Bacterial biofilms can make traditional antibiotics impenetrable and even promote the development of antibiotic-resistant strains. Therefore, non-antibiotic strategies to effectively penetrate and eradicate the formed biofilms are urgently needed. Here, we demonstrate the development of self-propelled biohybrid microrobots that can enhance the degradation and penetration effects for Pseudomonas aeruginosa biofilms in minimally invasive strategy. The biohybrid microrobots (CR@Alg) are constructed by surface modification of Chlamydomonas reinhardtii (CR) microalgae with alginate lyase (Alg) via biological orthogonal reaction. By degrading the biofilm components, the number of CR@Alg microrobots with fast-moving capability penetrating the biofilm increases by around 2.4-fold compared to that of microalgae. Massive reactive oxygen species are subsequently generated under laser irradiation due to the presence of chlorophyll, inherent photosensitizers of microalgae, thus triggering photodynamic therapy (PDT) to combat bacteria. Our algae-based microrobots with superior biocompatibility eliminate biofilm-infections efficiently and tend to suppress the inflammatory response in vivo, showing huge promise for the active treatment of biofilm-associated infections.

Liver cancer is a malignant tumor with a high mortality rate.With the continuous development of targeted drugs,immunotherapy and other technological means,translational therapy has become a consensus in the treatment of advanced liver cancer.The liver's inherent immune tolerance,tumor tissue,and various immune components constitute a dynamically changing liver cancer microenvironment.The immune escape in the microenvironment of liver cancer is the main obstacle to current immunotherapy.Cellular immunity is an important component of anti-tumor immunity,and the status and function of immune cells are closely related to cancer prognosis.This article reviews the progress of tumor infiltrating lymphocytes in the tumor microenvironment of hepatocellular carcinoma,in order to benefit the exploring of targeted antitumor therapy.

Objective:To summarise and analyse the experience in the diagnosis and management of abdominal aortic endograft infection in recent years.Methods:Retrospectively summarised and analysed the general data, clinical presentation, laboratory and imaging findings, causative organisms and treatment choices of 14 patients with abdominal aortic endograft infection treated in Beijing Friendship Hospital, Capital Medical University, from January 2018 to June 2024, and analysed the prognosis of the patients and the risk factors associated with prognosis.Results:Positive bacterial cultures were 10 out of 14 patients. One non-operatively treated patient died of infectious toxic shock. Thirteen surgically treated patients underwent axillary-bifemoral artery bypass, removal of the infected stent, and closure of the aortic stump. Four of the 13 cases had combined aortoenteric fistula, 3 cases underwent one-stage enterocutaneous fistula repair, 1 case only fistula drainage, 3 cases of gastrojejunal anastomosis, all of them underwent gastric or jejunal nutrient tube implantation. Two of the 13 patients had combined the infection foci spread to the renal artery openings. To save the kidney, intraoperative left kidney autologous renal transplantation was performed in 1 case, and autologous saphenous vein reconstruction from celiac trunk artery-left renal artery and superior mesenteric artery-right renal artery was performed in the other case. All 14 patients were retrospectively summarised and followed up in August 2024, with 5 deaths in the early postoperative period (< 3 months), 3 deaths in the mid- to long-term period (≥3 months), and 5 survivors, with a median follow-up time of 2 years (1-5 years) for surviving patients. Among the 13 operated patients, 4 cases were combined with aortoenteric fistula, and 3 cases died in the early postoperative period; 4 cases of abdominal aortic infection foci involving renal artery openings, 2 cases of early postoperative death; 4 cases with pleural effusion, 4 cases died in the early postoperative period; 2 cases of combined creatinine elevation, 2 cases of early postoperative death; 2 cases of postoperative infection of artificial blood vessels.Conclusions:Abdominal aortic endograft infection are aggressive. The risk of early death is increased in patients who are elderly, in poor general condition, with aortoenteric fistula or with pre-existing cardiac, pulmonary, hepatic and renal insufficiency, but surgery based on adequate anti-infective therapy remains an effective means of saving the patient′s life.

