In vitro biosynthesis of plasma proteins under ischemic conditions of closed-circuit perfusion of healthy and intoxicated rabbit liver

We are elaborating on the kinetics and mechanisms of septic rabbit liver to de novo biosynthesize acute-phase response (APR) proteins under in vitro conditions of deepening ischemia in reference to their in vivo prevalence in serum and cerebrospinal fluids (CSF) collected at predetermined times. The significance of the data is interpreted as relevant to grafting cadaveric liver into end-stage liver diseased patients and APR-induced ischemic heart diseases (IHD). Hepatic APR was induced by CCl(4)-intubation, and the administration of cholera toxin (CT) or scorpion venom (SV), or both, to rabbits. Hepatic functional efficiency, in terms of biosynthesis of APR proteins in closed circuit perfusion of the isolated intoxicated liver with oxygenated saline or L-15 media paralleled the two-dimensional immunoelectrophoresis (2D-IEP) spectrum of APR serum proteins at time of liver isolation. We are suggesting: (a) in vitro biosynthesis of plasma proteins by isolated perfused liver is the result of in vivo decoded and retained APR inflammatory signals; and (b) decoded inflammatory signals are expressed not withstanding the perfusate's organic composition. Furthermore, 90 min of ischemic perfusion in saline or L-15 medium precipitated mitochondrial aberrations which resulted in further deterioration of de novo biosynthesis of APR plasma proteins. Regardless of the nature of the inflammatory stimuli, mitochondrial aberrations rendered the perfused organ a biologically inert tissue mass that was incapable of resuming biological function upon perfusion with oxygenated L-15 medium. This is most likely due to ischemia-induced irreversible hepatic necrosis. Thus, in vitro aberrations of mitochondrial function(s) critically limit the capability of the isolated liver to resume its organic function to sustain biosynthesis of de novo plasma proteins. Extrapolation of these results to the surgical management of end-stage liver diseases points to the importance of the status and the handling protocol(s) of the cadaver donor liver prior to successful grafting. We conclude that although histology of a cadaver liver may reveal well-preserved hepatic cellular organelles with at least minimal intra- and intercellular communication required for viable hepatic function, we deem it essential to further define acceptable minimal capabilities to de novo biosynthesize plasma proteins by a cadaver liver as a measure of its functional viability and suitability for transplantation. Ultimately, this measure may improve the success of liver transplants with minimal surgical and drug interventions.     

消化道无线内窥镜便携式图像接收装置的硬件设计

消化道无线内窥镜便携式图像接收装置是在TMS320C6211DSP的基础上进行开发的。先对摄像胶囊发出的调制信号进行接收和解调，然后利用视频解码芯片SAA7114H的同步信号，经过时序逻辑变换，控制对断续视频信号的采集，并将其存储到CF卡中。此外．还利用高速DSP对图像信号进行预处理和压缩．可大大节约数据的存储空间和处理时间。     

RAGE: a new frontier in chronic airways disease

Asthma and chronic obstructive pulmonary disease (COPD) are heterogeneous inflammatory disorders of the respiratory tract characterized by airflow obstruction. It is now clear that the environmental factors that drive airway pathology in asthma and COPD, including allergens, viruses, ozone and cigarette smoke, activate innate immune receptors known as pattern-recognition receptors, either directly or indirectly by causing the release of endogenous ligands. Thus, there is now intense research activity focused around understanding the mechanisms by which pattern-recognition receptors sustain the airway inflammatory response, and how these mechanisms might be targeted therapeutically. One pattern-recognition receptor that has recently come to attention in chronic airways disease is the receptor for advanced glycation end products (RAGE). RAGE is a member of the immunoglobulin superfamily of cell surface receptors that recognizes pathogen- and host-derived endogenous ligands to initiate the immune response to tissue injury, infection and inflammation. Although the role of RAGE in lung physiology and pathophysiology is not well understood, recent genome-wide association studies have linked RAGE gene polymorphisms with airflow obstruction. In addition, accumulating data from animal and clinical investigations reveal increased expression of RAGE and its ligands, together with reduced expression of soluble RAGE, an endogenous inhibitor of RAGE signalling, in chronic airways disease. In this review, we discuss recent studies of the ligand–RAGE axis in asthma and COPD, highlight important areas for future research and discuss how this axis might potentially be harnessed for therapeutic benefit in these conditions.     

慢性阻塞性肺疾病患者SAA及IP-10与炎性因子水平相关性分析

目的 探讨慢性阻塞性肺疾病患者SAA及IP-10与炎性因子水平相关性分析.方法 选择慢阻肺患者78例,分为AECOPD组(A组)、COPD组(B组),并选择健康人群50例为对照组(C组),分别有31、47、50例,分别对各组SAA及IP-l0与炎性因子进行检测.结果 A组患者SAA及IP-10水平较B、C组均出现升高(P＜0.05),B组患者较C组SAA及IP-10均出现升高(P＜0.05).A组患者IL-1、IL-6、TNF-α较B、C组均出现升高(P＜0.05),B组患者较C组IL-1、IL-6、TNF-α均出现升高(P＜0.05).SAA与IL-6、NF-α显正相关(P＜0.05),与IL-1未见显著相关性(P＞0.05),IP-10与IL-1、IL-6、TNF-α正相关(P＜0.05).结论 SAA及IP-10水甲升高与炎性因子密切相关,共同参与慢阻肺患者病情进展.     

