Objective To investigate if Shikonin(SKI)can induce ferroptosis via the ROS/JNK pathway to inhibit the malignant behavior of pancreatic cancer.Methods Human pancreatic cancer PANC-1 or BxPC-3 cells were selected.Drug efficacy experiments were established with a blank control group(Con group)and low,medium,and high dose SKI groups(2,4,8 μmol/L).JNK-related mechanism experiments were categorized into a blank control group(Con group),SKI group,and SKI+JNK inhibitor group(SKI+SP600125 group).ROS-related mechanism experiments were divided into a blank control group(Con group),SKI group,and SKI+ROS scavenger group(SKI+NAC group).Cell viability was assessed using the CCK-8 method to calculate IC50;Transwell experiments evaluated cell migration and invasion capabilities;the C11 BODIPY 581/591 probe was utilized for flow cytometry to detect lipid peroxidation levels,while the FerroOrange fluorescent probe measured ferrous ion levels;ROS levels were determined using a ROS detection kit;the Western blot method identified ferroptosis-related key proteins(SLC7A11,GPX4),apoptosis-related proteins(Caspase3,PARP),and JNK pathway proteins(JNK,p-JNK);an in vivo xenograft tumor model was employed to assess tumor proliferation.Results SKI treatment significantly and dose-dependently inhibited PANC-1 cell viability(IC50:6.04 μmol/L,P<0.0001)and BxPC-3 cell viability(IC50:12.27 μmol/L,P<0.0001),and significantly reduced migrating and invasive cell numbers(P<0.0001),with migration cell numbers dropping to about 30%of the control group at 8 μmol/L SKI treatment(P<0.0001).Mechanistically,SKI induced increased intracellular lipid peroxidation,Fe2+accumulation,and significant ROS production(P<0.0001),significantly downregulated SLC7A11 and GPX4 protein expression(GPX4 protein expression reduced to 40%of that in the control group,P<0.0001),and activated JNK phosphorylation(p-JNK/JNK ratio increased to 2.8-fold,P<0.0001).Pretreatment with the JNK-specific inhibitor SP600125 or ROS scavenger NAC effectively reversed SKI's inhibition of cell viability and downregulation of SLC7A11/GPX4 protein(all P<0.01).SKI also inhibited pancreatic cancer tumor cell proliferation in vivo(P<0.0001).Conclusion SKI induces ferroptosis by activating the ROS/JNK pathway,thereby inhibiting pancreatic cancer proliferation,migration,and invasion.

Objective To investigate the predictive efficiency of combined uterine artery hemodynamic parameters and oxidative stress indicators in early pregnancy on hypertensive diseases in pregnancy (HDP). Methods A total of 90 HDP patients (case group) and 30 healthy pregnant women (control group) as research subjects. The case group included 30 patients with pregnancy-induced hypertension, 30 patients with preeclampsia, and 30 patients with severe preeclampsia, respectively, and were divided into pregnancy-induced hypertension group, preeclampsia group, and severe preeclampsia group. Serum levels of reactive oxygen species (ROS), superoxide dismutase (SOD), heme oxygenase-1 (HO-1), glutathione peroxidase (GSH-PX), malondialdehyde (MDA), and uterine artery hemodynamic parameters were compared between the two groups in early pregnancy (8 weeks to 13 weeks plus 6 days). The receiver operating characteristic (ROC) curve was used to evaluate the predictive efficiency of relevant indicators for HDP. Results The serum levels of SOD and GSH-PX were lower in the case group than that in the control group, and the serum level of MDA and the uterine artery pulsatility index (PI) were higher in the case group than that in the control group (P < 0.05). The serum levels of SOD and GSH-PX gradually decreased, and the serum levels of MDA and PI gradually increased in the pregnancy-induced hypertension group, the preeclampsia group, and the severe preeclampsia group (P < 0.05). The ROC curve showed that the combination of SOD, GSH-PX, MDA, and PI in early pregnancy had a higher predictive efficiency for HDP, with an area under the curve of 0.824, a sensitivity of 81.1%, and a specificity of 76.7%. Conclusion Patients with HDP have changes in oxidative stress indicators and uterine artery hemodynamic parameters in early pregnancy, and there are differences among patients with different disease severities. The combined detection of SOD, GSH-PX, MDA, and PI in early pregnancy can help predict HDP.

Biofilms are complex three-dimensional bacterial assemblages that attach to biotic or abiotic solid surfaces, and frequently embed within a self-produced matrix of extracellular polymeric substances. Biofilm formation is a microbial defense response to biotic and abiotic stresses, and a key factor for survival in adverse environments. A wide variety of microorganisms can colonize distant tissues of higher plants, such as leaves, vascular network and roots, and adhere to the surface of the tissues to form biofilms. The dynamic processes in forming biofilms in response to plant internal environment are key steps required for full virulence of phytopathogenic bacteria. Exploring the mechanisms involved in regulation of bacterial biofilms is important for understanding the plant-pathogens interactions. In this review, we summarized the research progresses related to the biofilms of bacterial phytopathogens, including biofilm characteristics, essential regulatory mechanisms and key signals affecting the transition between a planktonic lifestyle and multicellular behavior.

Fractures of the odontoid process in children are rare but account for the majority of all the cervical spine injuries in the infantile and young juvenile groups. The initial radiographic evaluation is often difficult so that the diagnosis-making is delayed or the fractures are missed. The management of the odontoid fractures of adults has long been controversial and varies with different spinal surgeons. By contrast, the diagnosis and treatment of odontoid fractures in skeletally immature children have not been frequently documented and not in details. This paper reviews the clinical characteristics, diagnosis, treatment principles, and long-term outcome of the odontoid fractures in a consecutive series of patients aged 14 years or younger.