Objective To analyse the pathogeny of pregnancy with virus hepatitis,the change of index of hepatic function and the clinical pathogenetic characteristic,and to explore the relationship between pregnancy and hepatitis.Methods The clinical datas of 96 pregnant patients with virus hepatitis were retrospectively analyzed,and compared with non-pregnancy during the reprodective age in the corresponding period.The pathogeny,index of hepatic function and clinical pathogenetic characteristic were compared.Results Virus hepatitis in the pregnancy were mostly type B hepatits,the morbility of hepatitis increased gradually along with the progress of pregnant weeks,the prothrombin time(PT) significantly prolonged in pregnancy with virus hepatitis,and the albumin decreased significantly,the complications of hepatocerebral disease and hepatorenal syndrome were more than non-pregnancy with virus hepatits,the incidence rate of serious hepatiti was higher than non-pregnancy with virus hepatitis(P

Objective To study the correlation between the level of serum ferritin(SF) and the degree of liver damagement with severe hepatitis B,and the clinical significance of SF changes in judging the prognosis.Methods The level of SF was detected by radioimmunoassay(RIA) from 62 cases with severe hepatitis B,the level of SF from acute hepatitis B,chronic hepatitis B,liver cirrhosis and normal men were served as contrast study.Results The level of SF from severe hepatitis B was significantly higher than those from acute hepatitis B,chronic hepatitis B,liver cirrhosis and normal men;the level of SF was positively correlated with total bilirubin(TB),prothrombin time(PT),total bile acid(TBA) and negatively with Alb,ALT,AST,CHE.The levels of SF of those who died were significantly higher than those of suvivals;the level of SF decreased as the disease controlled and increased as the disease deterio-rated.Conclusions There is a parallel correlationship between the level of SF and the degree of liver damagement with severe hepatitis B,the severer the hepatocyte damage was,the higher the ferritin was.It is helpful to judge the degree of damagement and prognosis of severe hepatitis by detecting the level of serum ferritin.

Pericytes are a kind of microvascular parietal cells, which constitute neurovascular units together with neurons, astrocytes, microglia, vascular endothelial cells and vascular smooth muscle cells to maintain the basic function of the brain. Pericyte dysfunction can lead to cerebral microcirculation dysfunction, which is related to the occurrence and development of a variety of nervous system diseases. This article reviews the characteristics, identification and subtypes of pericytes, their relations with cerebral microcirculation, and their correlation with central nervous system diseases.

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.