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AIM: To investigate the effect of hypercapnia on hypoxia-induced pulmonary hypertension and the changes of lysyl oxidase (LOX) and extracellular matrix collagen cross-links in the rat.METHODS: Sprague-Dawley rats were randomly divided into 4 groups: normoxia group, hypoxia group, hypercapnia group and hypoxia+hypercapnia group.LOX activity was detected by fluorescence spectrophotometry.LOX protein expression was detected by immunohistochemistry and Western blot.The mRNA expression of LOX in the pulmonary artery was detected by real-time PCR.RESULTS: The levels of mean pulmonary artery pressure (mPAP), RV/(LV+S) and WA/TA in hypoxia group were significantly higher than those in normoxia group (P<0.01).Moreover, the levels of mPAP and RV/(LV+S) in hypoxia+hypercapnia group were significantly lower than those in hypoxia group (P<0.01).However, no significant difference of mPAP and RV/(LV+S) between hypercapnia group and normoxia group was observed.In hypoxia group, the collagen cross-links in the lung tissue was significantly higher than that in normoxia group and hypercapnia group (P<0.01).Importantly, collagen cross-links in the lung tissue of hypoxia+hypercapnia group was significantly lower than that in hypoxia group (P<0.01).There was no significant difference in collagen cross-links between hypercapnia group and normoxia group.The expression of LOX at mRNA and protein levels and its activity in the pulmonary arteries of hypoxia group were significantly increased as compared with normoxia group (P<0.01).Furthermore, the expression of LOX at mRNA and protein levels and its activity in the pulmonary arteries in hypoxia+hypercapnia group were lower than those in hypoxia group (P<0.01).CONCLUSION: Hypoxia not only up-regulates LOX but also promotes collagen cross-linking in the rat lung, which contributes to the development of pulmonary hypertension.Hypercapnia inhibits hypoxia-induced LOX expression and collagen cross-linking, therefore impairing the progress in hypoxia-induced pulmonary hypertension.
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Objective To investigate the influence factors of left ventricular hypertrophy ( LVH) in incipient systemic lupus erythe-matosus (SLE) patients with lupus nephritis (LN).Methods A total of 210 LN patients in the authors′centre were enrolled in this cross-section study .General information , laboratory measurements , examinations of left ventricular hypertrophy by ultrasonography were col -lected.Patients were divided into two groups according to left ventricular mass index (LVMI):left ventricle thickening (LVT) group (n=89) and left ventricle normal group (n=121).General information and laboratory results of two groups were statistically analyzed .In-fluence factors of the patients were analyzed with Spearman rank correlation and multiple linear regression .Results Serum uric acid and hyper-sensitive C-reactive protein (hs-CRP) were higher in left ventricular thickening (LVT)group, as compared with those in left ventricle normal group .Hemoglobin and estimated glomerular filtration rate ( eGFR) in LVT group were significantly lower than those in left ventricle normal group (P<0.05).Spearman rank correction indicated that LVH was positively correlated with serum uric acid and hs-CRP (r=0.283、0.327, all P<0.05).LVH was negatively correlated with hemoglobin and eGFR (r=-0.232, -0.186, all P<0.05).Multiple linear regression showed hs -CRP and hemoglobin correlated with LVH (β=0.235、-0.206, all P<0.05).Conclu-sion Inflammatory state and anemia were risk factors of LVH in LN patients .
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AIM: B cells are likely to play critical roles in the pathogenesis of systemic lupus erythematosus (SLE). Our aim was to investigate the role of peripheral CD24(hi) CD27(+) CD19(+) B cells in Chinese patients with new-onset SLE. METHOD: Peripheral CD24(hi) CD27(+) CD19(+) B cells were analyzed in 55 new-onset lupus and 36 healthy controls by flow cytometry. All SLE cases were treated with prednisolone and hydroxychloroquine during a 1-year follow-up. Thirteen cases were added with cyclophosphamide or mycophenolate mofetil. The CD24(hi) CD27(+) CD19(+) B cells were analyzed at days 0, 7, 14 and months 1, 3, 6, 9 and 12. Interleukin-10 (IL-10)-producing B cell was detected in eight naïve lupus and 10 healthy controls. RESULTS: Compared to healthy controls, the frequency and number of primary circulating CD24(hi) CD27(+) CD19(+) B cells was significantly reduced in SLE cases (8.22 ± 3.48% vs. 31.67 ± 5.53%, P < 0.0001; 4.04 ± 2.85 vs. 38.66 ± 10.22 10(3) cells/mL, P = 0.0001) before treatment; IL-10(+) CD19(+) B cells and IL-10(+) CD24(hi) CD27(+) CD19(+) B cells also decreased in SLE. Interestingly, primary CD24(hi) CD27(+) CD19(+) B cells inversely correlated with SLE disease activity index (SLEDAI) score. Patients with arthritis and hematologic disorders had a lower primary CD24(hi) CD27(+) CD19(+) B cells. In 48 SLE cases who finished the 1-year follow-up, the frequency and number of CD24(hi) CD27(+) CD19(+) B cells increased from 8.26 ± 3.61% to 25.51 ± 4.56%; 3.99 ± 2.86 to 28.64 ± 11.81 10(3) cells/mm(3) (P < 0.0001), accompanied by a significantly decreased SLEDAI score. Of note, CD24(hi) CD27(+) CD19(+) B cells decreased in some flare cases with an elevated SLEDAI score. CONCLUSION: These results demonstrate that a lower primary CD24(hi) CD27(+) CD19(+) B cells may be an immunologic aspect of new-onset SLE. CD24(hi) CD27(+) CD19(+) B cells may be a useful tool to evaluate lupus activity and monitor the response to therapy.