The connection between tendons and bones is called the tendon bone connection. With the continuous improvement of national sports awareness, excessive exercises and the related intensity are prone to damage the tendon bone connection. Tendon bone healing is a complex repair and healing process involving multiple factors, and good tendon bone healing is a prerequisite for its physiological function. The complexity of tendon bone structure also poses great challenges to the repair of tendon bone injuries. In recent years, researches have found that stem cells, growth factors, macrophages, and other factors are closely related to the healing process of tendon bone injuries, among which macrophages play an important role in the healing process. The authors reviewed relevant research literature in recent years and summarized the role of macrophages in tendon bone healing, in order to provide new ideas and directions for treatment strategies to promote tendon bone healing.
Humans ; Macrophages/metabolism* ; Wound Healing ; Animals ; Tendons/physiology* ; Bone and Bones/injuries* ; Tendon Injuries

Myelin formation is considered the last true "invention" in the evolution of vertebrate nervous system cell structure. The rapid jumping pulse propagation achieved by myelin enables the high conduction speed that is the basis of human movement, sensation, and cognitive function. As a key structure in the brain, white matter is the gathering place of myelin. However, with age, white matter-associated functions become abnormal and a large number of myelin sheaths undergo degenerative changes, causing serious neurological and cognitive disorders. Despite the extensive time and effort invested in exploring myelination and its functions, numerous unresolved issues and challenges persist. In-depth exploration of the functional role of myelin may bring new inspiration for the treatment of central nervous system (CNS) diseases and even mental illnesses. In this study, we conducted a comprehensive examination of the structure and key molecules of the myelin in the CNS, delving into its formation process. Specifically, we propose a new hypothesis regarding the source of power for myelin expansion in which membrane compaction may serve as a driving force for myelin extension. The implications of this hypothesis could provide valuable insights into the pathophysiology of diseases involving myelin malfunction and open new avenues for therapeutic intervention in myelin-related disorders.
Myelin Sheath/metabolism* ; Humans ; Central Nervous System/metabolism* ; Animals

Lysosomes represent a promising target for cancer therapy and reducing drug resistance. However, the short treatment time and low efficiency of lysosomal targeting have limited the application in lysosome-targeting anticancer drugs. In this study, we proposed an adhesive-bandage approach and synthesized a new lysosomal targeting drug, namely long-term lysosome-targeting anticancer drug (LLAD). It contains a SLC38A9-targeting covalently bound moiety and an alkaline component both to prolong the inhibition of SLC38A9 in lysosomes and alkalinize lysosomes. Upon short term and low-dose treatment of HeLa cells, at passage 0, with LLAD, it rapidly alkalinized lysosomes and also can be detected in lysosomes even at passage 15. LLAD induced apoptosis in HeLa cells through long-term lysosomal damage, and showed better long-term anticancer effect than cisplatin in vivo. Overall, our study paves the way for developing long-term lysosomal targeting drugs to treat cancer and overcome the drug resistance of cancer cells, and also provides a candidate drug, LLAD, for treating cancer.

The incomplete degradation of tumour cells by macrophages (Mϕ) is a contributing factor to tumour progression and metastasis, and the degradation function of Mϕ is mediated through phagosomes and lysosomes. In our preliminary experiments, we found that overactivation of NADPH oxidase 2 (NOX2) reduced the ability of Mϕ to degrade engulfed tumour cells. Above this, we screened out liquiritin from Glycyrrhiza uralensis Fisch, which can significantly inhibit NOX2 activity and inhibit tumours, to elucidate that suppressing NOX2 can enhance the ability of Mϕ to degrade tumour cells. We found that the tumour environment could activate the NOX2 activity in Mϕ phagosomes, causing Mϕ to produce excessive reactive oxygen species (ROS), thus prohibiting the formation of phagolysosomes before degradation. Conversely, inhibiting NOX2 in Mϕ by liquiritin can reduce ROS and promote phagosome-lysosome fusion, therefore improving the enzymatic degradation of tumour cells after phagocytosis, and subsequently promote T cell activity by presenting antigens. We further confirmed that liquiritin down-regulated the expression of the NOX2 specific membrane component protein gp91 phox, blocking its binding to the NOX2 cytoplasmic component proteins p67 phox and p47 phox, thereby inhibiting the activity of NOX2. This study elucidates the specific mechanism by which Mϕ cannot degrade tumour cells after phagocytosis, and indicates that liquiritin can promote the ability of Mϕ to degrade tumour cells by suppressing NOX2.

