Standardized clinical trial reporting is crucial for ensuring the scientific validity,reproducibility,and clinical translational value of reported results.The Consolidated Standards of Reporting Trials(CONSORT)statement,an internationally recognized guideline for randomized controlled trials(RCTs),has become an important reference standard for writing research papers in medicine since the 2010 version of CONSORT was published.With advancements in scientific research methodologies and the emergence of new forms of clinical trials,the CONSORT working group released an updated version in April 2025,published in journals such as The BMJ.Herein,we provide a systematic interpretation of the core revisions of CONSORT 2025,as well as a comparison with CONSORT 2010 to highlight the key differences.By providing practical,example-based recommendations,we aim to help domestic researchers apply the new guidelines efficiently,thereby improving the quality of clinical trial reports authored by domestic researchers.

A high-quality clinical trial protocol is the cornerstone for ensuring the scientific integrity and ethical compliance of a study.The Standard Protocol Items:Recommendations for Interventional Trials(SPIRIT)has become the international benchmark for developing clinical trial protocols since its release in 2013.To adapt to the developing trends of open science and patient-centered principles,the SPIRIT group completed a comprehensive update in 2025.While retaining its core structure,this updated guideline introduces a new open science module and incorporates several new elements,including patient and public involvement,trial monitoring,and data sharing,alongside substantial revisions of five pre-existing items.In this article,we critically examine the core revisions in SPIRIT 2025 and,through analysis of representative case studies,illustrate the practical application of the new reporting guideline in drafting trial protocols.Our goal is to to provide Chinese researchers with a valuable reference for understanding and implementing this new reporting guideline,thereby enhancing the quality and rigor of clinical trial protocols developed in the country.

BACKGROUND:In the process of intervening in the development of osteoarthritis,platelet-rich plasma plays an important role by intervening in autophagy,apoptotic cytokines and signal transduction pathways.OBJECTIVE:To summarize the structure of cytokines and signaling pathways involved in the diagnosis of osteoarthritis by platelet-rich plasma in recent years,as well as its correlation with chondrocyte apoptosis and autophagy,in order to provide effective targets for the future treatment of osteoarthritis.METHODS:Literature search was conducted in CNKI,WanFang Data,VIP,PubMed,Web of Science,and Medline databases using "platelet-rich plasma,chondrocyte,apoptosis,autophagy,osteoarthritis,cytokines,signaling pathway" as Chinese and English search terms.A systematic summary and induction were made for the 66 included articles.RESULTS AND CONCLUSION:Current research has shown that platelet-rich plasma can promote cartilage repair and assist bone tissue healing through various pathways,mainly divided into three aspects:(1) Platelet-rich plasma regulates the extension,closure,and maturation of microautophagosomes,promotes chondrocyte megaautophagy and molecular chaperone-mediated cell autophagy under specific conditions,enhances the expression of autophagy-related factors such as LC3Ⅱ/Ⅰ and Beclin1,inhibits the expression of P62/SQSTM1.Currently,there is no clear research directly exploring the specific effect of platelet-rich plasma on heat shock proteins,and further research is needed in this field in the future.(2) The various growth factors released by platelet-rich plasma inhibit the expression of pro-apoptotic factors Caspase,interleukin-1β,and tumor necrosis factor alpha,promote the expression of anti-apoptotic factor Bcl-2,and prevent chondrocyte apoptosis and degeneration.(3) By activating the PI3K/AKT/mTOR signaling pathway,NF-κB signal transduction pathway,death receptor pathway,mitochondrial stress pathway and other pathways,platelet-rich plasma inhibits the expression of Bax and Caspase,and prevents the release of cytochrome c,thereby inhibiting the death and necrotic apoptosis of chondrocytes.In general,platelet-rich plasma promotes cartilage repair,supports cartilage regeneration,and plays an anti-inflammatory role,and its biological effect in chondrocytes usually depends on the regulation of autophagy and apoptosis-related cytokines and signaling pathways.

