Multi-output neural network model for predicting biochar yield and composition.

In biomass pyrolysis for biochar production, existing prediction models face computational challenges and limited accuracy. This study curated a comprehensive dataset, revealing pyrolysis parameters' dominance in biochar yield (54.8 % importance). Pyrolysis temperature emerged as pivotal (PCC = -0.75), influencing yield significantly. Artificial Neural Network (ANN) outperformed Random Forest (RF) in testing set predictions (R2 = 0.95, RMSE = 3.6), making it apt for complex multi-output predictions and software development. The trained ANN model, employed in Partial Dependence Analysis, uncovered nonlinear relationships between biomass characteristics and biochar yield. Findings indicated optimization opportunities, correlating low pyrolysis temperatures, elevated nitrogen content, high fixed carbon, and brief residence times with increased biochar yields. A multi-output ANN model demonstrated optimal fit for biochar yield. A user-friendly Graphical User Interface (GUI) for biochar synthesis prediction was developed, exhibiting robust performance with a mere 0.52 % prediction error for biochar yield. This study showcases practical machine learning application in biochar synthesis, offering valuable insights and predictive tools for optimizing biochar production processes.

Thermal Oxidative Aging and Service Life Prediction of Commercial Ethylene-Propylene-Diene Monomer Spacer Damping Composites for High-Voltage Transmission Lines.

The aging behavior and life prediction of rubber composites are crucial for ensuring high-voltage transmission line safety. In this study, commercially available ethylene-propylene-diene monomer (EPDM) spacer composites were chosen and investigated to elucidate the structure and performance changes under various aging conditions. The results showed an increased C=O peak intensity with increasing aging time, suggesting intensified oxidation of ethylene and propylene units. Furthermore, the surface morphology of commercial EPDM composites displayed increased roughness and aggregation after aging. Furthermore, hardness, modulus at 100% elongation, and tensile strength of commercial EPDM composites exhibited a general increase, while elongation at break decreased. Additionally, the damping performance decreased significantly after aging, with a 20.6% reduction in loss factor (20 °C) after aging at 100 °C for 672 h. With increasing aging time and temperature, the compression set gradually rose due to the irreversible movement of the rubber chains under stress. A life prediction model was developed based on a compression set to estimate the lifetime of rubber composites for spacer bars. The results showed that the product's life was 8.4 years at 20 °C. Therefore, the establishment of a life prediction model for rubber composites can provide valuable technical support for spacer product services.

Comparative metabolomics combined with genome sequencing provides insights into novel wolfberry-specific metabolites and their formation mechanisms.

Wolfberry (Lycium, of the family Solanaceae) has special nutritional benefits due to its valuable metabolites. Here, 16 wolfberry-specific metabolites were identified by comparing the metabolome of wolfberry with those of six species, including maize, rice, wheat, soybean, tomato and grape. The copy numbers of the riboflavin and phenyllactate degradation genes riboflavin kinase (RFK) and phenyllactate UDP-glycosyltransferase (UGT1) were lower in wolfberry than in other species, while the copy number of the phenyllactate synthesis gene hydroxyphenyl-pyruvate reductase (HPPR) was higher in wolfberry, suggesting that the copy number variation of these genes among species may be the main reason for the specific accumulation of riboflavin and phenyllactate in wolfberry. Moreover, the metabolome-based neighbor-joining tree revealed distinct clustering of monocots and dicots, suggesting that metabolites could reflect the evolutionary relationship among those species. Taken together, we identified 16 specific metabolites in wolfberry and provided new insight into the accumulation mechanism of species-specific metabolites at the genomic level.

Constructing Self-Healing Polydimethylsiloxane through Molecular Structure Design and Metal Ion Bonding.

