The 9th edition TNM staging system refines N2 subclassification into single-station (N2a) and multi-station (N2b) metastases, leading to substantial stage migration within the previously heterogeneous stage IIIA category. While the 9th edition has demonstrated improved overall prognostic performance, it remains unclear whether the newly defined stage IIIA category is prognostically homogeneous. This study aimed to address this question in a real-world cohort of resected occult N2 NSCLC. Data of NSCLC patients who underwent surgery at the Department of Thoracic Surgery, Fourth Hospital of Hebei Medical University from January 2014 to December 2017 were retrospectively analyzed. Patients were staged according to the 8th and 9th editions of the AJCC TNM guidelines. Kaplan-Meier analysis was used to assess the impact of clinicopathological factors on survival, and Cox regression analysis was performed for multivariate analysis. The Receiver Operating Characteristic (ROC) curve was utilized to evaluate the predictive performance of the two TNM staging systems. A retrospective study analyzed 550 T1-4N2M0 NSCLC patients post-surgery. 262 (47.6
INTRODUCTION:Hydroxysteroid 17-beta dehydrogenase 4 (HSD17B4) is involved in the progression of hepatocellular carcinoma (HCC). AIMS:This study aimed to investigate the inhibitory effect of gamma-tocotrienol (γ-T3) on the proliferation and growth of HSD17B4-overexpressing HepG2 cells. METHODS:HepG2 cells were transfected with empty or HSD17B4-overexpressing plasmids, followed by vitamin E (VE) or γ-T3 treatment. MTS assay, Western blotting, qRT-PCR, and flow cytometry were employed to assess cell proliferation, protein expression, mRNA levels, and apoptosis. HSD17B4 interaction with γ-T3 was assessed by quantifying γ-T3 in the collected precipitate of HSD17B4 using anti-flag magnetic beads. Tumor xenografts were established in NSG mice, and tumor growth was monitored. RESULTS:HSD17B4 overexpression significantly promoted HepG2 cell proliferation, which was effectively counteracted by VE or γ-T3 treatment in a dose-dependent manner. VE and γ-T3 did not exert their effects through direct regulation of HSD17B4 expression. Instead, γ-T3 was found to interact with HSD17B4, inhibiting its activity in catalyzing the conversion of estradiol (E2) into estrone. Moreover, γ-T3 treatment led to a reduction in cyclin D1 expression and suppressed key proliferation signaling pathways, such as ERK, MEK, AKT, and STAT3. Additionally, γ-T3 promoted apoptosis in HSD17B4-overexpressing HepG2 cells. In an in vivo model, γ-T3 effectively reduced the growth of HepG2 xenograft tumors. CONCLUSION:In conclusion, our study demonstrates that γ-T3 exhibits potent anti-proliferative and anti-tumor effects against HepG2 cells overexpressing HSD17B4. These findings highlight the therapeutic potential of γ-T3 in HCC treatment and suggest its role in targeting HSD17B4-associated pathways to inhibit tumor growth and enhance apoptosis.
Epigenetic modifications of chromatin, including histone acetylation, and tumor angiogenesis play pivotal roles in creating an immunosuppressive tumor microenvironment. In the randomized phase 2 CAPability-01 trial, we investigated the potential efficacy of combining the programmed cell death protein-1 (PD-1) monoclonal antibody sintilimab with the histone deacetylase inhibitor (HDACi) chidamide with or without the anti-vascular endothelial growth factor(VEGF) monoclonal antibody bevacizumab in patients with unresectable chemotherapy-refractory locally advanced or metastatic microsatellite stable/proficient mismatch repair (MSS/pMMR) colorectal cancer. Forty-eight patients were randomly assigned to either the doublet arm (sintilimab and chidamide, n=23) or the triplet arm (sintilimab, chidamide and bevacizumab, n=25). The primary endpoint of progression-free survival (PFS) rate at 18 weeks (18wPFS rate) was met with a rate of 43.8% (21 of 48) for the entire study population. Secondary endpoint results include a median PFS of 3.7 months, an overall response rate of 29.2% (14 of 48), a disease control rate of 56.3% (27 of 48) and a median duration of response of 12.0 months. The secondary endpoint of median overall survival time was not mature. The triplet arm exhibited significantly improved outcomes compared to the doublet arm, with a greater 18wPFS rate (64.0% versus 21.7%, P=0.003), higher overall response rate (44.0% versus 13.0%, P=0.027) and longer median PFS rate (7.3 months versus 1.5 months, P=0.006). The most common treatment-emergent adverse events observed in both the triplet and doublet arms included proteinuria, thrombocytopenia, neutropenia, anemia, leukopenia and diarrhea. There were two treatmentrelated fatalities (hepatic failure and pneumonitis). Analysis of bulk RNA sequencing data from the patients suggested that the triplet combination enhanced CD8+ T cell infiltration, resulting in a more immunologically active tumor microenvironment. Our study suggests that the combination of a PD-1 antibody, an HDACi, and a VEGF antibody could be a promising treatment regimen for patients with MSS/pMMR advanced colorectal cancer. ClinicalTrials. gov registration: NCT04724239.