BACKGROUND:In the process of intervening in the development of osteoarthritis,platelet-rich plasma plays an important role by intervening in autophagy,apoptotic cytokines and signal transduction pathways.OBJECTIVE:To summarize the structure of cytokines and signaling pathways involved in the diagnosis of osteoarthritis by platelet-rich plasma in recent years,as well as its correlation with chondrocyte apoptosis and autophagy,in order to provide effective targets for the future treatment of osteoarthritis.METHODS:Literature search was conducted in CNKI,WanFang Data,VIP,PubMed,Web of Science,and Medline databases using "platelet-rich plasma,chondrocyte,apoptosis,autophagy,osteoarthritis,cytokines,signaling pathway" as Chinese and English search terms.A systematic summary and induction were made for the 66 included articles.RESULTS AND CONCLUSION:Current research has shown that platelet-rich plasma can promote cartilage repair and assist bone tissue healing through various pathways,mainly divided into three aspects:(1) Platelet-rich plasma regulates the extension,closure,and maturation of microautophagosomes,promotes chondrocyte megaautophagy and molecular chaperone-mediated cell autophagy under specific conditions,enhances the expression of autophagy-related factors such as LC3Ⅱ/Ⅰ and Beclin1,inhibits the expression of P62/SQSTM1.Currently,there is no clear research directly exploring the specific effect of platelet-rich plasma on heat shock proteins,and further research is needed in this field in the future.(2) The various growth factors released by platelet-rich plasma inhibit the expression of pro-apoptotic factors Caspase,interleukin-1β,and tumor necrosis factor alpha,promote the expression of anti-apoptotic factor Bcl-2,and prevent chondrocyte apoptosis and degeneration.(3) By activating the PI3K/AKT/mTOR signaling pathway,NF-κB signal transduction pathway,death receptor pathway,mitochondrial stress pathway and other pathways,platelet-rich plasma inhibits the expression of Bax and Caspase,and prevents the release of cytochrome c,thereby inhibiting the death and necrotic apoptosis of chondrocytes.In general,platelet-rich plasma promotes cartilage repair,supports cartilage regeneration,and plays an anti-inflammatory role,and its biological effect in chondrocytes usually depends on the regulation of autophagy and apoptosis-related cytokines and signaling pathways.

BACKGROUND:In cartilage degeneration in osteoarthritis,cytokines and signaling pathways that target chondrocytes play an important role. OBJECTIVE:To review the latest research progress of osteoarthritis related cytokines and signaling pathways in recent years,such as the mechanism of action and treatment modalities,in order to provide a basis for future exploration of new therapeutic targets and modalities. METHODS:Literature search was conducted on CNKI,WanFang,VIP,PubMed,Web of Science,and Medline databases.Chinese search terms were"osteoarthritis,cytokines,signal pathway,chondrocyte,inflammation,treatment".Finally,60 papers were included for review. RESULTS AND CONCLUSION:(1)In current studies,it is believed that the specific mechanism of osteoarthritis is not clear,and a large number of studies have shown that osteoarthritis is strongly associated with cytokines and signaling pathways,which is a complex process of action.Relevant studies taking cytokines and signaling pathways as therapeutic breakthroughs are also the current hot spot.(2)The receptor antagonists of pro-inflammatory factors such as interleukin 1 are not effective in the treatment of osteoarthritis,and more studies turn to gene therapy.(3)The therapeutic methods of transforming growth factor β,recombinant factors of Wnt signaling pathway,gene therapy and mesenchymal stem cells have obtained positive research results.However,basic and clinical studies on safety and efficacy are likely to be conducted in future studies.(4)At present,relevant therapeutic methods such as platelet-rich plasma have been widely used in clinical practice,while recombinant factor,gene therapy and mesenchymal stem cell therapy are all in the research stage,among which mesenchymal stem cell therapy and gene therapy are expected to make breakthroughs in the field of cartilage repair and regeneration,and are worthy of expectation in the future.However,more clinical and basic studies are needed to verify its effectiveness and safety,explore its mechanism of action and scope of application,and set standards for its clinical use.