Self-healing polydimethylsiloxane (PDMS) has garnered significant attention due to its potential applications across various fields. In this study, a functionalized modification of PDMS containing di-aminos was initially conducted using 2,6-pyridinedicarbonyl chloride to synthesize pyridine-PDMS (Py-PDMS). Subsequently, rare earth metal europium ions (Eu3+) were incorporated into Py-PDMS. Due to the coordination interaction between Eu3+ and organic ligands, a coordination cross-linking network was created within the Py-PDMS matrix, resulting in the fabrication of Eu3+-Py-PDMS elastomer. At a molar ratio of Eu3+ to ligands of 1:1, the tensile strength of Eu3+-Py-PDMS reached 1.4 MPa, with a fracture elongation of 824%. Due to the dynamic reversibility of coordination bonds, Eu3+-Py-PDMS with a metal-to-ligand molar ratio of 1:2 exhibited varying self-healing efficiencies at different temperatures. Notably, after 4 h of repair at 60 °C, its self-healing efficiency reached nearly 100%. Furthermore, the gas barrier properties of Eu3+-Py-PDMS with a molar ratio of 1:1 was improved compared with that of Eu3+-Py-PDMS with a molar ratio of 1:1. This study provides an effective strategy for the design and fabrication of PDMS with high mechanical strength, high gas barrier properties, and exceptional self-healing efficiency.

m6A-dependent upregulation of DDX21 by super-enhancer-driven IGF2BP2 and IGF2BP3 facilitates progression of acute myeloid leukaemia.

BACKGROUND: Acute myeloid leukaemia (AML) is a haematological malignancy with unfavourable prognosis. Despite the effectiveness of chemotherapy and targeted therapy, relapse or drug resistance remains a major threat to AML patients. N6-methyladenosine (m6A) RNA methylation and super-enhancers (SEs) are extensively involved in the leukaemogenesis of AML. However, the potential relationship between m6A and SEs in AML has not been elaborated. METHODS: Chromatin immunoprecipitation (ChIP) sequencing data from Gene Expression Omnibus (GEO) cohort were analysed to search SE-related genes. The mechanisms of m6 A-binding proteins IGF2BP2 and IGF2BP3 on DDX21 were explored via methylated RNA immunoprecipitation (MeRIP) assays, RNA immunoprecipitation (RIP) assays and luciferase reporter assays. Then we elucidated the roles of DDX21 in AML through functional assays in vitro and in vivo. Finally, co-immunoprecipitation (Co-IP) assays, RNA sequencing and ChIP assays were performed to investigate the downstream mechanisms of DDX21. RESULTS: We identified two SE-associated transcripts IGF2BP2 and IGF2BP3 in AML. High enrichment of H3K27ac, H3K4me1 and BRD4 was observed in IGF2BP2 and IGF2BP3, whose expression were driven by SE machinery. Then IGF2BP2 and IGF2BP3 enhanced the stability of DDX21 mRNA in an m6A-dependent manner. DDX21 was highly expressed in AML patients, which indicated a poor survival. Functionally, knockdown of DDX21 inhibited cell proliferation, promoted cell apoptosis and led to cell cycle arrest. Mechanistically, DDX21 recruited transcription factor YBX1 to cooperatively trigger ULK1 expression. Moreover, silencing of ULK1 could reverse the promoting effects of DDX21 overexpression in AML cells. CONCLUSIONS: Dysregulation of SE-IGF2BP2/IGF2BP3-DDX21 axis facilitated the progression of AML. Our findings provide new insights into the link between SEs and m6A modification, elucidate the regulatory mechanisms of IGF2BP2 and IGF2BP3 on DDX21, and reveal the underlying roles of DDX21 in AML.

A Risk Model for 28-Day in-Hospital Mortality in 173 COVID-19 Patients Admission to ICU: A Retrospective Study.

Background: The surge in the number of patients diagnosed with COVID-19 since China's open-door policy has placed a huge burden on the public healthcare system, especially the intensive care system. This study's objective was to discover possible clinical outcome predictors in COVID-19 patients treated in intensive care units (ICUs) and to provide useful information for future preventative efforts and therapies. Methods: This retrospective study included 173 COVID-19 critically ill patients and reviewed the 28-day survival outcome in the First Affiliated Hospital of Nanjing Medical University. Competing risk analysis was performed to predict the cumulative incidence function (CIF) of mortality in hospital. The independent prognostic factors were identified by applying the Fine-Gray proportional subdistribution hazard model. Receiver operating characteristic (ROC) curves were used to evaluate model efficacy, and calibration curves were used to validate the model. Finally, we compared the competing risk model with the traditional proportional hazards model (Cox regression model) using CIF. Results: Of these 173 patients, 66 (38.2%) survived, 55 (31.8%) died, and 52 (30.0%) discharged. In univariate analysis, 12 variables were significantly correlated with mortality. In multivariate analysis, Age, Neutrophil ratio, Direct Bilirubin (DBIL) and Renal disease were independent predictors of 28-day outcome. The ROC curve of the multivariate prediction model showed an AUC (area under the curve) of 0.790. The results of the calibration curve and the concordance index (C-index) show that the model has good discriminatory power. The competing risk model we applied was more accurate than the Cox model. Conclusion: We presented a more accurate multivariate prediction model for 28-day in-hospital mortality for ICU COVID-19 patients using a competing risk model.

