Objective To investigate the effects of advanced oxidation protein products (AOPP) in type 2 diabetic ocular muscles palsy (DOMP). Methods 58 DOMP patients and 50 type 2 diabetes patients were included in the research. Hemoglobin A1c (HbA1c), blood glucose (FPG), fasting insulin (FINS) and triglycerides (TG), total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL) were measured and recorded. Homeostasis model assessment was performed to evaluate the status of insulin resistance (HOMA-IR), basal insulin secretion (HOMA-β) and the insulin sensitivity index (ISI). Serum AOPP was measured by enzyme linked immunosorbent assay. Unconditional logistic regression model was used to evaluate the influencing factors of DOMP. Results The DOMP group showed higher levels of plasma AOPP, TG, LDL, FPG, FINS, HbA1c and HOMA-IR, but lower levels of HDL, HOMA-β and ISI than those of the T2DM group. Unconditional logistic regression analysis revealed that AOPP was an independent risk factors for DOMP (OR =3.01, P = 0.002). Conclusion AOPP may be involved in the pathogenesis of DOMP. AOPP could be a useful indicator for monitoring the development of DOMP and for evaluating its severity.

Objective To explore the change of glyoxalase I in type 2 diabetic ocular muscles palsy (DOMP) and its associations with advanced oxidation protein products (AOPP) and oxidative stress. Methods 58 DOMP patients, 50 T2DM and 30 normal controls were enrolled in this study. Levels of blood lipids, fasting blood glucose, hemoglobin A1c, insulin, serum glyoxalase I, AOPP, malondialdehyde (MDA), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) were measured. Homeostasis model assessment was performed to evaluate the status of insulin resistance (IR). Results Levels of high-density lipoprotein cholesterol, SOD and T-AOC were positively correlated with glyoxalase I and inversely associated to AOPP. Levels of triglycerides , low-density lipoprotein cholesterol , fasting blood glucose , hemoglobin A1c , IR and MDA were negatively correlated with glyoxalase I and positively related to AOPP. AOPP had an inverse association with glyoxalase I (r = -0.823, P < 0.001). Multivariate regression analysis showed that serum levels of glyoxalase I (Sβ = 0.554) and AOPP (Sβ= -0.469) were influencing factors of groups. Conclusion Serum glyoxalase I levels were significantly decreased in DOMP and correlated with AOPP and levels of oxidative stress , which suggest that glyoxalase I could play crucial roles on the development of DOMP.

We detected the isoniazid resistance in clinical Mycobacterium tuberculosis isolates by high-resolution melting (HRM) curve analysis and assessed the application value of the assay.The isoniazid resistance of 49 M.tuberculosis isolates preserved in laboratory was analyzed by the drug sensitivity test (traditional proportion method).Further analysis was made on the sequencing of the isoniazid resistance determining region in these test strains,and their mutation sites were screened.Specific primers used in the HRM curve analysis were designed based on the screened mutation sites,DNA mutations were assayed in the isoniazid-resistant gene determining region by the HRM curve analysis,and an assessment was made of the detection efficiency of the assay in isoniazid resistance in M.tuberculosis.Results of the drug sensitivity test (proportion method) showed that,of the 49 test strains,there were 20 isoniazid-resistant strains,29 isoniazid-sensitive strains.Results of the sequencing analysis showed that:1) KatG gene had four mutation patterns,i.e.,point mutations at site 234,at sites 234 and 315,at sites 234 and 463,and at sites 234,315 and 463;2) there were three mutations were detected in inhA gene,i.e.,mutations in inhA-8,-15 and-152.Analysis of gene mutation in drug-resistant strains found that of the 20 isoniazid-resistant strains,11 (55 ％) were mutated at codon 315 of KatG gene;6 (30％) were mutated in inhA-15 (4/20),-8 (1/20) and-153 (1/20) of inhA gene;two (10％) were mutated at codon 315 of KatG gene and in inhA-15;in one strain (5％),no mutation was detected in KatG and inhA genes.Through the gene mutation detection,the sensitivity and specificity of isoniazid resistance in M.tuberculosis were 95 ％ and 100 ％,respectively.Results of HRM curve analysis of drug-resistance gene mutations in test strains showed gene mutations were present in 18 strains and absent in 24 ones;referring to DNA sequencing results,the sensitivity and specificity of the assay were 94.7％ and 80％,respectively.Judged by mutations as drug-resistance via the HRM curve analysis,19 resistant and 24 sensitive strains were tested.With the drug sensitivity test results by the proportion method as controls,the sensitivity and specificity of the assay were 95 ％ and 82.76 ％,respectively.Use of the HRM curve in the detection of resistance of M.tuberculosis to isoniazid is characterized by good sensitivity and short time consuming,and has certain value in the rapid diagnosis of isoniazid-resistant tuberculosis.

OBJECTIVE: To explore the clinical efficacy of decitabine for treatment of patients with myelodysplastic syndrome (MDS) and factors predicting the prognosis. METHODS: The clinical data of 87 patients with MDS treated with decitabine were analyzed retrospectively. The hENT1 mRNA expression and TP53 gene mutation were detected by Q-PCR and gene target sequencing, respectively. The relationship of clinical characteristics and molecular indicators with the clinical response to decitabine was analyzed. RESULTS: In treatment for median 4 (2-17) courses, a total 51 patients (58.6%) showed therapeutic responses, including CR in 17 cases, PR in 12 cases, mCR in 9 cases, HI in 13 cases; 36 (41.4%) patients showed non-response. Univariate analysis showed that the patients with the complex karyotype, monosomal karyotype, chomosome 7 abnormality and Plt count doubling after 1 course treatment had a high CR rate, while the patients with relative high risk by IPSS (intermediate risk 2+ high risk), complex karyotype and Plt count doubling after 1 course had much more high overall remission rate (ORR). The expression level of hENT1 mRNA in MDS patients with response was significantly higher than that in patients without response ［(1.78±1.45 (2) vs 0.96±0.97 (2)(P= 0.002)］. Among 51 patients with therapeutic response, the expression level of hENT1 mRNA in CR group was higher than that in non-CR group ［(2.58±1.44 (2) vs 1.39 ±1.3 (2), P= 0.005)］. Among 52 patients in relative high risk (intermediate risk 2 +high risk), the median OS time of patients with high hENT1 mRNA expression was significantly longer than that of patients with low hENT1 mRNA expression (31 vs 12 months)(P<0.001). Among 87 patients received decitabine treatment, the TP53 gene mutation occured in 11 (12.6%) patients. The ORR in patients with TP53 mutation was high (P=0.04), moreover the patients with TP53 mutation more easily gained CR (P<0.001). Multivariate logistic regression model showed that the complex karyotype, Plt count doubling after 1 course treatment, TP53 mulation and high expression of hENT1 mRNA were the independent prognostic factors for predicting the CR after decitabine treatment. CONCLUSION IPSS staging, complex karyotype, Plt count doubling after 1 course treatment and hENT1 mRNA expression, TP53 gene mutation can be used to predict the tharapeutic efficacy of dectitabine for treatment of MDS.
Decitabine ; therapeutic use ; Humans ; Myelodysplastic Syndromes ; drug therapy ; Prognosis ; Retrospective Studies ; Treatment Outcome