S100B is a class of acid calcium-binding protein. It mainly exists in neuroglial cells in the central nervous system, and it is one of the signs of astrocyte activation. S100B may reflect the function of neuroglial cells and regulate the complex interactions between the neurons and neuroglial cells. Studies in recent years have demonstrated that S100B protein is involved in the pathological processes of acute ischemic brain injury. Serum S100B protein can be used as an important marker for identifying the severity of cerebral infarction, progress and outcome.

Objective To investigate the effects of peroxisome proliferators-activated receptorγ(PPARγ)agonist pioglitazone on the expressions of glial fibrillary acidic protein (GFAP) and cyclin D1 in the hippocampal CA1 region after cerebral ischemia in rats.Methods Fifty-four Sprague-Dawley rats were randomly divided into 3 groups:sham operation group,ischemia/reperfusion group,and pioglitazone intervention group (18 in each group).A rat middle cerebral artery occlusion and reperfusion model was induced by the modified suture method.Continuous pioglitazone rosiglitazone gavage (0.65 mg/kg once a day) was conducted for 5 days before modeling in the pioglitazone intervention group.At day 1,3,and 7 after modeling the rats (6 at each time point) were sacrificed and their brains were removed.HE staining was used to detecte the pathological changes of neurons in the hippocampal CA1 region.Immunohistochemical staining was use to detect the expressions of GFAP and cyclin D1 in the hippocampal CA1 region.Results Compared to the sham operation group,at day 3 and 7 after ischemia/reperfusion,the number of neuronal survival in the hippocarmpal CA1 region in the ischemia/reperfusion group was significantly reduced (all P ＜ 0.01).The expressions of GFAP and Cyclin D1 at all time points were significantly upregulated (all P ＜ 0.01).At day 3 and 7 after ischemia/reperfusion,the numbers of neuronal survival in the hippocampal CA1 region in the pioglitazone intervention group were significantly increased (all P ＜0.01).Compared to the ischemia/reperfusion group,the expressions of GFAP and Cyclin D1 at all time points were significantly down-regulated (all P ＜ 0.01).Conclusions PPARγagonist pioglitazone has a significant protective effect on neuron in the hippocampal CA1 region after cerebral ischemia/reperfusion in rats.Its mechanism may be associated with inhibiting GFAP and cyclin D1 expressions.

The daily management of medical equipment in the shelter hospital of CAPF was explored, and some measures were put forward including completing administration, determining responsibilities, improving supervising system, creating management tools, strengthening application for military and civilian uses, enhancing professional awareness and etc. The problems were solved in the discrepancies between construction and management, application and maintenance as well as training and daily service, so that the equipment was improved in efficiency, service life, metrology and stability. References may be provided for the shelter hospital or other medical units of CAPF for daily management of medical devices.

Objective:To observe the intrinsic association between cognitive function in patients with Parkinson′s disease (PD) and retinal structural changes in retina nerve fiber layer thickness, macular volume and macular thickness.Methods:A total of 36 patients with PD and 12 normal controls matched with age and sex were selected randomly. Examinations of Montreal Cognitive Assessment (MoCA), Mini-Mental State Examination (MMSE), Unified Parkinson′s Disease Rating Scale Ⅲ (UPDRS-Ⅲ), Hoehn-Yahr stage were performed in all subjects. The PD patients were divided into three groups according to the score of MoCA: PD without cognitive impairment (PD-NCI; n=12), PD with mild cognitive dysfunction (PD-MCI; n=13) and PD dementia (PDD; n=11). The retinal nerve fiber layer thickness, macular volume and thickness which were corrected with body mass index (BMI) were determined and analyzed by optical coherence tomography imaging. Results:The total RNFL thickness (μm/BMI) of the PD with cognitive impairment group (PD-MCI group: 3.55±0.12 ( t=2.552, P=0.014), PDD group: 3.07±0.18 ( t=4.122, P=0.000)) was thinner than that of the normal control group (4.05±0.16). The RNFL thickness in each quadrant of the PD with cognitive impairment group (PD-MCI group and PDD group) was thinner than those of the normal control group. The RNFL thickness gradually became thinner with the cognitive impairment increasing ( r=0.558 3, P<0.001). The macular volume (mm 3/BMI) of PD group (PD-NCI group: 0.274±0.010 ( t=2.523, P=0.015), PD-MCI group: 0.268±0.010 ( t=2.848, P=0.007), PDD group: 0.266±0.010 ( t=2.604, P=0.013)) was smaller than that in the normal control group (0.316±0.010), and the macular volume gradually decreased with the severity of cognitive impairment ( r=0.234 1, P=0.024). The macula thickness in each subgroup of PD was thinner than that of the normal control group. The macula thickness gradually became thinner with the cognitive impairment increasing ( r=0.283 9, P<0.001). The macular thickness (normal controls: (10.67±0.12) μm/BMI, PD group: (9.51±0.07) μm/BMI, t=8.312, P<0.001) and volume (normal controls: (0.316±0.010) mm 3/BMI, PD group: (0.270±0.010) mm 3/BMI, t=3.570, P<0.001) became thinner and smaller in patients with PD. Conclusions:In patients with PD, the thickness of the retina nerve fiber layer, the volume and thickness of the macula become thinner/smaller with the severity of cognitive impairments increasing. Macular thickness and volume in patients with PD appear thinner/smaller, which can be used as a valuable biological marker in the early stage of PD. The retina nerve fiber layer thickness in patients with PD becomes thinner, which may be accompanied by cognitive impairment.

Chronic urticaria （CU） is a common skin disease worldwide， and its incidence is increasing year by year in various regions. Clinical manifestations such as severe itching can affect normal work， sleep， and daily life and increase the negative psychological burden caused by stress， anxiety， and depression. Mast cell activation and degranulation induced by immunoglobulin（Ig）E hypersensitivity is one of the core pathogenic mechanisms of CU， and there is no cure. Antihistamines such as cetirizine and loratadine are preferred for the clinical treatment of CU. Although they can effectively improve clinical manifestations such as itchiness， long-term application can increase the risk of adverse reactions and drug resistance. The phosphatidylinositol kinase/serine-threonine protein kinase B（PI3K/Akt） signaling pathway， as a classical signaling pathway regulated by phosphatidylinositol and tyrosine kinase receptor （RTK）， is a key target regulating the production and release of cytokines in macrophages and affecting the migration of leukocytes and the activation of mast cells and inflammation， and it can be involved in a variety of metabolic processes， such as mast cell activation and degranulation induced by IgE hypersensitivity and abnormal activation of the complement system so that the PI3K/Akt molecular pathway could be an important target for the future eradication of CU. However， the mechanism and potential role of the PI3K/Akt signaling pathway in the treatment of CU are less reported in China. Now， this paper reviewed the molecular mechanism of PI3K/Akt signaling pathway regulation in the treatment of CU and provided corroborative evidence and therapeutic strategy choices for the treatment of CU with traditional Chinese medicine （TCM） from the perspectives of molecular regulation and network pharmacology analysis.