Basic fibroblast growth factor(bFGF)is a polypeptide cell growth factor,which has exten- sive physiological functions.With the in-depth study,the exploration of relationship between basic fibroblast growth factor and tumor has been developing rapidly in recent years,It shows a good prospect in diagnosis and treatment of tumor.There is a brief overview about the molecular biology of bFGF,its expression in tumor and the relationship between bFGF and tumorigenesis.

As one of the most sensitive cells of endoplasmic retieulum stress (ERS), pancreatic β-cells have an a-bundance of endoplasmic reticulum. Fatty acids cause apoptosis of β-cells and might contribute to β-cell loss in type 2 diabetes mellitus via the induction of ERS. Glucose is an amplifier of the ERS response to fatty acid, leading to increased β-cell apoptosis. ERS response mediates glucolipotoxicity-induced β-cell apoptosis.

Aim To investigate the specific binding of folate conjugated PGA to FR-positive tumor cells.Method Folate-PGA and PGA were radiolabeled with 125I by the Iodogen method to examine the binding of PGA to FR positive HeLa cells and SKOV3 cells, or FR negative A549 cells. Results 125I-folate-PGA showed specific bound to HeLa cells and SKOV3 cells; Scatchard analysis of the data estimated the Kd of binding to be 0.11 nmol?L-1 and 0.25 nmol?L-1 respectively. 125I-folate-PGA showed virtually little specific binding to A549 cells which lack folate receptors. Conclusions folate-PGA displayed high affinity and good targeting activities for FR-positive tumor cells and the data warranted further studies for enzyme prodrug therapy.

Objective To expore the difference between magnetic resonance image ( MRI) expression of spinal tuberculosis and brku-cellare spondylitis. Methods Retrospectively analyzed the clinical data of 10 patients with tuberculous spondylitis and 12 patients with bru-cellar spondylitis from Jan. 2012 to Oct. 2013. All the patients were scanned by MRI, and the expression difference of MRI were compared. Results The vertebral body of spinal tuberculosis was destroyed severely, and it often accompanied by the kyphosis and multiple-level para-vertebral abscess, and even adjacent organs tuberculosis. The vertebral body of brucellar spondylitis was destroyed lightly,and the abscess is often limited. Conclusion We can distinguish spinal tuberculosis and brucellar spondylitis by the typical difference of the expression of MRI.

Objective To discuss the risk factors and outcome of abnormal lung function in adult congenital heart disease .Meth‐ods 327 patients with adult congenital heart disease undergoinglung function testing between January ,2009 to December ,2011 in our hospital were enrolled .Accorded to the severity of lung dysfunction based on predicted values of forced vital capacity (FVC) ,pa‐tients were divided into 3 groups :group A(normal lung function ,predicted FVC >70% ) ,group B(mildly impaired lung function , predicted FVC 60% -70% ) ,group C(moderately to severely impaired lung function ,predicted FVC <60% ) ,all the patients were followed‐up to January in 2013 ,the baseline characteristics and outcome were recorded ,the associate factors of moderately to se‐verely impaired lung function in adult congenital heart disease were analyzed through Logistic regression analysis ,the risk factors of death in adult congenital heart disease were analyzed through Cox regression analysis ,and Kaplan‐Meier curve compared survival rate of patients in the 3 groups .Results Lung function was abnormal in 167 patients(51 .1% ) with adult congenital heart disease , in which moderately to severely impaired were 96 patients(29 .4% ) .BMI ,smoke and enlarged cardiothoracic ratio were independent associate factors of moderately to severely impaired lung function in adult congenital heart disease (P<0 .05) .NYHA Ⅲ - Ⅳ and moderate to severe impairment of lung function were independent predictors of death in adult congenital heart disease .There were significant difference of the survival rate between group A and group C ,group B and group C(P<0 .05) ,but it was not significantly different between group A and group B(P>0 .05) .Conclusion Lung function impairment is common in patients with adult congen‐ital heart disease ,and moderate to severe impairment of lung function seriously impact the outcome of the patients .