Highest mediastinal lymph node (HMLN) involvement is a category of uncertain resection, yet the prognostic significance of HMLN involvement remains controversial. A total of 486 patients with pathological stage III-N2 disease who underwent radical resection were enrolled from January 2015 to December 2018. Patients were allocated into two groups—HMLN involvement (219 cases) and HMLN-negative (249 cases) groups. Kaplan–Meier analysis and Cox proportional hazard regression models were used to evaluate the impact of HMLN involvement on 5-year recurrence-free survival (RFS) and overall survival (OS). The proportion of patients with multiple N2 diseases (72.1
Lung cancer remains a leading cause of cancer-related deaths globally, with its incidence steadily rising each year, representing a significant threat to human health. Early detection, diagnosis, and timely treatment play a crucial role in improving survival rates and reducing mortality. In recent years, significant and rapid advancements in artificial intelligence (AI) technology have found successful applications in various clinical areas, especially in the diagnosis and treatment of lung cancer. AI not only improves the efficiency and accuracy of physician diagnosis but also aids in patient treatment and management. This comprehensive review presents an overview of fundamental AI-related algorithms and highlights their clinical applications in lung nodule detection, lung cancer pathology classification, gene mutation prediction, treatment strategies, and prognosis. Additionally, the rapidly advancing field of AI-based three-dimensional (3D) reconstruction in lung cancer surgical resection is discussed. Lastly, the limitations of AI and future prospects are addressed.
PBX/knotted 1 homeobox 2 (PKNOX2) has been implicated in tumorigenesis; however, its role in lung cancer (LC) remains unknown. The present study thus aimed to examine the expression, regulation, function and clinical implication of PKNOX2 in LC. A series of experiments were performed, including Cell Counting Kit-8 assay, cell cycle analysis, wound-healing assay, Transwell assay, methylation-specific PCR and western blotting. Bioinformatics analysis revealed that PKNOX2 was a LC-related gene, and a decrease in its expression was found in LC tissues from three public datasets. The results of reverse transcription-quantitative PCR assays also confirmed that PKNOX2 mRNA expression was markedly downregulated in LC tissues (n=60, P<0.01) and in five types of LC cell lines, and this was associated with the promoter methylation of PKNOX2. In addition, PKNOX2 expression was significantly associated with tumor invasion (P<0.0001), lymph node metastasis (P=0.0057) and TNM stage (P=0.0003); however, it was not associated with sex, age, pathological type or distant metastasis. The data obtained in vitro demonstrated that PKNOX2 silencing promoted LC cell proliferation and inhibited cell cycle arrest, accompanied by an increase in the expression levels of cell cycle-related proteins (cyclinD1, cyclinE1, CDK2 and CDK4), whereas PKNOX2 overexpression exhibited the opposite trend. In addition, PKNOX2 inhibited the migration and invasion of LC cells. Mechanistically, PKNOX2 knockdown activated the PI3K/AKT/mTOR signaling pathway by accelerating the phosphorylation of PI3K, AKT and mTOR, whereas PKNOX2 overexpression inactivated this signaling pathway. In conclusion, the findings of the present study suggested that PKNOX2 may suppress LC cell proliferation by inhibiting the PI3K/AKT/mTOR axis.
