Design, Synthesis, and Anti-Inflammatory Activity Evaluation of Novel Indanone Derivatives for the Treatment of Vascular Dementia.

Vascular dementia (VaD) is a neurodegenerative disease resulting from cerebral vascular obstruction, leading to cognitive impairment, and currently lacks effective treatment options. Due to its complex pathogenesis, multi-target drug design (MTDLs) strategies are considered among the most promising therapeutic approaches. In this study, we designed and synthesized a series of novel indanone derivatives targeting targets related to vascular health and dementia. The results indicated that compound C5 exhibited excellent acetylcholinesterase inhibitory activity (IC50 = 1.16 ± 0.41 µM) and anti-platelet aggregation activity (IC50 = 4.92 ± 0.10 µM) within ranges of 0.1-1000 µM and 0.03-300 µM, respectively, possibly mediated by molecular docking interactions. Furthermore, compound C5 demonstrated protective effects on cells at concentrations ≤50 µM, significantly reducing the release of nitric oxide (NO), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1ß) in a concentration-dependent manner, showcasing its potent neuroinflammatory inhibitory effects. Anti-inflammatory therapies are regarded as effective strategies for treating VaD. Therefore, compound C5 holds promise as a novel candidate drug for further investigation into the treatment of vascular dementia.

Total alkaloids in Fritillaria cirrhosa D. Don alleviate OVA-induced allergic asthma by inhibiting M2 macrophage polarization.

ETHNOPHARMACOLOGICAL RELEVANCE: Fritillaria cirrhosa D. Don (FCD) is a traditional Chinese medicine used to treat respiratory disorders, known for its effects in clearing heat, moistening the lungs, resolving phlegm, and relieving cough. Additionally, the total alkaloids extracted from FCD can alleviate asthma symptoms and reduce airway inflammation. However, no studies have investigated the effects of total alkaloids on lung macrophages. AIM OF THE STUDY: This study explored whether the total alkaloids of FCD (TAs-FCD) reduce M2 macrophage polarization and, consequently, attenuate airway remodeling in asthmatic mice. This study further elucidated its mechanism of action in treating allergic asthma. MATERIALS AND METHODS: The extracted TAs-FCD was analyzed for its composition using UPLC-Q-TOF/MS. Network pharmacology was employed to identify the active ingredients and potential mechanisms of TAs-FCD in the treatment of allergic asthma. A mouse model of ovalbumin-induced allergic asthma was established, adopted, and validated through in vivo experiments. Hematoxylin-eosin staining (H&E), immunohistochemistry (IHC), immunofluorescence staining (IF), enzyme-linked immunosorbent assay (ELISA), Western blotting (WB), and real-time fluorescence quantitative polymerase chain reaction (q-PCR) were used to investigate the role of TAs-FCD in inhibiting M2 macrophage polarization in the context of allergic asthma. RESULTS: A total of 66 active ingredients were screened from 116 compounds using SWISSADME. The targets of these 66 compounds were predicted by SwissTargetPrediction, resulting in 808 unique drug targets after excluding duplicates. Additionally, 1756 targets related to allergic asthma were identified from the DisGeNET, Genecard, and OMIM databases. This led to 267 cross-targets between the active ingredient targets and allergic asthma targets, including interleukin (IL)-1ß, tumor necrosis factor (TNF), and STAT3. Animal experiments demonstrated that TAs-FCD improved histopathological injury in mouse lungs, reduced peri-airway collagen fiber accumulation, airway mucus secretion, and airway smooth muscle proliferation. TAs-FCD also lowered IL-1ß, TNF-α and IL-4 levels in lung tissues and alleviated airway inflammation. Furthermore, TAs-FCD significantly reduced levels of Arg1 and CD206, which are closely associated with M2 macrophages, and downregulated the expression of p-STAT3 and p-JAK2. CONCLUSION: TAs-FCD may inhibit M2 macrophage polarization by regulating the JAK2/STAT3 pathway, thereby alleviating airway remodeling and inflammation in allergic asthmatic mice.

PARP1 acetylation at K119 is essential in regulating the progression and proliferation of cervical cancer cells.

