ObjectivesTo evaluate the effects of Pulmonary Embolism Response Team (PERT) on treatment strategies and long-term prognosis in patients with acute pulmonary embolism before and after the implementation of the first PERT in China. Methods The official start of PERT (July 2017) was took as the cut-off point, all APE patients who attended Beijing Anzhen Hospital of Capital Medical University one year before and after this cut-off time were included through the hospital electronic medical record system. The APE patients who received traditional treatment from July 5, 2016 to July 4, 2017 were recruited in the control group (Pre-PERT group), and the APE patients who received PERT mode treatment from July 5, 2017 to July 4, 2018 were recruited as the intervention group (Post-PERT group). Treatment methods during hospitalization were compared between the two groups. The patients were followed up for one year after discharge to evaluate their anticoagulant therapy, follow-up compliance and long-term prognosis. Results A total of 108 cases in the Pre-PERT group and 102 cases in the Post-PERT group were included. There was no significant statistical difference between the two groups in age and gender (both P>0.05). Anticoagulation therapy (87.3% vs. 81.5%, P=0.251), catheter-directed treatment (3.9% vs. 2.8%, P=0.644), inferior vena cava filters (1.0% vs. 1.9%, P=1.000), surgical embolectomy (2.0% vs. 0.9%, P=0.613), systemic thrombolysis (3.9% vs. 4.6%, P=0.582) were performed in both groups with no significant differences between the two groups. The use rate of rivaroxaban in the Post-PERT group was higher than that in the Pre-PERT group at one year of discharge, and the use rate of warfarin was lower than that of the Pre-PERT group (54.5% vs. 32.5%; 43.6% vs. 59.0%, P=0.043). The anticoagulation time of the Post-PERT group was longer than that of the Pre-PERT group (11.9 months vs. 10.3 months, P<0.001). The all-cause mortality within one year, hemorrhagic events and the rate of rehospitalization due to pulmonary embolism were not significantly different between the two groups, (10.4% vs. 8.6%), (14.3% vs. 14.8%), and (1.3% vs. 2.5%, χ2=3.453, P=0.485), respectively. Conclusions APE treatment was still dominated by anticoagulation and conventional treatment at the early stage of PERT implementation, and advanced treatment (catheter-directed treatment and surgical embolectomy) is improved, it showed an expanding trend after only one year of implementation although there was no statistical difference. At follow-up, there is no increase in one-year all-cause mortality and bleeding events with a slight increase in advanced treatment after PERT implementation.
ObjectivesTo systematically review the influence of single-stent versus double-stent strategy for coronary bifurcation lesions prognosis.MethodsPubMed, The Cochrane Library, EMbase, Web of Science, CBM, WanFang Data, VIP and CNKI databases were searched online to collect randomized controlled trials (RCTs) of single-stent versus double-stent strategy for coronary bifurcation lesions from inception to March, 2017. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies, then, meta-analysis was performed by using Stata 12.0 software.ResultsA total of 23 RCTs involving 7 391 patients were included. The results of meta-analysis showed that: compared to the double-stent strategy, the single-stent strategy significantly reduced the myocardial infarction rate (RR=0.61, 95%CI 0.50 to 0.73, P<0.001). There were no significant differences between two groups in all cause mortality, cardiac mortality, main adverse coronary event (MACE), target lesion revascularization (TLR) and stent thrombosis. The results of subgroup analysis showed that: single-stent strategy for coronary bifurcation lesions was associated with lower all-cause mortality at five-years follow-up (RR=0.59, 95%CI 0.40 to 0.88,P=0.01).ConclusionsCurrent evidence shows that single-stent strategy for coronary bifurcation lesions could reduce the myocardial infarction rate and five-year mortality compared to double-stent strategy. Due to limited quality and quantity of the included studies, more high quality studies are needed to verify above conclusion.