祖卡木颗粒联合利巴韦林治疗小儿急性上呼吸道感染的临床研究

目的探讨祖卡木颗粒联合利巴韦林治疗小儿急性上呼吸道感染的临床有效性和安全性。方法选取2016年3月—2017年3月在荆州市中医院就诊的小儿急性上呼吸道感染患儿141例,根据用药不同将患儿分成对照组(70例)和治疗组(71例)。对照组患儿静脉滴注利巴韦林注射液,10 mg/kg加入生理盐水稀释成1 mg/mL滴注,2次/d。治疗组患儿在对照组基础上口服祖卡木颗粒,1袋/次,3次/d。两组患儿均连续治疗5d。观察两组患儿临床疗效,同时比较治疗前后两组患者临床症状消失时间、血清淀粉样蛋白A(SAA)、白细胞计数(WBC)、超敏C反应蛋白(hs-CRP)水平及不良反应情况。结果治疗后,对照组和治疗组患儿临床有效率分别为85.71%和97.18%,两组比较差异具有统计学意义(P0.05)。治疗后,治疗组患儿体温恢复、咳嗽消失和咽喉红肿消失时间均明显早于对照组(P0.05)。治疗后,两组患儿血清SAA和hs-CRP水平均明显降低(P0.05),WBC水平明显升高(P0.05),且治疗组患儿血清SAA、hs-CRP和WBC水平明显优于对照组(P0.05)。治疗期间,治疗组患儿不良反应发生率为4.23%,明显低于对照组的15.71%,两组比较差异具有统计学意义(P0.05)。结论祖卡木颗粒联合利巴韦林治疗小儿急性上呼吸道感染临床疗效好、安全性高,具有一定的临床推广应用价值。     

Serum Amyloid A Protein in Acute Myocardial Infarction

ABSTRACT Tissue injury including myocardial infarction leads to a variety of changes in plasma proteins commonly referred to as “the acute phase response”. In this report the concentrations of serum amyloid A protein (SAA) were measured serially in 6 patients with myocardial infarction and 4 with angina. SAA was found to be increased in all patients with infarction, but in no patients with angina. Significantly increased SAA levels were detected 12 hours after the peak level of creatine kinase, and the concentrations of SAA seemed to correlate to the amount of damaged tissue. The SAA-response was both faster and more extensive than the response of C-reactive protein (CRP), but the correlation between SAA and CRP was very good.     

Effect of influenza vaccine on markers of inflammation and lipid profile

Despite wide use of the influenza vaccine, relatively little is known about its effect on the measurement of inflammatory markers. Because inflammatory markers such as C-reactive protein (CRP) are increasingly being used in conjunction with lipids for the clinical assessment of cardiovascular disease and in epidemiologic studies, we evaluated the effect of influenza vaccination on markers of inflammation and plasma lipid concentrations. We drew blood from 22 healthy individuals 1 to 6 hours before they were given an influenza vaccination and 1, 3, and 7 days after the vaccination. Plasma CRP, interleukin (IL)-6, monocyte chemotactic protein 1, tumor necrosis factor alpha, IL-2 soluble receptor alpha, and serum amyloid A were measured, and differences in mean concentrations of absolute and normalized values on days 1, 3, and 7 were compared with mean baseline values. There was a significant increase in mean IL-6 (P < .01 absolute values, P < .001 normalized values) on day 1 after receiving the influenza vaccine. The mean increases in normalized high sensitivity CRP values were significant on day 1 (P < .01) and day 3 (P = .05), whereas the mean increase in normalized serum amyloid A was significant only on day 1 (P < .05). No significant changes were seen in mean concentrations of IL-2 soluble receptor alpha, monocyte chemotactic protein-1, or tumor necrosis factor-alpha. Of the lipids, significant decreases in mean concentrations of normalized triglyceride values were seen on days 1 (P < .05), 3 (P < .001), and 7 (P < .05) after vaccination. Our findings show that the influenza vaccination causes transient changes in select markers of inflammation and lipids. Consequently, clinical and epidemiologic interpretation of the biomarkers affected should take into account the possible effects of influenza vaccination.     

Acute phase response in Chinese soft-shelled turtle (Trionyx sinensis) with Aeromonas hydrophila infection

Chinese soft-shelled turtle (Trionyx sinensis) is an important culture reptile. However, little is known about its acute phase response (APR) caused by bacteria. Serum amyloid A (SAA) is a major acute phase protein (APP). In this study, a turtle SAA homologue was identified and described in reptiles. The full-length cDNA of turtle SAA was 554 bp and contained a 381 bp open reading frame (ORF) coding for a protein of 127 aa. Similar to other known SAA genes, the turtle SAA gene contained three exons and two introns. The promoter region of turtle SAA gene contained the consensus binding sites for nuclear factor (NF)-κB and c-Rel. The turtle SAA amino acid sequence shared the highest identity to avian SAA sequences. Meantime, we present the first systematic study with expression levels of five genes encoding APPs in immune response caused by Aeromonas hydrophila infection. After infection, turtle SAA mRNA was induced in liver at 8 h, then increased more than 1200-fold at 2 d; in spleen and kidney, the SAA mRNAs were also induced during 8 h-7 d, but the level was far lower than that in the liver. The complement 3 (C3), fibrinogen-gamma chain (Fb-G) and cathepsin L (CathL) mRNAs were increased in liver at 2 d, whereas the albumin (ALB) mRNA was significantly decreased during 8 h-7 d. Our studies suggest that the APR in turtle with A. hydrophila infection is similar to that in mammals, and SAA is a major indicator of bacterial infection, especially at early stage, in reptiles. Additionally, the different expression patterns of five APP genes observed in present studies could provide clues for understanding the innate immune mechanisms in the APR of reptiles.