Objective:To compare the gait characteristics of cognitive and motor dual task walking (DTW) in patients with cerebral small vessel disease (CSVD), and determine the best gait parameters to diagnose CSVD and judge the severity of the disease.Methods:A total of 106 patients with CSVD and 21 healthy individuals were included from September 1, 2020 to July 1, 2021 in the Seventh Medical Center of Chinese People′s Liberation Army General Hospital. According to the Fazekas scores, the subjects were divided into mild ( n=34, 1 point), moderate ( n=34, 2 points), severe ( n=38,3 points) groups and control group ( n=21). Participants were recorded parameters under single task walking (STW) and DTW conditions, and calculated dual task effect (DTC) through the difference between single task and dual task. The differences in gait variances and their DTC were shown by generalized estimation equations when performed in STW and DTW and 4 groups of the severity of disease. Post-hoc comparisons were corrected using Bonferroni′s method. Spearman analyses were applied to explore the correlations between gait parameters and their DTC during STW or DTW and severity of disease. Based on the Logistic model, combining predictors or probabilities were gained and applied to establish receiver operating characteristic curve in order to calculate sensitivity, specificity, and the area under the curve. Results:In the control group, there was no statistically significant difference in gait parameters between STW and DTW. In the CSVD group, the gait parameters of STW were significantly better than cognitive or motor DTW (all P<0.05). In the control group, there was no statistically significant difference in basic gait parameters under different tasks (all P>0.05). In cognitive DTW, temporal gait parameters (stride frequency and stride time) deteriorated significantly only in moderate and severe groups [stride frequency:moderate group 100.220±1.795/min,severe group 94.525±2.139/min;stride time:moderate group (1.227±0.024) s, severe group (1.299±0.031) s], but spatial parameters [stride length: control group (1.050±0.021) m, mild group (0.974±0.022) m, moderate group (0.903±0.025) m, severe group (0.793±0.026) m; stride speed: control group (0.944±0.028) m/s, mild group (0.866±0.030) m/s, moderate group (0.751±0.027) m/s, severe group (0.606±0.022) m/s] were significantly different among all groups (except the control group and mild group;all P<0.05). The DTC of all gait parameters during cognitive DTW was higher than that during motor DTW (all P<0.05) for CSVD patients. While no any difference was found between cognitive DTW and motor DTW in the control group (all P>0.05). Similarly, the temporal parameters′ DTC of cognitive DTW was abnormal only in the late stage of disease, while the spatial parameters′ DTC showed statistically significant difference among all the groups (including the control group and the mild group;all P<0.05). Correlation coefficients of the spatial parameters and their DTC in condition of cognitive DTW were significantly higher than temporal parameters and their DTC (0.50< r<0.64 vs 0.15< r<0.39). The area under curve of the combined predictor was significantly higher than that of any single index. Conclusions:Cognitive DTW can better reflect the abnormal gait of CSVD patients. The spatial parameters and DTC of cognitive DTW could effectively diagnose CSVD and distinguish the disease of severity. And DTC might be better indicators. For diagnosis of CSVD, there was no significant discrepancy between the spatial parameters and DTC, but the combined predictor could significantly improve the sensitivity and reduce the false negative rate.
Background Lymph node dissection is essential for staging of pure solid lung adenocarcinoma and selection of treatment after surgical resection, particularly for stage I disease since the rate of lymph node metastasis can vary from 0 to 23.7%. Methods We retrospectively screened all adult patients (18 years of age or older) who underwent lobectomy for pure solid cT1N0M0 lung adenocarcinoma between January 2015 and December 2017 at our center. Cox proportional hazard regression was used to assess the association between the number of dissected lymph nodes and recurrence-free survival (RFS) and to determine the optimal number of dissected lymph nodes. Results The final analysis included 458 patients (age: 60.26 ± 8.07 years; 241 women). RFS increased linearly with an increasing number of dissected lymph nodes at a range between 0 and 9. Kaplan-Meier analysis revealed significantly longer RFS in patients with ≥ 9 vs. <9 dissected lymph nodes. In subgroup analysis, ≥ 9 dissected lymph nodes was not only associated with longer RFS in patients without lymph node metastasis (n = 332) but also in patients with metastasis (n = 126). In multivariate Cox proportional hazard regression, ≥ 9 dissected lymph nodes was independently associated with longer RFS (hazard ratio [HR], 0.43; 95% confidence interval [CI], 0.26 to 0.73; P = 0.002). Conclusions ≥9 Dissected lymph nodes was associated with longer RFS; accordingly, we recommend dissecting 9 lymph nodes in patients undergoing lobectomy for stage IA pure solid lung adenocarcinoma.
