Ventilator-associated pneumonia (VAP) is a common hospital acquired infection in neonatal intensive care unit with high incidence in China. There is no diagnostic gold standard of VAP. The risk factors include premature birth, low birth weight, dura-tion of mechanical ventilation, episodes of intubation, blood stream infections. The recommended precautions include rising head of bed, closed tracheal suction, sucralfate, selective decontamination in digestive tract, improvement of mechanical ventilation, oral and skin care, hand hygiene. However, it is controversial that sucralfate, selective decontamination in digestive tract, passive humidifiers, oral and skin care can reduce the incidence of VAP.

Age-related macular degeneration (AMD) is the leading cause of visual impairment among older population worldwide,and wet AMD is more threatened to vision because of the choroidal neovascularization.Some physical therapies are thought to destroy the lesions but can not improve the visual acuity.Therefore,anti-VEGF drug therapy is becoming a new approach to the management of wet AMD.Vascular endothelial growth factor(VEGF) is thought to play an important role in the complicated pathogenesis,which can be addressed by disease reduction strategies.Among the anti-VEGF drug therapies,anti-VEGF monoclonal antibodies are proved to maintain and improve visual acuity.Other therapies have been or now being developed for the treatment of neovascular AMD with the goal of inhibiting VEGF.These inhibitors include VEGF receptor decoy aflibercept,small interfering RNA-based therapies (bevasiranib) and tyrosine kinase inhibitors (vatalanib),which could offer the potential for further advances.To completely realize the active mechanism of VEGF in wet AMD is helpful for the rational use of anti-VEGF drugs.

Objective: To establish an experimental autoimmune encephalomyelitis (EAE) model in C57BL/6 mice, providing a basis for studying the immunopathological mechanism and experimental therapy of multiple sclerosis. Methods: Twenty-five C57BL/6 mice were immunized with both 300μg MOG35-55 in complete Freund's adjuvant (CFA) and 109/ml Bordetella pertussis vaccine (BPV) to establish EAE model. Mice in adjuvant group (n=8) were treated with CFA, BPV and normal saline; mice in control group (n=7) were treated with normal saline. The pathologic changes of the central nervous system were studied by H-E staining and Luxol Fast Blue (LFB) staining. Results: The clinic symptoms of EAE were present in 22 mice in model group since the 11th day post-immunization, with the incidence being 88%. There was no evident EAE symptom in CFA group and control group. Light microscopy showed there were abundant inflammatory cells infiltrated in the cerebral and spinal cord tissues in EAE mice, with evident demyelination in white matter. Conclusion: This method is easy to be carried out; the model established by it is stable and worth popularizing.

Aneuploidy ; Breast Neoplasms ; genetics ; metabolism ; pathology ; Carcinoma in Situ ; genetics ; metabolism ; pathology ; Carcinoma, Ductal, Breast ; genetics ; metabolism ; pathology ; Cell Movement ; DNA Methylation ; DNA, Neoplasm ; genetics ; Female ; Humans ; Membrane Proteins ; metabolism ; Neoplasm Invasiveness

Diagnostic Errors ; Female ; Humans ; Infant, Newborn ; Inhalation ; Male ; Organophosphate Poisoning ; Poisoning ; diagnosis

Acute Disease ; Humans ; Male ; Middle Aged ; Occupational Diseases ; therapy ; Plasma Exchange ; Propane ; analogs & derivatives ; poisoning

Antineoplastic Agents ; therapeutic use ; BRCA2 Protein ; metabolism ; Breast Neoplasms ; drug therapy ; metabolism ; pathology ; Cell Cycle Proteins ; metabolism ; physiology ; Centrosome ; metabolism ; Drug Screening Assays, Antitumor ; Female ; Humans ; Microtubule-Associated Proteins ; metabolism ; Neoplasm Invasiveness ; Nuclear Proteins ; metabolism ; Phosphorylation ; Prognosis ; Protein-Serine-Threonine Kinases ; metabolism ; physiology ; Proto-Oncogene Proteins ; metabolism ; physiology ; RNA, Small Interfering ; pharmacology ; Tumor Suppressor Protein p53 ; metabolism

Objective To investigate the effect of levosimendan on pulmonary artery pressure in patients with pulmonary hypertension undergoing mitral valve replacement.Methods Twenty-four ASA Ⅱ or Ⅲ and NY-HA class Ⅱ or Ⅲ patients,aged 35-60 yr,with mean pulmonary artery pressure (MPAP) ＞ 30 mm Hg,undergoing mitral valve replacement were randomly divided into 2 groups (n =12 each):control group (group C) and levosimendan group (group L).In group L,a loading dose of levosimendan 24 μg/kg was injected intravenously after aortic unclamping,followed by infusion of levosimendan at a rate of 0.2 μg· kg-1 · min-1 until 1 d after operation.Group C received the equal volume of normal saline.HR,MAP,MPAP,pulmonary capillary wedge pressure (PCWP),cardiac index (CI) were recorded at 5 min after induction (T0),at the end of CPB (T1) and at 1 h after operation (T2),and the pulmonary vascular resistance (PVR) and rate-pressure product (RPP) were calculated.The improvement in pulmonary hypertension was recorded.Results PCWP was significantly lower and CI higher at T1,2 in both groups,and HR was significantly higher at T1,2 and MPAP lower at T2 in group C,and MPAP and PVR were significantly lower at T1,2 in group L than at T0 (P ＜ 0.05).HR,MPAP and PVR were significantly lower and CI was significantly higher at T1,2,RPP was significantly lower at T2 and the improvement in pulmonary hypertension was higher in group L than in group C (P ＜ 0.05).Conclusion Levosimendan can improve pulmonary hypertension without increasing the myocardial oxygen consumption and with a significant increase in myocardial contractility in patients with pulmonary hypertension undergoing mitral valve replacement.

Objective To investigate a simple and dependable approach to establish the hypoxic-ischemic encephalopathy model in neonatal rat. Methods Twenty-one neonatal rats of 7 days old were randomly divided into control group,hypoxic group,and hypxic-ischemic group.Every group was randomly divided into 3 hours,6 hours,1 day,3 days,7 days, 14 days,and 21 days group,according to the time of killing.Left common carotid artery of neonatal rats at age of 7 days in hypoxic-ischemic group were ligated.Then,the rats in hypoxic and hypoxic-ischemic group were put in a state of 8% oxygen for 2.5 hours. Brain tissues of rats in 3 groups were observed with HE staining under light microscope.Results In hypoxic-ischemic group,there was found mild brain damage after hypoxic-ischomic 3 hours,the brain lesion was most severe at 1 day,glial cell proliferation was found at 3 days,much neur were losed at 14,21 days,and colloid scar was formed in cortex,striatum and hippocampi.Conclusion The method that left common carotid ontery of neonatal rats were ligated and then put in 8% oxygen for 2.5 hours is simple, rapid and dependable, which can be applied widely.