Late-stage guanine C8-H alkylation of nucleosides, nucleotides, and oligonucleotides via photo-mediated Minisci reaction.

Chemically modified nucleosi(ti)des and functional oligonucleotides (ONs, including therapeutic oligonucleotides, aptamer, nuclease, etc.) have been identified playing an essential role in the areas of medicinal chemistry, chemical biology, biotechnology, and nanotechnology. Introduction of functional groups into the nucleobases of ONs mostly relies on the laborious de novo chemical synthesis. Due to the importance of nucleosides modification and aforementioned limitations of functionalizing ONs, herein, we describe a highly efficient site-selective alkylation at the C8-position of guanines in guanosine (together with its analogues), GMP, GDP, and GTP, as well as late-stage functionalization of dinucleotides and single-strand ONs (including ssDNA and RNA) through photo-mediated Minisci reaction. Addition of catechol to assist the formation of alkyl radicals via in situ generated boronic acid catechol ester derivatives (BACED) markedly enhances the yields especially for the reaction of less stable primary alkyl radicals, and is the key to success for the post-synthetic alkylation of ONs. This method features excellent chemoselectivity, no necessity for pre-protection, wide range of substrate scope, various free radical precursors, and little strand lesion. Downstream applications in disease treatment and diagnosis, or as biochemical probes to study biological processes after linking with suitable fluorescent compounds are expected.

OsBCAT2, a gene responsible for the degradation of branched-chain amino acids, positively regulates salt tolerance by promoting the synthesis of vitamin B5.

Salt stress negatively affects rice growth, development and yield. Metabolic adjustments contribute to the adaptation of rice under salt stress. Branched-chain amino acids (BCAA) are three essential amino acids that cannot be synthesized by humans or animals. However, little is known about the role of BCAA in response to salt stress in plants. Here, we showed that BCAAs may function as scavengers of reactive oxygen species (ROS) to provide protection against damage caused by salinity. We determined that branched-chain aminotransferase 2 (OsBCAT2), a protein responsible for the degradation of BCAA, positively regulates salt tolerance. Salt significantly induces the expression of OsBCAT2 rather than BCAA synthesis genes, which indicated that salt mainly promotes BCAA degradation and not de novo synthesis. Metabolomics analysis revealed that vitamin B5 (VB5) biosynthesis pathway intermediates were higher in the OsBCAT2-overexpressing plants but lower in osbcat2 mutants under salt stress. The salt stress-sensitive phenotypes of the osbcat2 mutants are rescued by exogenous VB5, indicating that OsBCAT2 affects rice salt tolerance by regulating VB5 synthesis. Our work provides new insights into the enzymes involved in BCAAs degradation and VB5 biosynthesis and sheds light on the molecular mechanism of BCAAs in response to salt stress.

BCLAF1 is Expressed as a Potential Anti-oncogene in Bile Duct Cancer.

Validating the role of BCLAF1 in the development of Bile Duct Cancer. Differential expression of BCLAF1 in Bile Duct Cancer and normal tissues was analyzed bioinformatically, and immuno-infiltration analysis was performed by R. We also derived the correlation between the expression of BCLAF1 and HIF-1α by bioinformatics analysis and validated it by Western Blotting, qRT-PCR and scratch assays before and after hypoxia. Through bioinformatics analysis, we found that BCLAF1 mRNA was significantly higher in the tumor tissues of Bile Duct Cancer. The high expression of BCLAF1 implied a more advanced stage but a lower mortality rate. KEGG and GO enrichment analysis showed that BCLAF1 overexpression in Bile Duct Cancer was mainly associated with histone modification, peptidyl lysine modification, and macromolecular methylation. We used the TIMER algorithm to show that BCLAF1 expression in Bile Duct Cancer is associated with immune cell infiltration, which affects tumor progression and patient prognosis. We confirmed by normoxia and hypoxia qRT-PCR, Western Blotting and scratch assays that BCLAF1 and HIF-1α expression are positively correlated and that BCLAF1 may be expressed as anti-oncogene in Bile Duct Cancer. These findings demonstrate that BCLAF1 may act as anti-oncogene in Bile Duct Cancer and may be involved in immune cell infiltration in Bile Duct Cancer, suppressing the expression of HIF-1α.

