Bipolar disorder and obsessive-compulsive disorder comorbidity is becoming more and more common and has aroused clinical physicians' increasing interest. This review summarizes the epidemiology, clinical characteristics, neurobiochemistry, and treatment of comorbid bipolar disorder and obsessive-compulsive disorder and discusses the neurobiochemical mechanism. Findings from this review will provide evidence for identifying the clinical symptoms of bipolar disorder and obsessive-compulsive disorder comorbidity and for treatment of the comorbidity.

ObjectiveTo investigate protective effect of Arctium lappa root aqueous extract （ALR-AE） on hydrochloric acid/ethanol （HCl/EtOH）-induced acute gastric ulcer in rats based on protein kinase B/nuclear transcription factor-κB （Akt/NF-κB） signaling pathway. MethodRats were randomly divided into 5 groups， namely normal group， model group， ranitidine group （35 mg·kg^-1）， ALR-AE low dose group （50 mg·kg^-1， ALR-AE-L group） and ALR-AE high dose group （100 mg·kg^-1， ALR-AE-H group）. Different doses of ALR-AE were orally administered twice daily for three consecutive days before the animals were subjected to HCl/EtOH （60% ethanol in 150 mmol·L^-1 HCl） to induce acute gastric ulcer. For the gastric tissue samples， the ulcer surface was recorded by electronic imaging technique， and then the ulcer inhibition rate was calculated using ImageJ 1.8.0， hematoxylin-eosin （HE） and periodic acid-Schiff （PAS） staining were used to observe the pathological changes and mucoprotein distribution， respectively. The levels of oxidative stress factors of malondialdehyde （MDA）， superoxide dismutase （SOD） and glutathione peroxidase （GSH-Px） in rat gastric tissues were determined by colorimetric method， the levels of pro-inflammatory mediators of tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6） and IL-1β were determined by enzyme linked immunosorbent assay （ELISA）， protein levels of phosphorylation and non-phosphorylation of Akt， NF-κB p65， NF-κB inhibitor protein α （IκBα） and IκB kinase α （IKKα） were evaluated by Western blot. ResultCompared with the normal group， the gastric tissue of the model group was severely damaged， and the area of gastric ulcer were significantly enlarged （P<0.01）， the levels of MDA， TNF-α， IL-6 and IL-1β in gastric tissue were significantly increased （P<0.01）， levels of GSH-Px and SOD were significantly decreased （P<0.01）， and phosphorylation levels of Akt， NF-κB p65， IKKα and IκBα in gastric tissue were significantly increased （P<0.01）. Compared with the model group， ALR-AE significantly attenuated HCl/EtOH-induced gastric tissue damage， significantly increased ulcer inhibition rate （P<0.01）， and dose-dependently reduced the levels of MDA， TNF-α， IL-6 and IL-1β （P<0.05， P<0.01）， and elevated GSH-Px and SOD levels （P<0.01）， ALR-AE-L group could significantly inhibit the phosphorylation levels of Akt （P<0.05）， and ALR-AE-H group could significantly inhibit phosphorylation levels of Akt， NF-κB p65， IKKα and IκBα （P<0.05， P<0.01）. ConclusionALR-AE has a significant protective effect on HCl/EtOH-induced acute gastric ulcers in rats， and its mechanism may be related to the inhibition of inflammatory mediator expression and reduction of oxidative stress levels mediated by Akt/NF-κB signaling pathway.