ObjectiveThe antitumor activity of sesquiterpenoid M36 isolated from Myrrha against human hepatoma HepG2 cells was investigated in this study. MethodHepG2 cells were treated with M36 at different concentrations （0， 2， 4， 6， 8， 10 μmol·L^-1）. Firstly， the effects of M36 on the proliferation of human hepatoma HepG2 cells were detected by methyl thiazolyl tetrazolium （MTT）， colony formation assay， and EdU proliferation assay. Hoechst staining， flow cytometry analysis， and Western blot were used to explore the effect of M36 on the apoptosis of human hepatoma HepG2 cells. Acridine orange staining and western blotting were used to examine the effect of M36 on autophagy in HepG2 cells. Finally， Western blot was used to detect protein expression of cancer-related signaling pathways. ResultCompared with the blank group， M36 treatment significantly inhibited the proliferation of human hepatoma HepG2 cells （P<0.01）， and the half inhibitory concentration （IC₅₀） value of M36 for 48 h was 5.03 μmol·L^-1， in a dose- and time-dependent manner. M36 was also able to induce apoptosis and autophagy in human hepatoma HepG2 cells. After treatment with 8 μmol·L^-1 M36 for 48 hours， the apoptosis rate of HepG2 cells was （42.03±9.65）% （P<0.01）. Compared with the blank group， HepG2 cells treated with 4 and 8 μmol·L^-1 M36 for 48 h had a significant increase in cleaved poly ADP-ribose polymerase （cleaved-PARP） protein levels （P<0.01）. Acridine orange staining showed that autophagy was significantly activated in HepG2 cells treated with 4 and 8 μmol·L^-1 M36 for 48 h compared with the blank group （P<0.01）， which was further verified by the up-regulation of microtubule-associated protein 1 light chain 3 Ⅱ （LC3 Ⅱ）. Western blot results showed that compared with the blank group， the levels of phosphorylated extracellular regulated protein kinase （p-ERK）， phosphorylated p38 mitogen-activated protein kinase （p-p38 MAPK）， phosphorylated c-Jun N-terminal kinase （p-JNK）， and its downstream nuclear transcription factors c-Jun and p-c-Jun protein were significantly increased in M36 group （P<0.05， P<0.01）. The mechanism may be related to the up-regulation of MAPK signaling pathway. ConclusionThe sesquiterpenoid M36 isolated from Myrrha inhibits the proliferation of human hepatoma HepG2 cells and promotes apoptosis and autophagy， which may be related to the activation of the MAPK signaling pathway.

Objective:To investigate the application effect of WeChat group combined with case-based learning (CBL) in probation teaching of vascular surgery.Methods:A total of 128 intern doctors of the seven-year medical program in vascular surgery were selected and divided into experimental group (WeChat group combined with CBL teaching) and control group (CBL teaching alone), and a unified assessment method was used to evaluate the mastery degree of professional theories and clinical knowledge and assess the teaching effect of these two teaching modes in vascular surgery. SPSS 22.0 was used to perform the t-test. Results:Compared with the control group, the experimental group had significantly higher scores of theoretical examination [(86.36±7.42) vs. (84.71±6.72)] and clinical examination [(88.44±7.62) vs. (86.22±6.41)], as well as significantly higher degrees of satisfaction with learning interest, classroom climate, self-learning ability, clinical thinking ability, and teamwork spirit.Conclusion:The teaching mode of WeChat group combined with CBL can improve the effect of the probation teaching of vascular surgery and the self-learning and clinical thinking abilities of intern doctors.

Objective:To explore the mechanism of Ma-Xing Shi-Gan decoction combined with Xiao-Chai-Hu decoction (hereinafter referred to as " Sanyang combined treatment" ) in alleviating colon injury in mice infected with influenza virus by transcriptome sequencing technique.Methods:The mouse model of colonic injury caused by influenza virus was induced by intranasal drip of influenza A virus H1N1 suspension. The mice were divided into Control group, Model group, and Sanyang combined treatment (SCT) group. Model group and SCT group were fed with PBS and Ma-Xing Shi-Gan decoction combined with Xiao-Chai-Hu decoction respectively. Seven days later, the colon tissues of each group were taken, the colon length and pathological damage were observed, and the transcriptome was sequenced to screen the significantly different genes between the SCT group and model group for Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Set Enrichment Analysis(GSEA).Results:After the therapy with SCT, the length of the colon of mice was significantly improved and the pathological injury of the colon was reduced. There are 92 differentially expressed genes between the SCT group and the model group. GO analysis indicated that the differential genes were enriched in biological processes such as regulation of cytokine and chemokine production, inflammatory response, defense response, immune response, regulation of NF-κB inducing kinase(NIK)/Nuclear factor-κB(NF-κB) signal and Mitogen-activated protein kinase(MAPK) cascade, as well as cell components related to intestinal barrier such as brush border membrane, brush border and microvilli. KEGG analysis indicated that the differential genes were enriched in Toll-like receptor signaling pathway, intestinal immune network for IgA production, complement and coagulation cascade, and Peroxisome proliferator-activated receptor(PPAR) signaling pathway. GSEA indicated that the intestinal immune network for IgA production, PPAR signaling pathway, propionic acid metabolism and butyrate metabolism were significantly up-regulated after the intervention with SCT, while apoptosis and MAPK signaling pathway were significantly down-regulated.Conclusions:Sanyang combined therapy can protect the intestinal tract of mice infected with influenza virus mainly through immunity, inflammation and metabolism pathways.