Cervical cancer, CC, is one of the malignant cancers in women worldwide. Many studies about the genesis and progression of CC have been done at genomic, transcriptional, translational, and epigenetic levels. However, much less is done at post-translational modification (PTM) level. We first used pan-PTM antibodies to compare the pan PTM levels between clinical normal cervical tissues and CC tissues; we then sent the selected samples for label-free identification of acetylation sites. Next, we employed WT or K119A mutant PARP1-EGFP-STREPII plasmid transfection in Hela cells and examined various indexes including colony formation, wound healing, ROS generation, early apoptosis, and immunofluorescence and quantification of proliferation markers (Ki67, PCNA, and p-P53). Last, we examined the levels of multiple important kinases regulating cervical cancer progression. We found that pan-acetylation was the most downregulated in clinical CC samples, whereas the acetylation of PARP1, Poly(ADP-ribose) polymerase-1, was upregulated at K119. Next, we showed that PARP1-WT overexpression significantly suppressed the proliferation and progression in CC cell line Hela, while K119A overexpression didn't show any impact. Finally, PARP1-WT overexpression significantly decreased p-ERK1/2 while didn't affect the phosphorylation levels of other important kinases such as AKT, MTOR, and RPS6. This study discovered a new type of PTM of PARP1 in CC, and showed that PARP1 acetylation at K119 is essential in regulating the proliferation and progression of CC through ERK1/2. Further studies are required to investigate how PARP1 acetylation impact its function.

Computed tomography-based multi-organ radiomics nomogram model for predicting the risk of esophagogastric variceal bleeding in cirrhosis.

BACKGROUND: Radiomics has been used in the diagnosis of cirrhosis and prediction of its associated complications. However, most current studies predict the risk of esophageal variceal bleeding (EVB) based on image features at a single level, which results in incomplete data. Few studies have explored the use of global multi-organ radiomics for non-invasive prediction of EVB secondary to cirrhosis. AIM: To develop a model based on clinical and multi-organ radiomic features to predict the risk of first-instance secondary EVB in patients with cirrhosis. METHODS: In this study, 208 patients with cirrhosis were retrospectively evaluated and randomly split into training (n = 145) and validation (n = 63) cohorts. Three areas were chosen as regions of interest for extraction of multi-organ radiomic features: The whole liver, whole spleen, and lower esophagus-gastric fundus region. In the training cohort, radiomic score (Rad-score) was created by screening radiomic features using the inter-observer and intra-observer correlation coefficients and the least absolute shrinkage and selection operator method. Independent clinical risk factors were selected using multivariate logistic regression analyses. The radiomic features and clinical risk variables were combined to create a new radiomics-clinical model (RC model). The established models were validated using the validation cohort. RESULTS: The RC model yielded the best predictive performance and accurately predicted the EVB risk of patients with cirrhosis. Ascites, portal vein thrombosis, and plasma prothrombin time were identified as independent clinical risk factors. The area under the receiver operating characteristic curve (AUC) values for the RC model, Rad-score (liver + spleen + esophagus), Rad-score (liver), Rad-score (spleen), Rad-score (esophagus), and clinical model in the training cohort were 0.951, 0.930, 0.801, 0.831, 0.864, and 0.727, respectively. The corresponding AUC values in the validation cohort were 0.930, 0.886, 0.763, 0.792, 0.857, and 0.692. CONCLUSION: In patients with cirrhosis, combined multi-organ radiomics and clinical model can be used to non-invasively predict the probability of the first secondary EVB.

Early-Life Milk αS1-Casein Allergy Induces the Activation of Astrocytes in Mice and Leads to Stress Vulnerability in Adulthood.

In recent years, the incidence of food allergies in children has been increasing annually, significantly affecting the quality of life for patients and their families. It has long been suspected that childhood allergies might potentially lead to behavioral and psychological issues in adulthood, but the specific connection remains unclear. In this study, we established a model of young mice allergic to milk αS1-casein, conducted behavioral tests, and employed transcriptomics, immunohistochemistry, Golgi staining, and fecal microbiota transplantation to explore the link between early life allergies and adult psychological problems. The results showed that early life milk protein allergy significantly increased intestinal epithelial permeability in mice, leading to the translocation of gut microbiota metabolites. This process subsequently activated astrocyte lysosomes via SLC15a3, making astrocytes more susceptible. This susceptibility caused mice with early life milk protein allergy to have more activated astrocytes and excessive dendritic spine phagocytosis (normal group: 5.4 ± 1.26 spines/10 µm, allergy group: 3.2 ± 0.92 spines/10 µm) under acute stress in adulthood, leading to anxiety and depressive behaviors.

