BACKGROUND: Diabetic retinopathy is a commonly chronic-vascular complication in a course of diabetes mellitus (DM), and its relation with apoptosis and changes of ion level needs to be proved.OBJECTIVE: To observe apoptosis and changes of Na+ and K+ contents in retinal tissue of DM rats.DESIGN: Randomized controlled study.SETTING: Department of Ophthalmology, Liuzhou Municipal People's Hospital.MATERIALS: The experiment was completed at the Department of Ophthalmology, Liuzhou Municipal People's Hospital. A total of forty adult male Wistar rats, aged 20 months, weighing 320-350 g, were provided by Animal Center of Medical College Affiliated to Sun Yat-sen University.METHODS: Forth Wistar rats were randomly divided into control group and experimental group with 20 in each group. Streptozotocin was used to induce DM in the experimental group. Apoptosis and changes of Na+ and K+ contents in retinal tissue were measured on the 4th, 6th, 12th and 16th weeks after DM onset. Rats in the control group were injected only with the same volume of citrate buffer solution. Then, correlations on the aspect of fasting blood glucose (FBG), hemoglobin glycosylation (HbAlc), Na+ and K+ contents and DM course were analyzed between the two groups.MAIN OUTCOME MEASURES: ① Na+ and K+ contents; ② FBG concentra tion and HbAlc level; ③ changes of apoptosis; ④ correlations among markers.RESULTS: Apoptosis could be detected in retinal tissue in the experimental group at 4 weeks after DM onset, and with course elongating, level of apoptosis was aggravated gradually. Na+ concentration was increased in retinal tissue, but K+ concentration was decreased (P ＜ 0.01 or 0.05). Levels of apoptosis in retinal tissue in the experimental group were positive correlation with FBG concentration, HbAlc level, Na+ content and DM course (r=7.584, 7.844, 7.369, 6.246; P ＜ 0.01); however, they were negative correlation with K+ content in retinal tissue (r=7.658, P ＜ 0.01).CONCLUSION: There are apoptosis and abnormal Na+ and K+ contents in retinal tissue of DM rats. Moreover, these changes may be one of pathological bases of diabetic retinopathy.

Objective To explore the distribution and characteristics of initial PSA and PSA velocity in men younger than years without prostate cancer. Methods PSA in men younger than 50 years without prostate cancer from January 2001 to November 2009 were retrieved retrospectively from our computer center. PSA velocity was calculated if their PSA was measured twice or more. The distributions of initial PSA and PSA velocity were analyzed. The correlations between initial PSA, initial PSA age, and PSA velo-city were also analyzed. Kaplan-meier and log-rank tests were used to estimate the significant difference at the risk of PSA≥ 2.5 ng/ml after initial PSA measurement, stratified by median initial PSA (0.6 ng/ml). Results A total of 4206 men without prostate cancer were included. The median initial PSA value in these men was 0.6 ng/ml. Of these men, 1026 (24.4%), 177 (4.2%), and 90 (2.1%) had an initial PSA≥1.0, ≥2.5, and ≥4.0 ng/ml, respectively. A total of 417 men had their PSA measured these men, 25 (6.0%), 13 (3.1%), and 8 (1.9%) had a PSA velocity≥0.35, ≥0.75, initial PSA age and initial PSA, initial PSA age and PSA velocity, and initial PSA and PSA velocity (correlation coefficient r=0.019, -0.015, and -0.006, respectively; P=0.218, 0.754, and 0.897, respectively). After a follow-up of up to 7.1 years from baseline PSA measurement, the risk of PSA≥2.5 ng/ml, stratified by median initial PSA (0.6 ng/ml) was significantly different (log-rank test, P＜0.001). Conclusions The median baseline PSA and PSA velocity in men younger than 50 years old without prostate cancer are 0.6 ng/ml and 0.03 cancer with an initial PSA higher than median (0.6 ng/ml) have a subsequently higher risk of PSA value ≥2.5 ng/ml.

Forty patients with Hashimoto thyroiditis ( HT) and 20 healthy subjects with matched age-and sex-features ( NC) were selected. The patients with HT were further divided into normal thyroid function ( HT-A) and hypothyroidism ( HT-B) groups. Real-time PCR was performed to evaluate the expressions of Notch1, Dll4, and retinoid-related orphan receptor ( ROR )-γt mRNA. Flow-cytometry was used to detect the percentage of Th17 cells. Thyroid function, thyroid peroxidase antibody ( TPOAb) , and thyroglobulin antibody ( TgAb) were detected by electrochemiluminescence immunoassaies. The results showed that the Notch1, Dll4, ROR-γt mRNA levels and Th17 cell percentage were significantly increased in HT group compared with NC group (all P<0.01), especially in HT-B group. In HT patients, Notch1 and Dll4 mRNA expression levels were positively correlated with Th17 cell percentage and its transcription factor ROR-γt ( all P<0.01) . Besides, there were significantly positive correlations of Notch1 and Dll4 mRNA expressions with TPOAb and TgAb titers (P<0.05 or P<0.01). These results suggest that Notch1-Dll4 signaling pathway might be involved in the pathogenesis of thyroid-specific autoimmune damage by regulating Th17 cells in HT patients.

[Abstract] Objective: Toevaluatetheexpressionof6-phosphofructo-2-kinase/fructose-2, 6-biphosphatase 3(PFKFB3) in malignant glioma tissues and the effects of inhibitor of PFKFB3(PFK15) on the proliferation, migration, invasion, clone formation and tumorigenesis of H4 cells. Methods: Malignant brain glioma tissues and corresponding paratumor tissues from 31 patients, who were hospitalized in Department of Neurosurgery,Ankang Hospital of Traditional Chinese Medicine during February 1, 2015 to January 31, 2016 for operative treatment, were collected for this study. Immunohistochemistry and western blotting assays were applied to detect the expression of PFKFB3 in collected tissues. PFKFB3 in H4 cells were blocked by PFK15 (1.25, 2.5, 5.0 μmol/L). The effect of PFK15 on proliferation, migration, clone formation and tumorigenesis of H4 cells were determined by MTT assay, EdU incorporation assay, wound healing assay, Transwell assay, colone formation assay and in vivo xenograft bearing nude mice model respectively. Results: Positive expression rate of PFKFB3 was significantly higher in malignant glioma tissues compared with normal adjacent tissues[(80.60±8.98)% vs (41.57±10.16)%, P<0.05]. The results of MTT assay and EdU incorporation assay indicated that PEK15 significantly inhibited the proliferation of H4 cells in a concentration dependent manner. The migration, invasion and clone formation activity of H4 cells were significantly reduced by treatment with PFK15 (all P<0.05). In tumor bearing nude mice, the tumor volume of mice treated with PFK15 was significantly smaller than that of mice from control group ([254.15±154.25] vs [801.52±224.25] mm3, P<0.05). Conclusion: PFKFB3 was highly expressed in malignant glioma tissues. Blocking of PFKFB3 by PFK15 significantly reduced the malignant biological behaviors and tumorigenesis of H4 cells in vitro and in vivo, which may serve as a promising target for the treatment of malignant gliomas.