Objective To study the methodology and effect of auricle reconstruction with prefabricated expanded fascial flap in temporal and parietal area and skin flap in mastoid area, covered on the Medpor support. Methods Thirty cases of congenital vestigial auricle were involved in this study. The operations were divided into two stages: in the stage I,the temporal and parietal superficial fascia flap was cut with a vascular pedicle in the parietal and temporal superficial area, which was implanted under the skin of mastoid, and then both layers of those were expanded at the same time; in the stage II, this fascial skin flap was cut down and covered on the whole Medpor support to rebuild the man-made auricle. Results Thirty cases were successful after following-up for 6 months to 3 years. Their auricle shapes were vivid; their skin color was normal, and it had no any difference from all around skins, or no any appearance of the support. Conclusions With best understanding the biological characteristics of the Medpor support and choosing the suitable procedures and using the prefabricated expanded support, we could minimize the surgical complications in this operation. The results show that this procedure is satisfactory, without any necrosis of flap, swelling of contour, or appearance of the support. The combination of two flaps is the best method for the auricle reconstruction.

Background and purpose:Vascular endothelial growth factor(VEGF) is a potent angiogenic mediator and angiogenesis has important effects on tumor growth and metastasis.The present study was to investigate the relationship between genetic polymorphism of VEGF and heredity risk factor of lung cancer.Methods:VEGF genotypes were determined by PCR-RFLP method in 171 patients with lung cancer and 172 healthy controls.Software PHASE 1.0 was used to construct the haplotypes of every individual.Unconditional logistic regression model was used to analyze the statistical association of genotypes or haplotypes in the two groups adjusted by gender and age. Results:Individuals with at least one-2578A allele had a significantly decreased risk of lung cancer compared with those carrying-2578CC genotype.When the analyses were stratified by gender,the combined-2578 CA and AA genotype,were associated with a considerably reduced risk of lung cancer(P=0.001,OR=0.303,95%CI=0.15 3-0.601).The distribution of the two haplotypes(936C/-2578C and 936C/-2578A) among overall lung cancer cases was significantly different from that among the controls(P=0.016,0R=0.317,95%CI=0.124-0.809 and P=0.018,OR=0.547, 95%CI=0.331-0.903).When the cases were categorized by tumor histology,the distribution of C-C haplotype in the adenocarcinoma(AC) group was associated with a substantially lowered risk of AC(P=0.004,0R=0.237,95%CI=0.090- 0.627),compared with the reference haplotypes.Conclusion:VEGF polymorphism may be a critical risk for the genetic risk factor to lung cancer.

OBJECTIVETo detect the expression of miR-124 in colorectal carcinoma (CRC) cells and tissue specimens and analyze its association with the radiosensitivity of the cells.

METHODSThe expression of miR-124 in CRC cell lines and tissues were detected using qRT-PCR. The effect of miR-124 in modulating cell radiosensitivity was assessed in CRC cells with miRNA-124 overexpression and miRNA-124 knockdown, and bioinformatics prediction and dual luciferase reporter system were employed to identify the direct target of miR-124.

RESULTSs miR-124 expression was down-regulated in CRC cell lines and tissues. CRC cells over-expressing miR-124 showed an obviously enhanced radiosensitivity, whereas miR-124 knockdown resulted in a reduced radiosensitivity of the cells. Bioinformatics prediction and dual luciferase reporter system verified PRRX1 as a direct target of miR-124, which regulated the radiosensitivity of CRC cells by directly inhibiting PRRX1.

CONCLUSIONmiR-124 can enhance the radiosensitivity of CRC cells by directly targeting PRRX1, which provides a target for improving the therapeutic effect of radiotherapy of CRC.

Cell Line, Tumor ; Colorectal Neoplasms ; pathology ; radiotherapy ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Homeodomain Proteins ; genetics ; metabolism ; Humans ; Luciferases ; MicroRNAs ; genetics ; metabolism ; Radiation Tolerance

OBJECTIVEThe primary aim of this prospective study was to use serial (18)F-FDG PET-CT imaging to evaluate the trend of the tumor's maximum standardized uptake value (SUVmax) during radiotherapy (RT) for patients with nasopharyngeal carcinoma (NPC), and to explore the possibility of early evaluation of the tumor bio-metabolic response during radiotherapy.