BACKGROUND:Studies have shown that posterior cruciate ligament injuries are associated with the anatomical morphology of the knee joint. OBJECTIVE:To explore anatomical morphological risk factors for posterior cruciate ligament injury. METHODS:The imaging data of 142 patients who visited Affiliated Hospital of Binzhou Medical University for knee joint problems from January 2015 to August 2022 were retrospectively analyzed.They were divided into posterior cruciate ligament injury group(n=71,including 49 males and 22 females)and posterior cruciate ligament intact group(n=71,including 49 males and 22 females).Intercondylar notch width,intercondylar notch height,bicondyle width,notch width index,angle of intercondylar notch,Blumensaat's line inlication angle,medial tibial spine height,lateral tibial spine height,tibial spine width,tibiofemoral consistency index,tibial plateau anterior-posterior diameter,medial tibial depth and patellar tendon-tibial shaft angle were measured on MRI images.Posterior tibial slope was measured on X-ray images.The above indicators were included in the logistic regression analysis for investigation. RESULTS AND CONCLUSION:(1)Univariate logistic regression analysis in men showed that tibial spine width,tibiofemoral consistency index,medial tibial depth,and posterior tibial slope were associated with posterior cruciate ligament injury(P<0.05).Multivariate binary logistic regression analysis showed that tibiofemoral consistency index and medial tibial depth were associated with posterior cruciate ligament damage(P<0.05).(2)Univariate logistic regression analysis in women showed that medial tibial spine height,lateral tibial spine height,tibial spine width,and posterior tibial slope were associated with posterior cruciate ligament injury(P<0.05).Multivariate binary logistic regression analysis showed that posterior tibial slope was associated with posterior cruciate ligament damage(P<0.05).(3)The receiver operating characteristic curve showed that tibiofemoral consistency index,medial tibial depth and posterior tibial slope had a certain predictive value on posterior cruciate ligament damage.(4)These findings suggest that anatomical morphological risk factors for posterior cruciate ligament injury differ between men and women,and tibial spine width and posterior tibial slope are common risk factors.In the male population,abnormal tibial spine width,tibiofemoral consistency index,medial tibial depth,and posterior tibial slope are easy to induce posterior cruciate ligament injury.In the female population,abnormal medial tibial spine height,lateral tibial spine height,tibial spine width,and posterior tibial slope are easy to induce posterior cruciate ligament injury.Clinicians can use the above risk factors to identify abnormal knee morphology,assess people at risk of posterior cruciate ligament injury,and provide preventive advice and guidance for treatment.

Tuberculosis (TB) is an ancient infectious disease. Before the availability of effective drug therapy, it had high morbidity and mortality. In the past 100 years, the discovery of revolutionary anti-TB drugs such as streptomycin, isoniazid, pyrazinamide, ethambutol and rifampicin, along with drug combination treatment, has greatly improved TB control globally. As anti-TB drugs were widely used, multidrug-resistant (MDR) and extensively drug-resistant (XDR) strains of Mycobacterium tuberculosis emerged due to acquired genetic mutations, and this now presents a major problem for effective treatment. Genes associated with drug resistance have been identified, including katG mutations in isoniazid resistance, rpoB mutations in rifampin resistance, pncA mutations in pyrazinamide resistance, and gyrA mutations in quinolone resistance. The major mechanisms of drug resistance include loss of enzyme activity in prodrug activation, drug target alteration, overexpression of drug target, and overexpression of the efflux pump. During the disease process, Mycobacterium tuberculosis may reside in different microenvironments where it is expose to acidic pH, low oxygen, reactive oxygen species and anti-TB drugs, which can facilitate the development of non-replicating persisters and promote bacterial survival. The mechanisms of persister formation may include toxin-antitoxin (TA) modules, DNA protection and repair, protein degradation such as trans-translation, efflux, and altered metabolism. In recent years, the use of new anti-TB drugs, repurposed drugs, and their drug combinations has greatly improved treatment outcomes in patients with both drug-susceptible TB and MDR/XDR-TB. The importance of developing more effective drugs targeting persisters of Mycobacterium tuberculosis is emphasized. In addition, host-directed therapeutics using both conventional drugs and herbal medicines for more effective TB treatment should also be explored. In this article, we review historical aspects of the research on anti-TB drugs and discuss the current understanding and treatments of drug resistant and persistent tuberculosis to inform future therapeutic development.
Humans ; Pyrazinamide/therapeutic use* ; Isoniazid/therapeutic use* ; Antitubercular Agents/therapeutic use* ; Tuberculosis, Multidrug-Resistant/microbiology* ; Mycobacterium tuberculosis/genetics* ; Tuberculosis/drug therapy* ; Rifampin/therapeutic use* ; Mutation ; Drug Resistance, Multiple, Bacterial/genetics*

