·Corneal neovascularization ( CNV) is one of the most important causes that affecting corneal transparency, and it is a high risk factor of allogeneic corneal graft rejection. lt has become a research focus for the regulation of CNV. microRNAs are a class of endogenous non-protein-coding micromolecule RNAs which play a critical role in regulating a series of life process.Researches in recent years show a close correlation between microRNA and CNV.ln this article we reviewed the recent advances in these researches.

Objective To study the genotyping of clarithromycin-resistant Helicobacter pylori(Hp) isolates.Methods From March 2007 to October 2007,247 gastric mucosa specimens were collected by the endoscopy from the patients with peptic ulcer or gastritis at the affiliated hospital of Youjiang Medical College for Nationalities.A total of 126 Hp strains were isolated.Resistance to clarithromycin in Hp was determined by E-test.All of the resistant isolates were genotyped with REP-PCR and further clustered with NTsys_2 software.The clinical data was collected for these patients with clarithromycin-resistant Hp.Results The 26 clarithromycin-resistant isolates from the west of Guangxi were divided into six genotypea including Group Ⅰ,Group Ⅱ,Group Ⅲ,Group Ⅲ,Group Ⅳ,Group Ⅴ and Group Ⅵ according to the homology of 78%.Every group have 2,11,1,8,3,1 strains Hp,respectively.Strains of group Ⅱ were isolated from patients with peptic ulcer and most of them from Chuang patients.All strains of group Ⅳ were isolated from patients with gastritis.Conclusions The clarithromycin-resistant isolates were divided into six groups by REP-PCR Disease type.nationality of patients and family history of stomach diseases were associated with the genotypes.

objective To analyze the prevalence of Helicobacter pylori(Hp)strains resistant to clarithromycin and the relation of 23S rRNA genetic mutation with clarithromycin resistance.Methotis Hp strains were isolated from gastric mucosa biopsies of patients with peptic ulcer or gastritis.Resistanee of the isolates to elarithromycin wag determined using diffusion test.Mutations in elarithromyein resistant strains were identified by PCR-RFLP and gene sequencing.Results The prevalence of Hp strains resistant clarithromyein was 22.2%.10 of clarithromycin resistant strains had A2143G.A2144G point mutation in 23S rRNA gene,and none of the 10 susceptible strains had the A2143G or A2144G mutation,and the result was affirmed by measure sequencing.Conclusion The prevalence of Hp is higher than Beijing and Shanghai,mutations in 23S rRNA are associated with elarithromyein resistance in Hp.

Objective To evaluate the difference of internal diameter of bronchial artery in big lung cancer,small lung cancer,and normal lung with multiple slice CT.Methods MSCT angiographies of 44 patients with lung cancer confirmed by pathology were retrospectively analyzed,and 29 patients were with big lung cancer(≥3 cm)and 15 patients with small lung cancer(

OBJECTIVETo investigate the effect of antisense VEGF165 infection on the growth of A375 cells in nude mice.

METHODSA375 cells were injected s.c into the axilla of the nude mouse. After the tumor formed, we cut it into 16 pieces equally, then transplanted into another 15 nude mice. There were three groups: Group PBS, Group Ad-GFP, and Group Ad-aVEGF. Four weeks after interfere, the mice were sacrificed and their tumors were excised for naked eye and histological observation. The VEGF expression was checked with ISH and immunohistochemistry staining. The micro-vessel density (MVD) in tumor mass was counted by VIII factor immunohistochemistry staining.

RESULTSThe visible and palpable nodules had developed at all the injected sites. Tumor growth speed was more slowly in Group Ad-aVEGF than that in other groups. GFP gene could express effectively in tumor mass. Ad-aVEGF infection could suppress the growth of tumors, and there were no obvious side effects. Ad-aVEGF resulted more tissue necrosis, but it had no obvious effect on cell apoptosis. VEGF expression was inhibited significantly in Group Ad-aVEGF, and MVD was decreased accordingly.

CONCLUSIONSAd-aVEGF interfere may be a new method against human malignant melanoma, whose main mechanism is to induce ischemia, but not apoptosis.