Sepsis is a multiple organ dysfunction syndrome caused by a dysregulated host response to infection. The mortality rate remains high under current treatment methods, and there is an urgent need to explore new therapeutic targets. Ubiquitination modification, as a key posttranslational regulation mechanism of proteins, plays a central role in the occurrence and development of sepsis and multiple organ damage by regulating key pathological processes such as inflammatory response, cell death and barrier function. This article aims to systematically elucidate the molecular mechanism of ubiquitination modification system in sepsis related organ damage, summarize the latest research progress on treatment strategies targeting the ubiquitination pathway, and explore the challenges and future transformation directions faced in this field. Through comprehensive analysis of existing research, this review aims to provide new ideas and theoretical basis for precise treatment of sepsis.
ObjectiveTo summarize the clinical morphological classification feature of symptomatic spontaneous isolated celiac artery dissection (SICAD), basing on the relative diameter of the true lumen (TLRD) and type of lesion, and then summarize the reasonable clinical treatment strategies and timing of arterial reconstruction.MethodsRetrospectively analyzed the imaging data, treatment methods, perioperative complications, and follow-up results of 26 symptomatic SICAD patients admitted to the Department of Endovascular Surgery of The First Affiliated Hospital of Zhengzhou University from May 2012 to May 2019, patients were divided into conservative treatment group (n=12) and endovascular intervention group (n=14) according the treatment, and then compared the clinical data of the two groups.ResultsTwelve patients in the conservative treatment group had an average of 12.6 days (5–22 days) and discharged from hospital with better condition, of which 11 patients’ TLRD≥30%. In the endovascular intervention group, 2 patients continued to aggravate the symptoms at the 3rd day of admission and received endovascular intervention, the remaining 12 patients’ symptoms were not significantly relieved or the symptoms reappeared after averaged 11.4 days, whose TLRD<30% or diameter >1.5 cm. Compared with the endovascular intervention group, the duration of symptoms was shorter (P=0.04), proportions of back pain (P=0.02) and chest pain (P=0.04) were lower, TLRD value and proportion of TLRD value>30% (subtype of a) were higher (P=0.01, P=0.02). The average follow-up duration of 26 patients was 28.2 months (12–83 months). The follow-up results of all patients in the conservative treatment group were good and no relevant symptoms had appeared since discharge. One patient in the endovascular intervention group had transient liver function damage, 1 patient had severe deformation of the proximal end of the stent at 1 year after implantation of the celiac artery stent. The remaining patients were stable with no progress.ConclusionsFor symptomatic SICAD, if the clinical symptoms are stable after hospitalization, conservative medication and close imaging follow-up are preferred, if there is no relief of symptoms, continuous organ perfusion and other manifestations based on medication, endovascular intervention can be considered for arterial reconstruction, the early and medium follow-up results were satisfactory under this treatment algorithm. In addition, there are differences in TLRD value between the conservative treatment group and the endovascular intervention group, suggesting that TLRD as the morphological characteristics of the classification has a potential guiding significance for the development of clinical treatment strategy.
Acute kidney injury (AKI), as a complex and severe kidney disease, has always been the hotspot of research. The epidemiological research of AKI in China has made significant progress, including initially reports on the domestic incidence of AKI, geographical distribution and risk factors; however, accompanying challenges like AKI prevention and treatment emerge. For improvement of the diagnosis and treatment of the AKI, this article summarizes and analyses the two challenges: early warning biomarkers and AKI treatment strategies, based on new ideas and research progress. The aim is to make Chinese nephrology scholars and specialists realize the focus of AKI prevention and protection of renal function, to standardize the treatment strategy of AKI, and to put forward the direction of future research.
