Staging Sequential Treatment of Ischemic Stroke Based on Syndrome Differentiation of Deficiency and Excess in Eight Principles / 中国实验方剂学杂志

The core of diagnosing and treating diseases in traditional Chinese medicine lies in syndrome differentiation. The eight principles of syndrome differentiation serve as guidance for syndrome differentiation. As one of the eight principles of syndrome differentiation， the differentiation of deficiency and excess is the basic and critical method. Ischemic stroke is currently the leading cause harming the health of Chinese residents. Although the hypotheses about the cause of ischemic stroke have evolved from external wind to the later internal wind and to the modern theory of toxin damaging the brain collaterals， they all believe that this disease is rooted in internal deficiency and external excess. According to available studies， although stroke is characterized by complex pathogenesis and rapid progression of syndromes， the key cause evolution has a regularity， that is， from excess to deficiency. This article analyzes the historical evolution of the etiology， pathogenesis， and syndrome differentiation schemes of stroke. There are diverse schemes for the syndrome differentiation of stroke， which make it difficult to choose in clinical practice. In view of this problem， this paper puts forward a new approach of staging sequential treatment of ischemic stroke based on the differentiation of deficiency and excess according to the evolution law of the key cause of stroke. Furthermore， we conducted a randomized controlled study on 100 patients with ischemic stroke to evaluate this new approach. The results showed that the staging sequential treatment of ischemic stroke based on the differentiation of deficiency and excess demonstrated definite clinical efficacy. In addition， this article reviews the previous research results of our team and the research achievements of other teams to preliminarily explore the relationship between stroke syndromes and biomarkers， aiming to provide an objective basis for unveiling the pathogenesis of stroke. In summary， according to the key cause evolution （from excess to deficiency）， the treatment of ischemic stroke by stages based on differentiation of deficiency and excess can facilitate the rapid intervention and improve the clinical efficacy on ischemic stroke.

Retrospect and prospect of IP-10 in the pathogenesis of autoimmune diseases / 中华检验医学杂志

Interferon-γ-inducible protein 10 (IP-10),also known as chemokine (C-X-C motif) ligand 10(CXCL10),belongs to the CXC subfamily.IP-10 exerts its function by binding to chemokine (C-X-C motif) receptor 3 or Toll-like receptor 4.IP-10 plays an important role in the occurrence and development of autoimmune diseases.The expression of IP-10 in blood and body fluid is closely associated with the activity of autoimmune disease.IP-10 is expected to become a potential new marker and possess a significant application value in early screening,condition monitoring and therapeutic evaluation of autoimmune diseases.

Effects of valsartan on plasma resistin and microinflammation in patients with maintenance hemodialysis / 中华全科医师杂志

In total, 106 patients with maintenance hemodialysis (MHD) were divided into two groups based on their valsartan administration, and 53 healthy controls were recruited in the study. Plasma concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), resistin and high sensitivity C-reactive protein (hs-CRP) were measured by enzyme-linked immunosorbent assay (ELISA) before and after valsartan treatment. Plasma levels of resistin, IL-6, TNF-α and hs-CRP were all significantly increased in patients with MHD as compared to those in healthy controls (P＜0. 05). Among patients with MHD the plasma levels of resistin, IL-6 and hs-CRP in valsartan group were lower than those in non-valsartan group (P＜0. 05).

The effect of TNF-α in intracellular Ca2+-overload associated cardiac dysfunction / 临床儿科杂志

Objective To explore the effect of TNF-α in intracellular Ca~(2+)-overload associated myocardial injury. Methods Thirty Wistar rats were randomly divided into three groups:control group,Ca~(2+)+-paradox group,and pentoxifylline treatment group. The intracellular Ca~(2+)-overload rat model was established by pre-filling the rats with Langendorff for 20 minutes,isolated rat hearts subjected to Ca~(2+)-depletion for 5 minutes and Ca~(2+)-repletion for 30 minites(Ca~(2+)-paradox). Changes in hemodynamics indexes were monitored continuously. TNF-α in cardiac tissues was tested by ELISA method,and nuclear factor-κB(NF-κB)in cardiac tissues was detected with Western blot. Results Dramatic depression in left ventricle contraction function was found in the Ca~(2+)-paradox hearts:significant decrease in left ventricular diastolic pressure(LVDP),markedly elevated left ventricular end diastolic pressure(LVEDP),decreased dP/dt ratio,increased TNF-α content,decreased cytosolic/homogenate NF-κB ratio. All these changes in Ca~(2+)-paradox group were significantly attenuated upon the treatment with 100 μmol/L pentoxifylline. Conclusions Activation of NF-κB and increased production of TNF-α may play important roles in cardiac injury associated with intracellular Ca~(2+)-overload.