Z/E configuration controlled by a Taxus sesquiterpene synthase facilitating the biosynthesis of (3Z,6E)-α-farnesene.

Plant enzymes often present advantages in the synthesis of natural products with specific configurations. Farnesene is a pharmacologically active sesquiterpene with three natural Z/E configurations, among which the enzyme selectively responsible for the biosynthesis of (3Z,6E)-α-farnesene remains elusive. Herein, a sesquiterpene synthase TwSTPS1 biosynthesizing (3Z,6E)-α-farnesene as the major product was identified from Taxus wallichiana through genome mining. Utilizing molecular dynamics simulations and mutation analysis, the catalytic mechanism of TwSTPS1, especially Z/E configuration control, was explored. Moreover, the crucial residues associated with the specific catalytic activity of TwSTPS1 was elucidated through mutagenesis experiments. The findings contribute to our understanding of the Z/E configuration control by plant terpene synthases and also provide an alternative tool for manipulating (3Z,6E)-α-farnesene production using synthetic biology.

Pediatric Acute Myeloid Leukemia: Unraveling Complexities in Intensive Chemotherapy and the Emergence of Superbugs - A Case Study.

Background: This case report underscores the intricate challenges in managing paediatric patients with acute myeloid leukaemia (AML) undergoing intensive chemotherapy, particularly when complicated by the emergence of multidrug-resistant pathogens such as Carbapenem-Resistant Pseudomonas aeruginosa (CRPA). Case Presentation: An 11-year-old male with AML presented with skin purpura and persistent cough. Clinical and laboratory assessments revealed a high-risk AML profile with genetic mutations, leading to the initiation of intensive chemotherapy per the C-HUANA-AML-2015 protocol. Despite successful disease remission after initial chemotherapy courses, the patient experienced unexpected complications. Notably, septic shock, bone marrow failure, and the emergence of CRPA were encountered during the clinical course. Septic shock occurred following Course B3 chemotherapy, marked by a fever unresponsive to initial antibiotic therapy. Despite negative blood cultures, meropenem and vancomycin were initiated, successfully normalizing temperature. Subsequent challenges included persistent bone marrow suppression, perianal dermatitis, and the identification of CRPA in stool cultures, leading to altered antibiotic therapy guided by minimum inhibitory concentration (MIC) considerations. Whole-genome sequencing (WGS) of the CRPA strain revealed a highly virulent clone (ST-970) with numerous resistance and virulence genes. Conclusion: This case report offers new insights into the complexities of pediatric AML management, with a focus on the emergence of CRPA. The discovery of a high-risk CRPA clone with detailed genomic data underscores the growing challenge of antimicrobial resistance in pediatric oncology. The persistent presence of CRPA and ongoing bone marrow failure highlight the difficulties in managing these complications. This case calls for a reassessment of treatment strategies and encourages further research to improve outcomes in pediatric AML, emphasizing the need for a multidisciplinary approach to address infectious complications and antimicrobial resistance.

How big nanoparticles carry small ones into cells: Actions captured by transmission electron microscopy.

The mechanism of cellular uptake of nanoparticles (NPs) is critical for both bio-application and risk evaluation of NPs, but is still not fully understood due to many influencing factors, among which particle size is a major one. Recent studies show that there is an unusual interplay among differently-sized NPs when they simultaneously interact with cells, e.g., 100 nm silica NPs (SNP100) can promote the cellular uptake of 50 nm silica NPs (SNP50). However, the underlying mechanism is still unclear. Herein, we manage to capture individual endocytosis events in HeLa and A549 cells after co-exposure to SNP50 and SNP100 for 2 hours, using transmission electron microscopy (TEM). TEM images clearly show that there is a size threshold for SNPs to trigger clathrin-mediated endocytosis: One single SNP100 can efficiently trigger it, while it needs about 6 SNP50 to do so. Remarkably, TEM also captures how SNP100 triggers the endocytosis and carries nearby SNP50 into cells, and statistical data show that the average number of SNP50 carried by one SNP100 could be up to about 6. In addition, the mechanism was further verified by using mixed 60 nm SNPs (SNP60) and SNP100. This mechanism has an immediate implication for the design of drug-deliver nanocarriers, and as a proof-of-concept, more catalase functionalized SNP50 (CAT@SNP50) was delivered into HeLa cells by adding some SNP100, resulting in a more severe cell damage compared to CAT@SNP50 alone under same conditions. The findings have general impact on the nanotoxicity study of NP products that commonly have certain distributions in size, and provide new insights on designing efficient drug delivery systems by deliberately control the combinations of NPs of different sizes.

