OBJECTIVE: To review the research progress on the lower limb biomechanical characteristics of patients with discoid lateral meniscus (DLM) injury after surgery. METHODS: By searching relevant domestic and international research literature on DLM, the postoperative characteristics of knee joint movement biomechanics, tibiofemoral joint stress distribution, lower extremity force line, and patellofemoral joint changes in patients with DLM injury were summarized. RESULTS: Surgical treatment can lead to varying degrees of changes in the lower limb biomechanical characteristics of patients with DLM injury. Specifically, the kinematic biomechanics of the knee joint can significantly improve, but there are still problems such as extension deficits in the affected knee joint. The peak stress of the tibiofemoral joint decreases with the increase of the residual meniscus volume, and the degree of change is closely related to the residual meniscus volume. Preserving a larger volume of the meniscus, especially the anterior horn volume, helps to reduce stress concentration. The lower extremity force line will deviate outward after surgery, and the more meniscus is removed during surgery, the greater the change in the lower extremity force line after surgery. There are conditions such as cartilage degeneration, position and angle changes in the patellofemoral joint after surgery. CONCLUSION The changes in the lower limb biomechanical characteristics after DLM injury are closely related to the choice of surgical methods and rehabilitation programs. However, the mechanisms of biomechanical changes in multiple lower limb joints and individual differences still need to be further studied and clarified.
Humans ; Biomechanical Phenomena ; Tibial Meniscus Injuries/physiopathology* ; Menisci, Tibial/physiopathology* ; Knee Joint/surgery* ; Lower Extremity/physiopathology* ; Patellofemoral Joint/physiopathology* ; Range of Motion, Articular ; Knee Injuries/physiopathology*

Trauma can disrupt the body′s internal environment, resulting in organ dysfunction. This may manifest as symptoms such as acute respiratory distress, liver and kidney dysfunction, circulatory disorders and neurological damage. Mitochondrial quality control (MQC), encompassing processes like autophagy, dynamic changes, and biogenesis, plays an essential role in maintaining mitochondrial function. Stress responses following trauma can cause mitochondrial dysfunction and MQC imbalance, thereby exacerbating organ injury. Correcting MQC imbalance can improve organ function. Current researches on MQC in post-traumatic organ dysfunction mainly focuses on imbalance in specific MQC mechanism, lacking a systemic understanding of its incidence and progression. To this end, the authors reviewed the progress in researches on the impact of MQC imbalance on post-traumatic organ dysfunction, aiming to provide insights for clinical treatment.

Diabetic nephropathy(DN)ranks as a frequent and serious complication in diabetes mellitus,and it's a key factor in chronic kidney disease and end-stage renal disease(ESRD),greatly diminishing the life quality of patients.Presently,the conventional treatment approaches for DN mainly involve strict regulation of blood sugar and pressure,in conjunction with the application of renin-angiotensin-aldosterone system inhibitors.While these therapies can slow down the advancement of DN,they are ineffective in stopping its final development into ESRD.Lately,the involvement of the gut-kidney axis in the development and advancement of DN has attracted growing interest.Individuals suffering from DN show changes in the variety of gut microbiota,which are crucial in the development and management of DN due to metabolic interactions with the host.The goal of this analysis is to explore the fundamental processes of gut microbiota's role in DN and explore treatment approaches focusing on gut microbiota,aiming to offer new perspectives for the clinical handling of DN.

Diabetic nephropathy(DN)ranks as a frequent and serious complication in diabetes mellitus,and it's a key factor in chronic kidney disease and end-stage renal disease(ESRD),greatly diminishing the life quality of patients.Presently,the conventional treatment approaches for DN mainly involve strict regulation of blood sugar and pressure,in conjunction with the application of renin-angiotensin-aldosterone system inhibitors.While these therapies can slow down the advancement of DN,they are ineffective in stopping its final development into ESRD.Lately,the involvement of the gut-kidney axis in the development and advancement of DN has attracted growing interest.Individuals suffering from DN show changes in the variety of gut microbiota,which are crucial in the development and management of DN due to metabolic interactions with the host.The goal of this analysis is to explore the fundamental processes of gut microbiota's role in DN and explore treatment approaches focusing on gut microbiota,aiming to offer new perspectives for the clinical handling of DN.

Trauma can disrupt the body′s internal environment, resulting in organ dysfunction. This may manifest as symptoms such as acute respiratory distress, liver and kidney dysfunction, circulatory disorders and neurological damage. Mitochondrial quality control (MQC), encompassing processes like autophagy, dynamic changes, and biogenesis, plays an essential role in maintaining mitochondrial function. Stress responses following trauma can cause mitochondrial dysfunction and MQC imbalance, thereby exacerbating organ injury. Correcting MQC imbalance can improve organ function. Current researches on MQC in post-traumatic organ dysfunction mainly focuses on imbalance in specific MQC mechanism, lacking a systemic understanding of its incidence and progression. To this end, the authors reviewed the progress in researches on the impact of MQC imbalance on post-traumatic organ dysfunction, aiming to provide insights for clinical treatment.

