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paramamosain to pathogens. Apoptosis of hemocytes was higher in crabs treated with TnT-dsRNA compared with control crabs treated with phosphate-buffered saline. Knockdown of TnT increased apoptosis of hemocytes following VA infection, but reduced hemocyte apoptosis following WSSV infection. In summary, TnT may enhance the immune response of S. paramamosain to WSSV infection by regulating apoptosis, THC, PO activity and SOD activity. And TnT may play a positive role in the immune response against VA infection by regulating apoptosis, THC, SOD activity and PO activity. Rescue chemotherapy is usually the preferred treatment for patients with advanced estrogen receptor-positive (ER+) breast cancer with endocrinotherapy resistance. However, these patients often simultaneously show a poor response to cytotoxic drugs, and thus the detailed mechanism of this resistance needs to be further investigated. Our previous research indicated that the G-protein-coupled estrogen receptor (GPER) is a novel mediator of the development of multidrug resistance, including resistance to both endocrinotherapy and chemotherapy, and ATP binding cassette subfamily G member 2 (ABCG2) has been identified as an engine that confers cancer cells with chemoresistance by expelling xenobiotics and chemotherapeutics. Here, we are the first to show that the expression levels of GPER and ABCG2 are markedly increased in tamoxifen-resistant ER + metastases compared to the corresponding primary tumors. A plasma membrane expression pattern of GPER and ABCG2 was observed in patients with metastases. Furthermore, boresistance and provide a rationale for the GPER/ABCG2 signaling axis being a promising target for reversing chemoresistance in patients with advanced ER + tamoxifen-resistant breast cancer. Kisspeptin, encoded by the Kiss1 gene, and its receptor GPR54 have a central regulatory role in the male reproduction. However, their functions in peripheral tissues, such as testes, remain unclear. This study investigated the local expressions and function of Kiss1/GPR54 in goats' testes. The mRNA expression of Kiss1/GPR54 in pubertal goat Leydig cells was detected through reverse transcriptase PCR (RT-PCR), and its protein expression in Leydig cells or the testis was examined by immunohistochemistry and Western blot analysis. Isolated and cultured Leydig cells were treated with different concentration of kisspeptin (0, 1, 10 and 100 μM) and kisspeptin antagonist for 4, 24 or 72 h. The direct effect of kisspeptin on testosterone secretion and Kiss1/GPR54 mRNA expression was evaluated by ELISA and RT-PCR. Kiss1/GPR54 mRNA and protein were expressed in Leydig cells and spermatids, and GPR54 were expressed in Sertoli cells. Kisspeptin treatment significantly stimulated testosterone secretion in Leydig cells, with the highest levels found under 24 h of treatment with 10 μM kisspeptin. Treatment with kisspeptin + kisspeptin antagonist significantly reduced the kisspeptin-stimulated testosterone secretion in Leydig cells. Kisspeptin treatment significantly enhanced the expression of Kiss1/GPR54 mRNA in Leydig cells. These data suggest the local expressions of Kiss1/GPR54 in goats' testes and its autocrine role in Leydig cells, which is helpful in understanding the regulation role of kisspeptin/GPR54 system in other peripheral tissues. Spinocerebellar ataxia type 3, also known as Machado-Joseph disease (SCA3/MJD), is the most common type of autosomal dominant cerebellar ataxias. Few studies focused on the changes of the whole mitochondrial genomes of SCA3/MJD patients and its relationship with the pathogenesis of SCA3/MJD. We adapted one-step long-range PCR to amplify the entire mitochondrial DNA (mtDNA) followed by next-generation sequencing technology to investigate the information of whole mitochondrial genomes in 38 SCA3/MJD patients and 31 healthy controls from mainland China. Compared to the healthy control group, the mitochondrial variations in SCA3/MJD patients were more concentrated in the tRNA-transcribed genes which were further found to be potentially associated with the pathogenesis of SCA3/MJD by SKAT-O analysis. However, owning variations in tRNA-transcribed genes could not affect the age of onset (AO) of SCA3/MJD patients. We also noticed that the variant loads greater than 90% took up more in SCA3/MJD patients than in controls. Moreover, from our preliminary study, compared to the patients whose ages of onset were elder than 20, the mitochondrial genomes showed no difference in those AO less than 20. This is the first study to demonstrate the feasibility of using the next-generation sequencing technology for mtDNA variant analysis of SCA3/MJD patients from mainland China. And this research enriches the genetic information of SCA3/MJD and provides a direction for further investigations about the mitochondrial genomes in SCA3/MJD. OBJECTIVE The purpose of this study was to investigate the function of APC polymorphisms (D1822V and E1317Q) on the transition from polyps to colorectal cancer (CRC). METHODS 259 patients with polyps were included in the study. APC polymorphisms were genotyped via polymerase chain reaction (PCR) and subsequent sequencing. χ2 test was performed to analyze the relationship of APC polymorphisms or CRC occurrence with clinical features. COX regression was used to find out risk factors for CRC. Hazard ratio (HR) and 95% confidence interval (CI) represented the risk of CRC. RESULTS Clinical information on sex, regular physical activity, smoking history, alcohol use and polyps types was recorded. Neither D1822V nor E1317Q polymorphism was associated with these factors. In following analysis, we found significant difference in the frequency of males between CRC and non-CRC patients (87.4% vs. 58.7%, P  less then  0.001). Distinct difference in the distribution of D1822V polymorphism was also observed between CRC and non-CRC patients (P = 0.001). In COX analysis, sex was identified as a risk factor for transition from polyps to CRC (HR = 2.442, 95%CI = 1.281-4.654). EGFR tumor D1822V polymorphism tended to inhibit the transition process (HR = 0.286, 95%CI = 0.170-0.480). However, E1317Q seemed to have no significant effect on this process (HR = 1.042, 95%CI = 0.676-1.606). CONCLUSION In a word, APC D1822V polymorphism has strong effect on the transition from polyps to CRC.

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