To evaluate the visual performance of the patients with traumatic corneal astigmatism, after the treatment of topography guided off-flap epipolis laser in situ keratomileusi (off-flap Epi-LASlK).
●METHODS: This prospective clinical study was comprised of 21 eyes of 21 patients with irregular corneal astigmatism caused by trauma, they were treated by off-flap Epi - LASlK from July 2012 to December 2013. The data included uncorrected visual acuity ( UCVA), best spectacle - corrected visual acuity ( BSCVA ), contrast sensitivity 1, 6mo before and after surgery; the healing area percentage of corneal epithelia, the healing time of corneal epithelia and pain score at 3d after surgery.
●RESULTS: Postoperative 1mo both UCVA and BSCVA were improved significantly than that before surgery (t =15. 703, 4. 351, P< 0. 05); Compared with the 1mo after surgery, UCVA at 6mo after surgery raised significantly (t= 6. 867, P <0. 05). There was no statistical significance between 6 and 1mo after surgery about BSCVA (t= 1. 497, P = 0. 140 ). After surgery, mean spherical equivalent (SE) was reduced from -2. 43±3. 02D to -0. 23±0. 49D (P<0. 05), and the mean cylinder was reduced from -1. 86± 2. 23D to - 0. 46 ± 1. 03D (P< 0. 05). Postoperative 1mo,4 kinds of spatial frequency and contrast sensitivity had no significant difference compared with the preoperative (P>0. 05 ). Postoperative 6mo except the 3c/ d spatial frequency, the remaining 3 spatial frequency contrast sensitivity compared with those before operation were significantly improved ( P < 0. 05 ). The healing area percentage of corneal epithelia was 92. 46% ±8. 24% (80% -100%) at 3d after surgery; The healing time of corneal epithelia was 3. 50 ± 1. 56d; Pain scores at 3 and 7d after surgery was 1. 54±1. 32 and 0. 04±0. 64, respectively.
●CONCLUSlON: Topography-guided off-flap Epi-LASlK is safe and effective in treating the patients with traumatic corneal irregular astigmatism. The operation can improve both the contrast sensitivity and the visual performance.

BACKGROUND: Thyroid cancer stem cells are essential to the recurrence and metastasis of thyroid carcinoma. Leukemia inhibitory factor receptor (LIFR) shows a downward trend in a variety of malignant tumors, and its overexpression can inhibit the recurrence and metastasis of malignant tumors. OBJECTIVE:To explore the effect of LIFR on the stemness maintenance and lung metastasis of thyroid cancer stem cells in vivo. METHODS: Primary thyroid cancer cells TCLM were isolated from the lung metastases of a metastatic thyroid cancer patient. Serum-free suspension culture was used to form tumor cell balls. Flow cytometry was used to screen CD133+phenotype of metastatic thyroid cancer stem cell subpopulation TCLM-S. The overexpressed recombinant lentiviral plasmid containing LIFR and its negative control containing the empty plasmid were infected into thyroid cancer stem cells TCLM-S at the ratio of virus/cell number=20, and screened with 2.0 mg/L puromycin to construct TCLM-SLIFRand TCLM-Scontrolstem cells which stably expressed LIFR and its control. Real-time quantitative PCR (qRT-PCR) was used to detect the expression of LIFR in TCLM-SLIFRand TCLM-Scontrolstem cells. Flow cytometry was used to detect the percentage of CD133+phenotype cell subsets, western blot assay was used to detect the expression of tumor stemness related factors SOX2, Oct4, Nanog and tumor invasion and metastasis related proteins E-cadherin, matrix metalloproteinase (MMP)-2, MMP-7 in TCLM-SLIFRand TCLM-Scontrol stem cells. TCLM-SLIFRand TCLM-Scontrolstem cells were respectively injected into BALB/c nude mice by tail vein, and the lung metastasis model of thyroid cancer stem cells was constructed. The effect of LIFR overexpression on lung metastasis was observed. RESULTS AND CONCLUSION: Compared with TCLM-Scontrolcells, the expression of LIFR in TCLM-SLIFRcells was significantly increased, the proportion of CD133+phenotype stem cell subsets was significantly decreased, the expression of SOX2, Oct4 and Nanog were significantly decreased, the expression of E-cadherin was significantly increased, and the expression of MMP-2 and MMP-7 was significantly decreased. Moreover, the number of lung metastasis in nude mice given TCLM-SLIFRcells was significantly decreased as compared with those given TCLM-Scontrol cells.To conclude,LIFR overexpression can decrease the stemness and ability of lung metastasis in vivo.