BACKGROUND: Synovectomy has been introduced into total knee arthroplasty (TKA) with the aim of relieving pain and inflammation of the synovium. However, there are no long-term, comparative data to evaluate the effect of synovectomy in TKA. This study was aimed at assessing pain, function, and complications in patients undergoing synovectomy during TKA for osteoarthritis (OA) at long-term follow-up. METHODS: This was a prospective randomized controlled trial of 42 consecutive patients who underwent staged bilateral TKA. Patients undergoing the first-side TKA were allocated to receive TKA with or without synovectomy followed by a 3-month washout period and crossover to the other strategy for the opposite-side TKA. The overall efficacy of both strategies was evaluated by determination of blood loss, the Knee Society score (KSS), and knee inflammation conditions during a 3-month postoperative period. The postoperative pain, range of motion (ROM), and complications were sequentially evaluated to compare the two groups until 10 years after surgery. RESULTS: At the 10-year follow-up, both groups had a similarly significantly improved ROM (114.88 ± 9.84° vs. 114.02 ± 9.43°, t  = 0.221, P  = 0.815) and pain relief with no differences between the two groups (1.0 [1.0] vs. 1.0 [1.5], U  = 789.500, P  = 0.613). Similar changes in total blood loss, KSS, and knee inflammation were found in both groups during 3 months postoperatively ( P  > 0.05). Additionally, there was no significant difference regarding complications and satisfaction between the two groups ( P  > 0.05). CONCLUSIONS: Synovectomy in conjunction with TKA for primary OA does not seem to provide any benefit regarding postoperative pain, ROM, and satisfaction during a 10-year follow-up. In addition, it may not result in more blood loss and increased incidence of long-term complications. Based on our long-term findings, it should not be performed routinely. TRIAL REGISTRATION Chinese Clinical Trial Registry, ChiCTR-INR-16008245; https://www.chictr.org.cn/showproj.aspx?proj=13334 .
Humans ; Arthroplasty, Replacement, Knee/methods* ; Synovectomy/methods* ; Osteoarthritis, Knee/surgery* ; Prospective Studies ; Pain, Postoperative ; Inflammation/etiology* ; Range of Motion, Articular ; Knee Joint/surgery* ; Treatment Outcome ; Knee Prosthesis/adverse effects*

BACKGROUND: Cancer stem-like cells (CSCs) are a small subset of cells in tumors that exhibit self-renewal and differentiation properties. CSCs play a vital role in tumor formation, progression, relapse, and therapeutic resistance. B7-H3, an immunoregulatory protein, has many protumor functions. However, little is known about the mechanism underlying the role of B7-H3 in regulating gastric cancer (GC) stemness. Our study aimed to explore the impacts of B7-H3 on GC stemness and its underlying mechanism. METHODS: GC stemness influenced by B7-H3 was detected both in vitro and in vivo . The expression of stemness-related markers was examined by reverse transcription quantitative polymerase chain reaction, Western blotting, and flow cytometry. Sphere formation assay was used to detect the sphere-forming ability. The underlying regulatory mechanism of B7-H3 on the stemness of GC was investigated by mass spectrometry and subsequent validation experiments. The signaling pathway (Protein kinase B [Akt]/Nuclear factor erythroid 2-related factor 2 [Nrf2] pathway) of B7-H3 on the regulation of glutathione (GSH) metabolism was examined by Western blotting assay. Multi-color immunohistochemistry (mIHC) was used to detect the expression of B7-H3, cluster of differentiation 44 (CD44), and Nrf2 on human GC tissues. Student's t -test was used to compare the difference between two groups. Pearson correlation analysis was used to analyze the relationship between two molecules. The Kaplan-Meier method was used for survival analysis. RESULTS: B7-H3 knockdown suppressed the stemness of GC cells both in vitro and in vivo . Mass spectrometric analysis showed the downregulation of GSH metabolism in short hairpin B7-H3 GC cells, which was further confirmed by the experimental results. Meanwhile, stemness characteristics in B7-H3 overexpressing cells were suppressed after the inhibition of GSH metabolism. Furthermore, Western blotting suggested that B7-H3-induced activation of GSH metabolism occurred through the AKT/Nrf2 pathway, and inhibition of AKT signaling pathway could suppress not only GSH metabolism but also GC stemness. mIHC showed that B7-H3 was highly expressed in GC tissues and was positively correlated with the expression of CD44 and Nrf2. Importantly, GC patients with high expression of B7-H3, CD44, and Nrf2 had worse prognosis ( P = 0.02). CONCLUSIONS B7-H3 has a regulatory effect on GC stemness and the regulatory effect is achieved through the AKT/Nrf2/GSH pathway. Inhibiting B7-H3 expression may be a new therapeutic strategy against GC.
Humans ; Cell Line, Tumor ; Neoplasm Recurrence, Local ; NF-E2-Related Factor 2/metabolism* ; Proto-Oncogene Proteins c-akt/metabolism* ; Signal Transduction ; Stomach Neoplasms