Nonalcoholic steatohepatitis （NASH） is a chronic liver disease with the main pathological features of hepatic steatosis， inflammatory cell infiltration， and interstitial fibroplasia， and it is an important risk factor for liver fibrosis， liver cirrhosis， and hepatocellular carcinoma. NOD-like receptor protein 3 （NLRP3） inflammasome is the core of innate immunity， and the abnormal activation of NLRP3 inflammasome is closely associated with the development and progression of NASH， which involves multiple links such as inflammatory response and oxidative stress. A large number of studies have shown that the active ingredients of traditional Chinese medicine （TCM） and TCM compound prescriptions can improve oxidative stress， regulate lipid metabolism， and alleviate liver inflammation by regulating NLRP3 inflammasome. TCM treatment applied in clinical practice has achieved a good therapeutic effect， while inflammasome is one of the key pathways or targets for TCM in improving NASH. This article reviews the mechanism of action of NLRP3 inflammasome in NASH and the research advances in TCM intervention of NLRP3 inflammasome， in order to provide ideas for the clinical TCM treatment of NASH， as well as reference targets and research directions for the research and development of new TCM drugs.

Background Hexavalent chromium [Cr(VI)] exposure can cause structural disruption of intestinal flora and functional impairment. Vitamin C (VC) is one of the essential micronutrients, which plays an important role in promoting the growth of intestinal probiotics, improving the intestinal barrier, and maintaining the homeostasis of intestinal flora. However, the regulatory effect of VC on the intestinal flora disorders caused by Cr(VI) exposure remains to be investigated. Objective To investigate the effect of VC on intestinal flora disruption in mice due to Cr(VI) exposure. Methods Thirty-two SPF-grade C57BL/6 mice were acclimatized and fed for 3 d and randomly divided into control (Con), VC, potassium dichromate [K₂Cr₂O₇, Cr(VI)], and VC+K₂Cr₂O₇ [VC+Cr(VI)] groups. At 8:00 a.m. on day 4, the Con group (double-distilled water given by gavage and injected intraperitoneally), the VC group (VC given by gavage and double-distilled water injected intraperitoneally), the Cr(VI) group (double-distilled water given by gavage and K₂Cr₂O₇ solution injected intraperitoneally), and the VC+Cr(VI) group (VC given by gavage and K₂Cr₂O₇ solution injected intraperitoneally) were treated. The dose of VC was 200 mg·kg⁻¹, and the dose of K₂Cr₂O₇ was 1.25 mg·kg⁻¹. The mice were treated for 45 consecutive days and then executed, the contents of the colon were sampled in sterile freezing tubes, and three replicates were collected from each group. After labeling, the samples were immediately put into liquid nitrogen for rapid freezing. After all the samples were collected, they were transferred to a -80 ℃ ultra-low temperature refrigerator for storage. Samples of colon contents were analyzed for intestinal flora structure by high-throughput sequencing and bioinformatics software. Results The Cr(VI) exposure resulted in reduced body weight gain values in mice compared to the Con group. Pathological changes occurred in the ileal tissue of mice, with significant inflammatory cell infiltration in the Cr(VI) group and reduced inflammatory cell infiltration in the VC+Cr(VI) group. The number of operational taxonomic units (OTUs) of intestinal flora was altered in the Cr(VI) group of mice. In the α diversity analysis, the mean Sobs index in the Cr(VI) group was 240.333±67.796, the Chao index was 258.173±64.813, and the Ace index was 259.481±66.891, which were significantly lower than those in the Con group (P<0.05), the PD whole tree index in the Cr(VI) group was 27.863±2.399, which was significantly higher than that in the Con group (P<0.05), and the VC intervention significantly reversed the changes of the above indexes due to Cr(VI) exposure (P<0.05). In the β diversity analysis, the principal coordinates analysis (PCoA) results showed a significant separation between the Cr(VI) group and the Con group, and after the VC intervention, there was a retraction of the separation trend and the difference was reduced. The multi-sample similarity dendrogram results showed that the control and the VC groups clustered together first, then with the VC+Cr(VI) group, and finally with the Cr(VI) group. The abundances of Bacteroidetes, Saccharibacteria, and Tenericutes in the intestine of mice in the Cr(VI) group were decreased, and the abundance of Firmicutes was increased; the abundances of Lactobacillus, Alistipes, Bacteroides, and Ruminiclostridium were also increased. Included among these, Bacteroides showed a significantly higher abundance compared to the control mice (P<0.05). Changes in the abundances of phyla and genera of the above mentioned gut microorganisms were reversed after the VC intervention. Conclusion Cr(VI) exposure can lead to intestinal damage and disorganization of the intestinal flora structure in mice, while VC intervention can ameliorate the above changes to a certain extent and normalize the intestinal flora structure.

