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Lu Y.H.,Suzhou Municipal Hospital
Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics | Year: 2012

To compare differences in the intelligence and physical developmental levels of children with congenital hypothyroidism (CH) who received initial treatment at different times. Forty-nine children with CH diagnosed by neonatal screening between September 2008 and September 2011 were enrolled in this study. According to the timing of initial treatment with thyroid hormone, they were classified into two groups: <1 month and 1 to 3 months of life. At 6 months old, 1 year and 2 years old, their intelligence levels were evaluated by Gessell test. Their physical developmental levels were also measured. Their thyroid functions were examined with fluorescence immunoassay. With treatment, there were no significant differences in thyroid hormones (FT3, FT4 and TSH) between the two groups (P>0.05) at 6 months old, 1 year and 2 years old. However, heights and weights in the <1 month treatment group were significantly higher than in the 1 to 3 months treatment group at all time points (P<0.05). At 6 months old, intelligence developmental levels in the <1 month treatment group were better than the 1 to 3 months treatment group (P<0.05) but significant differences were not noted at 1 and 2 years old (P>0.05). The timing of initial treatment with thyroid hormone appears to be associated with the intelligence and physical development in children with CH. Treatment starting at less than 1 month of life contributes to improved physical and intelligence development compared with treatment starting at 1 to 3 months of life. Source

Zhong T.,Nanjing Medical University | Xu F.,Nanjing Medical University | Xu J.,Suzhou Municipal Hospital | Liu L.,Nanjing Medical University | Chen Y.,Nanjing Medical University
Biomedicine and Pharmacotherapy | Year: 2015

Aldo-keto reductase 1C3 (AKR1C3), one member of the aldo-keto reductase superfamily, is involved in a variety of cancers. Recently, AKR1C3 has been demonstrated to be related with the doxorubicin (DOX) resistance in human breast cancer. Here, we attempted to explore the resistance mechanism mediated by AKR1C3. First, one DOX resistant breast cancer cell line MCF-7/DOX was successfully established and an increased level of AKR1C3 was observed in the MCF-7/DOX cells compared to the parental MCF-7 cells. To investigate the contribution of AKR1C3 in the DOX resistance, we further established an AKR1C3 overexpression cell line, referred to MCF-7/AKR1C3. In the MCF-7/AKR1C3 cells, the DOX induced cytotoxicity, detected by CCK-8 cell viability assay and DAPI staining, was greatly reduced (3.2-fold increase in the IC50 value). Interestingly, a loss of tumor suppressor PTEN (phosphatase and tensin homolog deleted on chromosome 10) was observed when AKR1C3 was overexpressed. Secondary to the PTEN loss, the activated Akt also markedly increased. In addition, the AKR1C3 mediated DOX resistance can be conquered by the Akt inhibitor (LY294002). Furthermore, we found that the expression levels of AKR1C3 and PTEN had a negative relationship in the human breast tumor tissues (the standard correlation coefficient=-0.71; P=0.048). In conclusion, our data suggested that the AKR1C3 mediated DOX resistance might be resulted from the activation of anti-apoptosis PTEN/Akt pathway via PTEN loss. AKR1C3 may present a potential therapeutic target in addressing DOX resistance in breast cancer. © 2015 Elsevier Masson SAS. Source

Shi L.,Nantong University | Wu H.,Nantong University | Dong J.,Nantong University | Jiang K.,Nantong University | And 2 more authors.
British Journal of Ophthalmology | Year: 2015