ObjectiveTo investigate the mechanism of protective effect of ethanol extracts of Hemsleya chinensis （HC-EE） on hydrochloric acid/ethanol （HCl/EtOH）-induced acute gastric ulcer in rats. MethodLipopolysaccharide （LPS）-induced RAW264.7 cells were used to evaluate inhibitory effect of HC-EE on the production of inflammatory mediators in vitro. A rat acute gastric ulcer model induced by HCl/EtOH （60% ethanol in 150 mmol·L^-1 HCl） was used to evaluate protective effect of HC-EE on acute gastric ulcer. Rats were divided into five groups， including normal group， model group， HC-EE low dose （HC-EE 30， 30 mg·kg^-1） group， HC-EE high dose （HC-EE 60， 60 mg·kg^-1） group and ranitidine （35 mg·kg^-1） group. For model and drug-treated groups， vehicle solvent or drugs were orally administered twice daily for 7 consecutive days before the rats were subjected to HCl/EtOH to induce acute gastric ulcer. After being anesthetized， ulcer surface of each rat was obtained and recorded using electronic imaging technology， and the ulcer inhibition rate was calculated by ImageJ 1.8.0. Hematoxylin-eosin （HE） and periodic acid-Schiff （PAS） staining were used to observe the pathological histological changes in rats. Content of nitric oxide （NO） in cell culture medium was measured by the Griess method. The levels of interleukin-1β （IL-1β）， tumor necrosis factor-α （TNF-α）， IL-6， vascular cell adhesion molecule-1 （VCAM-1） and prostaglandin E₂ （PGE₂） in rat serum （or cell culture medium） were determined by enzyme linked immunosorbent assay （ELISA）. The protein expressions of phosphorylation （p）-p38 mitogen activated protein kinase （MAPK）/p38 MAPK and p-nuclear transcription factor-κB （NF-κB） p65/NF-κB p65 in rat gastric tissue were detected by Western blot. ResultIn vitro assay showed HC-EE could significantly down-regulate the expressions of NO， TNF-α， IL-1β， IL-6 and VCAM-1 in LPS-induced cells （P<0.05， P<0.01）. In vivo experimental results showed that， compared with the normal group， gastric tissue of the model group was severely damaged， and the area of gastric ulcer was significantly enlarged， levels of TNF-α， IL-6 were significantly increased （P<0.01）， and the level of PGE₂ was significantly decreased （P<0.01）， the phosphorylation levels of of p38 MAPK， NF-κB p65 in gastric tissue were significantly increased （P<0.01）. Compared with the model group， HC-EE dose-dependently improved HCl/EtOH-induced gastric tissue injury and inflammatory cell infiltration， and it could increase ulcer inhibition rate， significantly decreased the release of TNF-α and IL-6 （P<0.01）， HC-EE 60 group could increase the content of PGE₂ （P<0.05）， and significantly inhibit the phosphorylation levels of p38 MAPK and NF-κB p65 （P<0.05， P<0.01）. ConclusionHC-EE can exert protective effect on HCl/EtOH-induced acute gastric ulcer in rats， and its mechanism may be related to the inhibition of expression of inflammatory mediators mediated by p38 MAPK/NF-κB signaling pathway.

Microgravity in space will lead to the decline of astronauts'motor sensation,which will affect the ability of balance maintenance and posture control.Which limits the ability of astronauts to quickly get out of danger in case of extravehicular activities or landing emergencies,and seriously affects the completion of space missions and endangers the safety of astronauts.The current weightlessness countermeasure based on exercise can effectively alleviate the problems of skeletal muscle and cardiovascular system caused by weightlessness to a certain extent,but it cannot effectively prevent the motor sensory dysfunction after space flight.Therefore,new weightlessness countermeasures of special physical conditioning are needed to attenuate the decline of human balance control ability after long-term space flight.By reviewing the previous research results of space flight and simulated weightlessness experiments,this paper systematically analyzes the influencing factors of human body balance control,compares the balance control promotion schemes of special physical conditioning in the field of sports,and puts forward the potential protection strategies for weightlessness environment based on the integration of sports and medicine.The feedback regulation of muscle tension,tactile and proprioceptive play an important role in human posture balance and motion control.The unloading of human gravity load in space weightlessness environment will greatly reduce the input-output feedback regulation activity of the above senses which may lead to balance dysfunction.The post-flight balance control dysfunction may be improved by special physical conditioning,such as loading of z-axial load,enhancement of tactile feedback and proprioceptive response based on unstable mechanical stress stimulation during spaceflight.