METHODSSixty patients with biopsy-proven primary NPC were prospectively enrolled into the study. All patients underwent four (18)F-FDG PET-CT scans: one initial scan before RT/cisplatin based concurrent chemoradiotherapy, at the point of 50 Gy during RT, the end of RT, and one month after RT, respectively. Tumor (18)F-FDG uptake was analyzed according to the World Health Organization pathological type.

RESULTSThere was a significant difference (P < 0.001) of the mean of SUVmax of the primary site among pretreatment (11.20 ± 5.37) and posttreatment at the dose of 50 Gy (3.50 ± 1.59), at the end of RT (3.05 ± 1.56) and one month after RT (2.52 ± 1.46). There was also a significant difference (P < 0.001) of the mean of SUVmax of neck node site. However, there was a significant difference of the SUVmax between histological WHO type IIb and type IIa in the primary site (P = 0.046) [(67 ± 19)% reduction at dose 50 Gy for type IIb vs. (55 ± 24)% for type IIa] but not in the lymph nodes.

CONCLUSIONSEarly PET scan during or right after RT instead of conventional 3 months interval after RT is indicated to evaluate the tumor response and to develop individualized adaptive radiotherapy in NPC. Our next study will attempt to demonstrate the results based on long-term follow-up data.

Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Carcinoma, Squamous Cell ; diagnosis ; drug therapy ; pathology ; radiotherapy ; Chemoradiotherapy ; Cisplatin ; administration & dosage ; Female ; Fluorodeoxyglucose F18 ; Humans ; Lymphatic Metastasis ; Male ; Nasopharyngeal Neoplasms ; diagnosis ; drug therapy ; pathology ; radiotherapy ; Neoplasm Staging ; Positron-Emission Tomography ; methods ; Prospective Studies ; Radiopharmaceuticals ; Radiotherapy Dosage ; Radiotherapy, High-Energy ; Radiotherapy, Intensity-Modulated ; Tomography, X-Ray Computed

OBJECTIVEThe mechanism through which platelet activating factor (PAF) induces cardiac electrical activity and arrhythmia is not well understood and previous studies have suggested a potential involvement of ion channels in its action. The present study was aimed to clarify the role of PAF in fatal arrhythmias following acute myocardia infarction (AMI) and the underlying mechanism.

METHODS(1) Blood PAF levels were measured among 72 AMI patients at the time of diagnosis with AMI and 48 h later, and their electrocardiogram (ECG) was recorded continuously. (2) Ischemia simulation and surface electrocardiogram were conducted in 20 pigs and their PAF levels were measured. (3) PAF perfusion and standard microelectrode recording were performed on guinea pig papillary muscles.

RESULTSIn both humans and pigs, elevated PAF levels were detected in AMI and simulated ischemia, respectively, and even higher PAF levels were found when fatal arrhythmias occurred. In guinea pig myocardium, PAF induced a shortening of action potential duration at 90% level of repolarization (APD90)under non-ischemic conditions and a more pronounced shortening under early simulated ischemic conditions.

CONCLUSIONAMI and ischemia are associated with increased PAF levels in humans and pigs, which are further raised when fatal arrhythmia follows. The effects of PAF on the myocardium may be mediated by multiple ion channels.

Animals ; Arrhythmias, Cardiac ; blood ; etiology ; physiopathology ; Electrocardiography ; Female ; Heart ; physiopathology ; Humans ; Male ; Middle Aged ; Myocardial Ischemia ; blood ; complications ; physiopathology ; Platelet Activating Factor ; metabolism ; Swine

Adult ; Female ; Hepatitis ; complications ; diagnostic imaging ; mortality ; Humans ; Infant, Newborn ; Pregnancy ; Pregnancy Complications ; diagnostic imaging ; mortality ; Prognosis ; Ultrasonography

OBJECTIVETo assess the effects of apolipoprotein E (APOE) polymorphism on the susceptibility of depression and the efficacy of antidepressants.