To construct a rabies virus mutant, the psi region was replaced by the coding region of human cytochrome c gene, and the coding region for cytoplasmic domain of glycoprotein G was deleted in the full-length of genomic cDNA of rabies virus strain SRV9. The mutant plasmid and the plasmids with N, P, L and G structural proteins of wild type SRV9 were co-transfected into BHK-21 cells. It was shown by IFA that there were many specific fluorescence in the BHK-21 cells, and typical rabies virus virions were observed by electronic microscope. These results demonstrated that the mutant rabies virus was successfully rescued. The genetically modified SRV9 stain has promise to provide invaluable experimental tool to develop attenuated live rabies vaccine.
Animals ; Cell Line ; Cricetinae ; DNA, Complementary ; genetics ; DNA, Viral ; genetics ; Genome, Viral ; genetics ; Humans ; Microscopy, Immunoelectron ; Mutation ; Rabies virus ; genetics ; ultrastructure

Objective Radionuclide-labeled low molecular weight polypeptide is reeently advocated for the diagnosis and treatment of malignant tumor. The purpose of this study was to evaluate the anti-tumor effect of 131Ⅰ-Tyr-octreotide in nude mice bearing human non-small cell lung cancer (NSCLC). Methods 131Ⅰ-Tyr-octreotide was prepared by Ch-T method. The radiochemical purity was measured and biodistribution was evaluated. The nude mice models bearing human NSCLC were studied and divided into four groups: group A injected 131Ⅰ-Tyr-octreotide through tail vein, group B injected normal saline, group C injected 131Ⅰ-Tyroctreotide through stroma and group D injected 131Ⅰ through stroma. The radioactivity ratio of tumor to normal tissue (T/NT) was calculated over region of interest (ROI). The tumor cell cycle and cell apoptosis were analyzed by flow cytometry (FCM), terminal deoxynucleotidyl transferase mediated dUTP-biotion nick end labeling (TUNEL) and histopathological analysis. Statistical analysis was performed with SPSS 11.0, and the comparison for difference between groups performed with one-way ANOVA analysis. Results The labeled radiochemical purity was (95.23±1.67)% and specific activity of 3.5×106Bq/ug. The biodistributiou showed high uptake in kidney, and low uptake in liver and spleen. The radioactive uptake in group C was higher than the other groups, and the retention time was longer. The T/NT was 52.74±0.13 after 24 h, which was much higher than that the other groups (group D: 8.90±0.23, group A: 6.42±0.02, q=628.81 and 664.33, all P<0.05). The resuits of tmnor cell cycle determined by FCM showed that the G1 phase was blocked mast remarkably in group C than the other groups [group C: (83.17±6.86)%, group A: (57.02±18.81)%, group D: (49.29±7.80)%, group B: (45.88±5.13)%, q=5.29, 6.86, 7.55, 1.56, 2.26, 0.69, all P<0.05]. Apeptotic cells were observed by TUNEL, and apoptotic body was detected by immuno-histochemical examination. Conclusions 131Ⅰ-Tyr-octreotide was easily labeled by Ch-T. 131Ⅰ-Tyr-octreotide could induce tumor cell apoptosis and inhibit the tumor cell of NSCLC. It might be a potential target-directed agent in NSCLC.

Abdominal Wall ; Adenocarcinoma ; diagnosis ; Colonic Neoplasms ; diagnosis ; Female ; Histiocytoma, Malignant Fibrous ; diagnosis ; Humans ; Ileal Neoplasms ; diagnosis ; Ileocecal Valve ; Leiomyoma ; diagnosis ; Middle Aged ; Neoplasms, Multiple Primary ; diagnosis ; Soft Tissue Neoplasms ; diagnosis ; Uterine Neoplasms ; diagnosis

OBJECTIVETo investigate the clinical manifestations, pathologic features and laboratory findings in two Proteus syndrome patients with giant hemangiomas in the spleen and chronic DIC.

METHODSUltrasound imaging and magnetic resonance imaging (MRI) were used for analysing the characteristics of the giant hemangiomas in the spleen. The spleen specimen was examined pathologically for the feature of the hemangioma. Homostatic tests were performed by routine laboratory methods.

RESULTSTwo Proteus syndrome patients with giant hemangiomas in the spleen causing chronic DIC (Kasabach-Merritt syndrome) were first reported. They were recovered after splenectomy.

CONCLUSIONProteus syndrome when accompanied giant hemangioma could cause chronic DIC. Significantly decreased plasma fibrinogen level in this case might be helpful for the differential diagnosis from DIC caused by other diseases.

Adolescent ; Disseminated Intravascular Coagulation ; etiology ; Female ; Hemangioma, Cavernous ; complications ; diagnostic imaging ; surgery ; Humans ; Proteus Syndrome ; complications ; Splenectomy ; Splenic Neoplasms ; complications ; diagnostic imaging ; surgery ; Ultrasonography

OBJECTIVETo evaluate the prevalence of TET2 gene mutation in acute myeloid leukemia (AML) patients, and analyze their clinical characteristics and prognosis.

METHODSPolymerase chain reaction (PCR) and direct sequencing were used to sequence exon 3 to 11 of TET2 gene.