Objective:To discuss the clinical effect of endovascular treatment of 15 patients with spontaneous isolated superior mesenteric artery dissection(SISMAD).Methods:The clinical data of 15 patients with SISMAD treated with endovascular stent in Beijing Friendship Hospital Affiliated to Capital Medical University from January 2016 to July 2022 were collected and analyzed. The white blood cell, neutrophil percentage (NEUT%) and D-Dimer at admission, day 1 and day 3 after operation were analyzed and compared retrospectively. The time of abdominal pain at admission, YOO classification, angle from superior mesenteric artery to abdominal aorta(ASA), conservative treatment time, operation time, type and length of stent, vascular remodeling rate and long-term patency rate of stent were analyzed. The measurement data conforming to normal distribution was expressed as mean ± standard deviation ( ± s), t-test was used for comparison between the two groups. Measurement data of skewed distribution were expressed as M ( Q1, Q3), and non-parametric test was used for comparison between groups. Count data were expressed as rate or component ratio(%). The same variable was compared at different time points by repeated measurement data analysis of variance. Results:There were significant differences in white blood cell, NEUT% and D-Dimer between admission and postoperative day 3 in 15 patients. The time to admission for abdominal pain was 24.0(15.0, 78.0) hours. IVS type accounted for 46.7% of YOO type, and the ASA beyond 60° accounted for 66.7%. The conservative treatment time was (34.0±8.6) hours, moreover, the operation time was(153.0±37.8) min. Besides, self-expanding bare stent accounted for 85% of the stent types, moreover, the length of the stents beyond 60 cm was 50%. All patients were followed up for more than 24 months, and the vascular remodeling rate was(89.7±9.7)%.Conclusion:Endovascular self-expanding thin-wall stent placement has better vascular remodeling rate and patency rate for patients with IVS type.

METTL3 and METTL14 are two components that form the core heterodimer of the main RNA m6A methyltransferase complex (MTC) that installs m6A. Surprisingly, depletion of METTL3 or METTL14 displayed distinct effects on stemness maintenance of mouse embryonic stem cell (mESC). While comparable global hypo-methylation in RNA m6A was observed in Mettl3 or Mettl14 knockout mESCs, respectively. Mettl14 knockout led to a globally decreased nascent RNA synthesis, whereas Mettl3 depletion resulted in transcription upregulation, suggesting that METTL14 might possess an m6A-independent role in gene regulation. We found that METTL14 colocalizes with the repressive H3K27me3 modification. Mechanistically, METTL14, but not METTL3, binds H3K27me3 and recruits KDM6B to induce H3K27me3 demethylation independent of METTL3. Depletion of METTL14 thus led to a global increase in H3K27me3 level along with a global gene suppression. The effects of METTL14 on regulation of H3K27me3 is essential for the transition from self-renewal to differentiation of mESCs. This work reveals a regulatory mechanism on heterochromatin by METTL14 in a manner distinct from METTL3 and independently of m6A, and critically impacts transcriptional regulation, stemness maintenance, and differentiation of mESCs.
Animals ; Mice ; Methylation ; Chromatin ; Histones/metabolism* ; RNA, Messenger/genetics* ; Methyltransferases/metabolism* ; RNA/metabolism*

The prevalence and mortality of cancer have been on the rise， and it has been the global leading cause of death. The causes of cancer are diverse， such as heredity， radiation， and carcinogens. The abnormality of cell cycle regulation is also one of the causes. Cell cycle is a complex sequence of events through which a cell duplicates its contents and divides. Cell cycle is highly organized to ensure the integrity of genetic material. This process involves many regulatory genes and proteins. Cell cycle will be dysregulated when these proteins and genes change， resulting in the loss of control of cell proliferation， the inhibition of apoptosis， and finally the occurrence of tumor. At the moment， the therapies for cancer include traditional surgical resection， radiotherapy， chemical therapy， and targeted therapy. Chinese medicine has a wide range of sources and little side effect， which is worthy of further research and development. More and more studies have revealed that a variety of Chinese medicines play an anti-tumor role by inducing cell cycle arrest， so as to improve the quality of life and prolong the survival time of patients with advanced tumors. This article first introduces the characteristics and related regulatory factors of each phase of cell cycle， and enumerates the clinical and experimental examples of tumorigenesis caused by abnormal cell cycle. Then， we summarize the hot anti-tumor drugs targeting cell cycle in China and abroad， such as Cyclin-dependent kinase （CDK） inhibitors， cell division cycle 25 （CDC25） inhibitors， ataxia-telangiectasia-mutated-and-Rad3-related kinase （ATR） inhibitors， and checkpoint kinase 1 （CHK1） inhibitors. Finally， this article summarizes the recent research on the anti-tumor effect of Chinese medicine by inducing cell cycle arrest from the three aspects of cell cycle G₀/G₁ phase， S phase and G₂/M phase， in order to provide some reference for the research on the anti-tumor effect of Chinese medicine.

Diabetic cardiomyopathy is a myocardial complication associated with abnormal glucose metabolism and dyslipidiaemia, which increases the risk of death and heart failure in diabetic patients. Mitochondrial dysfunction is involved in the occurrence and development of diabetic cardiomyopathy. Recent studies have confirmed that scavenging damaged mitochondria in cardiomyocytes through mitophagy can restore mitochondrial homeostasis, reduce oxidative stress and improve diabetic cardiomyopathy. Therefore, this article provides a comprehensive review of the mechanisms and characteristics of mitochondrial autophagy in diabetic cardiomyopathy. It aims to offer new insights and theoretical basis for the prevention and treatment of diabetic cardiomyopathy.