OBJECTIVE To study the cell-mediated immune function among older inpatients with Pseudomonas aeruginosa pneumonia.METHODS T-cell subsets and expression of membrane molecule on activated T-cell in peripheral blood were measured in 35 cases with P.aeruginosa pneumonia by using immunofluorescence and flow cytometry,and compared with those of control healthy older people.RESULTS The expressions of CD4+ /CD3+ and CD25+ /CD3+ in P.aeruginosa pneumonia patients were lower than in control group(P0.05).CONCLUSIONS There are disfunctions of lymphocgte and immunity among P.aeruginosa pneumonia patients.

Objective This study aimed to investigate the role of pyrroloquinoline quinone (PQQ) in repairing oxidative nerve cells,and to study the antioxidant capacity of PQQ on the oxidative damage of rats caused by apolexis,as well as the effects on learning and memory abilities of apolexis rats.Methods Oxidative damage of PC12 was induced by H2O2,and the repairing rate of PQQ on oxidative PC12 cells was tested by methylthiazolyldiphenyl-tetrazolium bromide assay kit.The 18-month-old male SD rats were administered PQQ (0,10,20,40 mg/kg).After 4 weeks,Morris water maze test was used to test the learning and memory ability.After 6 weeks,serum and brain tissue related indicators and antioxidant capacity were recorded.Results The survival rate of PC12 cells increased from 59.1％ to 90.5％ with 200 nmol/L PQQ.Compared with the apolexis model group,the latency of the PQQ group (20,40 mg/kg) was shortened in the Morris water maze experiment,the swimming distance was reduced,pass-through counts were increased,and the first secure platform pass-through was reduced.Meanwhile,the levels of malondialdehyde and lipofuscin in serum and brain tissue of PQQ group decreased,the levels of superoxide dismutase,glutathione peroxidase vitality,antioxidant capacity of PQQ group (20,40 mg/kg) were enhanced.Conclusion PQQ could repair the oxidative damage of nerve cells,and it was confirmed that PQQ could play the same antioxidant effect in body and brain,and increase the learning and memory ability of apolexis rats.

Cerebral edema and its caused elevated intracranial pressure are one of the main causes of death in patients with acute ischemic stroke. The main pathogeneses of brain edema include cytotoxic edema, ionic edema, and angiogenic edema. At present, the treatment strategies used to control brain edema and reduce intracranial pressure are mainly osmotic drugs and hemicraniectomy decompression, which are symptomatic treatments to reduce intracranial pressure. In recent years, it has been proposed to inhibit the ion channel in the formation of brain edema as a therapeutic target, which provides a new direction for the treatment of brain edema.

In recent years, many studies have found that white matter hyperintensity (WMH) of presumed vascular origin is closely related to cognitive impairment, which reflects the negative effects of white matter macrostructure damage on cognition, while diffusion tensor imaging (DTI) can quantify white matter microstructure damage through different imaging parameters. A variety of DTI parameters are associated with cognitive impairment in WMH, and are of great value in early diagnosis, evaluation of progress risk and efficacy of cognitive impairment. On the basis of DTI, the relevant parameters of brain structural network obtained by joint the graph theory analysis method are also considered to be related to the cognitive impairment with WMH. This paper reviews the latest progress of DTI derived parameters, brain structural network parameters and their relations with WMH cognitive impairment.