Dual-Fuel Propelled Nanomotors with Two-Stage Permeation for Deep Bacterial Infection in the Treatment of Pulpitis.

Bacterial infection-induced inflammatory response could cause irreversible death of pulp tissue in the absence of timely and effective therapy. Given that, the narrow structure of root canal limits the therapeutic effects of passive diffusion-drugs, considerable attention has been drawn to the development of nanomotors, which have high tissue penetration abilities but generally face the problem of insufficient fuel concentration. To address this drawback, dual-fuel propelled nanomotors (DPNMs) by encapsulating L-arginine (L-Arg), calcium peroxide (CaO2 ) in metal-organic framework is developed. Under pathological environment, L-Arg could release nitric oxide (NO) by reacting with reactive oxygen species (ROS) to provide the driving force for movement. Remarkably, the depleted ROS could be supplemented through the reaction between CaO2 with acids abundant in the inflammatory microenvironment. Owing to high diffusivity, NO achieves further tissue penetration based on the first-stage propulsion of nanomotors, thereby removing deep-seated bacterial infection. Results indicate that the nanomotors effectively eliminate bacterial infection based on antibacterial activity of NO, thereby blocking inflammatory response and oxidative damage, forming reparative dentine layer to avoid further exposure and infection. Thus, this work provides a propagable strategy to overcome fuel shortage and facilitates the therapy of deep lesions.

Serum amyloid A aggravates endotoxin-induced ocular inflammation through the regulation of retinal microglial activation.

Serum amyloid A (SAA) are major acute-phase response proteins which actively participate in many inflammatory diseases. This study was designed to explore the function of SAA in acute ocular inflammation and the underlying mechanism. We found that SAA3 was upregulated in endotoxin-induced uveitis (EIU) mouse model, and it was primarily expressed in microglia. Recombinant SAA protein augmented intraocular inflammation in EIU, while the inhibition of Saa3 by siRNA effectively alleviated the inflammatory responses and rescued the retina from EIU-induced structural and functional damage. Further study showed that the recombinant SAA protein activated microglia, causing characteristic morphological changes and driving them further to pro-inflammatory status. The downregulation of Saa3 halted the amoeboid change of microglia, reduced the secretion of pro-inflammatory factors, and increased the expression of tissue-reparative genes. SAA3 also regulated the autophagic activity of microglial cells. Finally, we showed that the above effect of SAA on microglial cells was at least partially mediated through the expression and signaling of Toll-like receptor 4 (TLR4). Collectively, our study suggested that microglial cell-expressed SAA could be a potential target in treating acute ocular inflammation.

Repressing HIF-1α-induced HDAC9 contributes to the synergistic effect of venetoclax and MENIN inhibitor in KMT2Ar AML.