RESULTSAmong 96 AML patients, TET2 gene mutation was detected in 13 (13.54%) patients (95%CI 6.70% - 20.38%). The median age was 54 years in mutated group and 41 years in unmutated group (P = 0.010). Mutated and unmutated patients did not significantly differ in gender, white blood cells (WBC) count at diagnosis, platelet count, PB and BM blast percentage and chromosome karyotype, excepting for hemoglobin level 84 (70 - 108) g/L in mutated group versus 70 (55 - 87) g/L in unmutated group (P = 0.032). TET2 gene mutation had no significant correlation with C-KIT, FLT3, JAK2V617F mutations, but did with NPM1 mutation. TET2 mutated patients had lower CR1 rate and 2-year overall survival than unmutated in non-M(3) patients (P < 0.05).

CONCLUSIONSTET2 gene mutation is more prevalent in older AML patients and has a certain correlation with clinical characteristics and outcome. It may be a molecular marker for poor prognosis in AML.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; DNA Mutational Analysis ; DNA-Binding Proteins ; genetics ; Exons ; Female ; Humans ; Karyotype ; Leukemia, Myeloid, Acute ; genetics ; Male ; Middle Aged ; Proto-Oncogene Proteins ; genetics ; Young Adult

OBJECTIVETo identify and characterize a missence mutation Ser250 Phe underlying coagulation factor Ⅶ (FⅦ) deficiency in a Chinese patient and his family.

METHODSThe FⅦ gene (F7) was analyzed by DNA sequencing, and the FⅦ levels (including antigen and activity) in patient's plasma were determined with enzyme-linked immunoabsorbent assay (ELISA) and one stage prothrombin time based method. In addition, a FⅦ-250 Phe mutant corresponding to the identified mutation was expressed in HEK293 cells, and a subcellular localization experiment in CHO cells was performed to clarify the molecular mechanism of FⅦ deficiency caused by the FⅦ-250 Phe mutation.

RESULTSThe patient had a prolonged prothrombin time (PT: 36.5 s) and low levels of both FⅦ antigen and activity (130.2 ng/mL and 4.0%, respectively). Two heterozygous mutations were identified in the F7 gene (NG-009262.1), which included a g.15975 G>A mutation at the splice receptor site of intron 6 (IVS6-1G>A) and a novel g.16750 C>T mutation in exon 8, which resulted in replacement of Ser (TCC) 250 with Phe (TTC)250 in the vicinity of a charge-stablizing system. By gene expression experiments, the antigen and activity levels of FⅦ-250 Ser and FⅦ-250 Phe in the culture medium were (37.77 ± 2.30) ng/mL and (4.02 ± 0.52) ng/mL, respectively. ELISA and Western blotting analyses indicated that expression of the mutant FⅦ-250 Phe and wild type FⅦ-250 Ser was (130.51 ± 2.32) ng/mL and (172.45 ± 2.25) ng/mL, respectively. FⅦ-250 Phe was found in endoplasmic reticulum and Golgi apparatus, suggesting that the mutant FⅦ-250 Phe could be normally synthesized in the cells but was inefficiently secreted.

CONCLUSIONCompound heterozygous mutations in F7 gene (g.15975G>A and g.16750C>T) may be responsible for the FⅦ deficiency in this patient. The novel FⅦ 250 Phe can be transported from endoplasmic reticulum to Golgi apparatus, but may be degraded or inefficient.

Adult ; Animals ; CHO Cells ; Cricetinae ; Cricetulus ; Enzyme-Linked Immunosorbent Assay ; Factor VII ; genetics ; physiology ; Factor VII Deficiency ; genetics ; HEK293 Cells ; Humans ; Male ; Mutation, Missense

OBJECTIVETo identify gene mutations involved in five cases of inherited factor V (FV) deficiency.

METHODSActivity of FV was determined by one-stage clotting assay using FV-deficiency plasma, and FV antigen by an ELISA assay. All the exons and exon-intron boundaries of FV gene were amplified by PCR and then DNA sequencing. Restriction enzyme analysis was used to analyze the probands, their family members and healthy volunteers.

RESULTSBoth activity and antigen of FV in the 5 patients were extremely lower compared with that of normal mixed plasma. Six mutations were identified in these 5 patients, G69969T (G2079V), C45533T (R712Ter), C46796T (R1133Ter), G45366A (C656Y), C46253T (R952C) and G16088C (D68H), the latter three were novel mutations reported for the first time and the C46253T (R952C) was the first missense mutation reported in B domain. The result of sequencing or restriction enzyme analysis showed that the three novel missense mutations were not caused by single nucleotide polymorphisms.

CONCLUSIONGene mutations in 5 type I inherited FV deficiency of patients including 2 nonsense mutations and 4 missense mutations identified which led to the instability of FV protein and the reducing of FV: Ag in the plasma.

Adolescent ; Adult ; Child ; DNA Mutational Analysis ; Exons ; genetics ; Factor V ; genetics ; metabolism ; Factor V Deficiency ; blood ; genetics ; Female ; Humans ; Male ; Mutation ; Pedigree ; Phenotype ; Young Adult