Objective To elucidate the relationship between quality of life (QOL) and disease activity of systemic lupus erythematosus (SLE),as well as to reveal the factors impacting disease activity and the QOL of SLE utilizing the combination of SLE-specific quality of life questionnaire (SLEQOL) and the medical outcomes survey short form 36 (SF-36).Methods SLEQOL and SF-36 health survey questionnaire were applied.Information on gender,disease duration,age,education level were collected.Serum complement (C3 and C4) level and erythrocyte sedimentation rate (ESR) were measured.Patients were divided into inactive,mild active,moderate active and severe active respectively according to SLE disease activity index (SLEDAI).Pearson's product moment correlation coefficient was used to analyze the correlation between the activity of disease and the QOL.Multiple linear regression was employed to explore the factors which could impact on SLEQOL.Results The physical function of SLEQOL was positively correlated with SLEDAI (r=0.36; P＜0.05).The association between reported health transition of SF-36 and SLEDAI was positive (r=0.19; P＜0.05).Physical functioning,role-physical,role-emotional,body pain and vitality were all negatively correlated with SLEDAI (r:-0.20,-0.19,-0.19,-0.19,-0.21 respectively; P＜0.05).The scores of patients with severe disease activity were significantly increased in the physical functioning of SLEQOL than other three groups (18±10 vs 11±5,12±6,13±7; P＜0.05).Scores on the Health transition of patients with moderate and severe disease activity were lower than those of whom with mild disease activity (23±28.14±17 vs 34±39,P＜0.05).Patients with mild or severe disease activity had lower score than those of patieuts in disease inactive (30±41,34±39 vs 44±44,P＜0.05).Multiple linear regression analyses showed that disease duration and education level might be the influencing factors of SLEQOL.Conclusion QOL of patients with SLE is related to the level of disease activity and is impacted by disease duration and education.

OBJECTIVE: To demonstrate the mechanism of mechanical ventilation (MV) induced endoplasmic reticulum stress (ERS) promoting mechanical ventilation-induced pulmonary fibrosis (MVPF), and to clarify the role of angiotensin receptor 1 (AT1R) during the process. METHODS: The C57BL/6 mice were randomly divided into four groups: Sham group, MV group, AT1R-shRNA group and MV+AT1R-shRNA group, with 6 mice in each group. The MV group and MV+AT1R-shRNA group mechanically ventilated for 2 hours after endotracheal intubation to establish MVPF animal model (parameter settings: respiratory rate 70 times/minutes, tidal volume 20 mL/kg, inhated oxygen concentration 0.21). The Sham group and AT1R-shRNA group only underwent intubation after anesthesia and maintained spontaneous breathing. AT1R-shRNA group and MV+AT1R-shRNA group were airway injected with the adeno-associated virus one month before modeling to inhibit AT1R gene expression in lung tissue. The expressions of AT1R, ERS signature proteins [immunoglobulin heavy chain-binding protein (BIP), protein disulfide isomerase (PDI)], fibrosis signature proteins [collagen I (COL1A1), α-smooth muscle actin (α-SMA)] in lung tissues were detected by immunofluorescence and Western blotting. Hematoxylin-eosin (HE) staining was used to evaluate lung injury and Masson staining was used to evaluate pulmonary fibrosis. RESULTS: Compared with the Sham group, the degree of pulmonary fibrosis and lung injury were more significant in the MV group. In the MV group, the protein expressions of AT1R, BIP, PDI, COL1A1 and α-SMA were increased (AT1R/β-actin: 1.40±0.02 vs. 1, BIP/β-actin: 2.79±0.07 vs. 1, PDI/β-actin: 2.07±0.02 vs. 1, COL1A1/α-Tubulin: 2.60±0.15 vs. 1, α-SMA/α-Tubulin: 2.80±0.25 vs. 1, all P < 0.01). The number of E-cad⁺/AT1R⁺ and E-cad⁺/BIP⁺ cells in lung tissue increased, and the fluorescence intensity of COL1A1 and α-SMA increased. Compared with the MV group, the degree of pulmonary fibrosis and lung injury were significantly relieved in the MV+AT1R-shRNA group. In the MV+AT1R-shRNA group, the protein expressions of AT1R, BIP, PDI, COL1A1 and α-SMA were decreased (AT1R/β-actin: 0.53±0.03 vs. 1.40±0.02, BIP/β-actin: 1.73±0.15 vs. 2.79±0.07, PDI/β-actin: 1.04±0.07 vs. 2.07±0.02, COL1A1/α-Tubulin: 1.29±0.11 vs. 2.60±0.15, α-SMA/α-Tubulin: 1.27±0.10 vs. 2.80±0.25, all P < 0.01). The number of E-cad⁺/AT1R⁺ and E-cad⁺/BIP⁺ cells in lung tissue decreased, and the fluorescence intensity of COL1A1 and α-SMA decreased. There was no statistically significant difference in the indicators between AT1R-shRNA group and Sham group. CONCLUSIONS MV up-regulate the expression of AT1R in alveolar epithelial cells, activate the AT1R pathway, induce ERS and promote the progression of MVPF.
Mice ; Animals ; Pulmonary Fibrosis/chemically induced* ; Lung Injury ; Respiration, Artificial/adverse effects* ; Actins/metabolism* ; Tubulin ; Mice, Inbred C57BL ; Endoplasmic Reticulum Stress ; RNA, Small Interfering