Objective : To investigate the effects of dexmedetomidine on inflammatory factors and endoplasmic reticulum stress in myocardial ischemia reperfusion indu~ced brain injury. Methods : Twenty⁃four SPF⁃grade healthy male SD rats , weighing (200 220) g and aged (6 8) weeks , were divided into three groups (n = 8) by random number table method : sham operation group ( S group) myocardial ischemia reperfusion group ( IR group) and myocardial ischemia/reperfusion + Dex group (IR + Dex group) . After the rats were adapted to the feeding environment , the myocardial ischemia reperfusion injury model was established by ligating the anterior descending branch of the left coronary artery for 30 min and reperfusion for 120 min. At the beginning of reperfusion , IR + Dex group was given 25 μg/kg dexmedetomidine , S group and IR group were injected with equal volume normal saline. Rats were sacrificed by decapitation and brain tissue was taken and the changes of hippocampal cell structure of rats stained by HE were observed under light microscope. Serum inflammatory factors IL⁃6 , IL⁃8 and IL⁃10 were detected by ELISA. The expressions of Chop , Bip , p ⁃eif⁃2α and p ⁃perk in rat hippocampal tissues were determined by Western blot. Results : Compared with the S group , the IR group and the IR + Dex group showed aggravation of brain lesions , increased expression of inflammatory cytokines IL⁃6 and IL⁃8 (P < 0. 05) , and decreased expression of IL⁃10 ( P < 0. 05 ) . Hippocampal Chop , Bip , p ⁃eif⁃2α and p ⁃perk proteins were up⁃regulated ( P < 0. 05 ) . Compared with IR group , IR + Dex group showed reduced pathological injury , decreased expression of IL⁃6 and IL⁃8 (P < 0. 05) , increased expression of IL⁃10 (P < 0. 05) , and down⁃regulated expressions of Chop , Bip , p ⁃eif⁃2α and p ⁃perk in hippocampal tissues ( P < 0. 05 ) . Conclusion Dexmedetomidine preconditioning can reduce the brain injury caused by myocardial ischemia reperfusion , and its mechanism may be related to the inhibition of systemic inflammatory response and endoplasmic reticulum stress.

