Objective:To explore the relationship among blood glucose,blood lipid levels,peripheral blood white cells and slow coronary flow (SCF).Methods:Clinical data of 183 patients receiving angiography in our hospital from Apr 2010 to Apr 2013 were retrospectively analyzed.Patients with TIMI grade 2 or lower coronary blood flow were defined as SCF;patients were divided into SCF group (n=93)and normal control group (n=90).Levels of blood lipid,glycosylated haemoglobin (HbA1c),hematocrit,and peripheral blood white cell levels were measured and compared between two groups.Results:Compared with normal control group,there was significant reduction in high density lipoprotein cholesterol (HDL-C) level [(1.21 ± 0.26)mmol/L vs.(1.12 ± 0.28)mmol/L,P =0.043],and significant rise in HbA1c level [(5.41±0.50)% vs.(5.83±0.45)%,P =0.01],hematocrit [(0.41 ±0.04)vs.(0.43±0.07),P =0.01]and white blood cell count [(6.1±1.6)109/L vs.(6.7±1.7)109/L,P <0.05]in SCF group.Logistic analysis indicated that white cell count was the risk factor of SCF (OR 1.920,95% CI 1.234~2.987,P =0.004).Conclusion:Levels of high density lipoprotein cholesterol,glycosylated haemoglobin, hematocrit and white blood cell count are related to slow coronary flow,and elevated white blood cell count may be a risk factor aggravating slow coronary slow.

Circulating nitric oxide(NO)and endothelin (ET) levels were determined in 30 normal subjects and 63 diabetic patients.The results showed that:serum NO level was significantly higher in DM I group(68.66?12.37?mol/L)and DM Ⅱ group(63.43?11.09?mol/L)than in normal subjects(44. 92?9.04?mol/L,P0.05).Plasma ET level was markedly elevated in DM Ⅰ group(68.92?11.96ng/L,P

Heart sound signals acquisition is the primary basis for achieving non-invasive diagnosis of coronary heart disease. In this paper, a digital signal processor (DSP)-based on miniaturized circuit of heart sound signals acquisition and analysis platform was designed to achieve the functions of filtering, collecting, processing, displaying and the communicating with PC. With the self-developed experimental platform, we collected 228 cases of heart sounds of clinical data, and processed the signals using de-noising method with wavelet transform. These experimental results indicated that the db6 wavelet has the most obvious de-noising effect among the four most commonly used wavelets, i.e., haar, db6, sym8, and coif5. One wavelet at different levels possessed different de-noising effects, with level-5 db6 decomposition obtaining the most desirable result.
Algorithms ; Auscultation ; Heart Sounds ; Humans ; Phonocardiography ; methods ; Signal Processing, Computer-Assisted ; Wavelet Analysis

Heparinase III is an enzyme that specifically cleaves certain sequences of heparan sulfate. Previous reports showed that this enzyme expressed in Escherichia coli was highly prone to aggregation in inclusion bodies and lacks detectable biological activity. In this paper, we fused a glutathione-S-transferase (GST) tag to the N-terminus of heparinase III gene and expressed the fusion protein in Escherichia coli to develop an expression system of soluble heparinase III. As a result, approximately 80% of the fusion protein was soluble. The protein was then purified to near homogeneity via one-step affinity chromatography. A 199.4-fold purification was achieved and the purified enzyme had a specific activity of 101.7 IU/mg protein. This represented 32.3% recovery of the total activity of recombinant GST-heparinase III. The maximum enzyme production was achieved when bacteria were induced with 0.5 mmol/L isopropyl-beta-D-thiogalactoside at 15 degrees C for 12 h. The enzyme showed maximum activity at 30 degrees C and pH 7.5. And the enzyme activity was stimulated by 1 mmol/L Ca2+ and 150 mmol/L NaCl.
Escherichia coli ; genetics ; metabolism ; Flavobacterium ; enzymology ; genetics ; growth & development ; Glutathione Transferase ; biosynthesis ; genetics ; Heparin Lyase ; biosynthesis ; genetics ; isolation & purification ; Recombinant Fusion Proteins ; biosynthesis ; genetics ; isolation & purification

Purpose: The role of vacuolar protein sorting 34 (Vps34), an indispensable protein required for cell vesicular trafficking, in the biological behavior of hepatocellular carcinoma (HCC) has yet to be studied. Materials and Methods: In the present study, the expression of Vps34 in HCC and the effect of Vps34 on HCC cell invasion was detected both in vivo and in vitro. Furthermore, by modulating the RILP and Rab11, which regulate juxtanuclear lysosome aggregation and recycling endosome respectively, the underlying mechanism was investigated. Results: Vps34 was significantly decreased in HCC and negatively correlated with the HCC invasiveness both in vivo and in vitro. Moreover, Vps34 could promote lysosomal juxtanuclear accumulation, reduce the invasive ability of HCC cells via the Rab7-RILP pathway. In addition, the deficiency of Vps34 in HCC cells affected the endosome-lysosome system, resulting in enhanced Rab11 mediated endocytic recycling of cell surface receptor and increased invasion of HCC cells. Conclusion Our study reveals that Vps34 acts as an invasion suppressor in HCC cells, and more importantly, the endosome-lysosome trafficking regulated by Vps34 has the potential to become a target pathway in HCC treatment.

Pancreatic ductal adenocarcinoma (PDAC) is characterized by the highest mortality among carcinomas. The pathogenesis of PDAC requires elevated autophagy, inhibition of which using hydroxychloroquine has shown promise. However, current realization is impeded by its suboptimal use and unpredictable toxicity. Attempts to identify novel autophagy-modulating agents from already approved drugs offer a rapid and accessible approach. Here, using a patient-derived organoid model, we performed a comparative analysis of therapeutic responses among various antimalarial/fungal/parasitic/viral agents, through which econazole (ECON), an antifungal compound, emerged as the top candidate. Further testing in cell-line and xenograft models of PDAC validated this activity, which occurred as a direct consequence of dysfunctional autophagy. More specifically, ECON boosted autophagy initiation but blocked lysosome biogenesis. RNA sequencing analysis revealed that this autophagic induction was largely attributed to the altered expression of activation transcription factor 3 (ATF3). Increased nuclear import of ATF3 and its transcriptional repression of inhibitor of differentiation-1 (ID-1) led to inactivation of the AKT/mammalian target of rapamycin (mTOR) pathway, thus giving rise to autophagosome accumulation in PDAC cells. The magnitude of the increase in autophagosomes was sufficient to elicit ER stress-mediated apoptosis. Furthermore, ECON, as an autophagy inhibitor, exhibited synergistic effects with trametinib on PDAC. This study provides direct preclinical and experimental evidence for the therapeutic efficacy of ECON in PDAC treatment and reveals a mechanism whereby ECON inhibits PDAC growth.