KMT2A-rearranged acute myeloid leukemia (KMT2Ar-AML) is an aggressive subtype of AML with poor response and prognosis. KMT2Ar-AML has been demonstrated to be sensitive to BCL2 inhibitor venetoclax (VEN), but these patients are unable to benefit from current VEN-based regimen (VEN plus azacitidine or low dose-cytarabine), so a novel and KMT2A rearrangement-specific targeting partner is required, and MENIN inhibitor (MEN1i) is a promising one. Herein, we investigated the effect and mechanism of VEN plus MEN1i in KMT2Ar-AML. Our results showed that VEN and MEN1i exhibited a striking synergistic effect in KMT2Ar-AML cell lines (in vitro), primary KMT2Ar-AML cells (ex vivo), and MOLM13 xenotransplantation model (in vivo). Furthermore, we found that VEN plus MEN1i significantly enhanced apoptotic induction in KMT2Ar-AML cell lines. VEN or MEN1i monotherapy disrupted balance of BCL-2/BCL-XL or down-regulated HOXA9/MEIS1, respectively, but these mechanisms were not further strengthened by their combination. RNA-Sequencing identified that HDAC9 was specifically repressed by VEN plus MEN1i rather than monotherapy. We demonstrated that HDAC9 was indispensable for KMT2Ar-AML proliferation and its repression contributed to proliferation inhibition of VEN plus MEN1i. Moreover, we found that hypoxia induced HDAC9 expression in KMT2Ar-AML, and VEN plus MEN1i inhibited hypoxia pathway, especially HIF-1A, and its target HDAC9. As our results indicated, VEN plus MEN1i-mediated HDAC9 down-regulation was partially dependent on HIF-1A repression in KMT2Ar-AML. Hypoxia induction sensitized KMT2Ar-AML to VEN plus MI-503-mediated proliferation inhibition and apoptosis induction. Therefore, repressing HIF-1A-induced HDAC9 contributed to the synergistic effect of VEN and MEN1i in KMT2Ar-AML.

Targeting mitochondrial quality control for diabetic cardiomyopathy: Therapeutic potential of hypoglycemic drugs.

Diabetic cardiomyopathy is a chronic cardiovascular complication caused by diabetes that is characterized by changes in myocardial structure and function, ultimately leading to heart failure and even death. Mitochondria serve as the provider of energy to cardiomyocytes, and mitochondrial dysfunction plays a central role in the development of diabetic cardiomyopathy. In response to a series of pathological changes caused by mitochondrial dysfunction, the mitochondrial quality control system is activated. The mitochondrial quality control system (including mitochondrial biogenesis, fusion and fission, and mitophagy) is core to maintaining the normal structure of mitochondria and performing their normal physiological functions. However, mitochondrial quality control is abnormal in diabetic cardiomyopathy, resulting in insufficient mitochondrial fusion and excessive fission within the cardiomyocyte, and fragmented mitochondria are not phagocytosed in a timely manner, accumulating within the cardiomyocyte resulting in cardiomyocyte injury. Currently, there is no specific therapy or prevention for diabetic cardiomyopathy, and glycemic control remains the mainstay. In this review, we first elucidate the pathogenesis of diabetic cardiomyopathy and explore the link between pathological mitochondrial quality control and the development of diabetic cardiomyopathy. Then, we summarize how clinically used hypoglycemic agents (including sodium-glucose cotransport protein 2 inhibitions, glucagon-like peptide-1 receptor agonists, dipeptidyl peptidase-4 inhibitors, thiazolidinediones, metformin, and α-glucosidase inhibitors) exert cardioprotective effects to treat and prevent diabetic cardiomyopathy by targeting the mitochondrial quality control system. In addition, the mechanisms of complementary alternative therapies, such as active ingredients of traditional Chinese medicine, exercise, and lifestyle, targeting mitochondrial quality control for the treatment of diabetic cardiomyopathy are also added, which lays the foundation for the excavation of new diabetic cardioprotective drugs.

Determination of key factors affecting biofilm formation on the aged Poly(ethylene terephthalate) during anaerobic digestion.

Biofilm formation on plastic surface is a growing concern because it can alter the plastic surface properties and exacerbate the ecological risk. Identifying key factors that affecting biofilm formation is critical for effective pollution control. In this study, the poly (ethylene terephthalate) (PET) was aged in water and air conditions with UV irradiation, then incubated in the digestate of food waste anaerobic digestion to allow biofilm formation. Surface analysis techniques, including scanning electron microscopy (SEM), atomic force microscopy (AFM), and Fourier-transform infrared spectroscopy with attenuated total reflection (FTIR-ATR), were utilized to investigated the changes in the topography, roughness, hydrophily, and functional groups change of the PET surface during the aging process. Confocal laser scanning microscopy (CLSM) was used to determine the distribution of microorganisms on the PET surface after incubation in the digestate. This study focused on understanding the interactions between the PET surface and biofilm to identify critical surface factors that affect biofilm formation. Results showed that the four months aging process decreased the contact angle of the PET surface from 96.92° to 76.08° and 68.97° in water and air conditions, respectively, corresponding to an increase of 44% and 70% in the surface energy. Additionally, aging in air conditions led to a rougher surface compared to water conditions. The arithmetic roughness average (Ra) of the PET-Water was 11.0 nm, comparable to that of the pristine PET, while the value of PET-Air was much higher (43.9 nm). The results further indicated that biofilm formation during anaerobic digestion was more sensitive to roughness than hydrophily. The PET surface aged in air conditions provided a more suitable environment for microbial reproduction, leading to the aggradation of living cells.

