathophysiological mechanisms. Methods We measured fasting blood glucose (FBG) and insulin (FINS) in a rat model of T2DM. Expression of members of the TLR4/MyD88/NF-κB signaling pathway as well as downstream cytokines was investigated. Levels of mRNA and protein were assessed using quantitative real-time polymerase chain reaction and western blotting, respectively. Protein content of tissue homogenates was assessed using enzyme-linked immunosorbent assays. Results Diabetic rats had lower body weights, higher FBG, higher FINS, and higher intraperitoneal glucose tolerance than normal rats. In addition, biochemical indicators related to heart and liver function were elevated in diabetic rats compared with normal rats. TLR4 and MyD88 were involved in the occurrence of T2DM as well as T2DM-related heart and liver complications. TLR4 caused T2DM-related heart and liver complications through activation of NF-κB. Conclusions TLR4/MyD88/NF-κB signaling induces production of tumor necrosis factor-α, interleukin-6, and monocyte chemoattractant protein-1, leading to the heart- and liver-related complications of T2DM.

Soluble α-synuclein aggregates varying in size, structure, and morphology have been closely linked to neuronal death in Parkinson’s disease. However, the heterogeneity of different co-existing aggregate species makes it hard to isolate and study their individual toxic properties. Here, we show a reliable non-perturbative method to separate a heterogeneous mixture of protein aggregates by size. We find that aggregates of wild-type α-synuclein smaller than 200 nm in length, formed during an in vitro aggregation reaction, cause inflammation and permeabilization of single-liposome membranes and that larger aggregates are less toxic. Studying soluble aggregates extracted from post-mortem human brains also reveals that these aggregates are similar in size and structure to the smaller aggregates formed in aggregation reactions in the test tube. Furthermore, we find that the soluble aggregates present in Parkinson’s disease brains are smaller, largely less than 100 nm, and more inflammatory compared to the larger aggregates present in control brains. This study suggests that the small non-fibrillar α-synuclein aggregates are the critical species driving neuroinflammation and disease progression. α-synuclein aggregates cause neuronal damage, but their heterogeneity complicates studying their toxic properties. Here, the authors analyze α-synuclein aggregates in vitro and study post-mortem brain samples, providing evidence that small aggregates are the main culprit for neuronal death in Parkinson’s disease.

Background Interstitial pneumonitis (IP) is a severe adverse event in patients receiving immunotherapy. Although PD-1/PD-L1 inhibitors and bevacizumab have been widely used in patients with non-small cell lung cancer (NSCLC), the interaction between their combination and IP is less known. Methods To investigate the interaction between bevacizumab and PD-1/PD-L1 inhibitors on IP, an observational study between January 2012 and June 2023, US, from the Food and Drug Administration Adverse Event Reporting System (FAERS) database including 55,673 NSCLC patients was performed. The reported proportions of PD-1/PD-L1 inhibitor-associated IP in patients receiving and not receiving bevacizumab treatment were compared. Results A total of 23,790 and 4753 patients were treated with PD-1/PD-L1 inhibitors and bevacizumab, among whom 1693 were treated with both PD-1/PD-L1 inhibitors and bevacizumab. The proportions of IP were 7.3% (95% CI 7.1 to 7.5%) in the total population of patients with NSCLC, 11.1% in patients treated with PD-1/PD-L1 inhibitors, and 4.4% in patients treated with bevacizumab. The reported IP proportion was 15.4% for PD-1 inhibitors with bevacizumab, which was greater than the 9.1% for PD-1 inhibitors without bevacizumab, while the opposite trend was observed for PD-L1 inhibitors (4.4% for bevacizumab vs 19.6% for PD-L1 inhibitors without bevacizumab). Conclusions Our study showed that bevacizumab was associated with a higher reported proportion of PD-1 inhibitor-associated IP but a lower reported proportion of PD-L1 inhibitor-associated IP. Although this was a post-marketing, observational study with many limitations, bevacizumab might be a proper combination with PD-L1 inhibitors in consideration of IP, especially in patients at high risk of IP. However, this relationship still needs further clinical validation.