Enhanced photocatalytic CO2 conversion over 0D/2D CsPbBr3/BiOCl S-scheme heterojunction via boosting charge separation.

The stable contact of heterogeneous interfaces and the substantial exposure of active sites are crucial for enhancing the photocatalytic performance of semiconductor catalysts. However, most reported two-dimensional (2D)/2D CsPbBr3 and BiOCl heterostructures are fabricated using electrostatic self-assembly methods, which exhibit significant deficiencies in precise interface quality control and effective active site exposure. In this study, we fabricate a zero-dimensional (0D)/2D CsPbBr3/BiOCl heterojunction via a two-step calcination method, achieving an efficient direct S-scheme configuration. Optimizing interfacial contact and band alignment between CsPbBr3 quantum dots and BiOCl nanosheets enhances cross-plane charge transfer, promoting superior charge separation. This 0D/2D CsPbBr3/BiOCl heterojunction exhibits enhanced carrier mobility and high conversion rates without cocatalysts or sacrificial agents. The mechanism underlying the accelerated S-scheme charge transfer is comprehensively elucidated through a combination of analytical techniques and density functional theory (DFT) calculations. This study offers a novel approach for managing charge carrier segregation and mobility in CO2 reduction photocatalysts.

Arctium lappa L. polysaccharides alleviate oxidative stress and inflammation in the liver and kidney of aging mice by regulating intestinal homeostasis.

Arctium lappa L. polysaccharide (ALP) is a prominent bioactive compound renowned for its multifaceted functional properties, including anti-inflammatory, antioxidant, antifibrotic, immunomodulatory, and pro-apoptotic effects. This study evaluated the aging-delaying effect of ALP and its mechanisms using a D-galactose (D-gal)-induced aging model. After an 8-week treatment, ALP significantly ameliorated D-gal-induced inflammation and oxidative stress in the liver, kidneys, and intestines. Notably, ALP administration led to a marked reduction of the pathogenic bacterium Desulfovibrio and a substantial increase in the beneficial bacterium Muribaculum. These microbial shifts were associated with upregulated expression of intestinal tight junction proteins and intestinal mucins, leading to enhanced intestinal barrier integrity. Consequently, the leakage of enterotoxins and inflammatory mediators was effectively reduced. The findings indicate that ALP alleviates tissue inflammation and oxidative stress, while also delaying aging in mice. This effect is achieved through the regulation of intestinal ecological homeostasis and the repair of the intestinal immune barrier.

The Effect of a Caffeine and Nicotine Combination on Nicotine Withdrawal Syndrome in Mice.

Nicotine dependence is an important cause of excessive exposure to tobacco combustion compounds in most smokers. Nicotine replacement therapy is the main method to treat nicotine dependence, but it still has its shortcomings, such as the inability to mitigate withdrawal effects and limited applicability. It has been hypothesized that a combination of low-dose nicotine and caffeine could achieve the same psychological stimulation effect as a high dose of nicotine without causing nicotine withdrawal effects. To establish a model of nicotine dependence, male C57BL/6J mice were subcutaneously injected four times a day with nicotine (2 mg/kg) for 15 days and fed with water containing nicotine at the same time. They were randomly divided into four groups. After 24 h of withdrawal, different groups were injected with saline, nicotine (0.25 mg/kg or 0.1 mg/kg), or nicotine (0.1 mg/kg) and caffeine (20 mg/kg). Behavioral and physiological changes were evaluated by an assessment of physical signs, open field tests, elevated plus maze experiments, forced swimming tests, hot plate tests, and new-object-recognition tests. The changes in dopamine release in the prefrontal cortex (PFC) and ventral tegmental area (VTA) in the midbrain were analyzed using ELISA. The results showed that a combination of caffeine and nicotine could effectively relieve nicotine withdrawal syndrome, increase movement ability and pain thresholds, reduce anxiety and depression, enhance memory and cognitive ability, and increase the level of dopamine release in the PFC and VTA. Thus, caffeine combined with nicotine has potential as a stable and effective treatment option to help humans with smoking cessation.

