Alzheimer's disease (AD) is a neurodegenerative disease of the central nervous system that starts slowly and progressively leads to cognitive impairment.Clusterin,as an apolipoprotein,is usually widely expressed in mammalian brain tissue.In previous studies,below theories have been demonstrated:clusterin influences the aggregation,clearance and neurotoxicity of β-amyloid;compared to healthy people,AD patients show higher clusterin level in plasma and cerebrospinal fluid;the polymorphisms of clusterin gene encoding clusterin can enhance the incidence risk of AD.In addition,regulating the expression of clusterin in AD animals model has certain therapeutic effect on AD.Further investigating intrinsic relationship between clusterin and AD will help clarify the pathogenesis and establish a new therapeutic target of AD thus contributing to the prevention of Alzheimer's disease.

Aquaporin 4 (AQP4) is the most abundant aquaporin type in the brain.It is mainly expressed in the perivascular end feet of astrocytes.A large number of studies have shown that AQP4 is involved in the formation and elimination of brain edema in intracerebral hemorrhage,and plays important roles in the maintenance of the integrity of blood-brain barrier,secondary neuroinflammation,and apoptosis after intracerebral hemorrhage.More and more studies focus on the roles and mechanisms of AQP4 in intracerebral hemorrhage,however,the results are not completely consistent.This article reviews the roles and mechanisms of AQP4 in intracerebral hemorrhage

The central nervous system inflammatory response plays an important role in the pathogenesis of AD.Pro-inflammatory cytokines can induce inflammatory reactions in the body,enhance the neurotoxic effects caused by Aβ,promote the pathogenesis of AD and anti-inflammatory factors can down-regulate the inflammatory response,play a protective role and promote the reconstruction of damaged tissue.However,due to the existence of genetic polymorphisms,the influence of inflammatory factors on AD is complicated,especially in different population groups.Studing and clarifying the relationship between gene polymorphisms of inflammatory factors and and the pathogenesis of AD will promote the study of the mechanism of AD and provide a new method for the treatment of AD.Therefore,this article mainly reviews this.

Objective To observe the effect and molecular mechanism of lipopolysaccharide (LPS) on activation and differentiation of microglia (MG) cells. Methods Routinely in vitro cultured BV2 microglia cells were divided into control group and LPS group: BV2 microglia cells in the LPS group were treated with 200 ng/mL LPS; cells in the control group were added the same amount of medium. Six h after treatment, real-time quantitative (qRT)-PCR and enzyme-linked immunosorbent assay (ELISA) were used to detect the inflammatory factors, interleukin (IL)-1β and tumor necrosis factor (TNF)-α mRNA and protein expressions in supernatant of cell culture medium. The iNOS, CD32, Arg1 and CD206 mRNA and protein expressions were detected by qRT-PCR and immunofluorescence, respectively. The mRNA and protein expressions of Notch1, Hes1 and Hes5 were detected by qRT-PCR and Western blotting. Results After LPS stimulation, BV2 microglia cells were activated and the morphological changes were observed. The IL-1β and TNF-α protein and mRNA expressions in the LPS group were significantly increased as compared with those in the control group (P<0.05). The iNOS and CD32 protein and mRNA expressions in the LPS group were significantly increased as compared with those in the control group (P<0.05). The Arg1 and CD206 mRNA and protein expressions showed no significant differences between the two groups (P>0.05). The Notch1 and Hes1 mRNA and protein expressions in the LPS group were significantly increased as compared with those in the control group (P<0.05), while no significant differences on Hes5 mRNA and protein expressions were noted between the two groups (P>0.05). Conclusion LPS activates MG cells, which may regulate the differentiation of MG cells into M1 through Notch signaling pathway and promote inflammatory response; therefore, Notch signaling pathway may be a target for regulating MG cells differentiation and reducing inflammatory damage.

Objective To establish a risk prediction model,and to observe its value for predicting retained cesarean scar pregnancy(CSP)after ultrasound-guided curettage.Methods Data of 401 CSP patients who received ultrasound-guided curettage were retrospectively analyzed.The patients were randomly divided into training set(n=264)or validation set(n=137)at a ratio of 7:3.According to whether there was retained CSP at the lower segmental scar of uterine after ultrasound-guided curettage,the patients were divided into retained group or non-retained group.The variables with the biggest predictive value for retained CSP after ultrasound-guided curettage were selected with LASSO regression,and the independent risk factors were screened using multivariate logistic regression,and then a nomogram model was established.Results The results of LASSO regression and multivariate logistic regression indicated that embedded depth of gestational sac in cesarean scar more than 1.13 cm,convexity of gestational sac,rich blood supply(Adler degree Ⅱ-Ⅲ),and pre-curettage serum β-human chorionic gonadotropin(HCG)more than 33 063.50 U/L were all independent risk factors for retained CSP after curettage(all P＜0.05).The calibration curve of nomogram predictive model established based on the above indexes was basically consistent with the ideal curve,and the model had good clinical benefits.Conclusion The established nomogram predictive model had good predictive ability for retained CSP after curettage.