Adenoviridae ; Animals ; Genetic Therapy ; Genetic Vectors ; Humans ; Male ; Melanoma ; genetics ; pathology ; Melanoma, Experimental ; genetics ; pathology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; genetics ; Skin Neoplasms ; genetics ; Vascular Endothelial Growth Factor A ; genetics

Objective To investigate the frequency and mutational status of JAK2V617F mutation in Chinese patients with chronic myeloproliferative disorders(CMPD) and to study the relative quantification of mutated JAK2 mRNA and the clinical significance. Methods JAK2V617F mutation and the mutational status were screened with amplification-refractory mutation system polymerase chain reaction(ARMS-PCR), the relative quantification of mutated JAK2 mRNA was studied by using capillary electrophoresis. Results A higher prevalence of JAK2V617F in either the heterozygotc or homozyote status in essential thrombocythemia (ET) was observed in elderly patients with ET (P<0.05). The presence of JAK2V617F was found to be significantly correlated with the age at diagnosis (P<0.05); patients with age ≥ 60 years showed significantly higher JAK2 mutated RNA levels than those with age < 60 years (P<0.05); the presence of JAK2V617F in polycythemia vera (PV) and ET was found to be significantly associated with higher hemoglobin level and higher leukocyte count (P< 0.05). In addition, higher leukocyte count was observed in homozygous ET patients than in heterozygous ET patients (P<0.05). The frequency of JAK2V617F mutation and the prevalence of homozygote in PV patients were higher than those in ET patients (P<0.05). The differences of JAK2V617F mRNA levels among PV, ET and chronic idiopathic myelofibrosis (IMF) were not significant. Conclusions ARMS-PCR technique can be used to detect the frequency and mutational status of JAK2V617F mutation owing to its sensitivity and along with capillary electrophoresis, quantitative assay for mutated JAK2 mRNA, diagnosis of CMPD and judgement of prognosis become possible.

OBJECTIVETo explore the prevalence of IDH gene (IDH1 and IDH2) mutations, types of mutations in patients with acute myeloid leukemia (AML), correlation with the internal tandem duplication(ITD) mutation of FLT3 gene, NPM1 gene mutation and some clinical characteristics.

METHODSThe mutations of IDH1 and IDH2 gene at exon 4, NPM1 gene at exon 12 and FLT3-ITD at exon 14 and 15 in 163 newly diagnosed AML patients were detected by PCR amplification followed by direct sequencing of genomic DNA.

RESULTS(1) IDH mutations were found in 25 patients (25/163), and all were heterozygous, of which IDH1 in 7 patients (4.29%) and IDH2 in 18 (11.04%). A total of 4 types of IDH1 mutations were identified (c.395G→A, p.R132H, n = 4; c.394C→A, p.R132S, n = 1; c.394C→G, p.R132G, n = 1; c.315C→T, n = 1). The IDH1 mutation caused substitutions of residue R132 except for one (c.315C→T). All IDH2 mutations caused changes of R140 (c.419G→A, p.R140Q, n = 18). The incidence of IDH2 mutation was significantly higher than that of IDH1 mutation (11.0% v 4.3%, P = 0.022). Both IDH1 and IDH2 mutation were detected in one patient, while IDH1 was synonymous substitution (c.315C→T). IDH-mutated cases showed a significantly higher frequency of concurrent FLT3-ITD mutation compared with wildtype cases (34.6% vs 11.9%, P = 0.003), so did IDH mutations concurrent NPM1 mutation vs NPM1 wildtype (28.1% vs 12.7%, P = 0.033), of which the frequency of concurrent NPM1 and FLT-ITD mutations cases with the IDH mutation was significantly higher than that of NPM1 and FLT-ITD negative (45.5% vs 11.7%, P = 0.002). IDH mutation incidence was significantly higher in normal karyotype cases than in abnormal ones (20.5% vs 5.8%, P = 0.020). Patients with IDH mutations were significantly older than wildtype patients(P < 0.001), whereas, there were no statistically significant differences in gender, peripheral blood (PB) count at diagnosis between two groups.

CONCLUSIONSThe incidence of IDH mutation is higher in patients with de novo AMLs, of which IDH2 mutation more frequently, and the patients associated with older age, normal karyotype at diagnosis. IDH mutation has a strong association with NPM1 and FLT3-ITD mutations, suggesting that IDH mutation has synergistic effect with the latter gene on leukemogenesis.

Adolescent ; Adult ; Aged ; DNA Mutational Analysis ; Female ; Genotype ; Humans ; Isocitrate Dehydrogenase ; genetics ; Leukemia, Myeloid, Acute ; genetics ; Male ; Middle Aged ; Young Adult