Cognitive frailty in relation to vitamin B12 and 25-hydroxyvitamin D in an elderly population: a cross-sectional study from NHANES.

Background: Nutritional support has been identified as a potential intervention for cognitive frailty; however, the association between 25-hydroxyvitamin D [25-(OH)D], vitamin B12, and cognitive frailty remains ambiguous. Methods: This study utilized data from two cycles (2011-2012, 2013-2014) of the National Health and Nutrition Examination Survey (NHANES) to investigate this relationship. The researchers constructed a 41-item frailty index encompassing diverse aspects of physical functioning, psychological evaluation, and medical conditions, and evaluated each participant individually. The study utilized Spearman's rank correlation coefficient and univariate ordered logistic regression to assess the relationships between variables and cognitive frailty. Recursive feature elimination and cross-validation methods were employed to identify the most influential variables for building and optimizing multivariate ordered logistic regression models. Subgroup analyses and interaction tests were further conducted to validate the identified correlations. Results: The findings of this study confirm a negative linear correlation between 25-(OH)D levels and cognitive frailty in older adults. Specifically, a one-unit increase in 25-(OH)D levels was associated with a 12% reduction in the risk of cognitive frailty. The result was further supported by subgroup analyses and interaction tests. Conclusion: The existence of a negatively correlated linear association between 25-(OH)D levels and cognitive frailty in older adults is plausible, but further rigorously designed longitudinal studies are necessary to validate this relationship.

[Effect of Xiongcan Yishen Formula on ferroptosis in mouse TM3 Leydig cells after oxidative stress injury].

OBJECTIVE: To investigate the effects of Xiongcan Yishen Formula (XYF) on ferroptosis in mouse TM3 Leydig cells after oxidative stress injury (OSI) induced by H2O2.　Methods: An oxidative stress injury model was established in mouse TM3 Leydig cells using H2O2 induction. The modeled TM3 cells were randomly divided into OSI group, XYF group, the ferroptosis inhibitor Ferrostatin-1 (F-1) group, and F-1+XYF group, which were respectively intervened with blank serum, 20% drug-containing serum, 2µmol/L F-1, and 2µmol/L F-1+ 20% drug-containing serum. A control group (normal TM3 cells + blank serum) was also set up. The morphology of cells in each group was observed, and the levels of testosterone, superoxide dismutase (SOD), reactive oxygen species (ROS), malondialdehyde (MDA), ferritin heavy chain 1 (FTH1), solute carrier family 7 member 11 (SLC7A11), glutathione (GSH), glutathione peroxidase 4 (GPX4), fatty acid CoA ligase 4 (FACL4), total iron ions, and ferrous ions were detected. RESULTS: Compared with the model group, the control group showed significantly decreased expression of ROS, MDA, FACL4, total iron, and ferrous ions (P<0.05), and significantly increased levels of testosterone, SOD, GSH, FTH1, SLC7A11, and GPX4 (P<0.05). The male silkworm kidney-tonifying formula group significantly promoted testosterone secretion by TM3 cells and upregulated the expression of FTH1, SLC7A11, GPX4, GSH, and SOD in TM3 cells (P<0.05), while significantly downregulating ROS, MDA, FACL4, total iron ions, and ferrous ions (P<0.05). CONCLUSION: Following H2O2 exposure, oxidative stress can induce ferroptosis in mouse TM3 Leydig cells. XYF can antagonize OSI and ferroptosis in TM3 cells by activating the SLC7A11/GSH/GPX4 axis, which may underlie the mechanism of XYF in the treatment of male late-onset hypogonadism.

[Ferroptosis in male reproductive system diseases: Progress in research].