In this study, we explored the mechanism of Huganning tablet (HGNP) in the treatment of nonalcoholic fatty liver disease (NAFLD) based on network pharmacology and computer-aided drug design. Firstly, the potential ingredients and targets of HGNP were identified from TCMSP database, Swiss Target Prediction database, Chinese pharmacopoeia (2015) and literatures, and then the targets of HGNP intersected with NAFLD disease targets that obtained in GeneCards database to acquired potential targets. The bioconductor bioinformatics package of R software was used for gene ontology (GO) enrichment and Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis. The network of “potential ingredient-key target-pathway” was formed in Cytoscape software to study the interactions between potential ingredients of HGNP, key targets, pathways and NAFLD. Based on the results of network pharmacology, the molecular docking analysis of the key targets and potential active ingredients in HGNP tablets with top degree in the network was conducted using Discovery Studio 2020 software, followed by molecular dynamics simulations, binding free energy calculation, drug-likeness properties analysis and ADMET (absorption, distribution, metabolism, excretion and toxicity) properties prediction. In vitro, HepG2 cells were used to establish steatosis model, and the effects of five key compounds on hepatocyte steatosis were analyzed by oil red O staining and triglyceride (TG) content determination. The results showed that 141 ingredients and 151 potential targets were obtained. A total of 2 526 items and 151 pathways were identified by GO and KEGG enrichment analysis. The molecular docking suggested that five components, isorhamnetin, salvianolic acid B, emodin, resveratrol and rhein, exhibited strong binding ability with key targets [retinoic acid receptor RXR-alpha (RXRA), tumor necrosis factor (TNF), glycogen synthase kinase-3 beta (GSK3B), serine/threonine-protein kinase 1 (AKT1)]. It was further verified that isorhamnetin and salvianolic acid B bind to key targets with good structural stability and binding affinity based on molecular dynamics simulations and binding free energy calculations. The drug-likeness properties, pharmacokinetic properties and toxicity of five key compounds were more comprehensively analyzed through drug-likeness properties analysis and ADMET properties prediction. In vitro, all five compounds, isorhamnetin, salvianolic acid B, emodin, resveratrol, and rhein, improved hepatocyte steatosis of HepG2 cells, confirming the reliability of the present study. In conclusion, based on network pharmacology, computer-aided drug design and in vitro validation, this study investigated the mechanism of HGNP for the treatment of NAFLD at multiple levels and provided a basis for its clinical application.

As one of the major sources of infection, viruses could infect all organisms including bacteria, plants, animals, and humans. Infectious diseases caused by viruses pose a great threat and damage to human health and economic activities all over the world. Adaptor-associated protein kinase 1 (AAK1) is a member of the Ark1/Prk1 family of serine/threonine kinases and a specific key kinase regulating the phosphorylation of AP-2 protein μ2 subunit T156. In the past, AAK1 has been regarded as a feasible biological target for the treatment of nerve pain. Recently, scientists have found that inhibiting AAK1 can regulate endocytosis and inhibit virus invasion into cells. Therefore, AAK1 could be the potential target of anti-virus therapy. This paper reviews the research progress of small molecule AAK1 inhibitors in the field of antiviral, analyzes the future research directions and challenges, and provides new ideas for the development of antiviral drugs targeting AAK1.

In this study we present our experiences with the reverse sural fasciocutaneous flap to reconstruct the distal lower limb soft tissue defects caused by traumatic injuries. These flap graftings were carried out from Oct. 2010 to Dec. 2012 in our department. The series consisted of 36 patients, including 21 men and 15 women with an average age of 46.2 years (14-83 years) and with a medium follow-up period of 18 months (12-24 months). Of all the cases of acute trauma, there were 10 cases of trauma of distal tibia, 9 cases of trauma of perimalleolus, and 17 cases of trauma of midfoot and forefoot. Related risk factors in the patients were diabetes (2 cases), advanced age (>65 years, 3 cases) and cigarette smoking (6 cases). The reverse flow sural island flap irrigation depended on lower perforators of the peroneal artery. The fasciocutaneous pedicle was 3-4 cm in width and the anatomical structures consisted of the superficial and deep fascia, the sural nerve, short saphenous vein, superficial sural artery together with an islet of subcutaneous cellular tissue and skin. The most proximal border of the flap was only 1.5 cm away from the popliteal skin crease and the pivot point was 5-7 cm above the tip of the lateral malleolus. All the flaps survived. No arterial crisis occurred in any case. The venous congestion occurred in 2 cases and got better after raising the limbs and bloodletting. Only in an old man, 1.5 cm necrosis of distal margin of his flap occurred and finally healed after continuous dressing change. One-stage skin grafting was performed, and all the donor sites were sutured and successfully healed. It was concluded that the reverse sural fasciocutaneous flap is safe and reliable to extend to the proximal third even near the popliteal skin crease. We also concluded this flap can be safely and efficiently used to treat patients with large and far soft-tissue defects from the distal leg to the forefoot with more versatility and it is easier to reach the recipient sites.

Objective To observe the regulatory effect of bFGF and TGF-β1 for the proliferation of mesenchymal progenitor cells ( MPCs) derived from primary osteoarthritis cartilage, and to provide theoretical evidence in preventing and curing primary OA. Methods Different concentrations of bFGF and TGF-β1 ( alone or combined) were used to treat primary OA cartilage and their effects on proliferation of MPCs were tested by MTT method. Results Either bFGF (10. 0~50. 0 ng/mL) or TGF-β1 (0. 1 ~1. 0 ng/mL) alone can significantly promote the proliferation of MPCs derived from primary OA cartilage (P<0. 05). But with their increased concentration,the proliferation rate was of no significant changes (P>0. 05). The combination of 10. 0 ng/mL bFGF and 1. 0 ng/mL TGF-β1 significantly increased the prolifer-ation of MPCs from primary OA (P<0. 05). Conclusion Both bFGF and TGF-β11 play important roles in the proliferation of MPCs in primary OA cartilage,and they can increase the proliferation in different degree with different concentrations. There must be feasible methods of gene technology to promote cell proliferation and differentiation of MPCs for repairing articular car-tilage injury.