Abrogation of ARF6 in promoting erastin-induced ferroptosis and mitigating capecitabine resistance in gastric cancer cells

BackgroundADP ribosylation factor 6 (ARF6) is a member of the Rat sarcoma virus (RAS) superfamily that is involved in the regulation of vesicular trafficking, membrane lipid remodeling, and signaling pathways. Our earlier work discovered that ARF6, as a downstream effector of the Kirsten rat sarcoma viral oncogene (Kras)/extracellular signal-regulated kinases (ERK) signaling pathway, may increase proliferation and induce the Warburg effect in gastric cancer (GC) cells. Additionally, ARF6 appears to be a potential biomarker for predicting the prognosis of GC. Ferroptosis has recently been described as a type of nonapoptotic iron-dependent cell death that is strongly associated with the Kras mutation. Therefore, it is critical to continue investigating the link between ARF6 and ferroptosis.MethodsWe first created ARF6 silenced cancer cell lines with lentivirus transfection. The knockdown efficiency was confirmed through quantitative polymerase chain reaction (qPCR) and western blotting. Subsequently, we used Cell Counting Kit-8 (CCK-8) and malondialdehyde (MDA) assay for lipid peroxidation measurement. Following this, qPCR and western blotting were conducted to clarify the mechanism involved. Finally, immunohistochemistry was used to stain human GC samples.ResultsOur findings established that, whereas ARF6 did not directly regulate lipid peroxidation, it did render GC cells susceptible to oxidative stress, particularly erastin-induced lipid peroxidation. Additionally, our research demonstrated that ARF6 may control capecitabine resistance via several routes.ConclusionsARF6 may play a critical role in the development of GC.     

Survival and prognostic factors for postoperative primary appendiceal cancer: a retrospective cohort study based on the Surveillance,Epidemiology, and End Results database

BackgroundThe factors affecting the postoperative survival of patients with primary appendiceal cancer (PAC) have yet to be fully explored. And there are no clear guidelines for adjuvant treatment after appendectomy. Whether chemotherapy can prolong patient survival after appendectomy, is critical in guiding postoperative medications. The majority of studies on appendiceal cancer are single case reports, and they focused on the incidence of appendiceal cancer. The present study aimed to investigate the survival characteristics of patients with primary appendiceal cancer after surgery using the Surveillance, Epidemiology, and End Results (SEER) database.MethodsThe data of 2,891 cases of primary appendiceal cancer between 2004 to 2015 were obtained from the SEER database and subjected to survival analysis using the Kaplan-Meier method and Cox proportional-hazards model. The annual percentage change (APC) was calculated using the weighted least squares method.ResultsThe overall age-adjusted incidence rate per 100,000 population steadily increased from 0.58 in 2004 to 1.63 in 2015. For patients who received chemotherapy, the median overall survival (OS) was 65 months and the 5-year OS rate was 51.9%, and for patients who did not receive chemotherapy or whose chemotherapy status was unknown, the median OS was not reached and the 5-year OS rate was 78.9%. Age [35< age <69: hazard radio (HR) =2.147; 95% confidence interval (CI): 1.442–3.197, P<0.001; age >69: HR =5.259; 95% CI: 3.485–7.937, P<0.001], race (White race: HR =0.728; 95% CI: 0.590–0.899, P=0.003), histologic type (mucinous neoplasm: HR =0.690; 95% CI: 0.580–0.821, P<0.001; malignant carcinoid: HR =0.657; 95% CI: 0.536–0.806, P<0.001), grade (II: HR =1.794; 95% CI: 1.471–2.187, P<0.001; III: HR =2.905; 95% CI: 2.318–3.640, P<0.001; IV: HR =3.128; 95% CI: 2.159–4.533, P<0.001), and stage (localized: HR =0.236; 95% CI: 0.194–0.287, P<0.001; regional: HR =0.425; 95% CI: 0.362–0.499, P<0.001) were identified as independent predictors of survival. And after adjusting for known factors (age, sex, race, tumor size, marital status, histologic type, grade, stage), chemotherapy (HR =1.220; 95% CI: 1.050–1.417, P=0.009) was revealed to be an independent indicator of poor prognosis.ConclusionsThere was an increasing trend in the incidence of appendiceal cancer in the United States between 2004 and 2015. Chemotherapy was revealed to be an independent indicator of poor prognosis, which provide valuable insight into the therapy of primary appendiceal cancer. Large clinical trials of chemotherapy and targeted therapy for appendiceal cancer are urgently needed.     