Molecular Structure and Properties of Sulfur-Containing High Refractive Index Polymer Optical Materials.

High refractive index polymers (HRIPs) are widely used in lenses, waveguide, antireflective layer and encapsulators, especially the advanced fields of augmented/virtual reality (AR / VR) holographic technology and photoresist for chip manufacturing. In order to meet the needs of different applications, the development of HRIPs focuses not only on the increase in refractive index but also on the balance of other properties. Sulfur-containing high refractive index polymers have received extensive attention from researchers due to their excellent properties. In recent years, not only ultrahigh refractive index sulfur-containing polymers have been continuously developed, but also low dispersion, low birefringence, high transparency, good mechanical properties, and machinability have been studied. The design of HRIPs is generally based on formulas and existing experience. In fact, molecular structure and properties are closely related. Mastering the structure-property relationship helps researchers to develop high refractive index polymer materials with balanced properties. This review briefly introduces the preparation methods of sulfur-containing high refractive index polymers, and summarizes the structure-property relationship between the sulfur-containing molecular structure and optical properties, mechanical properties, thermal properties, etc. Finally, the important role of synergistic effect in the synthesis of HRIPs and the prospect of future research on HRIPs are proposed.

Silencing of peroxiredoxin III inhibits formaldehyde-induced oxidative damage of bone marrow cells in BALB/c mice.

BACKGROUND: Formaldehyde (FA) is associated with the occurrence of leukemia, and oxidative stress is considered to be a major reason. As an endogenous biomarker of oxidative stress, few studies focus on the relationship between peroxiredoxin III (PrxIII) and FA toxicity. Our previous research observed high expression of PrxIII occurred in the process of apoptosis of bone marrow cells (BMCs) induced by FA, however the exact mechanism is unclear. Therefore, this paper aimed to explore the possible association between FA toxicity and PrxIII gene. METHODS: We first, used a Cell Counting Kit-8 (CCK-8) to detect the viability of BMCs after they were exposed to different doses of FA (50, 100, 200 µmol/L) for different exposure time (12, 24, 48 h), then chose 24 h as an exposure time to detect the expression of PrxIII for exposing different doses of FA by Quantitative reverse transcription-PCR (qRT-PCR) and Western blot analysis. Based on our preliminary experimental results, we chose 100 µmol/L FA as an exposure dose to expose for 24 h, and used a small interfering RNA (siRNA) to silenced PrxIII to examine the cell viability by CCK-8, reactive oxygen species (ROS) level by DCFH-DA, apoptosis by Annexin V/PI double staining and cell cycle by flow cytometry (FCM) so as to explore the possible regulatory effect of PrxIII silencing on FA-induced bone marrow toxicity. RESULTS: High expression of PrxIII occurred in the process of FA-induced oxidative stress. Silencing of PrxIII prevented FA from inducing oxidative stress, thus increasing cell viability, decreasing ROS level, rescuing G0 -G1 and G2 -M arrest, and reducing cell apoptosis. CONCLUSION: PrxIII silencing might be a potential target for alleviating FA-induced oxidative damage.

The Combination of Quantitative Proteomics and Systems Genetics Analysis Reveals that PTN Is Associated with Sleep-Loss-Induced Cognitive Impairment.

