Objective To discuss the predictive value of multiple ultrasonic features combination in diagnosis of thyroid papillary carcinoma (PTC) more than 1.0 cm in diameter. Methods The ultrasonic features of 258 PTC nodules from 251 patients and 207 nodular goiter (NG) nodules from 190 patients in the First People′s Hospital of Hangzhou were retrospectively analyzed. All the nodules were confirmed by pathological examination after surgery. The ultrasonic features included the shape of nodules, internal echo,anteroposterior/transverse diameter ratio (A/T), and microcalcification. The χ2 test was used to analyze the differences of ultrasonic features between PTC and NG. Multi-variate analyses (Logistic regression) was used to analyze the predictive risk ultrasonic features of PTC. The sensitivity and specificity of ultrasonic features were analyzed based on the gold standard of pathological results. Results There were significantly differences between 258 PTC nodules and 207 NG nodules in irregular shape, hypoechogenicity,A/T > 1 and microcalcification (χ2 values were 121.511, 105.411, 41.483, 121.072, all P < 0.01). The results of Logistic regression showed that irregular shape, hypoechogenicity, A/T>1 and microcalcification were risk ultrasonic features of PTC. And their OR values were 5.013 (95%CI 2.919-8.610), 5.811 (95%CI 3.411-9.901), 15.399 (95%CI 7.576-31.301), 4.141 (95%CI 1.687-10.164) respectively. The sensitivity and specificity of single ultrasonic feature were 26.0%-79.5% and 71.5%-96.1%; the sensitivity and specificity of two ultrasonographic features combination were 11.2%-57.0% and 92.3%-99.0%; and the sensitivity and specificity of three or four ultrasonographic features combination were 8.1%-31.8% and 99.0%-99.5%.Conclusions Irregular shape, hypoechogenicity, A/T> 1 and microcalcification of thyroid neoplasm are important ultrasonic features of PTC. Although the sensitivity of single ultrasonic feature in diagnosing PTC is higher than that of multiple features combination, it has a lower specificity. Therefore, combination of multiple ultrasonographic features can improve the specificity in diagnosing PTC and reduce the misdiagnosis of PTC.

Objective To investigate the clinical characteristics and treatment strategies of arachnoid cyst combined with chronic subdural hematoma.Methods Seventeen patients with arachnoid cyst combined with chronic subdural hematoma,who received treatment in our hospital from February 2008 to March 2016,were chosen in our study;13 of them were performed burr hole irrigation and drainage,2 received craniotomy for removing hematoma and cystectomy,and 2 received endoscopic cyst excision and hematoma removal surgery.A retrospectively analysis of clinical characteristics and treatment strategies of these patients was performed.Results Follow up for 0.5-2 years was performed in the 13 patients performed burr hole irrigation and drainage,and no hematoma relapse was noted;one was found rebleeding in the cyst associated with a small amount of subdural hematoma on the 5th d of surgery,and the subdural hematoma was absorbed during the follow-up observation;one was found that the cyst and subdural hematoma both disappeared in the postoperative check,while the cyst reappeared 40 days after surgery,and during the follow-up observation,the cyst was not enlarged and the chronic subdural hematoma was not relapsed.Two patients recovered after receiving the craniotomy for removing hematoma and cystectomy;two patients recovered after receiving the endoscopic cyst excision andhematoma removal surgery.Conclusion For patients with arachnoid cyst associated with chronic subdural haematoma,burr-hole irrigation and drainage are generally selected;for patients with reappeared cyst or hematoma,there is no need to burr hole again or perform the surgery aiming at the cyst in a haste,and follow-up observation is suggested;for patients whose symptoms in the cyst have appeared before hemorrhage or whose hemorrhage appeared recurrently in the cyst,surgery of hematoma removal and cyst excision can be chosen at the same time.

Objective To investigate the effect of inhibiting tumor suppressor gene phosphatase and tensin homology deleted on chromosome ten (PTEN) on growth of neurons cultured in inhibitive microenvironment.Methods Primary cortical neurons were separated from fetal rats and cultured with adult rat brain-derived myelin membrane proteins as inhibitory substrate.Cells were divided into 3 groups:normal control group,inhibitory control group (myelin membrane proteins as inhibitory substrate) and bpv treatment group (200 nmol/L bpv+myelin membrane proteins).Real-time quantitative-PCR was performed to detect the expressions of PTEN and mammalian target ofrapamycin (mTOR) genes,and immunofluorescence staining was used to observe the growth ofneurites 24,48 and 72 h,and 5 d after inoculation.Results Immunofluorescence staining revealed that significant differences of the growth of neurites at the four observation time points existed among the 3 groups (P＜0.05); during the early days of culture (24,48 and 72 h),cells in normal control group had the longest neurite (43.5±12.2,94.9±23.6 and 154.3±35.4 μm),those in the bpv treatment group enjoyed the second prize (28.8±10.2,75.4±22.5 and 136.8±40.8 μm) and those in the inhibitory control group was obviously inhibited (17.4±5.8,46.3± 13.7 and 78.4 ±29.8 μm).But the difference on the 5th d of cultivation changed into bpv treatment group＞normal control group＞inhibitory control group with the neurite length of (225.9±50.6),(218.4±58.1) and (173.6±48.7) μm,respectively (P＜0.05).PCR revealed no significant difference in expressions of PTEN and mTOR genes of the three groups between each two time points (P＞0.05); while at the same time point,significantly increased expressions ofmTOR and PTEN in the bpv treatment group were noted as compared with those in the normal control group and inhibitory control group (P＜0.05).Conclusions Growth of neurons in inhibitive microenvironment is improved on condition that the tumor suppressor gene PTEN is inhibited,which is probably related to the activation of PI3K/AKT/MTOR pathway.