Gastric cancer is a common gastrointestinal malignancy worldwide, with a high mortality rate and poor prognosis. Multidrug resistance remains a major obstacle to successful treatment for patients. Hence, it is of great significance to develop novel therapies to potentiate the anti-tumor effect. In this study, we have investigated the effect of estradiol cypionate (ECP) on gastric cancer in vitro and vivo. Our data show that ECP inhibited the proliferation, promoted apoptosis, and caused G1/S phase arrest of gastric cancer cells. The mechanism by which ECP promoted apoptosis of gastric cancer cells was related to the downregulation of AKT protein expression caused by the increased ubiquitination modification levels of AKT, which finally inhibited the over-activation of the PI3K-AKT-mTOR signaling pathway. In vivo tumorigenesis experiments showed that ECP significantly inhibited the growth of gastric cancer cells, showing promise for clinical application. The above findings indicate that ECP inhibited the growth of gastric cancer and induced apoptosis through the PI3K /Akt/mTOR pathway. In summary, the efficacy showed in our data suggests that ECP is a promising anti-tumor compound for gastric cancer.
目的 研究脑小血管病患者影像学标志物与跌倒风险之间的关系.方法 纳入2020年9月至2021年12月在解放军总医院第七医学中心神经内科住院的脑小血管病患者142例,分为有跌倒风险组58例和无跌倒风险组84例.所有患者行影像学标志物分析,包括脑白质高信号、腔隙性脑梗死、脑微出血,采用唐顿跌倒风险指数(DFRI)进行跌倒风险评估,DFRI≥3分为有跌倒风险.采用logistic回归分析法研究DFRI与神经影像标志物的相关性.结果 有跌倒风险组与无跌倒风险组年龄、性别、受教育年限、心绞痛、心肌梗死、糖尿病以及偏头痛比较,差异无统计学意义(P>0.05).有跌倒风险组高血压、高脂血症、中重度脑白质高信号比例明显高于无跌倒风险组(82.8%vs 48.8%,84.5%vs 56.0%,75.9%vs 41.7%,P<0.01).2组脑小血管病总负荷评分比较,差异有统计学意义(P<0.01).2组脑微出血和腔隙性脑梗死比例比较,差异无统计学意义(P>0.05).校正高血压、高脂血症等有意义的混杂因素后,中重度脑白质高信号是DFRI升高的危险因素(OR=4.136,95%CI:1.299~13.169,P=0.016).结论 对于脑小血管病患者而言,脑白质高信号的严重程度更能预测患者的跌倒风险.
背景 程序性死亡受体配体1(programmed?cell?death?1?ligand?1,PD-L1)和微卫星不稳性(microsatellite?instability,MSI)的表达被认为能够有效评估晚期胃癌(advanced?gastric?cancer,AGC)患者免疫治疗预后.但目前仍没有公认且有效的生物标志物可以识别AGC免疫治疗的受益人群.目的 探讨衍生中性粒细胞与淋巴细胞比率(derived?neutrophil-to-lymphocyte?ratio,dNLR)与AGC免疫治疗预后的关系.方法 纳入2014年12月-?2018年11月解放军总医院肿瘤中心学部接受免疫治疗的123例AGC患者.根据国外大型临床研究选取dNLR=3为临界值,分析不同dNLR水平组AGC患者免疫治疗后的中位总生存(overall?survival,OS)和中位无进展生存(progression-free?survival,PFS).采用Kaplan-Meier和Cox比例风险回归模型进行生存分析.结果 AGC患者中位年龄58岁,女性31例,男性92例.中位OS为9.4个月,中位PFS为3.8个月.dNLR高水平组中位PFS为4.6个月,dNLR低水平组为2.6个月(HR:1.952,95%?CI:1.248?~?3.053,P=0.008).dNLR高水平组OS为11.2个月,dNLR低水平组为4.8个月(HR:0.59,95%?CI:1.691?~?4.188,P<0.001).dNLR高、低水平组的客观缓解率(25.0%?vs?24.2%,P=0.932)、疾病控制率(46.4%vs?48.4%,P=0.853)差异无统计学意义.结论 治疗前dNLR水平是独立预测AGC患者免疫治疗后PFS和OS的生物标志物.基线dNLR低水平组患者或许可以从免疫治疗中获益.
