Objective:To study the relation between low density lipoprotein and macrophage myeloperoxidase.Methods:Using the reaction that MPO catalyze the oxidation of o dianisidin hydrochloride,MPO activity was determined.Using reverse transcription polymerase chain reaction(RT PCR),MPO gene expression was determined.The two methods were used to observe the relationship between low density lipoprotein and macrophage myeloperoxidase activity.Results:LDL was able to accelerate the hoist of MPO activity, but its effect is less than LPS OX LDL have no this effect When the time of LDL effect was prolonged, MPO activity was enhancing little by little When the concentration of LDL effect was increased, MPO activity was enhancing to max little by little, then it come to plateau Conclusion:LDL non especially induced the hoist of MPO activity and the swelling of MPO secretion The reason of the hoist of MPO activity was likely to make MPO into action and enhance its secretion, but not MPO gene expression

The progression of liver fibrosis directly affects treatment options and prognosis.Early diagnosis and classification of liver fibrosis and dynamic monitoring are clinically needed.Noninvasive diagnostic techniques can avoid or reduce liver biopsy to enable early identifica-tion of liver fibrosis and to dynamically monitor the progression of fibrosis.But various limitations have restricted its application.Noninvasive diagnostic techniques,such as liver transient elastography using the different probe mode,controlled attenuation parameter,spleen stiffness measurement,ultrasound-based transient elastography for the early prediction of hepatic fibrosis,and risk assessment of hepatitis B virus-related hepatocellular carcinoma,have been applied in clinical studies.In order to better understand and apply these diagnostic models,the progress in clinical studies of noninvasive diagnosis of liver fibrosis,as well as the limitations,is reviewed.

OBJECTIVE：To study the effcet of Nitric oxide (No) on transcriptional expression of c-fos and c-jun oncogene of cultured rabbit arterial smooth muscle cells (ASMC),and its mechanism.METHODS:(1)To culture rabbit ASMC from explants;(2) To determine if NO,FeSO4,and methylene blue have toxic effect on ASMC by cell counting;(3)RNA isolation from ASMC by Guanidinium Thiocyanate-phenol-chloroform method;(4)RNA-DNA blot hybridization.RESULTS:Under the condition of no toxic effects,NO inhibited the expression of c-fos and c-jun oncogene of ASMC apparently,FeSO4 and methylene blue antagonized the inhibition effcet.CONCLUSION:NO inhibited the expression of c-fos and c-jun oncogene of ASMC through cGMP.This may be related to the important mechanism that NO inhibits the proliferation of ASMC.

AIM: To investigate the influences of native and oxidized lipoprotein(a) on human arterial smooth muscle cell (SMC) proliferation, change of intracellular free calcium concentration ([Ca 2+ ] i) and the protective effect of sodium ferulate(SF). METHODS: Lp(a) was oxidized by Cu 2+ and the extent of oxidation was assessed by the MDA content.Human SMC were incubated in culture media with SF for 12 h, then exposed to Lp(a) and oxidized-Lp(a), respectively. MTT colorimetry and flow cytometry were used to evaluated the proliferation of SMC and flurorescent indicator Fura-2/AM was used to determined [Ca 2+ ] i. RESULTS: ox-Lp(a) significantly promoted proliferation of SMC and increased[Ca 2+ ] i compared with Lp(a). SF(40,80 mg/L) remarkedly inhibited SMC proliferation and decreased the rising of [Ca 2+ ] i induced by ox-Lp(a) in a dose-dependent manner, but no effect on SMC proliferation and the increase in [Ca 2+ ] i induced by Lp(a).CONCLUSION: ox-Lp(a) induces the strong growth-promoting effect in SMC through increasing in [Ca 2+ ] i, which might be one of the cellular mechanisms responsible for the higher atherogenic potential of ox-Lp(a) compared with Lp(a), and this process can be prevented by inhibiting of oxidation by SF.

