The present invention provides a power factor improvement method and device used in an LED lighting system. The device comprises: a rectifier bridge and a power factor improvement module. The rectifier bridge comprises two alternating current input ends and two direct current output ends. The power factor improvement module is connected between the two direct current input ends of the rectifier bridge. The power factor improvement module comprises: a resistor group formed of a first resistor (R1), a second resistor (R2), and a third resistor (R3) connected in series sequentially; a logic control circuit, a first input end thereof being connected between the first resistor (R1) and the second resistor (R2), and a second input end thereof being connected between the first resistor (R1) and the second resistor (R2); a drive circuit, an input end thereof being connected to the logic control circuit, and an output end thereof being connected to multiple switches and used for controlling on/off of the multiple switches; and a current control module, an input end thereof being connected to the logic control circuit, and an output end thereof being connected to multiple switches.
Chen, Kehong
Wang, Yong-tang
Gu, Wei
Zeng, Ling
Jiang, Dong-po
Du, Ding-yuan
Hu, Ping
Duan, Zhao-xia
Liu, Qing
Huang, S. N.
Jiang, Jian-xin
Objective: Toll-like receptor 4 is an important signaling receptor for lipopolysaccharide in mammals, and the variation of the promoter may affect the activity of toll-like receptor 4 expression. Although 12 single nucleotide polymorphisms have been identified in the toll-like receptor 4 promoter, little is known about the functional significance of these single nucleotide polymorphisms. Design: Genetic functional and association studies. Setting: National Key Laboratory of Trauma and Departments of Traumatic Surgery in two teaching hospitals. Subjects: Three hundred seventy-nine healthy volunteers and 303 patients with major trauma. Interventions: None. Measurements and Main Results: Five single nucleotide polymorphisms identified in the toll-like receptor 4 promoter in the Chinese Han population were selected. Three of them revealed a close relationship with transcription factor binding sites. Among the three single nucleotide polymorphisms, only the T-2242C polymorphism significantly increased transcriptional activities of the toll-like receptor 4 promoter, as shown by reporter gene assay. Results from flow cytometry and ex vivo responsiveness of peripheral blood leukocytes indicated that the T-2242C polymorphism was well-associated with increased expression of toll-like receptor 4 protein and production of tumor necrosis factor-alpha. The clinical relevance of these single nucleotide polymorphisms was then investigated in 303 patients with major trauma. The peripheral blood leukocytes of trauma patients with the variant C allele revealed greater capacity to produce tumor necrosis factor-alpha and interleukin-6 on the admission day. Furthermore, the toll-like receptor 4/-2242 polymorphism was significantly associated with higher sepsis morbidity rates and multiple organ dysfunction scores in patients with major trauma. Conclusions: The toll-like receptor 4/-2242 polymorphism is a functional variant and might be used as a relevant risk estimate for organ dysfunction and sepsis in trauma patients. (Crit Care Med 2010; 38:1292-1299)
To determine the clinical relevance of 13 reported common single-nucleotide polymorphisms (SNPs) of cytokine genes in patients with major trauma. Thirteen SNPs in nine key cytokine genes were selected for association study in 308 patients with major trauma on the basis of previous functional or association data. An allele-specific oligonucleotide array was developed and used to genotype 308 patients with major trauma. The clinical relevance of the 13 SNPs was assessed by observation of cytokine production and outcome of trauma patients. Results from the allele-specific oligonucleotide array indicated that 8 [interleukin-1 beta (IL-1 beta)/-1470, IL-1 beta/-511, IL-1 beta/-31, IL-4/-589, IL-6/-572, IL-8/-251, IL-10/-819, and tumor necrosis factor alpha (TNF alpha)/-308] out of the 13 SNPs were associated with respective ex vivo cytokine production by peripheral leukocytes in response to lipopolysaccharide (LPS) stimulation at admission, or risk of development of sepsis or organ dysfunction in major trauma patients. Patients with more than four risk alleles of the eight SNPs had more than 50% sepsis morbidity and more severe organ dysfunction. Polymorphisms of IL-1 beta/-1470, IL-1 beta/-511, IL-1 beta/-31, IL-4/-589, IL-6/-572, IL-8/-251, IL-10/-819, and TNF alpha/-308 are susceptibility loci for the development of sepsis and organ dysfunction in major trauma patients.
Tubulointerstitial inflammation plays a key role in the development of diabetic nephropathy (DN). Cytokines in the IL-1 family are the key pro-inflammatory cytokines of tubulointerstitial inflammation. Extracellular ATP can cause P2X receptors to activate the NOD-like receptor 3 (NLRP3) inflammasome and cause IL-1 beta and IL-18 maturation and release. We investigated the role of ATP-P2X4 signaling in NLRP3 inflammasome activation and renal interstitial inflammation characteristic of DN. Ex vivo studies, P2X4 showed increased expression in renal tubule epithelial cells in patients with nephropathy due to type 2 diabetes compared to those in the control group. Linear correlation analysis shows that P2X4 expression was positively related with urine IL-1 p and IL-18 levels. Moreover, P2X4 expression was co-localized with NLRP3, IL-1 beta, and IL-18 expression. In vitro culture experiments showed NLRP3 protein expression, cleavage of caspase-1 and IL-1 beta, and release of IL-1 beta, IL-18 and ATP in HK-2 cells significantly increased after high glucose stimulation. However, apyrase, which consumes extracellular ATP, completely blocked the changes caused by high glucose. The P2 receptor antagonist suramin, P2X receptor antagonist TNP-ATP, P2X4 selective antagonist 5-BDBD, and P2X4 gene silencing attenuated NLRP3 expression, cleavage of caspase-1 and IL-1 beta, and release of IL-1 beta and IL-18 induced by high glucose. Taken together, these results suggest that ATP-P2X4 signaling mediates high glucose-induced activation of the NLRP3 inflammasome, regulates IL-1 family cytokine secretion, and causes the development of tubulointerstitial inflammation in DN. (C) 2013 Elsevier Ltd. All rights reserved.
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