This paper presents a new method for QRS complex self-assortment based on mathematical morphology, which measures the comparability of QRS complex with weighted Hausdorff distance. Beginning with the traditional Hausdorff distance, this paper introduces the weighted Hausdorff distance of planar object and the detailed algorithm of self-assortment of QRS complex. The evaluation results of this algorithm by MIT-BIHECG database show that this method has high self-assortment capability.

Objective To establish and identify the induced pluripotent stem cell(iPSC) line reprogrammed from human umbilical cord mesenchymal cells(HuMSCs).Methods HuMSCs were cultured by adhesion method,and OCT4,SOX2,KLF4,c-Myc,NANOG,LIN-28 were transfected into HuMSCs with lentiviral victor to reprogramme HuMSCs into iPSC.Morphological observation,pluripotency genes (SOX2,TDGF1,THY-1,OCT4,REX1 and TERF1) expression,alkaline phosphatase detection,karyotype analysis,embryonic stem cells (ESC) specific proteins (NANOG,OCT4,SSEA-4,TRA-1-81) immunofluorescence staining,differentiated into teratomas in vivo(inject the iPSC into SCID mice) and embryniod bodies in vitro were performed to exam the pluripotency of the iPSC.Results Four days after being infected by lentivirus,the HuMSCs became round-shape; 10 days after infection,some embryonic stem(ESC)-like colonies appeared.Fourteen days after infection,picked up the regularly shaped colonies and cultured several passages.About 1.25％ HuMSCs were reprogrammed into iPSC.The iPSC presented clone-like growth like ESC.All the cells were positive to alkaline phosphatase staining and expressed the pluripotency genes.The iPSC also expressed the ESC specific proteins,and karyotype analysis showed normal chromosome caryotype (46,XY).Furthermore,the iPSC could form embryoid bodies in vitro,expressed alpha fetoprotein(AFP),smooth muscle actin(SMA) and β-tubulin.The iPSC could alsoform teratomas in vivo.Conclusion OCT4,SOX2,KLF4,c-Myc,NANOG,LIN-28 can reprogram HuMSCs into iPSC efficiently.

ObjectiveTo explore the histopathological changes of bile duct,liver and local tissue for injurious biliary stricture(IBS). MethodTo observe the morphological and pathological changes of bile duct, local tissue and liver in different periods with dogs as the established animal model for IBS. ResultBile duct obstruction due to injury can expand the proximal bile duct up to 18.91 ±1.85 mm as the pressure goes up. Damage to local tissue triggers acute inflammation. In early injury phase (within 10 d), inflammatory cell infiltration and proliferation appears on the wall of the duct with increased mucosal edema as well as thickening of the biliary ductile wall. In the late injury phase (15 d), the degree of infiltration of inflammatory cells, edema and mucosal thickness were reduced whereas fibroblast and collagen tissue were proliferated extensively. The wall of biliary duct also becomes fibrotic and thickens. Quantitative analysis of the inflammatory edema shows the most severe outcome on the 5th day (HE staining WBC count of 54.2±5.8 unit) and its severity progressively subsides on the 15th day. (HE staining WBC count of 41.7±7.2 vs 54.2±5.8 a, P＜0.0,5). In the early obstruction (5 d and 10 d), the liver cells showed mild to moderate swelling and its degeneration is often associated with steatosis and sinusoidal expansion and congestion. As the obstruction time increases in the 20 d and 30 d group, liver cells starts to show extensive vacuolation and sinusoidal occlusion. ConclusionsEarly phase (5 days) of acute bile duct obstruction due to injury shows rapid expansion of the bile duct, edema in the bile duct itself as well as its surrounding tissue and liver damage. After 15 days, the local inflammatory edema is greatly reduced and is replaced by hyperplasia of fibers and collagen. Liver damage appears to be irreversible after 20 days. Considering local environmental and systemic conditions, the optimal time frame to repair obstruction of bile duct surgically is between 10-20 days.

Objective To explore the optimal timing of operation for experimental obstructive jaundice in a dog model. Method A dog model of bile duct stricture (BDS) was established. Dogs were divided into (n = 12 in each group) 6 groups, ie control, BDS days 5, 10, 15, 20, and 30. In each dog,the morphology and local histopathology of the bile duct, and the liver function in different periods were observed. At the time of surgery biopsy was taken and Roux-en-Y hepaticojejunostomy performed. Surgical complications and survival were evaluated. Result After bile duct obstruction, the proximal bile duct dilated continuously. The diameter of bile duct was 15.6 ± 1.7 mm at the 10th day. The injury bile ductshowed the acute inflammation change. In the early time (in 10 days), inflammatory cells increased in the tissues, mucous edema aggravated, the wall was edematous thickening, it was most severe ( WBC counting 54 ±6) in the 5th day. In the later period (10 -30 days), inflammatory cells reduced, bile duct wall became fibrosis, which was most obvious in the 15th day (42 ± 7 vs 54 ± 6, P ＜ 0.05 ). During the development of jaundice, serum bilirubin reached the highest level in the early period ( BDS days 5 group),then presented a platform time, and then rised extremely at the last stage of the experiment ( BDS day 30 group) . Changes of ALT and AST paralleled that of bilirubin before the 20th day of obstruction and then plummeted. BDS was repaired successfully in 57 dogs. Ten dogs died postoperatively due to bile leakage within 10 days, 3 dogs in BDS days 5 group (3/11), 4 in BDS days 10 group (4/12), one each in other groups. Postoperatively 13 BDS dogs died of malnutrition and organ failure within 3 months, including one each in days 5 and days 10 group, two each in days 15 and days 20 group, and 7 in days 30 group (P＜0. 05). Conclusion Considering the changes of morphology, physical function and result of follow up.The period between 10 and 20 days after acute bile duct injury is optimal for surgical repair.

OBJECTIVETo establish a mice model with selective inactivation adenosine A2A receptors (A2ARs) in peripheral white blood cells (PWBC).

METHODSA2ARs were selectively inactivated in PWBCs by transplanting bone marrow cells (BMCs) from A2AR knockout (KO) mice into their wild type (WT) littermates after a single total body irradiation of 9.5 Gy or fractionated total body irradiation of 6.2 Gy x 2. The efficiency of reconstitution of bone marrow-derived cells in chimeric mice was assessed.

RESULTSPCR band patterns changed from the recipient pattern (one band of 330 bp) to the donor (two bands of 300 and 330 bp) pattern. Immunohistochemistry analysis showed that 10.21% of cells were A2AR+ in PWBCs in KO--> WT mice, whereas 96.72% of cells were A2AR+ in WT mice. The survival rates of mice irradiated with 6.2 Gy x 2 and transplanted with more than 6 x 10(6) BMCs were about 91%.

CONCLUSIONA murine model of selective inactivation adenosine A2A receptors in PWBCs was established successfully.

Animals ; Gene Deletion ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Animal ; Receptor, Adenosine A2A ; genetics