0.05).10% FBS induced -TdR incorporation increased by 87.5%(vs control,P

Objective:In the past study, a plasmid of pcDNA3 hCG? C3d3 had been constructed. It was suggested that the fusing protein be expressed by the pcDNA3 hCG? C3d3 plasmid both in the transient expression system in COS 7 cells, and the stable expression system in CHO cells. In the present research, it would be testified that the C3d molecular adjuvant could improve the immunogenicity of the hCG? DNA immunization or not. Methods:BALB/C mice of 6 weeks old were immunized intramuscularly two times at interval of 3 weeks by the plasmid pcDNA3, pcDNA3 hCG?, pcDNA3 hCG? C3d3 at dosage of 5, 10, 20 pmol, respectively. The anti hCG? antibody titers were determined by indirect ELISA in 6 weeks of last immunization. Results:The result showed that the C3d molecular adjuvant could increase significantly the titer of anti hCG? antibody in a dose dependent manner after DNA immunization.Conclusion:The C3d molecular adjuvant does improve the humoral immunity of the hCG? DNA immunization, which would be helpful for technical progress and clinical trial of the contraceptive vaccine. [

AIM: To investigate the effects of hypoxia-inducible factor-1 (HIF-1) on cardioprotection of hypoxic preconditioning (HPC) and its mechanisms. METHODS: In the model of hypoxia/reoxygenation (H/R) of cardiomyocytes from neonatal Spargue-Dawley rats, delayed cardioprotective effects of HPC on lethal H/R were observed. Whole cell extracts were prepared for determining activities of extracellular signal-regulated protein kinases (ERKs) and HIF-1? phosphorylation. RESULTS: HPC significantly promoted survival and membrane integrity of cardiomyocytes subjected to sustained H/R. SDS-PAGE mobility shift experiments showed increased phophorylation level of HIF-1? in hypoxic preconditioned cardiomyocytes. ERK1/2 were activated at 10 min after HPC and returned to the control level at 60 min. CONCLUSION: HPC protects neonatal cardiomyocytes from H/B injury. HIF-1? phosphorylation induced by ERKs might contribute to the cardioprotection of HPC.

Objective To investigate the correlation between expression of four adhesion molecules in sera and in skin lesions of patients with psoriasis vulgaris, as well as their relevance to clinical severity of the disease. Methods Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum levels of ICAM-1, ICAM-3, VCAM-1 and ELAM-1 in 36 patients with plaque type psoriasis vulgaris and 36 healthy controls. Avidin biotin immunoperoxidase staining system was employed to quantitate expression of the four adhesion molecules in psoriatic skin lesions before and after treatment. Results Significantly increased expression of four adhesion molecules was found in psoriatic skin lesions (P

Objective:To explore the relationship among clinical manifestations ,SⅠ QⅢ TⅢ feature of ECG ,plasma level of D‐dimer (DD) and diagnosis of pulmonary embolism (PE) .Methods :Clinical data of 212 inpatients ,who received pulmonary CT angiography (CTA) in our hospital from Jun 2012 to May 2014 ,were retrospectively ana‐lyzed .According to pulmonary CTA results ,patients were divided into PE group (n=56) and non‐PE group (n=156) .Basic hospitalization data ,including clinical manifestations ,ECG features and plasma DD level ,were collect‐ed and compared between two groups .Results:Compared with non‐PE group ,there were significant rise in percent‐ages of dyspnea (44.87% vs .75% ) and prolonged bedridden time (3.85% vs .14.29% ) ,significant reduction in percentage of no clinical manifestations (38.46% vs .3.57% ) in PE group , P<0.01 all .Percentage of ECG SⅠQⅢTⅢ feature in PE group was significantly higher than that of non‐PE group (50% vs .23.08% ) , P<0.01. Compared with non‐PE group ,percentage of plasma DD>10μg/ml significantly rose (19.23% vs .32.14% ) in PE group ,P<0.05 .Conclusion:Patients with dyspnea and/or prolonged bedridden time ,that cannot be explained by other car‐diopulmonary diseases ,and SⅠ QⅢ TⅢ feature of ECG ;plasma DD level significant rising (> 10 μg/ml) should be considered to be PE .

OBJECTIVETo apply single nucleotide polymorphism (SNP) microarray for delineation of small supernumerary marker chromosome (sSMC) in two newborns.

METHODChromosome karyotyping was performed on newborns who were born in Jan. 2013 and Jan. 2014 in Haidian Maternal and Child Health Hospital because of the abnormalities found in pregnancy checkups. SNP microarray analysis was carried out on 2 newborns with de novo sSMCs (one was mos 47,XY, + mar[45]/46,XY[5] and the other was mos 47, XY, + mar [30]/46, XY [20]), which could not be determined by conventional banding techniques. Genomic DNA was extracted from cord blood samples, amplified, tagged and hybridized following the manufacturer' s protocol. Data were collected and analyzed.

RESULTThere was a 78. 6 Mb duplication in chromosome 8 for Newborn A, which was associated with 8p22 duplication syndrome; and a 32. 7 Mb duplication in chromosome 13 for Newborn B, which was not yet reported definitely as pathogenic. The newborn A was identified with agenesis of the corpus callosum, obvious right eyelid drooping, the onset of low muscle tone and mental developmental lag behind their peers, while the newborn B had normal findings on physical and mental evaluation.