高原地区青少年无氧代谢阈值的特征及其影响因素的探讨

目的探讨不同海拔低氧环境对移居青少年无氧代谢阈值的影响。方法使用Jae-ger自行车功量仪,心阻抗仪,用逐级运动负荷法分别测定移居海拔2 260 m、3 417 m和4 280 m三个海拔高度,13~16岁青少年的无氧代谢阈值(AT),同步测定动脉血氧饱和度(SaO2)和心输出量(CO),分析其间的相互关系。结果AT值随海拔高度的上升而下降,以氧耗量表示,分别为(27.44±6.50)、(22.88±5.38)和(16.95±5.97)m l/m in.kg。AT值的降低与SaO2和CO的降低呈正相关。结论SaO2和CO是影响AT值的重要因素。长期移居高海拔的青少年AT值降低,海拔越高,降低越明显。     

博心通软胶囊的制备工艺考察

目的：研究博心通软胶囊的制备工艺。方法：采用CO2超临界流体萃取技术对葱白有效部位进行提取;以胶囊内容物的流动性、均匀性、沉降体积比及囊壳的软硬度,粘连性等为指标,确定软胶囊处方及制备工艺。结果：胶囊内容物的处方为葱白提取物：PEG400：丙二醇：吐温80：聚维酮K30=10：20：1：0．2：0．6（w／w）,囊壳处方为明胶：甘油：水：氧化铁：尼泊金乙酯：1：0．4：1：适量：适量（w／w）。结论：所确定的处方工艺稳定可靠,重复性好,适合工业生产。     

UPLC(超高效液相色谱)/MS/MS联用技术测定全血中的西罗莫司

目的 建立全血中西罗莫司的UPLC（超高效液相色谱）／MS／MS测定方法,方法 全血样品中加入他克莫司（FK506）作内标，用叔丁基甲醚进行提取。以乙腈与含千分之五甲酸的水溶液为流动相（40：50），色谱柱为AcquityUPLCTMBEHC。（50mm×2．1mm，1．7μm），流速0．5ml／min。三重四极杆质谱采用正离子模式，离子采集方式为多反应监测模式（MRM），离子源温度105℃，离子源电离电压为3300V，雾化气流速500L／h。采集离子（母离子／子离子）西罗莫司为931．2／864．1，FK506为822．0／577．0。结果 西罗莫司在1～240腿／L浓度范围内呈良好的线性（n=0．9995）。日内、日间精密度均在15％以内，提取回收率大于75．0％，方法回收率为95．0％～98．5％，最低检测限为0．2μg／L。结论 本方法灵敏、准确，适合临床西罗莫司的全血分析。     

血、尿中安眠酮及其代谢物的测定

通过一例安眠酮中毒病人血、尿中安眠酮及其代谢物的测定,描述了用紫外光谱(uv)、气相色谱(GC)和气相色谱质谱(GC/MS)法测定安眠酮及其代谢物的系统分析方法。样品的提取净化采用液一液萃取和固相萃取两种方法,都得到了很好的结果。紫外光谱用于测定血、尿中安眠酮和其代谢物的总量;气相色谱用于测定血、尿中安眠酮原药的含量;气相色谱质谱则用于鉴定血、尿中的安眠酮及其代谢物。除安眠酮外,血、尿中共检出10种安眠酮代谢物,其中包括两种乙酰化代谢物。此法还为临床救治提供指导。     

利用近红外图谱比对法及一致性检验模型鉴别健胃消食片

目的 在不破坏药品包装的情况下,利用近红外光谱快速鉴别健胃消食片(江中药业股份有限公司).方法 在12000～4000 cm-1波段范围内,对同一厂家的健胃消食片进行全谱扫描,通过图谱比对,建立一致性检验模型.结果 正品健胃消食片与伪品健胃消食片的近红外光谱在5500～9000 cm-1波长范围内存在较大差别,通过建立该品种的一致性近红外模型,可对健胃消食片进行初筛.结论 该方法快速简便、准确有效,为基层打假提供有效方法.     

