Objective To investigate the current situation of the flow maternal health management in Jinyun ,and propose in‐tervention strategies according to the results .Methods Medical records of maternal in 18 confinements hospitals in Jinyun during October 2009 to September 2013 were selected and retrospectively analyzed ,including 16 ,430 cases of household registered mater‐nal and 1 ,301 non‐household registered maternal .Maternal health management of household registered maternal and non‐household registered maternal were compared;and maternal health care management satisfaction survey were implemented for 100 cases in each group .Results The household registration book built rate ,early build rates ,system management rate ,postpartum visit rates were 99 .2% (16 297/16 430) ,96 .7% (15 882/16 430) ,95 .8% (15 733/16 430) ,and 97 .7% (16 ,057/16 430) in household regis‐tered maternal ,while which were 74 .5% (969/1 301) ,64 .0% (832/1 301) ,59 .0% (768/1 301) and 65 .5% (852/1 301) in non‐household registered maternal ,the difference was statistically significant (P<0 .05);3 cases were not satisfied during the childbirth hospitalization in household registered maternal ,the dissatisfied rate was 1 .5% ,12 cases were not satisfied during the childbirth hospitalization in non‐household registered maternal ,the dissatisfied rate was 6 .0% ,the difference was statistically significant (P<0 .05) .Conclusion There is a considerable gap in maternal Jinyun flow maternal health management and local residence ,and we should strengthen the flow of maternal health care management ,making it a fair quality of health care management and opportuni‐ties ,thus contributing to local economic and social development .

Objective:To investigate the effect of infliximab (IFX) on neurological function in mice after traumatic brain injury (TBI) and the role of nuclear factor-κB (NF-κB)/inducible nitric oxide lyase (iNOS) signaling in it.Methods:Seventy-two healthy adult male C57BL/6 mice were randomly divided into sham-operated group, TBI group, and TBI+IFX group ( n=24). The mouse TBI models were established by controlled cortical impact method. IFX (dissolved in normal saline at a concentration of 2.5 mg/mL and a dose of 10 μg/g) was administered intraperitoneally into the mice of TBI+IFX group 30 min after modeling once daily for 3 d; mice in the sham-operated group and TBI group were given the same amount of saline intraperitoneally at the same time points for 3 d. Neurological deficits (Garcia scores) were assessed one, 3 and 7 d after modeling; blood-brain barrier permeability was detected by Evans blue staining, and brain tissue water content was measured by dry and wet weight method; Nissl staining was used to detect the percentage of injured neurons in brain tissues; the percentage of apoptotic neurons was detected by Tunel staining; immunofluorescent double-labeling was used to detect the expressions of caspase-3 and neuronal nuclear antigen (NeuN) in neurons; immunohistochemical staining was used to detect the microglia marker ionized calcium binding adaptor molecule-1 (IBa-1) expression; ELISA was used to detect the expressions of inflammatory factors (tumor necrosis factor [TNF]-α, interleukin [IL]-1β, IL-6, interferon [IFN]-γ) and free radicals (oxygen free radicals [ROS], nitrogen free radicals [RNS]) in the brain tissues; and immunofluorescent staining and Western blotting were used to detect the expressions of nuclear factor (NF)-κB/inducible nitric oxide synthase (iNOS). Results:(1) One, 3 and 7 d after modeling, the Garcia scores showed significant differences among the three groups ( P<0.05); as compared with the TBI group, the TBI+IFX group had significantly increased Garcia scores 3 and 7 d after modeling ( P<0.05). (2) Three d after modeling, as compared with those in the TBI group, Evans blue leakage ([18.45±1.32] μg/g vs. [16.38±1.25] μg/g), brain water content ([81.56±0.96]% vs. [79.97±0.79]%), percentage of injured neurons ([79.50±5.85]% vs. [68.81±7.47]%), and percentage of apoptotic neurons ([41.93±7.49]% vs. [30.59±8.60]%) in mice of the TBI+IFX group were significantly deceased ( P<0.05). Three d after modeling, immunofluorescent double labeling showed that the relative caspase-3 expression in the TBI+IFX group (0.76±0.16) was significantly decreased as compared with the TBI group (1.11±0.23, P<0.05). Immunohistochemical staining and ELISA results showed that as compared with those in the TBI group, the Iba-1 staining scores, TNF-α, IL-1β, IL6 and IFN-γ levels, and ROS and RNS contents in TBI+IFX group were significantly decreased ( P<0.05). Immunofluorescent staining and Western blotting showed that as compared with the TBI group, the TBI+IFX group had significantly decreased expressions of NF-κB p65, iNOS and phosphorylated nuclear factor-κB inhibitor-α, and statistically inhibited nuclear translocation of NF-κB ( P<0.05). Conclusion:IFX can reduce inflammatory response and oxidative stress response, and play a neuroprotective role, which is related to its inhibition of downstream NF-κB/iNOS pathway activation.