Current Issue : January - March Volume : 2019 Issue Number : 1 Articles : 6 Articles
Selecting excellent oocytes is required to improve the outcomes of in vitro fertilization (IVF). Cumulus cells (CCs) are an integral\npart of the oocyte maturation process. Therefore, we sought to identify differentially expressed genes in CCs to assess oocyte\nquality and embryo development potential. We divided the participantsâ?? embryos into the high-quality embryo group and lowquality\nembryo group by the information including age, bodymass index, and the levels of luteinizing hormone, follicle-stimulating\nhormone, estradiol, and progesterone.We analyzed a total of 7 CC samples after the quality control in RNA sequencing.We found\nthat 2499 genes were unregulated and 5739 genes were downregulated in high-quality embryo group compared to the low-quality\nembryo group (Padj < 0.05). Interestingly,MSTN, CTGF, NDUFA1, VCAN, SCD5, and STAR were significantly associated with the\nquality of embryo. In accordance with the results of RNA sequencing, the association of the expression levels of MSTN, CTGF,\nNDUFA1, VCAN, SCD5, and STAR with the embryo quality was verified by quantitative reverse-transcription polymerase chain\nreaction (RT-qPCR) in 50 CC samples. Despite the small sample size and lack of validation in animal models, our study supports\nthe fact that differential gene expression profile of human CCs, including MSTN, CTGF, NDUFA1, VCAN, SCD5, and STAR, can\nserve as potential indicator for embryo quality....
Mercury compounds are known to cause central nervous system disorders; however\nthe detailed molecular mechanisms of their actions remain unclear. Methylmercury increases the\nexpression of several chemokine genes, specifically in the brain, while metallothionein-III (MT-III)\nhas a protective role against various brain diseases. In this study, we investigated the involvement\nof MT-III in chemokine gene expression changes in response to methylmercury and mercury vapor\nin the cerebrum and cerebellum of wild-type mice and MT-III null mice. No difference in mercury\nconcentration was observed between the wild-type mice and MT-III null mice in any brain tissue\nexamined. The expression of Ccl3 in the cerebrum and of Cxcl10 in the cerebellum was increased by\nmethylmercury in the MT-III null but not the wild-type mice. The expression of Ccl7 in the cerebellum\nwas increased by mercury vapor in the MT-III null mice but not the wild-type mice. However,\nthe expression of Ccl12 and Cxcl12 was increased in the cerebrum by methylmercury only in the\nwild-type mice and the expression of Ccl3 in the cerebellum was increased by mercury vapor only in\nthe wild-type mice. These results indicate that MT-III does not affect mercury accumulation in the\nbrain, but that it affects the expression of some chemokine genes in response to mercury compounds....
Both type 1 and type 2 diabetes are conditions that are associated with the loss of\ninsulin-producing ... cells within the pancreas. An active research therefore aims at regenerating\nthese ... cells with the hope that they could restore euglycemia. The approaches classically used\nconsist in mimicking embryonic development, making use of diverse cell sources or converting\npre-existing pancreatic cells. Despite impressive progresses and promising successes, it appears that\nwe still need to gain further insight into the molecular mechanisms underlying ... cell development.\nThis becomes even more obvious with the emergence of a relatively new field of research, epigenetics.\nThe current review therefore focuses on the latest advances in this field in the context of ... cell\n(neo-)genesis research....
Neurodegenerative diseases (NDs) have a profound impact on human health worldwide\nand their incidence is predicted to increase as the population ages. ND severely limits the quality\nof life and leads to early death. Aside from treatments that may reduce symptoms, NDs are almost\ncompletely without means of therapeutic intervention. The genetic and biochemical basis of many\nNDs is beginning to emerge although most have complex etiologies for which common themes remain\npoorly resolved. Largely relying on progress in vector design, gene therapy is gaining increasing\nsupport as a strategy for genetic treatment of diseases. Here we describe recent developments in the\nengineering of highly defective herpes simplex virus (HSV) vectors suitable for transfer and long-term\nexpression of large and/or multiple therapeutic genes in brain neurons in the complete absence of\nviral gene expression. These advanced vector platforms are safe, non-inflammatory, and persist in\nthe nerve cell nucleus for life. In the near term, it is likely that HSV can be used to treat certain NDs\nthat have a well-defined genetic cause. As further information on disease etiology becomes available,\nthese vectors may take on an expanded role in ND therapies, including gene editing and repair....
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Chemoresistance is a challenge for management of ovarian cancer, and therefore the response of resistant cells to nanosecond\nelectric pulses (nsEP) was explored. Human ovarian cancer cell line COC1 and the cisplatin-resistant subline COC1/DDP were\nsubjected to nsEP (32 ns, 10 kV/cm, 10Hz pulse repletion frequency, and 10min exposure duration), and then the cellular responses\nwere followed. Thepercentages of dead cells and of comet-formed cells in the alkaline assay displayed two peak levels (i.e., 2 and 8 h\nafter nsEP exposure), with the highest value noted at 8 h; the percentage of comet-formed cells in the neutral assay was increased\nat 8 h; the apoptotic percentage was increased at 8 h, with collapse of the mitochondrial membrane potential and the activation\nof caspase-3 and caspase-9. The comet assay demonstrated DNA single-strand break at 2 h and double-strand break at 8 h. nsEP\nresulted in lower cytotoxicity in COC1/DDP cells compared with COC1 cells. These findings indicated that nsEP induced early\nand late phases of DNA damage and cell death, and these two types of cell death may have distinct applications to treatments of\nchemoresistant ovarian cancers....
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