Ferroptosis is an iron-dependent form of programmed cell death triggered by the excessive accumulation of lipid peroxides on the cell membrane. Recent studies have found that ferroptosis can be induced by exposure of the testis tissue and germ cells to some high-risk factors, accompanied by various characteristic reproductive system injuries, including changes in cell morphology, ferroptosis-related physicochemical indicators and gene expressions. This review focuses on the association of ferroptosis with male reproductive system diseases from three key aspects: iron metabolism abnormalities, Cystine/GSH/GPX4 axis imbalance, and lipid peroxidation.

Interventional Effect of Donkey Bone Collagen Peptide Iron Chelate on Cyclophosphamide Induced Immunosuppressive Mice.

Immunodeficiency can disrupt normal physiological activity and function. In this study, donkey bone collagen peptide (DP) and its iron chelate (DPI) were evaluated their potential as immunomodulators in cyclophosphamide (Cytoxan®, CTX)-induced Balb/c mice. The femoral tissue, lymphocytes, and serum from groups of mice were subjected to hematoxylin and eosin (H&E) staining, methylthiazolyldiphenyl-tetrazolium bromide (MTT) cell proliferation assays, and enzyme-linked immunosorbent assay (ELISA), respectively. Furthermore, a non-targeted metabolomics analysis based on UPLC-MS/MS and a reverse transcription polymerase chain reaction (RT-qPCR) technology were used to explore the specific metabolic pathways of DPI regulating immunocompromise. The results showed that CTX was able to significantly reduce the proliferative activity of mouse splenic lymphocytes and led to abnormal cytokine expression. After DP and DPI interventions, bone marrow tissue damage was significantly improved. In particular, DPI showed the ability to regulate the levels of immune factors more effectively than Fe2+ and DP. Furthermore, metabolomic analysis in both positive and negative ion modes showed that DPI and DP jointly regulated the levels of 20 plasma differential metabolites, while DPI and Fe2+ jointly regulated 14, and all 3 jointly regulated 10. Fe2+ and DP regulated energy metabolism and pyrimidine metabolism pathways, respectively. In contrast, DPI mainly modulated the purine salvage pathway and the JAK/STAT signaling pathway, which are the key to immune function. Therefore, DPI shows more effective immune regulation than Fe2+ and DP alone, and has good application potential in improving immunosuppression.

Ovarian cancer derived extracellular vesicles promote the cancer progression and angiogenesis by mediating M2 macrophages polarization.

BACKGROUND: Extracellular vesicles (EVs) are mediators between cancer cells and other types of cells, such as tumor-associated macrophages (TAMs), in the tumor microenvironment. EVs can remodel the tumor microenvironment and regulate tumor progression. However, the underlying molecular mechanism of these interactions remains unclear. METHODS: First, we explored the effect of TAMs on the survival prognosis of patients with ovarian cancer. Next, we isolated EVs derived from ovarian cancer cells (OV-EVs) through ultracentrifugation and analyzed the capacity of OV-EVs to regulate macrophage polarization in ovarian tumors and in whole peripheral blood. Moreover, we explored the roles of OV-EVs-induced macrophages in tumor progression through in vitro and in vivo assays. RESULTS: OV-EVs were encapsulated by macrophages and induced the polarization of macrophages toward the M2 phenotype. Moreover, OV-EVs-induced M2 macrophages promoted angiogenesis and cancer progression both in vitro and in vivo. In addition, OV-EVs-induced macrophages increased the expression level of VEGF and increased the expression level of VEGFR in tumors, which resulted in angiogenesis in ovarian cancer. CONCLUSIONS: The present study demonstrated that OV-EVs induce M2 polarization in macrophages and promote the progression of ovarian cancer. This study provides novel insight into the mechanism of ovarian cancer progression.

Fully sp2 Carbon-Conjugated Covalent Organic Frameworks with Multiple Active Sites for Advanced Lithium-Ion Battery Cathodes.