Objective:To study the combined use of neoadjuvant chemotherapy and immunotherapy in patients with borderline resectable pancreatic cancer.Methods:The clinical data of patients with pancreatic cancer who were planned to undergo perioperative treatment before surgical treatment at the Fifth Medical Center of PLA General Hospital from January 2019 to June 2021 were retrospectively studied. Of 22 patients with pancreatic cancer, there were 10 males and 12 females, aged (56.0±10.2) years old. Preoperative treatment with chemotherapy (nab-paclitaxel and S-1, AS) and immunotherapy regimen before surgery were given. The baseline characteristics, treatment efficacy, surgical pathology and prognosis were analyzed.Results:Of 22 patients who were treated with neoadjuvant chemotherapy combined with programmed death-1 (PD-1) monoclonal antibody, 11 patients (50%) had tumors in the head, neck and uncinated process of pancreas. On radiographic assessment, one patient achieved CR (4.5%, 1/22), 9 patients PR (40.9%, 9/22), and 11 patients SD (50.0%, 11/22). All patients subsequently underwent R 0 resection. The postoperative pTNM staging showed 91% (20/22) of patients were in stage IA-IIB, 31.8% (7/22) of patients had pT2, 63.6% (14/22) had N0, and 1 patient had pCR. Thirteen patients (54.2%, 13/22) received postoperative adjuvant therapy. The median recurrence-free survival (RFS) was 6.4 months and the median time to progression (TTP) was 12.8 months. The median overall survival of patients was not reached. Postoperative pathology TNM staging IIA to III ( HR=3.63, 95% CI: 1.18-11.20, P=0.025) and postoperative pathology T2-3 stage ( HR=2.02, 95% CI: 1.01-5.05, P=0.049) were significantly associated with RFS. Postoperative pathology TNM stages IIA to III ( HR=2.39, 95% CI: 1.04-5.50, P=0.041) and postoperative pathology T2-3 stage ( HR=2.53, 95% CI: 1.26-5.09, P=0.009) were significantly associated with TTP. Conclusion:AS combined with PD-1 monoclonal antibody showed good efficacy as a neoadjuvant therapy for patients with borderline-resectable pancreatic cancer.
Increasing evidence from epidemiological studies indicate that Alzheimer's disease (AD) has a negative relationship with the incidence of cancers. Whether the Alzheimer's genetic risk factor, named as fermitin family homolog-2 (FERMT2), plays a pivotal part in the progressive process of colorectal carcinoma (CRC) yet remains unclear. This study revealed that FERMT2 was upregulated in CRC tissues which predicted an unfavorable outcome of CRC using the PrognoScan web tool. FERMT2 was co-expressed with a variety of genes have been linked with CRC occurrence and implicated in the infiltration of immune cell in CRC tissues. Overexpressing FERMT2 promoted CRC progression with upregulation of Wnt/β-catenin signaling. Knockdown of FERMT2 suppressed the cell multiplication, colony formation rate, migration and invasion, along with the epithelial to mesenchymal transition (EMT) with downregulation Wnt/β-catenin proteins in cells of CRC, while overexpressing β-catenin reversed the inhibitory effects of silencing FERMT2 on the migration or invasion of CRC cells. Furthermore, Aβ1-42 treated HT22 cells induced downregulation of FERMT2 and inhibited the migration, invasion and EMT in co-cultured CT26 cells through Wnt/β-catenin signaling. Our results revealed that the downregulated FERMT2 gene during AD is prominently activated in CRC, which promotes its progression via Wnt/β-catenin pathway.
