Objective To investigate clinical significance and function of microRNA-106b (miR-106b) in retinoblastoma tissues and cells.Methods We detected miR-106b expression in 51 samples of thyroid cancer and the adjacent non-tumor tissues using qRT-PCR.The expression of miR-106b was altered by corresponding vectors in thyroid cancer cells,and then BrdU cell proliferation and flow cytometry assay were performed to examine the proliferation and apoptosis of thyroid cancer cells.Results The expression of miR-106b in thyroid cancer tissues was significantly lower than that in normal tumor-adjacent tissues (0.36±0.029 vs 0.98±0.034,P＝ 0.004).MiR-106b expression in tumor tissues was significantly associated with tumor size and tumor number.MiR-106b was obviously inhibited by miR-106b inhibitor in PTC-I cells (0.96±0.025 vs 0.29±0.032,P＝0.001),and inhibition of miR-106b resulted in significantly increased proliferation (89.33±5.67 vs 136.67±10.33,P＝0.03) and decreased apoptosis (16.33±3.20 vs 7.67±2.45,P＝0.04).On the contrast,over-expression of miR-106b using miR-106b mimics led to significantly decreased proliferation (98.00±4.65 vs 76.33±2.87,P＝0.03) and increased apoptosis (22.54±2.13 vs 32.45±4.34,P＝0.04).Conclusions Decreased expression of miR-106b is correlated with the adverse clinicopathological features of thyroid cancer.MiR-106b can inhibit cell proliferation and apoptosis of thyroid cancer cells,suggesting miR-106b plays a suppressive role in development and progression of thyroid cancer.

Objective To analyses the magnetic resonance imaging(MRI)findings of different clinical patterns of neurosyphilis(NS).Methods Clinical records and MRI of 26 patients with NS were retrospectively studied.Results Abnormal MRI was found in 17 patients of 26 patients with NS.In 7 patients were with meningo-vascular syphilis,the MRI commonly showed multiple cerebral ischemia focus and cerebral infarction focus,very few similar to those of encephalitis;Six patients had general paresis,who presented cerebral MRI abnormalities of frontal and temporal atrophy,and few simultaneously with cerebral ischemia focus,granular apendymitis and hippocampus sclerosis;Three patients had syphilitic myelitis,their MRI showed mild tumefaction with multiple ischemic focus all the way through lower cervical spinal cord to lower thoracic spinal cord:One patient was with tabes dorsalis,whose cerebral MRI showed ischemic locus.Another 9 patients had normal MRI,of whom 4 patients with meningitis NS and 5 with tabes dorsalis.Conclusion The MRI of neurosyphilis has diverse presentations,and clinicians should pay much attention to it.

AIM:To explore the influence of ethyl(2,4,6-trimethylbenzoyl)phenylphosphinate(TPOL)on cell apoptosis and its potential mechanism.METHODS:HEK293T cells sensitive to TPOL were treated with different concentrations of TPOL with or without exposure to light radiation,before treatment with various inhibitors,N-acetyl-L-cysteine(NAC),pifithrin-α and Z-DVED-FMK.Cell viability was measured by CCK-8 assay.Annexin V/propidium io-dide staining was used to count the number of apoptotic cells.DCFH-DA staining was used to detect reactive oxygen spe-cies(ROS)levels,and JC-1 staining was used to assess mitochondrial membrane potential by flow cytometry.The expres-sion of apoptosis-related proteins and cell cycle-regulated molecules was measured by Western blot.RESULTS:TPOL enhanced the apoptosis of HEK293T cells in a dose-dependent manner(P<0.05),with a decrease in Bcl-2 and increases in Bax and cytochrome C(Cyto C),followed by up-regulation of activated caspase-9 and caspase-3,and the cleavage of PARP(P<0.05).The TPOL-enhanced cleavage of caspase-3 and PARP was rescued by Z-DVED-FMK(P<0.01).TPOL also led to a rapid increase in ROS,a reduction in mitochondrial membrane potential,and the release of Cyto C(P<0.01),all of which could be reversed by the ROS scavenger NAC.Moreover,the TPOL-caused alterations in p21,p27,Rb,and CDK2 were also recovered by the p53 inhibitor pifithrin-α(P<0.05).The TPOL-induced changes in Bax,Bcl-2,cleaved caspase-9,activated caspase-3,and cleaved PARP were subsequently rescued by pretreatment with pifithrin-α(P<0.05).CONCLUSION:TPOL can induce cellular apoptosis with ROS-mediated mitochondrial membrane damage through the activation of a ROS-dependent p53/p21/p27/Rb/Bax/Cyto C/caspase-mediated signal axis.