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1.
Endocrine ; 63(3): 422-429, 2019 03.
Artigo em Inglês | MEDLINE | ID: mdl-30652236

RESUMO

PURPOSE: Postoperative hemorrhage and hematoma formation is a potentially lethal complication in thyroid surgery, although the patterns and treatment of hemorrhage after total endoscopic thyroidectomy (TET) via breast approach has not been reported previously. We aim to share our experience about postoperative bleeding. METHODS: A retrospective analysis of 1932 patients who underwent TET from April 2008 to May 2018 in our institution was carried out. The patterns of postoperative hemorrhage and hematoma formation that need surgical treatment were summarized and focused on the relation to the source of bleeding and the time interval between first surgery and hemorrhage. Related risk factors were analyzed by univariate or multivariate analysis processes. RESULTS: The overall rate of hemorrhage and hematoma occurrence was only 0.724% (14 in 1932 patients). Of them, 12 occurred in the first 24 h after surgery, and the other two occurred after withdrawal of the drainage tube. The principle independent risk factors for postoperative hemorrhage and hematoma were age (older than 35 years old) and lateral compartment dissection (LCD) revealed by multivariate regression. During re-exploration, obvious bleeding points were detected in 13 patients. Among them, 12 bled from the vessels in the main trocar cavity and another 1 bled from a broken vein located between the two heads of the sternocleidomastoid (SCM) muscle with LCD. CONCLUSIONS: Hemorrhage after TET usually occurs within 24 h, and the main video trocar cavity was the area most likely to bleed. Age and LCD may increase the bleeding risk. Appropriate dissection level is the main solution to prevent postoperative hemorrhage.


Assuntos
Endoscopia/efeitos adversos , Hematoma/etiologia , Hemorragia Pós-Operatória/etiologia , Tireoidectomia/efeitos adversos , Adulto , Endoscopia/métodos , Feminino , Humanos , Estudos Retrospectivos , Tireoidectomia/métodos
2.
Oncotarget ; 8(14): 22954-22967, 2017 Apr 04.
Artigo em Inglês | MEDLINE | ID: mdl-28086241

RESUMO

Recent studies have indicated that long non-coding RNAs play crucial roles in numerous cancers, including thyroid cancer, while their function in the mechanism of thyroid cancer 131I resistance has not been elucidated to date. The present study identified a functional long non-coding RNA, SLC6A9-5:2, which was involved in the radioactive therapy resistance of thyroid cancer. We demonstrated that SLC6A9-5:2 was remarkably downregulated in 131I-resistant thyroid cancer cell lines and 131I-insensitive patients and was positively correlated with Poly (ADP-ribose) polymerase 1 (PARP-1) expression and its activation. After downregulating SLC6A9 or blocking PARP-1 artificially, the sensitive thyroid cancer cells mostly displayed a tolerant phenotype under 131I exposure. Furthermore, SLC6A9-5:2 overexpression was positively correlated with PARP-1 mRNA and protein levels, which restored the sensitivity of resistant thyroid cancer cells. The present study further revealed that cancer cell death was primarily caused by ATP exhaustion in excessive DNA repair with high PARP-1 activity. In patients with thyroid cancer, a positive correlation between SLC6A9-5:2 and PARP-1 was identified, and low SLC6A9-5:2 expression was associated with a worse prognosis of papillary thyroid carcinoma. Hence, our data provide a new lncRNA-mediated regulatory mechanism implying that SLC6A9-5:2 can be used as a novel therapeutic target for 131I-resistant thyroid cancer.


Assuntos
Carcinoma/genética , Carcinoma/radioterapia , Poli(ADP-Ribose) Polimerase-1/biossíntese , RNA Longo não Codificante/genética , Neoplasias da Glândula Tireoide/genética , Neoplasias da Glândula Tireoide/radioterapia , Carcinoma Papilar , Linhagem Celular Tumoral , Proliferação de Células/genética , Proliferação de Células/efeitos da radiação , Regulação para Baixo , Feminino , Proteínas da Membrana Plasmática de Transporte de Glicina/genética , Humanos , Radioisótopos do Iodo , Masculino , Poli(ADP-Ribose) Polimerase-1/genética , RNA Longo não Codificante/biossíntese , Tolerância a Radiação , Câncer Papilífero da Tireoide , Transfecção
3.
J Zhejiang Univ Sci B ; 17(7): 515-25, 2016 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-27381728