Objective:To observe the effects of electroacupuncture(EA)on sleep electroencephalogram(EEG)and event-related potential(ERP)in patients with somatoform disorders(SFD). Methods:Seventy-five SFD patients were recruited as an EA group to receive EA at Shenting(GV24)and Baihui(GV20)once daily,30 min each time,with 6 straight days as a treatment course,and 4 courses were conducted at 1-day intervals.Before treatment,patients underwent a survey using a physical symptom checklist on their primary symptoms.Before and after treatment,their sleep EEG was monitored using Quisi,and the ERP mismatch negativity(MMN)and P300 were detected.The Quisi sleep EEG and ERP were also examined among 40 normal volunteers as the normal group data. Results:During the trial,13 cases were removed from the EA group due to incomplete data,and 62 cases were finally included for statistical analyses.Of the 62 SFD patients,the main disturbing symptoms were cognitive impairments,sleep disorders,respiratory symptoms,digestive symptoms,five-sense organ problems,and cardiovascular symptoms in order.Before treatment,the EA group had increased MMN and P300 latencies and decreased amplitudes compared with the normal control group(P<0.01 or P<0.05);according to Quisi,the EA group also had reduced total sleep time(TST),shorter rapid eye movement sleep(REM)latency(RL)and REM time(RT),smaller number of REM period(NRP),extended sleep latency(SL),longer awaking time(AT),lower sleep efficiency(SE),larger percent of non-rapid eye movement sleep(NREM)stage 1(S1)and smaller percent of NREM stage 2(S2),and the percent of slow wave sleep(SWS),i.e.NREM stage 3(S3)plus stage 4(S4),also went down,all presenting significant differences between groups(P<0.01 or P<0.05).After 4 courses of treatment,the MMN and P300 latencies were reduced,and their amplitudes became larger in the EA group compared with the baseline(P<0.05);they had insignificant differences compared with the normal control group(P>0.05).Quisi showed that the TST and RL increased,and the SL and AT decreased in the EA group,and the predominant change in sleep architecture was reduced S1 percent,increased S2,and improved SE,all showing significant intra-group differences(P<0.01 or P<0.05);however,the intra-group difference in the NRP was statistically insignificant(P>0.05).Except the TST,RT,S1 percent,and SWS,there was no statistical significance in comparing the other Quisi parameters(including RL,NRP,SL,AT,SE,and S2 percent)between the two groups(P>0.05). Conclusion:SFD patients have a variety of clinical symptoms,and most of them show abnormal sleep EEG and ERP;EA can correct abnormal sleep EEG parameters and the MMN and P300 of ERP in SFD patients.

Objective To explore the value of probe-based confocal laser endomicroscopy(pCLE)in the differential diagnosis of fundic gland polyps.Methods A total of 63 patients who underwent conventional white light image(WLI)and suggested with gastric polyps in our gastroenterology endoscopy center during June and December 2023 were enrolled,and their clinical data,WLI,narrow band images(NBI),pCLE images and postoperative histopathological findings were collected.The characteristics of fundic gland polyps under pCLE were statistically verified,and the sensitivity,specificity,accuracy and consistency of different endoscopic diagnoses were calculated respectively.Results Under pCLE,fundic gland polyps were mainly manifested as elongated gastric pit opening,"hand-in-hand"gastric pit opening,well-arranged blood vessels around the pit opening,and no luciferin oozing.The sensitivity,specificity,accuracy of WLI were 72.73％,75.00％,73.13％and 0.343 for fundic gland polyps,and 81.82％,71.43％,71.64％and 0.354 for hyperplastic polyps,respectively.While,the above values of NBI were 87.27％,83.33％,86.57％and 0.673 for fundic gland polyps,and 81.82％,85.71％,85.07％and 0.554 for hyperplastic polyps;and those of pCLE were 92.73％,91.67％,92.53％and 0.769 for fundic gland polyps,and 90.91％,94.64％,94.03％and 0.797 for hyperplastic polyps pCLE had better sensitivity,specificity and accuracy than WLI and NBI,and had the results consistent with histopathological findings.Conclusion pCLE can be used in the differential diagnosis of fundic gland polyps.