奥美拉唑不同途径、不同剂量给药抑制胃酸的效果

目的 :研究不同途径、不同剂量奥美拉唑抑制胃酸的效果 ,指导临床合理用药。方法 :将 10 0例内窥镜证实为活动期消化性溃疡病人分成A组 4 0例 ,静脉推注奥美拉唑 4 0mg ,bid ;B组 36例 ,口服奥美拉唑 2 0mg ,bid ;C组 2 4例 ,口服奥美拉唑 2 0mg ,qd。监测用药后d 3～ 5胃内 2 4hpH值变化 ,对A ,B 2组中各 10例 (为A2 ,B2 组 )测定了首次给药后的药物起效时间。结果 :A ,B组的抑酸效果相仿 (P >0 .0 5) ,胃内 pH值分别为 7.0 7±s0 .15和6 .9± 0 .6 ,与C组胃内 pH值 5.8± 1.4相比 ,差异有非常显著意义 (P <0 .0 1) ;A2 组起效时间为 (0 .7± 0 .6 )h ,B2 组为 (4.8± 1.0 )h ,差异有非常显著意义 (P <0 .0 1)。结论 :不同途径 3种剂量的奥美拉唑均有良好的抑酸效果 ,A ,B组更佳 ;静脉用药起效更迅速     

IL-4/STAT6在变应性鼻炎豚鼠鼻黏膜的表达及鼻用糖皮质激素对其表达的影响

目的:研究IL-4/STAT-6在变应性鼻炎豚鼠鼻黏膜的表达和丙酸氟替卡松鼻喷雾剂对其表达的影响,进一步探讨变应性鼻炎的发病机制。方法:45只豚鼠随机分为对照组(NC组)、变应性鼻炎无干预组(AR组)和变应性鼻炎糖皮质激素干预组(Glu组),每组15只。其中AR、Glu组采用卵清白蛋白致敏法制备变应性鼻炎豚鼠模型;NC组用生理盐水替代卵清白蛋白进行同步处理。动物建模后用丙酸氟替卡松鼻喷雾剂(每次50μl/侧)治疗,每天2次,连续5d。观察各组大鼠行为学改变及鼻黏膜病理学改变,免疫组织化学法检测各组豚鼠鼻黏膜中IL-4、STAT6蛋白的表达并观察其变化情况及相关性。结果:与NC组比较,AR组豚鼠喷嚏及搔鼻次数明显增加,IL-4、STAT6表达增强;与AR组比较,Glu组激素干预后豚鼠喷嚏及搔鼻次数明显减少,IL-4、STAT6表达减弱,NC组与Glu组相比结果无明显差异。结论:IL-4/STAT6在Th2分化中起关键作用,丙酸氟替卡松鼻喷雾剂干预后可以通过影响IL-4/STAT6的表达发挥治疗作用。     

计算机辅助鼻额区域影像解剖学研究

OBJECTIVE: To evaluate the value of Advantage Windows 3.1 (AW 3.1) software for anatomical study of nasofrontal region, and to study the CT characteristics of nasofrontal region which related to the frontal sinus surgery. METHODS: Eighty patients underwent axial consecutive computed tomography scans and these data were studied with AW 3.1 software which provided reconstructional imaging of continuous coronal, sagittal, axial sections. Some related structures of nasofrontal region were studied and measured. RESULTS: AW 3.1 software could identify and measure the following structures accurately: The diameter of frontal sinus was (22.5 +/- 8.6) mm in height, (16.3 +/- 6.8) mm in depth, (23.8 +/- 9.8) mm in breadth. The diameter of frontal sinus ostium: the anterior-posterior diameter was (7.3 +/- 1.7) mm, the transverse diameter was (8.5 +/- 1.9) mm. The width of nasal beak of frontal bone(5.9 +/- 1.4 ) mm. The distance of frontal sinus ostium to the floor of columella nasi and the corresponding angle to the nasal floor were (60.8 +/- 4.2) mm and (70.1 +/- 4.7) degrees. The superior attachment sites of the uncinate process were as follows: lamina papyracea 41%, posteromedial wall of agger nasi cell 11%, middle turbinate 19%, anterior skull base 16%, superior bifurcation 13%. The cells could impinge on the frontal recess to cause obstruction (terminal recess 38.8%, anterior ethmoid cell 27.6%, agger nasi cells 24.5%). The accessory cells could impinge on the frontal sinus (perifrontal cells 32.7%, superaorbital cells 38.8%, intersinus septal cells 32.0%). There was significant difference between two groups of characteristics of nasofrontal region. CONCLUSIONS: AW 3.1 software is a helpful and powerful new tool for anatomical study of nasofrontal region and for preoperative evaluation. The structures of nasofrontal region are complex and various, frontal sinusitis almost always results from the obstruction of frontal sinus outflow tract. These results of anatomical study of nasofrontal region are helpful in directing the functional endoscopic surgery in frontal sinus.