ObjectiveTo elucidate the correlation between radiological tumor size (RTS) and pathological tumor size (PTS), and to evaluate the accuracy of clinical T staging. Methods Data on patients who underwent complete resection between September 2018 and June 2019 were retrospectively collected. The correlation between RTS and PTS was analyzed by and we assessed the agreement between clinical and pathologic T staging. Results Finally, 1 880 patients were included. There were 778 males and 1 102 females at average age of 57±11 years. In the entire cohort, the RTS and PTS was 19.1±13.5 mm and 17.7±14.0 mm, respectively (P<0.001). The RTS and PTS showed a strong linear correlation with the Pearson’s correlation coefficient calculated as 0.897. The mean RTS was significantly larger than PTS (P<0.001) in tumors≤3 cm, but significantly smaller in tumors>4 cm. The overall concordance rate between clinical and pathological T staging was 65.6%. Clinical staging failed to detect T4 disease in 29.4% (5/17) of patients. Male patients and the presence of cavities within nodules were independent significant factors leading to inaccurate clinical T staging. Conclusions The correlation between the tumor sizes measured on thin-section computed tomography and pathologic specimens varies with the real tumor size. Methods and techniques for improving clinical T staging accuracy is in urgent need.
Mast cell (MC) play a crucial role in non-allergic fundus diseases, including uveitis, diabetic retinopathy, and age-related macular degeneration. MCs can profoundly influence the pathological processes of these diseases by regulating inflammatory responses, promoting angiogenesis, and facilitating tissue remodeling through the degranulation and release of mediators such as histamine, cytokines, and enzymes. The application of MC-associated inhibitors has been shown to effectively mitigate or inhibit the progression of these pathologies, offering a promising strategy for treating ocular diseases. Understanding the current state of MC research in fundus diseases will enhance our insight into their role in the pathophysiological mechanisms of these conditions and encourage further research aimed at providing more effective treatment options for patients.
ObjectiveTo systematically elucidate the resistance mechanism of targeted drug therapy for breast cancer and to discuss future direction of optimized treatment strategies. MethodA literature review on targeted therapy for breast cancer had been conducted based on recent domestic and international research. ResultsContemporary breast cancer targeted therapies mainly comprised human epidermal growth factor receptor 2 (HER2)-directed agents, CDK4/6 inhibitors, phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin pathway blockers, poly (ADP-ribose) polymerase inhibitors, and immune checkpoint modulators, etc. While these agents had conferred subtype-specific survival benefits, resistance developed through target mutations, compensatory signaling, epigenetic alterations, drug efflux pumps, among other mechanisms. Emerging strategies for reversing drug resistance included dual-targeted approaches (such as trastuzumab in combination with pertuzumab), dynamic monitoring of drug-resistant gene mutations by liquid biopsy, epigenetic modulators, etc. ConclusionsDrug resistance remains a key bottleneck limiting long-term efficacy of breast cancer targeted therapy. Future research should integrate multi-omics approaches to decipher tumor heterogeneity, implement combinatorial multi-target inhibition with real-time monitoring of multidimensional interventions, and leverage artificial intelligence to predict resistance evolution. This integrated strategy is expected to enable personalized combination therapies, ultimately overcoming drug resistance and improving patient survival outcomes.
ObjectiveTo summarize a comprehensive overview of the mechanism of ferroptosis and its associated microRNAs in the occurrence and development of hepatocellular carcinoma (HCC), and to offer novel insights and potential avenues for tumor marker screening and targeted treatment in clinical hepatocellular carcinoma patients. MethodThe literatures on the basic and clinical application research of ferroptosis and related microRNA in the occurrence, development and prognosis of HCC at home and abroad in recent years were reviewed and summarized, and the research progress of microRNA regulating ferroptosis in HCC was summarized. ResultsMicroRNA, a type of non-coding small RNA, had the ability to regulate gene expression at the post-transcriptional and translational levels. It held promising potential in the diagnosis and treatment of HCC. Ferroptosis, on the other hand, was a form of cell death triggered by iron-dependent lipid peroxidation. It played a crucial role in the development of HCC. A series of miRNAs related to ferroptosis might act as HCC growth regulators to regulate the growth of cancer cells, or reverse the drug resistance of cancer cells, thereby promoting or inhibiting the occurrence and progression of HCC. ConclusionsMicroRNA can regulate the occurrence and development of HCC through the ferroptosis pathway and may become tumor markers for the early diagnosis of HCC. Additionally, microRNA may also serve as a related therapeutic target and provide a new treatment option for HCC.