OBJECTIVE: To study the correlation of hematomorphology, bone marrow cytogenetics and clinical biochemical parameters with the prognosis of non-Hodgkin's lymphoma with bone marrow invasion. METHODS: Morphological analysis of bone marrow cells was performed by routine bone marrow puncture.Chromosome samples were prepared by short-term bone marrow culture. Karyotype analysis was carried out by R-banding in 28 patients. P53 gene was detected by fluorescence in situ hybridization (FISH). Serum lactate dehydrogenase (LDH) of all patients was determined and compared. RESULTS: In all patients, bone marrow morphology showed invasion of lymphoma. Chromosome analysis revealed abnormal karyotypes in 19 cases, which yielded an incidence of 67.85%. The proportion of lymphoma cells in bone marrow among those with an abnormal karyotype was much higher than those with a normal karyotype (60.2% vs. 33.5%, P<0.05). FISH assay showed that 9 (32.14%) patients had P53 gene deletion. And the deletion was much more common among those with an abnormal karyotype (42.11% vs. 11.11%, P<0.05). The serum LDH level in patients with an abnormal karyotype was significantly higher compared with whose with a normal karyotype (1464.37 U/L vs. 294.33 U/L, P<0.05). CONCLUSION Patients with abnormal karyotypes have a higher rate of P53 gene deletion, and their LDH level is significantly higher than those with a normal karyotype, which predicted a relatively poor prognosis.
Adult ; Bone Marrow ; Child ; Chromosome Aberrations ; Humans ; In Situ Hybridization, Fluorescence ; Karyotyping ; Lymphoma, Non-Hodgkin

OBJECTIVETodelineate the clinical and genetic features of a patient with myeloproliferative neoplasm (MPN) in association with PDGFRA and EVI1 genes rearrangements.

METHODSClinical data of the patient was collected. Conventional cytogenetics, fluorescence in situ hybridization (FISH) and nested PCR were carried out for the patient.

RESULTSThe patient has featured recurrent rash, joint pain, and intermittent fever. Laboratory tests showed hyperleukocytosis and marked eosinophilia. Physical examination revealed splenomegaly. His karyotype was 46,XY,t(3;5)(q26;q15)[6]/46,XY[10]. FISH assay showed that both PDGFRA and EVI1 genes were rearranged. Molecular studies of the mRNA suggested that there was a in-frame fusion between exon 12 of the PDGFRA gene and exon 9 of the FIP1L1 gene. Imatinib was initiated at a dosage of 200 mg, and after 10 months, the signal of the FIP1L1-PDGFRA fusion gene was undetectable in bone marrow sample. However, the expression of EVI1 mRNA was stable, with no significant difference found between the patient and 10 healthy controls.

CONCLUSIONMPN in association with PDGFRA and EVI1 genes rearrangements have unique clinical and genetic features. Genetic testing is helpful for early diagnosis. Imatinib may be effective for the treatment.

Antineoplastic Agents ; therapeutic use ; Base Sequence ; Chromosome Banding ; Chromosomes, Human, Pair 3 ; genetics ; Chromosomes, Human, Pair 5 ; genetics ; DNA-Binding Proteins ; genetics ; Gene Rearrangement ; Humans ; Imatinib Mesylate ; therapeutic use ; In Situ Hybridization, Fluorescence ; Karyotyping ; MDS1 and EVI1 Complex Locus Protein ; Male ; Myeloproliferative Disorders ; drug therapy ; genetics ; Proto-Oncogenes ; genetics ; Receptor, Platelet-Derived Growth Factor alpha ; genetics ; Transcription Factors ; genetics ; Translocation, Genetic ; Treatment Outcome ; Young Adult

OBJECTIVETo assess the correlation of cytogenetic changes with serum vascular endothelial growth factor (VEGF) and serum tartrate resistant acid phosphatase (TRacp-5b) levels among elderly patients with multiple myeloma (MM).

METHODSChromosomal changes were analyzed with a modified culturing method in the presence of IL-6. Serum levels of VEGF and TRacp-5b were determined with enzyme-linked immunosorbent assays (ELISA).

RESULTSAmong the 60 MM patients, chromosomal abnormalities were found in 27 cases, including 22 with numerical abnormalities and 15 with structural abnormalities. Many patients had both numerical and structural abnormalities. For 33 patients with a normal karyotype, the levels of VEGF and TRacp-5b were 117.35 ± 55.26 pg/mL and 4.15 ± 2.15 U/L, respectively, while for 27 patients with an abnormal karyotype, the levels of VEGF and TRacp-5b were 190.26 ± 85.74 pg/ml and 5.96 ± 2.24 U/L, respectively. The difference between the two groups was significant (P<0.05).

CONCLUSIONCompared with MM patients with a normal karyotype, the levels of VEGF and TRacp-5b are higher in those with cytogenetic abnormalities.

Aged ; Aged, 80 and over ; Chromosome Aberrations ; Cytogenetic Analysis ; Female ; Humans ; In Situ Hybridization, Fluorescence ; Karyotype ; Male ; Multiple Myeloma ; blood ; diagnosis ; genetics ; Tartrate-Resistant Acid Phosphatase ; blood ; Vascular Endothelial Growth Factor A ; blood