Objective: To screen for differentially expressed genes associated with the development and progression of human growth hormone adenoma, so as to lay a foundation for future study. Methods: The whole genome oligonucleotide microarray (Affymetrix 133 plus 2.0) was used to examine gene profiles of 8 growth homone adenoma samples and 2 normal pooled pituitary samples. Differentially expressed genes were subjected to bioinformatics analysis. Real-time qPCR was used to verify the microarray result of a randomly selected candidate gene. Results: A total of 187 up-regulated genes and 899 down-regulated genes associated with growth hormone adenoma were screened out, with their functions mainly associated with molecular binding, apoptosis/tumor, metabolism, signal transduction, cell cycle, and transportation activities. Conclusion: Microarray technology can be used for preliminary screen of growth hormone adenoma associated genes. The development and progression of growth homone adenoma are complex processes involving multiple genes, molecules, and pathways.

The practice and exploration of bilingual teaching for the course of microbiology has been made in order to improve the students foreign lingual level and to meet the higher requirement on tip-top person with the social development. As a result,bilingual teaching is welcome,and the teaching effect is so distinct that the aim was reached to either study the fundamental knowledge or enhance the English level.

Adult ; Arsenic ; pharmacology ; Chromosome Aberrations ; chemically induced ; Dose-Response Relationship, Drug ; Female ; Humans ; Lymphocytes ; drug effects ; metabolism ; Male ; Middle Aged

OBJECTIVETo evaluate whether or not administration of folic acid and resveratrol have preventive effects on cleft palate formation as well as the comparison of the two drugs' s effects.

METHODSPregnant mice were randomly divided into 9 groups, with 8 mice in each group. The TCDD group mice were dosed with TCDD 28 microg/kg body weight on gestation day 10 (GD 10) animals in folic acid group were respectively dosed with folic acid 15, 10, 5 mg/kg and TCDD 28 microg/kg; resveratrol treated mice were divided into 3 groups: resveratrol 50 mg/kg were orally administered for 6 consecutive days, from gestational day GD 8 to GD13 in resveratrol (GD8-13 ) group; resveratrol 50 mg/kg were orally administered for 6 consecutive days, from gestational day GD 8 to GD13, followed hy an oral administered with TCDD on GD10 in resveratrol (GD8-13) + TCDD group; resveratrol 50mg/kg and TCDD 28 microg/kg were used by gavage administration at GD10 in resveratrol (GD10) + TCDD group. Control mice were treated with the same volume of water for 6 consecutive days from GD8 to GD13 and were given a single dose of corn oil on GD10. The pregnant mice weight and embryos, the number of live, cleft palate, dead and resorption fetal mice were recorded on GD 17.5. The coronal sections of the fetal mice heads were prepared at GD 17.5 and observed by microscopy.

RESULTSTotal frequency of clefts was 92.86% in TCDD group, 84.00% (15 mg), 73.08% (10 mg), 84.00% (5 mg) in folic acid + TCDD groups, 0% in resveratrol (GD10) group, 74.51% (GD10), 57.78% (GD8-13) in resveratrol + TCDD groups. The frequency of cleft was 0% in the control group. Compared with the control and the TCDD groups, there were significant differences in the number of live, dead and resorption fetal mice in TCCD + resveratrol (GD8-13) group (P < 0.05). No significant differences in embryonic weight, live fetuses weight, the number of live, dead and resorption fetal mice were found in the other groups (P > 0.05).

CONCLUSIONTest dose of folic acid and resveratrol both had certain antagonistic effect on cleft palate in mice induced by TCDD, with folic acid 10 mg/kg, resveratrol 50 mg/kg GD8-13 doses having stronger antagonistic action. Effects of both the two drugs have no significant difference, but resveratrol (50 mg/kg, GD8-13) significantly affects the fetal mice's growth and development under TCDD exposure in utero.

Abnormalities, Drug-Induced ; prevention & control ; Animals ; Cleft Palate ; chemically induced ; prevention & control ; Female ; Fetus ; Folic Acid ; administration & dosage ; pharmacology ; Humans ; Mice ; Mice, Inbred C57BL ; Polychlorinated Dibenzodioxins ; antagonists & inhibitors ; Pregnancy ; Random Allocation ; Stilbenes ; administration & dosage ; pharmacology ; Teratogens

OBJECTIVETo explore a method to repair nasal side mucosa of wide incomplete cleft palate and reduce the tension of wound by using oral mucosa flap in the top of fissure.

METHODS27 cases of wide incomplete cleft palatal were included in the study. On the basis of two-flap palatoplasty, the triangular oral mucosa flap in the top of fissure was turned and sewed with side mucosa to repair nasal side mucosa of wide palatal cleft.

RESULTSWithout postoperative active bleeding, airway obstruction and wound infection, 27 cases had been repaired satisfactorily by this procedure. 1-3 months followed up demonstrated that all the wounds healed well without wound dehiscence or fistulas and the scars in the palate were not severe.

