The effect of 131I therapy for primary and metastatic lesions of thyroid carcinoma depends on the ability of iodine uptake.The loss or down-regulation of iodine-metabolizing genes represents dedifferentiation of DTC,which results in the disability to take up and accumulate 131I and eventually leads to radioiodine-refractory DTC (RR-DTC).The management of RR-DTC is extremely difficult and the prognosis is poor.It is important for the treatment and prognosis of RR-DTC to investigate the mechanism of redifferentiation.The up-regulation of thyroid iodine-metabolizing genes expression,inhibition of the changes in epigenetic modifications and intervention of the abnormal activation of signaling pathways are reviewed in this article.

OBJECTIVE: To discuss the role of carbon nanoparticles in the protection of parathyroid during thyroid carcinoma surgery. METHOD: Seventy-two patients with thyroid carcinoma who had initial surgery were randomly divided into two groups: carbon nanoparticles group and the control group. Emulsion of carbon nanoparticles was injected into the thyroid gland of carbon nanoparticles group patients. After thirty minutes,the excision of thyroid carcinoma and VI group neck dissection were performed in carbon nanoparticles group patients, the control group directly underwent operation. The black stained tissue in the dissection specimen of carbon nanoparticles group was separated. The number of total lymph node,metastasis lymph node and parathyroid gland in the tissure black stained or not in two groups were counted respectively. RESULTS: There were 312 lymph nodes in the black stained tissue of central compartment dissection specimen of carbon nanoparticles group. No parathyroid gland was found in the black stained tissue. Fifteen lymph nodes containing four parathyroid glands were found in the non black stained tissue in carbon nanoparticles group while there were 202 lymph nodes containing 13 parathyroid glands in the control group. There were statistical difference between the amount of lymph node in black stain tissue and the specimen of the control group. Parathyroid glands were not stained black,and no parathyroid gland was found in the black-stained tissue. CONCLUSION The carbon nanoparticles could be used to identify the lymph node and the parathyroid gland for protecting the parathyroid gland in thyroid surgery.
Carbon ; Carcinoma ; Coloring Agents ; Dissection ; Humans ; Lymph Nodes ; Lymphatic Metastasis ; Nanoparticles ; Neck Dissection ; Parathyroid Glands ; Thyroid Neoplasms ; pathology ; surgery

Objective To investigate the efficiency of Trichostatin A (TSA) in inducing cell apoptosis and altering the Notch pathway genes expression in PANC-1 cells line.Methods The survival rate and apoptosis of PANC-1 cells were measured by MTT assay and Hoechst 33258 staining,respectively.mRNA expression levels of the genes,numb,gcn512,dll3,hes6,eaf2,cytohesins,in PANC-1 cells were assessed by real-time quantitive PCR.Western blot was used to measure the expression of bcl-2,bax,actived caspase-3 and NICD protein which was the biologically active form of Notch-1.Results After culturing with 0.1,0.2,and 0.4 μmol/L TSA for 24 hours,the cellular survival rate of PANC-1 cells significantly decreased to 72％,58％ and 39％,respectively.The survival rate of PANC-1 was negatively correlated to time length of culture with TSA.Increased apoptosis of PANC-1 cells after 12,24 and 36 h culture with TSA was detected by Hoechst 33258 staining.Western blotting showed that the expression of bax,actived caspase-3 and NICD protein increased while the bcl-2 protein decreased after culture with TSA.In real time quantitive PCR assessment,the mRNA expression of numb and hes6 in PANC-1 cells were upregulated by TSA (P ＜ 0.05),while the mRNA expression of gcn512 and dll3 were down-regulated by TSA (P ＜ 0.05).While mRNA expressions of eaf2 and cytohesin1,2,3,4 were not affected by TSA.Conclusions TSA induces apoptosis of pancreatic cancer cell line PANC-1.The Notch signal pathway may be involved in inducing cellular apoptosis of PANC-1 when cultured with TSA.

Objective To develop an LC-MS/MS method for simultaneous determination of metolazone and valsartan in beagle dog plasma.Methods The chromatographic separation was achieved on an Agilent Poroshell 120(2.1 mm ×30 mm × 2.7 μm)analytical column.The multiple reaction monitoring mode operating in positive ion was adopted in MS detection, and precursors to the product ion transitions of m/z 366.2/259, 436.2/291 and 423.4/207 were used to measure metola-zone, valsartan and internal standard ( losartan potassium) .Results The method was linear over the concentration range of 0.5 ng/ml-100 ng/ml for metolazone and 5-5000 ng/ml for valsartan, with the correlation coefficients ( r2 ) of 0.9937 and 0.9939, respectively.The average intra-day precision values ( RSD) were 2.09% -8.85% for metolazone and 2.36%-13.12%for valsartan.The matrix effect values were 87.73%-98.62%for metolazone and 99.03%-137.35%for valsartan.The average recovery was 75.74%-81.82%for metolazone and 83.89%-95.64%for valsartan.Conclu-sion This analytical method for metolazone and valsartan is simple, accurate and sensitive, so it can be used for pharma-cokinetic research of metolazone and valsartan immediate release tablets in beagle dogs.

Objective To investigate the impact of lncRNA DSCAM-AS1 on the malignant biological behaviors of thyroid cancer(TC)cells by regulating the miR-150-5p/BRAF axis.Methods The expression of DSCAM-AS1 in TC cells was detected by qRT-PCR,and the best intervention cell line was screened.;the relationship between DSCAM-AS1,BRAF and miR-150-5p targeting regulation was verified by FISH,pull down and double Luciferase reporter gene experiment;The proliferation,migration and invasion of SW579 cells were detected;Western blot was applied to detect the expression of BRAF,E-Cadherin,and vimentin proteins;the tumor formation experiment in mice was applied to verify the effect of DSCAM-AS1 on TC tumor growth.Results DSCAM-AS1 was highly expressed in TC tissue and cells(P<0.05);There is a targeted regulation relationship between DSCAM-AS1,BRAF and miR-150-5p;inhibition of DSCAM-AS1 expression or overexpression of miR-150-5p obviously inhibited the proliferation,migration,invasion,and EMT of SW579 cells(P<0.05);Inhibition of miR-150-5p expression or overexpression of BRAF reversed the inhibitory effect of inhibition of DSCAM-AS1 expression or overexpression of miR-150-5p on the malignant behavior of SW579 cells(P<0.05);in vivo experiments showed that inhibiting the expression of DSCAM-AS1 obviously inhibited the growth of transplanted tumors in mice(P<0.05).Conclusion DSCAM-AS1 is up-regulated in TC cells,inhibiting the expression of LncRNA DSCAM-AS1 can inhibit the malignant progression of TC by regulating the miR-150-5p/BRAF signaling axis.