Objective To observe the macular morphology and circumpapillary retinal nerve fiber layer thickness (RNFL) in Parkinson's disease (PD) evaluated by spectral-domain optical coherence tomography (SD-OCT). Methods A total of 37 patients (74 eyes) with PD were in the PD group, 32 age-and sex-matched healthy subjects (64 eyes) in the control group. All subjects underwent SD-OCT examination with 5 line scanning, macular cube 512×128 scanning and optic disc volume 200×200 scanning. The retinal thickness, central foveal thickness (CFT), macular volume and thickness of circumpapillary, superior, inferior, nasal, and temporal of RNFL between two groups were comparatively analyzed. The relationship between SD-OCT parameters and age, disease duration, scores of Hoehn-Yahr and unified PD rating scale (UPDRS) in PD patients was analyzed by Pearson correlation analysis. Results Both of the retinal thickness and macular volume in PD group were significantly reduced than those in control group (t=?2.546,?3.410;P=0.012, 0.001). There was no difference of CFT (t=?0.463, P=0.644) and the thickness of circumpapillary (t=?1.645, P=0.102), superior (t=?0.775, P=0.439), inferior (t=?1.844, P=0.067), nasal (t=?0.344, P=0.732) and temporal (t=?0.541, P=0.590) of RNFL between two groups. The retinal thickness, macular volume, CFT and the thickness of circumpapillary, superior, inferior, nasal, temporal of RNFL had no relationship with age, disease duration and scores of Hoehn-Yahr and UPDRS in PD patients (P>0.05). Conclusions In PD patients, the retinal thickness and macular volume are decreased, however, the circumpapillary RNFL have no obvious alterations.

Objective To investigate the effects of sevoflurane pretreatment on the inflammatory response in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB) and the mechanism of myocardial protection.Methods Twenty NYHA class Ⅱ or Ⅲ patients of both sexes,aged ＜ 60 yr,undergoing cardiac valve replacement with CPB,were randomly divided into 2 groups (n=10 each): sevoflurane group (group S) and control group (group C).The patients were premedicated with intramuscular morphine 0.1 mg/kg and scopolamine 0.3 mg.Anesthesia was induced with iv injection of midazolam 0.05-0.08 mg/kg,fentanyl 10-15 μg/kg and pipecuronium 0.08-0.10 mg/kg.The patients were tracheal intubated and mechanically ventilated.Anesthesia was maintained with intermittent iv boluses of midazolam0.03-0.06 mg/kg,fentanyl 5-10μg/kg and pipecuronium 0.04-0.08 mg/kg.Sevoflurane was inhaled before aortic clamping and the end-tidal concentration was rapidly adjusted to 1.0％ and maintained at this level for 30 min in group S.Blood samples were taken from the central vein before skin incision,immediately after aortic clamping,immediately after aortic unclamping and at 30 min after aortic unclamping,at 2,6,12 and 24 h (T1-8) after operation for determination of the concentrations of plasma tumor necrosis factor-α (TNF-α),interleukin-6 (IL) and interleukin-8 (IL-8),intercellular adhesion molecule-1 (ICAM-1),cardiac troponin I (cTnI) and activity of creatine kinase MB (CK-MB).The requirement for cardiovascular drugs was recorded after release of aortic cross clamp.Results Compared with group C,the plasma concentrations of TNF-α,IL-6 and IL-8 were significantly decreased at T3-8,the plasma concentrations of ICAM-1 and cTnl were significantly decreased at T4-8,the activity of plasma CK-MB was significantly decreased at T8,and the requirement for cardiovascular drugs was significantly reduced after release of aortic cross clamp in group S (P ＜0.05).Conclusion Sevoflurane pretreatment can inhibit the inflammatory response and provide myocardial protection to some extent in patients undergoing cardiac valve replacement with CPB.

