A study on the rapid diagnosis of chronic heart failure by measuring the difference in pulse oxygen saturation before and after arm compression.

BACKGROUND: Clinically, the pulse oxygen saturation of patients with chronic heart failure does not decrease significantly, and the clinical manifestations of labor-related dyspnea are not typical. As such, it is difficult to make a rapid diagnosis. OBJECTIVE: To investigate changes in pulse oxygen saturation in patients with chronic heart failure and examine the relationship between B-type natriuretic peptide (BNP) and normal pulse oxygen saturation. METHODS: A total of 80 hospitalized patients with chronic heart failure and increased BNP were randomly selected as the study group; the family members of 60 patients without dyspnea were randomly selected as the control group. The researchers measured the value of pulse oxygen saturation before and after upper arm compression, calculating the difference and analyzing the correlation between this difference and BNP values. The data were statistically analyzed using the SPSS Statistics 17.0 program. RESULTS: The decrease in pulse oxygen saturation in the study group was greater than in the control group; the decrease in pulse oxygen saturation of patients with chronic heart failure positively correlated with BNP. CONCLUSION: The value of pulse oxygen saturation in patients with chronic heart failure decreased more than in the control group, and this difference positively correlated with BNP. The measurement of pulse oxygen saturation before and after upper arm compression is a simple and effective method for diagnosing and evaluating chronic heart failure.

IL-17A induces pro-inflammatory cytokines production in macrophages via MAPKinases, NF-κB and AP-1.

BACKGROUND: Interleukin (IL)-17A, a newly identified cytokine, may participate in the transition of a stable plaque into an unstable plaque. Macrophages play a critical role in the destabilization of atherosclerotic plaque. METHODS: RAW 264.7 cells were stimulated with IL-17A. The mRNA expression of inflammatory cytokines was determined by RT-PCR. The cytokines production in the supernatants was measured by ELISA. Small interfering RNA (siRNA) was used to confirm that IL-17A-induced pro-inflammatory cytokines production via IL-17RA signaling. The western blot assay was used to detect the phosphorylation of MAPKinases including p38 and ERK1/2. The DNA binding activity of nuclear factor NF-κB and AP-1 were detected by EMSA. RESULTS: IL-17A induced the production of pro-inflammatory cytokines in macrophages in a time- and dose-dependent manner, such as tumor necrosis factor (TNF)-α, IL-1ß, and IL-6. Meanwhile, IL-17A resulted in the phosphorylation of p38 and ERK1/2 and increased DNA-binding activity of NF-κB and AP-1. Pharmacological inhibitors of p38 and ERK1/2 partly attenuated IL-17A-induced TNF-α, IL-1ß, and IL-6 production. Either NF-κB inhibitor or AP-1 inhibitor also partly decreased the IL-17A-induced cytokine production. CONCLUSIONS: IL-17A induces pro-inflammatory cytokines production in macrophages via MAPKinases, NF-κB and AP-1 pathway.

Inhibition of IL-17A in atherosclerosis.

OBJECTIVE: To determine the effects of interleukin (IL)-17A inhibition on experimental atherosclerosis. METHODS AND RESULTS: ApoE(-/-) mice were treated with either rat anti-mouse IL-17A, mouse anti-mouse IL-17A or isotype-matched control antibodies for 12 weeks (n=8-10 per group). Ldlr(-/-) mice were transplanted with IL-17A-deficient or wild type bone marrow (n=8 per group). Rat anti-mouse IL-17A treatment obviously reduced plaque size by 43% (p<0.01) without evidence of reduced IL-17A signaling. In contrast, mouse anti-mouse IL-17A treatment and IL-17A deficiency in bone marrow cells did not alter lesion size despite significant reduction of IL-17A production. CONCLUSIONS: Inhibition of IL-17A signaling does not alter lesion development in Th1-biased C57BL/6 ApoE(-/-) and Ldlr(-/-) mice with already low levels of IL-17A production. Alteration of lesion development after repeated injections of rat anti-mouse IL-17A antibody in ApoE(-/-) mice could not be attributed to blockade of IL-17A signaling.

The Th17/Treg functional imbalance during atherogenesis in ApoE(-/-) mice.

OBJECTIVE: Atherosclerosis is a chronic inflammatory disease regulated by T lymphocyte subsets. Recently, CD4(+) CD25(+) Foxp3(+) regulatory T (Treg) cells and Th17 cells have been described as two distinct subsets and have the opposite effects on autoimmunity. Clinical observation has revealed that the Th17/Treg imbalance exists in patients with acute coronary syndrome. We investigated whether the Th17/Treg functional imbalance existed during atherogenesis in ApoE(-/-) mice. METHODS AND RESULTS: Th17/Treg functions at different levels including cell frequencies, related cytokine secretion and key transcription factors were investigated comparatively between ApoE(-/-) mice and their age-matched C57BL/6J mice. The results demonstrated that ApoE(-/-) mice revealed significantly increased secretion of Th17 related cytokines (IL-17 and IL-6) and expression of transcription factor (RORgammat) levels and obviously decreased number in Treg cells, secretion of Treg related cytokines (TGF-beta(1)) and expression of transcription factor (Foxp3) levels as compared with age-matched C57BL/6J mice. Th17 related mediators reached their maximum expression values at the early stage (8-16weeks of age) in ApoE(-/-) mice, and then followed by continuous depression of their expression levels. Meanwhile, the expression of Treg related mediators was much lower in ApoE(-/-) mice than in their age-matched wild-type littermates. CONCLUSIONS: Th17/Treg functional imbalance exists during atherogenesis in ApoE(-/-) mice, suggesting a potential role of Th17/Treg imbalance in the formation and progression of atherosclerosis.