BACKGROUND:Circular RNAs (circRNAs) can act as key regulators in human cancers, including esophageal squamous cell carcinoma (ESCC). However, the role and mechanism of circ_0005231 in ESCC have not previously been reported. METHODS:RNA levels and protein levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot assay, respectively. Cell proliferation was assessed by colony formation assay and 5-ethynyl-2'-deoxyuridine (EdU) assay. Wound healing and transwell assays were used to assess cell migration and invasion, respectively. The intermolecular interaction was predicted by bioinformatic analysis and verified by RNA immunoprecipitation (RIP), RNA pulldown and dual-luciferase reporter assays. Xenograft tumor model was used for exploring the biological function of circ_0005231 in vivo. RESULTS:Circ_0005231 was upregulated in ESCC plasma, tissues and cells. Cell proliferation, migration and invasion were significantly restrained by knockdown of circ_0005231 in ESCC cells. Circ_0005231 acted as a sponge of miR-383-5p, and circ_0005231 regulated ESCC cellular behavior by sponging miR-383-5p. Moreover, miR-383-5p directly targeted KIAA0101, and circ_0005231 positively regulated KIAA0101 expression by sponging miR-383-5p. Furthermore, circ_0005231 knockdown suppressed the malignant behavior of ESCC cells by downregulating KIAA0101. Importantly, knockdown of circ_0005231 blocked xenograft tumor growth in vivo. CONCLUSION:Circ_0005231 acted as a sponge of miR-383-5p to promote ESCC progression by upregulating KIAA0101, which provided a potential therapeutic strategy for ESCC treatment.
背景 胃癌伴2型糖尿病患者行远端胃切除术后,哪种重建方式短期疗效更好尚不明确.目的 比较远端胃切除BillrothⅠ(B-Ⅰ)与Roux-en-Y(R-Y)两种重建方式对胃癌伴2型糖尿病患者术后短期疗效的影响.方法 回顾性分析2010年1月-2020年12月在解放军总医院第一医学中心行远端胃切除的259例胃癌伴2型糖尿病患者的临床资料,其中B-Ⅰ组109例,R-Y组150例,采用倾向性评分匹配的方法 平衡两组间变量,以手术时间、术后住院时间、术后早期并发症发生率等为结局指标对比两种重建方式的短期疗效.结果 经倾向性评分匹配后共有170例纳入后续分析,其中B-Ⅰ组和R-Y组各85例,匹配后两组术前临床资料和病理资料的差异均无统计学意义(P>0.05).R-Y组手术时间长于B-Ⅰ组[Md(IQR):210(184,242.5)min vs 190(164,235)min,P=0.028],术后住院时间长于B-Ⅰ组[Md(IQR):10(8,12.5)d vs 9(7,11.5)d,P=0.023],Ⅱ级以上术后早期并发症发生率高于B-Ⅰ组[41.2%(35/85)vs 20.0%(17/85),P=0.003],术后胃瘫发生率高于B-Ⅰ组[15.3%(13/85)vs 4.7%(4/85),P=0.021].两组术后第1?3?5?7天的晨起空腹血糖差异均无统计学意义(P>0.05).结论 胃癌伴2型糖尿病患者行远端胃切除术后,与R-Y重建相比,B-Ⅰ重建能够缩短手术时间?加快术后恢复,B-Ⅰ重建在降低Ⅱ级以上术后早期并发症发生率?术后胃瘫的发生率方面更有优势.
目的 为满足应急救援需求,设计一种一体化便携式通用生命支持系统,为伤员提供多参数监护和生命支持治疗.方法 把关键急救设备与器械进行微型化、轻量化和集成化设计,将多种急救设备的功能集成于一台设备上实现,系统主要包括机械通气、输液、监护、供氧、供电等模块;外形、结构、显示和操控界面充分考虑人机交互设计,采取外接氧源供氧,可接高压氧源和低压氧源;采用内部电池和外接交/直流电源供电.结果 该系统满足人机工程要求,体积更小、重量更轻,可实现呼吸支持、输液、多参数生命体征监护等功能,各项技术参数都高于研制总要求,具有更强的多环境适应性,可以在高寒、高原、雨淋、颠簸等多种野外环境下正常工作.结论 研制的微型化、轻量化便携式通用生命支持系统性能可满足重症患者救治需求,环境适应性强,可广泛用于事故救援、灾害救援等.