Objective:To investigate the risk factors of intraspinal cement leakage in the treatment of osteoporotic vertebral compression fracture by percutaneous vertebroplasty (PVP).Methods:From January 2018 to December 2021, 156 patients with OVCF who received surgical treatment in Beijing Tongzhou Integrated Traditional Chinese and Western Medicine Hospital were enrolled in this retrospective case-control study. The postoperative CT imaging results were analyzed, and the patients were divided into two groups according to the occurrence of intraspinal cement leakage: leakage group ( n=28) and non-leakage group ( n=128). Measurement data was expressed as mean±standard deviation ( ± s), and t-test was used for comparison of visual analogue score (VAS) between groups; the count data was expressed as the number of cases and percentage (%); univariate and multivariate Logistic regression analysis were used to evaluate the risk factors of postoperative intraspinal cement leakage. Results:All the patients were treated by PVP successfully, without obvious adverse reactions and serious complications occurred during and after the operation. Univariate Logistic regression analysis showed that higher bone mineral density ( P=0.005), OVCF combined with posterior vertebral wall injury ( P<0.001) and higher bone cement dosage ( P=0.013) were the risk factors leading to intraspinal cement leakage. Multivariate Logistic regression analysis showed that higher bone mineral density ( P=0.009, 95% CI: 0.152-0.762, OR=0.340), OVCF combined with posterior vertebral wall injury ( P=0.001, 95% CI: 2.134-15.780, OR=5.803), and higher bone cement dosage ( P=0.005, 95% CI: 1.175-2.505, OR=1.715) were the independent risk factors of intraspinal cement leakage. Conclusion:Intraspinal cement leakage was common complication after PVP. Higher bone mineral density, OVCF combined with posterior vertebral wall injury, and higher bone cement dosage were the independent risk factors affecting intraspinal cement leakage.

Inhibiting the death receptor 3(DR3)signaling pathway in group 3 innate lymphoid cells(ILC3s)pre-sents a promising approach for promoting mucosal repair in individuals with ulcerative colitis(UC).Paeoniflorin,a prominent component of Paeonia lactiflora Pall.,has demonstrated the ability to restore barrier function in UC mice,but the precise mechanism remains unclear.In this study,we aimed to delve into whether paeoniflorin may promote intestinal mucosal repair in chronic colitis by inhibiting DR3 signaling in ILC3s.C57BL/6 mice were subjected to random allocation into 7 distinct groups,namely the control group,the 2％dextran sodium sulfate(DSS)group,the paeoniflorin groups(25,50,and 100 mg/kg),the anti-tumor necrosis factor-like ligand 1A(anti-TL1A)antibody group,and the IgG group.We detected the expression of DR3 signaling pathway proteins and the proportion of ILC3s in the mouse colon using Western blot and flow cytometry,respectively.Meanwhile,DR3-overexpressing MNK-3 cells and 2％ DSS-induced Rag1-/-mice were used for verification.The results showed that paeoniflorin alleviated DSS-induced chronic colitis and repaired the intestinal mucosal barrier.Simultaneously,paeoniflorin inhibited the DR3 signaling pathway in ILC3s and regulated the content of cytokines(interleukin-17A,granulocyte-macrophage colony stimulating factor,and interleukin-22).Alternatively,paeoniflorin directly inhibited the DR3 signaling pathway in ILC3s to repair mucosal damage indepen-dently of the adaptive immune system.We additionally confirmed that paeoniflorin-conditioned me-dium(CM)restored the expression of tight junctions in Caco-2 cells via coculture.In conclusion,paeoniflorin ameliorates chronic colitis by enhancing the intestinal barrier in an ILC3-dependent manner,and its mechanism is associated with the inhibition of the DR3 signaling pathway.