Objective To determine the diagnostic accuracy of telemedicine in various clinical levels of diabetic retinopathy (DR) and diabetic macular oedema (DME). Methods PubMed, EMBASE and Cochrane databases were searched for telemedicine and DR. The methodological quality of included studies was evaluated using the Quality Assessment for Diagnostic Accuracy Studies (QUADAS-2). Measures of sensitivity, specificity and other variables were pooled using a random effects model. Summary receiver operating characteristic curves were used to estimate overall test performance. Metaregression and subgroup analyses were used to identify sources of heterogeneity. Publication bias was evaluated using Stata V.12.0. Results Twenty articles involving 1960 participants were included. Pooled sensitivity of telemedicine exceeded 80% in detecting the absence of DR, low-or high-risk proliferative diabetic retinopathy (PDR), it exceeded 70% in detecting mild or moderate nonproliferative diabetic retinopathy (NPDR), DME and clinically significant macular oedema (CSME) and was 53% (95% CI 45% to 62%) in detecting severe NPDR. Pooled specificity of telemedicine exceeded 90%, except in the detection of mild NPDR which reached 89% (95% CI 88% to 91%). Diagnostic accuracy was higher with digital images obtained through mydriasis than through non-mydriasis, and was highest when a wide angle (100-200°) was used compared with a narrower angle (45-60°, 30° or 35°) in detecting the absence of DR and the presence of mild NPDR. No potential publication bias was detected. Conclusions The diagnostic accuracy of telemedicine using digital imaging in DR is overall high. It can be used widely for DR screening. Telemedicine based on the digital imaging technique that combines mydriasis with a wide angle field (100-200°) is the best choice in detecting the absence of DR and the presence of mild NPDR. Source

OBJECTIVE: To detect the changes of expressions of II type collagen and matrix metalloproteinases-7 (MMP-7) of acetabular cartilage in early DDH (developmental dysplasia of hip) and to investigate the relevance between II type collagen and MMP-7 and the retrogression mechanism of acetabular cartilage. METHODS: The animal model of DDH was successfully established in 8 rabbits by applying the method of knee extension in which left lower extremity as experimental group and right one as control group. And the stains of HE and toluidine blue were applied on the samples of acetabular cartilage to observe the changes of chondrocytes and extracellular matrix (ECM). The techniques of immunohistochemical staining and Western blot were employed to respectively qualify and quantitate the expression of II type collagen and MMP-7. RESULTS: Pathohistological observation indicated the signs of retrogressive changes of acetabular cartilage in experimental group, including a loss of ECM in toluidine blue stain and a cluster of chondrocytes in HE stain. The positive numbers of II type collagen and MMP-7 by immunohistochemical staining in experimental group were both higher than that of control group. The quantitative amounts of II type collagen and MMP-7 by Western blot in experimental group were both higher than that of control group. Both significant differences existed between two groups (P < 0.05). CONCLUSION: The expression of II type collagen and MMP-7 is correlated to a retrogression of acetabular cartilage and increases obviously in early DDH. The amount and intensity of II type collagen and MMP-7 are probably the rationale of differential retrogression of cartilage. Source

Xu W.,Soochow University of China | Jiang K.,Soochow University of China | Shen M.,Soochow University of China | Qian Y.,Soochow University of China | Peng Y.,Suzhou Municipal Hospital
Biological Chemistry | Year: 2015

Lung cancer has been the most prolific cancer in China - as in the rest of the world - with a high death rate and low 5-year survival rate. Previous evidence showed that JMJD2A is over-expressed in human non-small cell lung cancer (NSCLC) tissues compared to adjacent normal tissues, and that high level of JMJD2A predicts poor overall and disease-free survival. However, the mechanism by which JMJD2A is regulated in human NSCLC is not fully understood. In the present study, we identified that the SIRT2 as an anti-oncogenic protein in NSCLC was down-regulated. JMJD2A as a target of SIRT2 was negatively correlated with SIRT2 level in NSCLC. SIRT2 bound to the promoter region of JMJD2A and negatively regulated JMJD2A expression. In addition, we found that SIRT2 inhibited NSCLC cells proliferation, colony formation and tumor growth in vitro and in vivo in a JMJD2A-dependent manner. In summary, our findings implicate that SIRT2 suppresses non-small cell lung cancer growth through targeting JMJD2A and SIRT2 activator may serve as candidate drug for NSCLC therapy. © 2015 by De Gruyter. Source

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