CONCLUSIONSNP-array can identify sSMCs of newborns at the DNA level, and can be used as an important supplement to the conventional karyotype analysis, but the pathogenicity of positive outputs need further verification.

Objective To investigate the correlation between neural tube defects (NTDs) and DACT1 gene, and provide the basic data for disease diagnosis and genetic counseling. Methods Blood samples were obtained from 163 NTDs patients and 480 unrelated healthy individuals. Mutation detection of DACT1 gene and DNA direct sequencing was carried out by PCR amplification. Bioinformatics analysis of these mutated loci was performed. Results Six mutations were found in NTDs patients, including 4 missense mutations (p.R45W, p.D142G, p.N356K and p.V702G). But these mutations were not found in 480 healthy individuals. Three mutated amino acid residues (p.45R, p.142D and p.356N) were highly conservative in evolution, and the mutated carriers were female patients, and suffered from anencephaly. Conclusion DACT1 gene mutation may be a risk factor of NTDs in Han population of northern China.

Objective To carry out a molecular screening of Chinese common deafness gene mutations in Chinese pregnant women group,so as to expatiate on the content,provide molecular epidemiological data,reduce the birth rate and provide a theoretical basis to the deaf children. Methods The molecular detection was done to the pregnant women underwent normal antenatal care in our hospital,using gene chips to screen the four com?mon deaf genes(GJB2,GJB3,SLC26A4 and mitochondrial 12S rRNA)in China;then,the newborn infants carrying mutations were treated with the hearing screening,using the methods of Otoacoustic Emissions(OAE)and Brainstem Auditory Evoked Potentials(BAEP),and the husbands of mutation carrying pregnant women were adopted molecular testing of the deaf susceptibility genes in order to investigate the correlation of the rate of pregnant women carrying the mutant genes and newborn infants deafness. Results Totally 2 067 cases of pregnant women were accepted to do the molecular screening,there were 110 cases of deafness mutations detected(5.320%),in which GJB2 gene(67 cases),GJB3 gene(6 cases), SLC26A4gene(33 cases),mitochondrial 12SrRNAgene(4 cases)mutation detection rates were 3.240%,0.290%,1.600%and 0.190%,respec?tively;especially:GJB2gene 235 del C,GJB2gene 299 del AT double mutant 1 case;GJB2gene 299 del AT,GJB3gene 538 C>T double mutant 1 case;GJB2 gene 235 del C,SLC26A4 gene IVS7?2 A>G double mutant 1 case. About 108 cases children newborn accepted to do the hearing screening,in which 3 cases had problems with the left ear,3 cases with the right ear,and 4 cases with the double ears. Conclusion The use of ge?netic deafness gene chip to do the molecular diagnostics in pregnant women can be convenient,fast and efficient for prenatal diagnosis of deafness, which provides a theoretical basis and good method for reducing the birth rate of deaf children and should be popularized more widely.

AIM: To investigate the effects of human urotensin Ⅱ (hUII) on in vivo mesenteric microcirculation in rats. METHODS: For recording of microcirculation images in the mesentery, the intestinal loop was mounted on the stage of an intravital microscope equipped with a TV camera. Video images of microcirculation were stored by a video cassette recorder. Temporal changes in internal diameter and microcirculatory velocity of microvesseles were measured by computer using the ImagePro software. The blood flow in intestinal wall was measured with PIMII laser Doppler perfusion Imager (Lisca Sweden). RESULTS: The internal diameters of arterioles and venules in control group were (21.4?2.3) ?m and (38.1?3.6) ?m,respectively. In UII group, the arterioles and venules contracted immediately after treated with UII and up to the peak at 1 min [(14.1?1.4) ?m and (22.2?5.2) ?m vs control,P0.05). The blood flow in intestinal wall increased 1 min after treated with UII and up to high peak at 5 min(6.4?1.1 perfusion unit vs control 4.2?0.9,P

AIM:To study whether ischemic preconditioning(IPC) has a protective effect against ischemia/reperfusion(I/R) injury in brain, and the possible relationship between IPC and the regulating function of microcirculation. METHODS: The I/R models were established both in I/R and IPC groups of Sprague-Dawley rats. Additional procedure was performed of short term cerebral ischemic preconditioning in IPC group 24 hours before I/R. Skull windows were performed through which microcirculation features were measured before ischemia, during ischemia, and reperfusion. Finally, brains were cut into slices and stained with red tetrazoline(TTC). RESULTS: Most TTC stained brains in I/R group presented irregular palely red areas which were few in IPC group. Compared with I/R group, IPC group presented relatively increase in accumulated length of capillaries, mean cerebral microcirculatory perfusion, and microcirculatory velocity in ischemic and reperfusion phase. There was no-reflow phenomenon in I/R group in reperfusion phase, which was substituted by the course of increasing reperfusion in IPC group. CONCLUSIONS:IPC could relieve the reduction of tissue perfusion during ischemia and the no-reflow phenomenon during reperfusion by improving the regulating function of microcirculation, which relatively promote the opening of capillaries and accelerating of microvascular flow, therefore protect brain from I/R injury.