CONCLUSIONUsing oral mucosa flap in the top of fissure to repair nasal side mucosa of wide palatal cleft can get a reduced tension and correspondingly increase the width of mucoperiosteal flaps so as to decrease incidence rate of palatal fistulas and reduce formation of scars.

Cleft Palate ; Female ; Humans ; Mouth Mucosa ; Nasal Mucosa ; Reconstructive Surgical Procedures ; Surgical Flaps

To investigate the transduction efficiency of recombinant adeno-associated virus 2 (rAAV-2) in human umbilical cord blood CD34(+) hematopoietic stem/progenitor cells, the CD34(+) cells sorted by the method of magnetic cell sorting from human cord blood were infected with the rAAV-2 expressing the green fluorescent protein (GFP) gene. After transduction for 19 hours, the expression of GFP was detected under fluorescence microscope. The results showed that 43% CD34(+) cells expressed the GFP gene at a multiplicity of infection of 2 x 10(5). It is concluded that the rAAV-2 can transduce human cord blood CD34(+) hematopoietic stem/progenitor cells efficiently.
Antigens, CD34 ; analysis ; Dependovirus ; genetics ; Fetal Blood ; cytology ; Genetic Therapy ; Green Fluorescent Proteins ; Hematopoietic Stem Cells ; metabolism ; Humans ; Luminescent Proteins ; genetics ; Recombination, Genetic ; Transduction, Genetic

Objective To explore the expression and function of correlative genes in the happening and developing of human pituitary adenoma-subtypes.Methods The whole genome oligonucleotide microarray (Affymetrix 133 plus 2.0) was used to examine the gene expressions of pituitary adenoma tissue in 8 patients with pituitary adenoma (2 with growth hormone adenomas,2 with prolactinomas,2 with gonadotroph adenomas and 2 with null cell adenomas) and normal pooled pituitary tissue.Differentially expressed genes were analyzed by Hierarchical method and bioinformatics.A candidate gene was selected to verify the microarray analyzed result by real-time quantitative PCR.Results Compared with associated genes with normal control,associated genes with pituitary adenoma mainly involved in the following biological processes analyzed from the view of function: binding,apoptosis-or-tumor correlation,metabolism,signal-transducer-activity,cell cycle,transcription-regulator-activity and transporter-activity.The specificity of expression in several differential genes was connected to the development of pituitary adenoma-subtypes.Conclusion The development of pituitary adenoma is a complex regulation process involving lots of genes,molecules and pathways.However,the molecular mechanism related to the individual pituitary adenoma-subtypes is different.

OBJECTIVETo explore the mechanism of cleft palate in mice induced by 2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin (TCDD).

METHODSOn gestation day 10 (GD 10), 12 pregnant mice were randomly divided into two groups as the treated group and the control group with 6 mice in each group. The mice in the treated group received intragastric administration with 64 microg TCDD/kg, while the mice in the control group received equivalent corn oil. The embryos were examined under stereomicroscope to detect the incidence of cleft palate on GD 18.5. Another 18 pregnant mice were randomly divided into two groups (treated group and control group) on GD 10 with 9 pregnant mice in each group. Then each group was divided into 3 subgroups: GD 13.5, GD 14.5 and GD 15.5, with 3 pregnant mice in each subgroup. The palatal shelves were dissected from the embryos for RNA and DNA extraction on GD 13.5, GD 14.5 and GD 15.5. At last the expression of Smad 2-4 and Smad 7 mRNA was investigated by RT-PCR, and the TGF-beta3 promoter methylamine levels were investigated by methylation specific PCR (MSP).

RESULTSThe cleft palate mice model was established successfully by exposing pregnant C57BL/6J mice to TCDD. Total frequency of clefts was 100% in TCDD group, and the frequency of clefts was 0 in the control group. The relative expression of Smad 2 mRNA was 0.263 +/- 0.088, 0.296 +/- 0.016 and 0.159 +/- 0.027 in TCDD group, 0.180 +/- 0.042, 0.282 +/- 0.029 and 0.165 +/- 0.018 in control group. The relative expression of Smad 3 mRNA was 0.453 +/- 0.153, 0.551 +/- 0.160 and 0.328 +/- 0.049 in TCDD group, 0.375 +/- 0.126, 0.510 +/- 0.145 and 0.259 +/- 0.035 in control group. The relative expression of Smad 4 mRNA was 0.675 +/- 0.174, 0.577 +/- 0.070 and 0.396 +/- 0.066 in TCDD group, 0.557 +/- 0.138, 0.587 +/- 0.080 and 0.441 +/- 0.054 in control group. The relative expression of Smad 7 mRNA was 0.283 +/- 0.050, 0.320 +/- 0.068 and 0.169 +/- 0.045 in TCDD group, 0.207 +/- 0.043, 0.288 +/- 0.051 and 0.155 +/- 0.040 in control group. There was no significant difference between the TCDD treated mice and the control (P > 0.05). The TGF-beta3 promoters were at the un-methylation state both in the TCDD treated and control group.