Objective To investigate the effects of sevoflurane pretreatment on the myocardial injury in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Twenty NYHA class Ⅱ or Ⅲ patients,aged ＜ 60 yr,undergoing cardiac valve replacement with CPB,were randomly divided into 2 groups (n =10 each):sevoflurane group (group S) and control group (group C).The patients were premeditated with intramuscular morphine and scopolamine.Anesthesia was induced with iv injection of midazolam 0.05-0.08 mg/kg,fentanyl 10-15 μg/kg and pipecuronium 0.08-0.10 mg/kg.Anesthesia was maintained with intermittent iv boluses of midazolam,fentanyl and pipecuronium and in addition sevoflurane was inhaled before aortic clamping and the end-tidal concentration was rapidly increased to 1.0％ and maintained at the level for 5 min in group S.Blood samples were taken from the central vein before skin incision (T1),immediately after aortic clamping (T2 ),at 0 and 30 min after aortic unclamping (T3-4),and at 2,6,12 and 24 h after operation (T5-8) for determination of the concentration of serum cardiac troponin Ⅰ (cTnI) and activities of creatine kinase (CK) and creatine kinase isoenzyme-MB (CK-MB).Myocardial specimens were taken from right auricle before aortic clamping and at 10 min after aortic unclamping for electron microscopic examination.Results The concentration of serum cTnI and activities of CK and CK-MB were significantly increased at T4-8 in both groups ( P ＜ 0.05).The serum cTnI concentration at T4-8 and the activities of CK and CK-MB at T8 were significantly lower in group S than in group C ( P ＜0.05).Different degrees of mitochondrial swelling were observed after aortic unclamping in both groups,but the changes were milder in group S than in group C.Conclusion Sevoflurane pretreatment can attenuate the myocardial injury in patients undergoing cardiac valve replacement with CPB.

Objective To investigate the effects of basic fibroblast growth factor (bFGF) on pericytes in the blood brain barrier at acute stage after traumatic brain injury (TBI) in mice.Methods A total of 90 mice with a C57BL/6 background were randomly divided into sham group,TBI group,and TBI + bFGF group,with 30 rats per group.The models of moderate TBl were established using the controlled cortical impactor.After 24 hours,the changes of nerve function were evaluated by Garcia neurological score.Each mouse received an intraperitoneal injection of Evans blue dye for measuring the permeability of blood brain barrier.Western blot was used to test the related indices of pericytes after the cerebral cortex was quickly dissected:platelet-derived growth factor receptor beta (PDGFR-β),aminopeptidase N (CD13),desmin,neurogliocyte 2 (NG2),and glyceraldehyde-3-phosphate dehydrogenase (GAPDH).Paraffin sections were prepared for HE staining and morphological changes were observed.Immunofluorescence assay was used to test the related indices of pericytes:PDGFR-β,CD13,and cell surface glycoprotein MUC18 (CD146).Results Garcia neurological score revealed that the score in TBI group was significantly decreased compared with that in sham group (P ＜ 0.01),but the score of TBI + bFGF group was significantly increased compared with that of TBI group (P ＜ 0.05).Permeability of blood brain barrier in TBI group was significantly increased compared with that in sham group (P ＜0.01),but in TBI + bFGF group this parameter significantly reduced compared with that in TBI group (P ＜ 0.01).Western blot analysis revealed that the expressions of PDGFR-β,CD13,desmin,NG2 proteins in TBI group were significantly decreased compared with those in sham group (P ＜0.05),while the expressions of PDGFR-β,CD13,desmin,NG2 proteins in TBI + bFGF group were significantly increased compared with those in TBI group (P ＜ 0.05).HE staining revealed injury of brain parenchyma in TBI group was the severest compared with both sham group and TBI + bFGF group.Immunofluorescence staining results revealed that the proteins expressions of PDGFR-β,CD13,and CD146 in TBI group were significantly decreased compared with those in sham group (all P ＜0.01),and those in TBI + bFGF group were significantly increased compared with those in TBI group (all P ＜ 0.05).Conclusions bFGF can prevent pericyte death via protecting its proteins to conserve blood-brain barrier,bFGF can also significantly ameliorate the injury of brain parenchyma.