Covalent organic frameworks (COFs) hold great promise for rechargeable batteries. However, the synthesis of COFs with abundant active sites, excellent stability, and increased conductivity remains a challenge. Here, chemically stable fully sp2 carbon-conjugated COFs (sp2c-COFs) with multiple active sites are designed by the polymerization of benzo[1,2-b:3,4-b':5,6-b'']trithiophene-2,5,8-tricarbaldehyde) (BTT) and s-indacene-1,3,5,7(2H,6H)-tetrone (ICTO) (denoted as BTT-ICTO). The morphology and structure of the COF are precisely regulated from "butterfly-shaped" to "cable-like" through an in situ controllable growth strategy, significantly promoting the exposure and utilization of active sites. When the unique "cable-like" BTT-ICTO@CNT is employed as lithium-ion batteries (LIBs) cathode, it exhibits exceptional capacity (396 mAh g-1 at 0.1 A g-1 with 97.9 % active sites utilization rate), superb rate capacity (227 mAh g-1 at 5.0 A g-1), and excellent cycling performance (184 mAh g-1 over 8000 cycles at 2.0 A g-1 with 0.00365 % decay rate per cycle). The lithium storage mechanism of BTT-ICTO is exhaustively revealed by in situ Fourier transform infrared, in situ Raman, and density functional theory calculations. This work provides in-depth insights into fully sp2c-COFs with multiple active sites for high-performance LIBs.

Diffuse large B-cell lymphoma with central nervous system symptoms during the maintenance therapy of acute lymphoblastic leukemia: a case report and literature review.

BACKGROUND: Diffuse large B-cell lymphoma (DLBCL) secondary to acute lymphoblastic leukemia (ALL) is a rare disease with poor prognosis, usually attributed to delayed diagnosis. To date, only four cases of ALL developing DLBCL have been reported, while none of them exhibiting central nervous system (CNS) symptoms. CASE DESCRIPTION: Here, we report an unusual case of a 15-year-old boy diagnosed with ALL and treated based on the SCCLG-ALL 2016 protocol. While he was receiving maintenance treatment, the patient developed dizziness and vomiting. An Epstein-Barr virus (EBV)-positive DLBCL with CNS involvement was diagnosed from inguinal lymph nodes biopsy, EBV DNA tests and head magnetic resonance imaging (MRI). Meanwhile, a dramatic decrease of immune cells and immunoglobulin was detected in the occurrence of DLBCL. He received therapy based on SCCCG-NHL-2017 protocol immediately after the diagnosis. CONCLUSIONS: We present the first retrospective report of four cases of non-Hodgkin lymphoma (NHL) secondary to ALL between 1990 and 2022. The pathogenesis of secondary DLBCL may be related to infection, immunodeficiency, genetic susceptibility, and treatment. Thus, the detection of EBV DNA during the full course of ALL therapy and genetic tests were needed in the occurrence of secondary DLBCL. Given to the rare rate and insufficient treatment experience, longer follow-up and enough sample size are needed.

Case report: Clinical features of pediatric acute myeloid leukemia presenting with cardiac tamponade: a case series study and literature review.

Objective: This study aims to elucidate the clinical features observed in cases of pediatric acute myeloid leukemia (AML) initially presenting with cardiac tamponade and to share treatment experiences. Materials and methods: Five pediatric patients were initially diagnosed with AML accompanied by cardiac myeloid sarcoma (MS). The diagnosis was established by examining our hospital records and reviewing pertinent literature from 1990 to July 2023, accessible through MEDLINE/PubMed. We comprehensively assessed the clinical characteristics and treatment modalities employed for these patients. Result: Five pediatric patients presented with acute symptoms, including shortness of breath, malaise, cough, and fever, leading to their hospitalization. Physical examination revealed irritability, hypoxia, tachypnea, tachycardia, and hypotension. Initial detection utilized chest X-ray or echocardiogram, leading to subsequent diagnoses based on pericardial effusion and/or bone marrow examination. Two patients received chemotherapy at the time of initial diagnosis, one with cytarabine and etoposide, and the other with cytarabine and cladribine. Post-treatment, their bone marrow achieved remission, and over a 2.5-year follow-up, their cardiac function remained favorable. Unfortunately, the remaining three patients succumbed within two weeks after diagnosis, either due to receiving alternative drugs or without undergoing chemotherapy. Conclusion: This is the first and largest case series of pediatric AML patients with cardiac MS, manifesting initially with cardiac tamponade. It highlights the rarity and high mortality associated with this condition. The critical factors for reducing mortality include identifying clinical manifestations, conducting thorough physical examinations, performing echocardiography promptly, initiating early and timely pericardial drainage, and avoiding cardiotoxic chemotherapy medications.