目的 探索建立一套医院院内就医导航系统,协助患者高效、准确地找到就诊目的 地,使有限的医疗资源得到充分利用[1-3].方法 基于区域三维地理和Floyd算法等技术与当今广泛使用的二维码技术相结合,设计并构建一套院内导航应用系统,患者通过扫码获取当前位置同时进入导航系统,完成医院区域内导航[3-4].结果 在不增加医院投入,不引入、不升级硬件设备的前提下,通过区域三维地理和Floyd算法可建立院内虚拟三维地图,将院内地理信息通过更加直观的方式展现在患者面前,选择二维码扫码的方式更加精准地定位当前位置,结合自建地图实现室内精准导航,满足目标需求.结论 应用移动信息技术建立院内导航系统可提高患者就医效率,降低在院滞留时间,改善患者就医体验,同时提升医疗服务智能化、智慧化服务水平.
Objective To improve doctors' understanding of giant perivascular space (PVS) in the brain. Methods A case of giant intracranial polycystic PVS was analyzed retrospectively by searching the databases of PubMed and Medline, combining with literature reports, the anatomy, pathophysiology, clinical manifestations, imaging changes, and treatment principles of giant PVS were summarized. Results A 19-year-old male solder was admitted due to intermittent occipital distension pain for 2 weeks. The brain MRI showed multiple cystic lesions in the right cerebral hemisphere without enhancement. The head-carotid artery CT angiography found no abnormality. The diagnosis was polycystic giant PVS in the brain. His headache was relieved after 3 days of oral compound paracetamol tablets. During a regular follow-up period for 3.5 years, he complained no discomfort. Until October 13, 2020, there were only 41 English articles about brain polycystic giant PVS collected in PubMed, including total of 46 cases. The clinical manifestations were not specific, depending on whether the nerve tissue around PVS was compressed or not. Headache accounted for 32.6%, and hydrocephalus for 43.5%. The MRI of PVS was characterized by its round, oval or tubular structure with a clear, smooth and homogeneous edge, its signal intensity was equal to that of cerebrospinal fluid (CSF) without enhancement. It is called giant or huge PVS when its diameter is more than 15 mm. There was no special treatment unless the giant PVS causes surrounding tissue oppression or hydrocephalus, if so, neurosurgical operation could be help to improve patient's status. Conclusions Characteristics of giant PVS appeared on all sequences of MIR is a CSF-like intensity cystic lesion without enhancement. Clinical attention should be paid to differential diagnosis and follow-up and. If space-occupying effect or hydrocephalus development, it can be intervened by neurosurgery, otherwise no special treatment. DOI: 10.11855/j.issn.0577-7402.2021.01.10
Targeted molecular therapy is the most effective treatment for cancer. An effective therapeutic target for colorectal cancer (CRC) is urgently needed. However, the mechanisms of CRC remain poorly understood, which has hampered research and development of CRC-targeted therapy. TRIM29 is a ubiquitin E3 ligase that has been reported as an oncogene in several human tumors. In this study, we show that increased levels of TRIM29 were detected in CRC compared with normal tissues and were associated with poor clinical outcome, advanced stage and lymph node metastasis, particularly those with right-sided colorectal cancer (RSCC). Notably, GATA2 (GATA Binding Protein 2) transcriptionally repressed TRIM29 expression. The loss of GATA2 and high expression of TRIM29 occur more frequently in RSCC than in left-sided colorectal cancer (LSCC). Functional assays revealed that TRIM29 promotes the malignant CRC phenotype in vitro and in vivo. Mechanistic analyses indicate that TRIM29 promotes pyruvate kinase (mainly PKM1) degradation via the ubiquitin-proteasome pathway. TRIM29 directly targets PKM1 to reduce PKM1/PKM2 ratio, which results in PKM2-mediated aerobic glycolysis (Warburg effect) acting as the dominant energy source in CRC. Our findings suggest that TRIM29 acts as a tumor promoter in CRC, especially in RSCC, and is a potential therapeutic target for CRC treatment.