Objective:To evaluate the role of protein O-linked beta-N-acetylglucosaminylation (O-GlcNAcylation) modification in oxidative stress injury in nerve cells of mice subjected to oxygen-glucose deprivation and restoration (OGD/R).Methods:The standard mouse hippocampal neuron cell line was inoculated on a culture plate or dish at a density of 5×10 4 cells/ml and divided into 4 groups ( n=20 each) using a random number table method: normal group (N group), O-(connection)N-acetylglucosamine hydrolase (OGA) inhibitor Thiamet G group (T group), OGD/R group (D/R group) and Thiamet G+ OGD/R complex sugar group (T-D/R group). The cells were exposed to a mixed gas of 94% N 2-5% CO 2-1% O 2 for 6 h in a low-glucose medium, then medium was replaced with a common medium for restoring oxygen and glucose, and the cells were cultured for 12 h. Thiamet G at a final concentration of 1 mmol/L was added to the culture medium at 4 h before OGD/R in T-D/R group, and the medium was replaced with a medium containing Thiamet G at a final concentration of 1 mmol/L at 4 h before extraction of cellular proteins.After oxygen and glucose restoration was completed, the accumulation of cellular ROS was measured using DCFH-DA staining, mitochondrial membrane potential was measured using Jc-1 staining, O-GlcNAc modification was determined by immunofluorescence, and the expression of nuclear factor E2-related factor 2 (Nrf2), c-Jun N-terminal kinase (JNK), phosphorylated JNK (p-JNK), and p53 tumor suppressor gene (p53) was detected using Western blot. Results:Compared with group N, the expression of O-GlcNAc in nerve cells was significantly up-regulated in group T, and the accumulation of ROS in nerve cells was significantly increased, JC-1 monomer was increased, JC-1 polymer was decreased, Nrf2 expression was down-regulated, and the expression of p-JNK and p53 was up-regulated in group D/R, and the expression of O-GlcNAc in nerve cells was up-regulated, the accumulation of ROS was increased, the polymerization of JC-1 monomer and JC-1 was increased, Nrf2 expression was down-regulated, and the expression of p-JNK and p53 was up-regulated in group T-D/R ( P<0.05). Compared with group D/R, the expression of O-GlcNAc in nerve cells was significantly up-regulated, the accumulation of ROS was decreased, JC-1 monomer was decreased, JC-1 polymer was increased, the expression of Nrf2 was up-regulated, and the expression of p-JNK and p53 was down-regulated in group T-D/R ( P<0.05). Conclusion:When mouse nerve cells are subjected to OGD/R, the protein O-GlcNAc modification as an endogenous protective mechanism is enhanced, which can reduce oxidative stress injury, and the mechanism may be related to regulating the Nrf2-mediated JNK pathway.

Objective:To evaluate the relationship between silence information regulator 1 (SIRT1) and signal transducers and activators of transcription 3 (STAT3) acetylation during high glucose-induced cardiac microvascular endothelial cell injury.Methods:Cardiac microvascular endothelial cells of Sprague-Dawley rats were cultured.The cells at the logarithmic growth phase were selected and divided into 3 groups ( n=24 each) using a random number table method: control group (C group), high glucose group (HG group) and high glucose+ SIRT1 agonist SRT1720 group (HG+ SRT group). The cardiac microvascular endothelial cells were seeded in a 6- or 96-well cell culture plate at a density of 2×10 5 cells/ml.When the cell density reached 50%, the culture medium was then replaced with high-glucose (glucose 33 mmol/L) DMEM culture medium containing with 10% fetal bovine serum and 1% double antibody in HG and HG+ SRT groups.In group HG+ SRT, 20 μmol/L SRT1720 was added simultaneously, and the cells were cultured at 37 ℃ in an incubator with 5% CO 2 for 24 h. The cell viability was determined by CCK-8 assay, the activity of superoxide dismutase (SOD) was detected using a spectrophotometer, the levels of lactic dehydrogenase (LDH), interleukin-6 (IL-6) and tumor necrosis factor-β (TNF-β) in the supernatant were detected by enzyme-linked immunosorbent assay, and the expression of SIRT1, acetylated STAT3 (ac-STAT3) and phosphorylated STAT3 (p-STAT3) was determined by Western blot. Results:Compared with C group, the cell viability and SOD activity were significantly decreased, levels of LDH, IL-6 and TNF-β in the supernatant were increased, expression of SIRT1 was down-regulated, and expression of ac-STAT3 and p-STAT3 was up-regulated in group HG and group HG+ SRT ( P<0.05). Compared with group HG, the cell viability and SOD activity were significantly increased, levels of LDH, IL-6 and TNF-β in the supernatant were decreased, expression of SIRT1 was up-regulated, and expression of ac-STAT3 and p-STAT3 was down-regulated in group HG+ SRT ( P<0.05). Conclusion:SIRT1 can alleviate high glucose-induced cardiac microvascular endothelial cell injury by promoting STAT3 deacetylation.