AIM and METHODS: To observe the effects of glucose-free and Mg 2+ -free in the extracellular fluid on the changes of [Ca 2+ ] i in the cerebro-cortical neurons damaged by 1 mmol/L glutamate using laser confocal scanning microscope. RESULTS: Both frequency and amplitude of neuronal calcium oscillation induced by glutamate were lowered in glucose-free and Mg 2+ -free buffers. The basic [Ca 2+ ] i concentration was lowered in the former case , but it was elevated in the latter case. CONCLUSION: Mg 2+ -free aggravates [Ca 2+ ] i overload induced by 1 mmol/L glutamate ,under certain conditions the glucose-free might resist damage role of glutamate and Mg 2+ -free.

AIM: The purpose of the present study was to detect intracellular Ca 2+ changes in living brain slices during focal cerebral ischemia/reperfusion (I/R) and reveal the role of intracellular Ca 2+ in the cerebral I/R injury. METHODS: The model of focal cerebral I/R was established in rats by reversible inserting a nylon thread, and dynamic change of intracellular Ca 2+ in brain slices was determined using laser confocal imaging system. RESULTS: ① Ca 2+ gradually enhanced with increase in ischemic time in cortex and striatum. ②At 1 h ischemia/ 10 min reperfusion, Ca 2+ increased significantly in striatum, but Ca 2+ decreased at 3 h reperfusion compared with 10 min reperfusion. ③ Ca 2+ markedly enhanced at 6 h ischemia compared with 1 h ischemia, and after 3 h reperfusion Ca 2+ decreased, but was still higher than that in sham-operation group. ④The striatum is more sensitive than cortex to ischemia/reperfusion. CONCLUSION: Ca 2+ overload in the area of cortex and striatum may play an important role in cerebral ischemia/reperfusion injury in rats.

AIM: To observe whether arachidonic acid (AA) could induce apoptosis in mouse fibroblast cell line L929 and the potential mechanism involved. METHODS: The viability and damaged degree of L929 was monitored by MTT and the release of lactate dehydrogenase (LDH). Lipid peroxidation in L929 was measured as malondialdehyde (MDA) content by colorimetric assay. Hoechst 33258 staining was used to observe AA-induced morphological changes. Agarose gel electrophoresis was used to detect DNA fragmentation. RESULTS: Treatment of L929 cell with AA for 24 h, in the range of 40-160 ?mol/L, caused a great decrease in cell survival and increased MDA contents and the release of LDH simultaneously( P

To investigate the CT appearances in early stage of clustering lung paragonimiasis,9 cases of two clustering lung paragonimiasis caused by eating raw stone-crab and laboratory examination were included in the study.Eight cases consulted by doctors in the hospital and their appearances were retrospectively analyzed.There were pleural effusion of varying degree (n=8) and random distribution sub-pleural pulmonary infiltrative lesions (n=7).The accompany appearances of the latter had lunar halo sign,characteristic tunnel sign (n=1) and peri-bronchitis (n=1).If CT detects pulmonary infiltrative lesions of random distribution within sub-pleura or tunnel sign,combining with the history of eating raw stone crabs and other freshwater fishes,with the rise of eosinophilic granulocytes in peripheral blood,the diagnosis of paragonimiasis should be suggested.

Although etiological treatment has reduced the incidence and mortality rates of liver cirrhosis complications, some patients may still experience disease progression. It is of great importance for further reducing mortality rate to accurately predict the clinical endpoints of liver cirrhosis and strengthen intervention. Therefore, this article discusses the prediction of clinical endpoints of liver cirrhosis from the aspects of liver pathology, noninvasive markers, imaging, and methodology, in order to help with early screening of the high-risk population, establish accurate predictive models, and further reduce the incidence rate of clinical endpoints of liver cirrhosis.

Achieving HBV DNA negative transformation and HBsAg clearance with effective antiviral therapy can reduce the incidence of HCC, but some patients are still at risk of developing HCC. Therefore, screening high-risk patients for close monitoring is essential to reduce the incidence of HCC. This paper reviews the occurrence of HCC, risk factors and risk prediction models of HBV DNA negative transformation and HBsAg clearance, and provides a basis for screening and follow-up management of high-risk group of HCC with chronic hepatitis B.