Sleep loss is associated with cognitive dysfunction. However, the detailed mechanisms remain unclear. In this study, we established a para-chlorophenylalanine (PCPA)-induced insomniac mouse model with impaired cognitive function. Mass-spectrometry-based proteomics showed that the expression of 164 proteins was significantly altered in the hippocampus of the PCPA mice. To identify critical regulators among the potential markers, a transcriptome-wide association screening was performed in the BXD mice panel. Among the candidates, the expression of pleiotrophin (Ptn) was significantly associated with cognitive functions, indicating that Ptn-mediates sleep-loss-induced cognitive impairment. Gene co-expression analysis further revealed the potential mechanism by which Ptn mediates insomnia-induced cognitive impairment via the MAPK signaling pathway; that is, the decreased secretion of Ptn induced by insomnia leads to reduced binding to Ptprz1 on the postsynaptic membrane with the activation of the MAPK pathway via Fos and Nr4a1, further leading to the apoptosis of neurons. In addition, Ptn is genetically trans-regulated in the mouse hippocampus and implicated in neurodegenerative diseases in human genome-wide association studies. Our study provides a novel biomarker for insomnia-induced cognitive impairment and a new strategy for seeking neurological biomarkers by the integration of proteomics and systems genetics.

Efficacy and safety of non-pharmacological therapy under the guidance of TCM theory in the treatment of anxiety in patients with myocardial infarction: A protocol for systematic review and meta-analysis.

BACKGROUND: With the increasing pressures of modern life and work, combined with a growing older population, the incidence of comorbid anxiety and myocardial infarction (MI) is increasing. Anxiety increases the risk of adverse cardiovascular events in patients with MI and significantly affects their quality of life. However, there is an ongoing controversy regarding the pharmacological treatment of anxiety in patients with MI. The concomitant use of commonly prescribed selective serotonin reuptake inhibitors (SSRIs) and antiplatelet medications such as aspirin and clopidogrel may increase the risk of bleeding. Conventional exercise-based rehabilitation therapies have shown limited success in alleviating anxiety symptoms. Fortunately, non-pharmacological therapies based on traditional Chinese medicine (TCM) theory, such as acupuncture, massage, and qigong, have demonstrated promising efficacy in treating MI and comorbid anxiety. These therapies have been widely used in community and tertiary hospital settings in China to provide new treatment options for patients with anxiety and MI. However, current studies on non-pharmacological TCM-based therapies have predominantly featured small sample sizes. This study aims to comprehensively analyze and explore the effectiveness and safety of these therapies in treating anxiety in patients with MI. METHOD: We will systematically search six English and four Chinese databases by employing a pre-defined search strategy and adhering to the unique rules and regulations of each database to identify studies that fulfilled our inclusion criteria, to qualify for inclusion, patients must be diagnosed with both MI and anxiety, and they must have undergone non-pharmacological TCM therapies, such as acupuncture, massage, or qigong, whereas the control group received standard treatments. The primary outcome measure will be alterations in anxiety scores, as assessed using anxiety scales, with secondary outcomes encompassing the evaluations of cardiopulmonary function and quality of life. We will utilize RevMan 5.3 to conduct a meta-analysis of the collected data, and subgroup analyses will be executed based on distinct types of non-pharmacological TCM therapies and outcome measures. RESULTS: A narrative summary and quantitative analysis of the existing evidence on the treatment of anxiety patients with MI using non-pharmacological therapies guided by Traditional Chinese Medicine theory. CONCLUSION: This systematic review will investigate whether non-pharmacological interventions guided by TCM theory are effective and safe for anxiety in patients with MI, and provide evidence-based support for their clinical application. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42022378391.

circSLC25A13 acts as a ceRNA to regulate AML progression via miR-616-3p/ADCY2 axis.

Circular RNAs (circRNAs), a type of endogenous noncoding RNA (ncRNA), exert vital roles in leukemia progression and are promising prognostic factors. Here, we report a novel circRNA, circSLC25A13 (hsa_circ_0081188), which was increased in acute myeloid leukemia (AML) patients with poor overall survival (OS) comparing to patients with good prognosis. Knockdown of circSLC25A13 in AML cells inhibited proliferation and increased cell apoptosis in vitro and in vivo. Enhanced circSLC25A13 expression promoted the survival of AML cells. Mechanistically, circSLC25A13 played as a microRNA sponge of miR-616-3p, which inhibited the expression of adenylate cyclase 2 (ADCY2). Downregulation of miR-616-3p and overexpression of ADCY2 partially rescued circSLC25A13 deficient induced cell growth arrest. In summary, through competitive absorption of miR-616-3p and thereby upregulating ADCY2 expression, circSLC25A13 promoted AML progression. Moreover, circSLC25A13 may represent a potential novel biomarker for the prognosis of AML and offer a potential therapeutic target for AML treatment.