RESUMO

We have investigated comprehensively the effects of thyroid function on gallstone formation in a mouse model. Gonadectomized gallstone-susceptible male C57BL/6 mice were randomly distributed into three groups each of which received an intervention to induce hyperthyroidism, hypothyroidism, or euthyroidism. After 5 weeks of feeding a lithogenic diet of 15% (w/w) butter fat, 1% (w/w) cholesterol, and 0.5% (w/w) cholic acid, mice were killed for further experiments. The incidence of cholesterol monohydrate crystal formation was 100% in mice with hyperthyroidism, 83% in hypothyroidism, and 33% in euthyroidism, the differences being statistically significant. Among the hepatic lithogenic genes, Trß was found to be up-regulated and Rxr down-regulated in the mice with hypothyroidism. In contrast, Lxrα, Rxr, and Cyp7α1 were up-regulated and Fxr down-regulated in the mice with hyperthyroidism. In conclusion, thyroid dysfunction, either hyperthyroidism or hypothyroidism, promotes the formation of cholesterol gallstones in C57BL/6 mice. Gene expression differences suggest that thyroid hormone disturbance leads to gallstone formation in different ways. Hyperthyroidism induces cholesterol gallstone formation by regulating expression of the hepatic nuclear receptor genes such as Lxrα and Rxr, which are significant in cholesterol metabolism pathways. However, hypothyroidism induces cholesterol gallstone formation by promoting cholesterol biosynthesis.


Assuntos
Cálculos Biliares/etiologia , Hipertireoidismo/complicações , Hipotireoidismo/complicações , Animais , Peso Corporal , Colesterol/sangue , Cálculos Biliares/patologia , Fígado/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Hormônios Tireóideos/sangue
4.
J Huazhong Univ Sci Technolog Med Sci ; 33(1): 117-121, 2013 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-23392719

RESUMO

A retrospective study was performed to explore the relationship between molecular subtypes and clinicopathological features of breast cancer in Chinese women. Six hundred and twenty-eight Chinese women with breast cancer were classified into four molecular subtypes according to their estrogen receptor (ER), progesterone receptor (PR) and Her-2 status. The prevalence rate of each molecular subtype was analyzed. Relationship between the subtypes and clinicopathologic features was determined. The distribution of molecular subtypes was as follows: luminal A 46.5%, luminal B 17.0%, basal 21.5%, HER2/neu 15.0%. The subtypes had no significant difference under different menopausal status. However, in the age-specific groups, the age group of ≤35 years was more likely to get basal cell-like cancer (36.9%). Statistically significant differences were found among molecular subtypes by age, nuclear grade, tumor size, lymph node (LN) metastasis, tumor stage by American Joint Committee on Cancer (AJCC), radiotherapy but not by chemotherapy, types of surgery. After adjusting for several relative confounding factors, the basal subtype more likely had lower nodal involvement in both the incidence of LN metastasis (≥1 positive LN) and incidence of high-volume LN metastasis (≥4 positive LN). The HER2/neu subtype had higher nodal involvement in the incidence of high-volume LN metastases. After adjusting for relative confounding factors, the HER2/neu subtype more likely had higher AJCC tumor stages. It was suggested that there existed close relationship between molecular subtypes and clinicopathological features of breast cancer. In addition, the breast cancer subtypes have been proven to be an independent predictor of LN involvement and AJCC tumor stage. These findings are very important for understanding the occurrence, development, prognosis and treatment of breast cancer in Chinese population.


Assuntos
Biomarcadores Tumorais/metabolismo , Neoplasias da Mama/metabolismo , Neoplasias da Mama/patologia , Receptor ErbB-2/metabolismo , Receptores de Estrogênio/metabolismo , Receptores de Progesterona/metabolismo , Neoplasias da Mama/classificação , Neoplasias da Mama/epidemiologia , China/epidemiologia , Feminino , Humanos , Pessoa de Meia-Idade , Técnicas de Diagnóstico Molecular/estatística & dados numéricos , Prevalência
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