With the improvement of people's living standard and changes of their lifestyle, the incidence of coronary artery disease (CAD) has increased quite significantly, which has attracted great concern. Examination methods for CAD are more and more advanced, while the cost of inspection is rising. As a traditional test, the exercise treadmill test (ETT) is convenient, safe, and cheap. ETT can be conducted in almost every hospital as it doesn't need advanced equipments. The values of some new evaluation indexes for diagnosis and prognosis of CAD are reviewed in this article.

Objective: To investigate the role of HIV-1 envelope protein gp120 in cognitive impairment induced by neuronal damage. Methods: Western blot and immunofluorescence assay were used to detect microglia activation, inflammatory factor expression and neuronal damage after gp120 treatment. Neuronal damage and neurocognitive performance in gp120-transgenic mice were evaluated using immunohistochemical staining and behavioral analysis, respectively. Results: In vivo and in vitro experiments showed that HIV-1 gp120 significantly induced the expression of caspase-1 and IL-1β, and indirectly caused neuronal synaptic shortening and neuronal damage (P<0.05). Compared with wild-type mice, gp120-transgenic mice showed significant cortical and hippocampal glial activation, neuronal loss, dendritic damage and neurocognitive disorders. Conclusions HIV-1 gp120 might cause neuronal damage through activating the release of inflammatory factor by microglia and involve in neurocognitive impairment.

OBJECTIVE: To construct a HIV-1 gp120 transgenic mouse model (gp120) with 7 nicotinic acetylcholine receptor (7nAChR) gene knockout. METHODS: The 7nAChR gene knockout mice (7R) were crossed with HIV-1gp120 transgenic mice (gp120) to generate F1 generation mice. We selected the F1 mice with the genotype of 7R/gp120 to mate to obtain the F2 mice. The genotypes of the F3 mice were identified by PCR, and the protein expressions in the double transgenic animal model was analyzed by immunohistochemistry. BV2 cells were treated with gp120 protein and 7nAChR inhibitor, and the expressions of IL-1β and TNF- were detected using ELISA. RESULTS: The results of PCR showed the bands of the expected size in F3 mice. Two F3 mice with successful double gene editing (7R/gp120) were obtained, and immunohistochemistry showed that the brain tissue of the mice did not express 7 nAChR but with high gp120 protein expression. In the cell experiment, treatment with gp120 promoted the secretion of IL-1β and TNF- in BV2 cells, while inhibition of 7nAChR significantly decreased the expression of IL-1β and TNF- ( < 0.001). CONCLUSIONS By mating gp120 Tg mice with 7R mice, we obtained gp120 transgenic mice with 7nAChR gene deletion, which serve as a new animal model for exploring the role of 7nAChR in gp120-induced neurotoxicity.
Animals ; Disease Models, Animal ; Glycoproteins ; Mice ; Mice, Knockout ; Mice, Transgenic ; Tumor Necrosis Factor-alpha ; alpha7 Nicotinic Acetylcholine Receptor ; metabolism