CONCLUSIONIt suggests that TCDD could induce a stable formation of cleft palate, but it is not through the TGF-beta/Smad signaling nor through the modification of TGF-beta3 promoter methylation.

Animals ; Cleft Palate ; chemically induced ; DNA Methylation ; Female ; Mice ; Mice, Inbred C57BL ; Polychlorinated Dibenzodioxins ; toxicity ; Pregnancy ; Promoter Regions, Genetic ; Signal Transduction ; Smad Proteins ; metabolism ; Teratogens ; toxicity ; Transforming Growth Factor beta3 ; metabolism

OBJECTIVETo detect changes of Foxp3 expression in the decidua in patients with preeclampsia and investigate the correlation of Foxp3-924 (rs2232365) polymorphisms with preeclampsia.

METHODSFrom October 2011 to December 2012, 252 normal pregnant women and 156 preeclampsia patients of Han nationality from the same geographic region were tested for Foxp3-924 genotypes by polymerase chain reaction with sequence-specific primer (PCR-SSP). Sixty-eight of the patients with preeclampsia (33 with mild and 35 with severe preeclampsia) and 30 of the normal pregnant women were also examined for Foxp3 expression in the decidua using immunohistochemical method.

RESULTSFoxp3 positive expression rates in the decidua was 51.52% in mild preeclampsia and 28.57% in severe preeclampsia cases, significantly lower than that in the control group (86.67%, P<0.05). In preeclampsia patients, the frequencies of Foxp3-924G/G, G/A, and A/A genotypes were 0.1346, 0.4615 and 0.4038, respectively, and the frequencies of Foxp3-924A and Foxp3-924 G were 0.6346 and 0.3654, respectively. The genotype frequencies of Foxp3-924G/G, G/A and A/A in the control group were 0.1508, 0.4087 and 0.4405, respectively, and the frequencies of Foxp3-924 A and Foxp3-924 G were 0.6448 and 0.3552, respectively. No significant differences were found in the gene frequencies of Foxp3-924G/A between preeclampsia patients and the control group (P>0.05).

CONCLUSIONThe expression level of Foxp3 in the placental tissue of preeclampsia patients is significantly lower than that in normal pregnant women, suggesting that lowered Foxp3 expression decreases the immunosuppressive function and causes imbalance of immune tolerance between maternal-fetal to induce preeclampsia. Foxp3-924 polymorphisms is not significantly correlated with the occurrence of preeclampsia.

Case-Control Studies ; Female ; Forkhead Transcription Factors ; genetics ; metabolism ; Gene Frequency ; Genotype ; Humans ; Placenta ; metabolism ; Polymorphism, Genetic ; Pre-Eclampsia ; genetics ; Pregnancy

BACKGROUNDEverlasting cellular proliferation is the fundamental feature during gliomagenesis and Ki-67 is one of the classical proliferation markers in human glioblastoma multiforme (GBM). However, the driver genes or core pathways for cellular proliferation in GBM have not been elucidated systematically.

METHODSWe evaluated by immunohistochemistry the prognostic value of Ki-67 expression in the clinical outcome of 156 Chinese patients with GBM and a total of 64 GBM samples were selected for further Agilent genome-wide microarray analysis. On the basis of the microarray data from Tiantan (n = 64) and The Cancer Genome Atlas (TCGA) (n = 202) database, differentially expressed genes between the GBM subgroups with high or low level of Ki-67 expression were identified using Significance Analysis of Microarrays (SAM). Gene Ontology (GO) and KEGG Pathway analyses were then undertaken for the Ki-67 associated genes to identify the most significant biological processes and signaling pathways.

RESULTSWe confirmed that Ki-67 was an independent prognostic indicator in the largest Chinese patient cohort of 156 GBM samples via immunohistochemical staining. Survival analysis of Ki-67 over-expression revealed a highly significant association with a worse clinical outcome (P = 0.010 for progression-free survival; P = 0.007 for overall survival). Comparative and integrated analysis between Tiantan and TCGA database identified a 247-gene "proliferation signature" (205 up-regulated and 42 down-regulated genes) that distinguished Ki-67 expression phenotypes. GO and KEGG Pathway analyses further indicated that Ki-67 expression phenotype was associated with distinct changes in gene expression associated with the regulation of cellular growth and proliferation.

CONCLUSIONSProliferation marker Ki-67 is an independent prognostic indicator in Chinese GBM patients. And Ki-67 associated proliferation signature identified through genome-wide microarray analysis may provide potential targets for anti-proliferation therapy in GBM.

Cell Proliferation ; Computational Biology ; Gene Expression Profiling ; methods ; Glioblastoma ; genetics ; metabolism ; Humans ; Immunohistochemistry ; In Vitro Techniques ; Ki-67 Antigen ; genetics ; metabolism ; Oligonucleotide Array Sequence Analysis