METHODSA total of 275 patients with depression, who met the diagnostic criteria of both CCMD-3 and DSM-4, were randomly assigned into venlafaxine group (n=136)and paroxetine group(n=139). Another 202 healthy subjects were enrolled as the control group. Hamilton Rating Scale for Depression (HAMD)-17 was adopted as the primary rating instrument to evaluate the severity of depression on the baseline and the end of the 1st, 2nd, 4th, 6th week after treatment, respectively. HAMD scores ≤7 was defined as remission, and the reduction of HAMD scores ≥50% was defined as response while <50% was defined as invalid. PCR-restriction fragment length polymorphisms (PCR-RFLP) was applied to detect the genetic polymorphism of the APOE in the case groups and control group.

RESULTSIn the venlafaxine group, the remission rate was 52.9%(n=72), the response rate was 26.5%(n=36), and the invalid rate was 20.6%(n=28), whereas the corresponding data in the paroxetine group wee 42.4%(n=59), 31.7%(n=44), and 25.9% (n=36), respectively. There were no significant differences in the efficacy between the two groups(p>0.05). In the venlafaxine group, there were no significant differences in the genotypes and the allele distribution frequency of APOEΕ2/Ε3/Ε4 between the remitters, nonremitters, and healthy controls at the end of the 6th week(p>0.05), but there was significant differences in the allele distribution frequency between the nonremitters and healthy controls(p=0.02). In paroxetine group, there were no significant differences in the genotypes and the allele distribution frequency of APOEΕ2/Ε3/Ε4 among the remitters, nonremitters and healthy controls at the end of the 6th week(p>0.05), but there were significant differences in the allele distribution frequency between the nonremitters and healthy controls (p=0.04); in addition, there were also significant differences in Ε2/Ε3 and Ε4 allele between the two groups (p=0.014).

CONCLUSIONSThe APOE gene may not play a major role in the pathogenesis of major depression. The efficacy of venlafaxine is same as paroxetine after treatment for six weeks. The APOE (Ε2+Ε3) allele may be an indicator of the bad efficacy of paroxetine treatment.

Adolescent ; Adult ; Aged ; Antidepressive Agents ; therapeutic use ; Apolipoproteins E ; genetics ; Cyclohexanols ; therapeutic use ; Depression ; drug therapy ; genetics ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Middle Aged ; Paroxetine ; therapeutic use ; Polymorphism, Genetic ; Treatment Outcome ; Venlafaxine Hydrochloride ; Young Adult

Adolescent ; Adult ; Female ; Humans ; Male ; Mercury ; urine ; Middle Aged ; Reference Values ; Spectrophotometry, Atomic

To investigate the mechanisms of serine/threonine kinase Pim-3 inhibition of fulminant hepatic apoptosis. Thirty-two rats were randomly divided into four groups (n = 8 each): normal controls (A); pretreatment with Ringer's solution (B), vector plasmid (C), or Pim-3 recombinant plasmid (D) by hydrodynamics-based procedure followed by intraperitoneal injections of lipopolysaccharide (LPS) and D-galactosamine (D-GalN) after one day. At 8 h after the LPS/D-GalN injections, liver tissues were collected from all groups of mice and analyzed for cell apoptosis by detecting caspase-3 activity (measured in relative fluorescence units, RFU). Changes in expression of relevant genes were determined by RT-PCR and Western blotting. Caspase-3 activity was induced in response to LPS/D-GalN injection. Pim-3-pretreated rats showed a lower level of caspase-3 activity than the Ringer's-pretreated or vector plasmid-pretreated rats [(141.7+/-13.7)RFU vs. (508.1+/-32.0) or (493.5+/-33.1) RFU; all P less than 0.01]. High expressions of the liver injury marker gene, iNOS, and the apoptosis-induced genes, p53 and Bax, were found after LPS/D-GalN challenge, and were suppressed by exogenous Pim-3 gene injection. In addition, exogenous Pim-3 gene injection induced high expression of the liver anti-apoptosis protein, Bcl-2, but had no effect on Bax protein expression. The Pim-3 gene can block fulminant hepatic apoptosis by affecting the expression of the iNOS liver injury gene and the p53, Bax and Bcl-2 apoptosis-related genes.
Animals ; Apoptosis ; Caspase 3 ; metabolism ; Liver ; metabolism ; pathology ; Liver Failure ; metabolism ; pathology ; Male ; Protein-Serine-Threonine Kinases ; genetics ; Rats ; Rats, Wistar

0.05).The cubitus varus incidence evaluation was done by follow-up study,2 cases were in operation group and 8 cases in non-operation group,there was a significant difference between the 2 groups(P