Cholestatic liver disease is a common disease that causes bile flow dysfunction due to various reasons. The etiology of cholestatic liver disease is complexed, and therapeutic drugs are extremely limited. To date, ursodeoxycholic acid is the only FDA-approved drug for treating primary biliary cirrhosis, whereas its efficacy is limited to early stage of the disease, therefore novel drugs are urgently needed. Nuclear receptors become therapeutic hotspot target in cholestasis since these receptors play a key role in regulating bile acid homeostasis. Peroxisome proliferator-activated receptor (PPAR) is an important nuclear receptor involved in regulating multiple mechanisms of cholestasis in vivo. It can improve intrahepatic cholestasis by inhibiting bile acid synthesis, reducing bile acid toxicity, affecting the expression of bile acid metabolic enzymes and transporters, and can play an anti-inflammatory, anti-oxidation and anti-fibrosis role. A number of studies have shown that PPAR agonists represented by fibrates alone or in combination can improve liver function indexes, inflammatory factors and fibrosis markers in patients with cholestasis. This review analyzes and summarizes the lastest advances in the molecular mechanism of PPAR as a therapeutic target for cholestasis and drug treatment in development or have been used in clinical.

OBJECTIVE：To investigate the effects of gypenosides （GPs）on gene expression of major urinary proteins （Mups） in liver tissue of hypercholesterolemia model mice. METHODS ：C57BL/6J mice were divided into control （ND）group，model （HFD）group and GPs therapy （GP）group according to body weight （BW），with 11 mice in each group. Except for ND group ， other groups were given high-lipid diet to induce hypercholesterolemia model. From the 17th week of feeding ，ND group and HFD group were given constant volume of 0.1％CMC-Na solution intragastrically ；GP group were given GPs suspension （250 mg/kg） intragastrically，once a day ，for consecutive 22 weeks. BW ，the levels of blood glucose （BG）and blood lipid （TC，LDL-C）were detected in each group. Total RNA of liver tissue was extracted ，and reverse transcription library was constructed and RNA-seq sequencing was performed. The differentially expressed genes were screened by PCA ，volcano map and scatter plot. RT-qPCR was used for verification for differentially expressed genes. The correlation between the expression of differentially expressed genes and the above pharmacodynamic indexes was analyzed by bivariate analysis. RESULTS ：Compared with ND group ，BW，the levels of BG，TC and LDL-C in HFD group were increased significantly （P＜0.05）. Compared with HFD group ，above indexes of GP group were decreased significantly except for BW （P＜0.05）. PCA showed that the data of ND group and HFD group distributed in different quadrants ，and the data distribution of GP group was between above two groups. mRNA of Mup4，Mup5，Mup11，Mup15 and Mup21 in liver tissue of mice were increased significantly after treated with high-fat diet （P＜0.05）. mRNA of Mup3，Mup4， Mup5，Mup8，Mup12 and Mup21 were decreased significantly after treated with GPs （P＜0.05）. In ND group vs. HFD group and HFD group vs. GP group ，mRNA of Mup4，Mup5 and Mup21 genes changed significantly and the trend was opposite. Results of RT-qPCR verification showed that compared with ND group ，relative mRNA expression of Mup4，Mup5 and Mup21 gene were increased significantly in HFD group （P＜0.05）. Correlation analysis revealed that mRNA expression of Mup5 was positively correlated with the levels of TC and BG （r＝0.727 1，0.670 6，P＜0.05），mRNA expression of Mup4 and Mup21 were positively correlated with the level of BG （r＝0.737 8，0.721 5，P＜0.05）. CONCLUSIONS ：GPs can regulate the expression of Mups genes in liver tissue of hypercholesterolemia model mice ， and reduce glucose and lipid level through regulating the mRNA over-expression of Mup4，Mup5 and Mup21.

Objective:To investigate the relationship between painful tonic spasm (PTS) and spinal cord injury in patients with neuromyelitis optica spectrum disorder (NMOSD).Methods:The clinical data, serum AQP4-IgG antibody levels and magnetic resonance data of 138 patients with NMOSD were analyzed. Those with spinal cord involvement were assessed using the American Spinal Injury Association Impairment Scale (AIS) to investigate the relationship between PTS and spinal cord injury.Results:The prevalence of PTS among the NMOSD patients was 36% (51/138), and all of the 51 NMOSD patients with PTS showed spinal cord lesions, an incidence significantly different from those without PTS. However, there were no significant differences in the age of onset, gender, disease duration, AQP4-IgG levels, lesion location, range of spinal cord lesions, or AIS grade between the NMOSD patients with and without PTS.Conclusion:PTS is a prevalent concomitant of NMOSD. As a common symptom of remission and recurrent remission, PTS is associated with myelopathy. This study failed to find any correlation between PTS and the affected spinal cord site or segment range. There was also no correlation between PTS and AIS grading among these subjects.