Air Embolism during Upper Endoscopy: A Case Report

Yin Fang,Junbei Wu,Feng Wang,Lihong Cheng,Yunhong Lu,Xiaofei Cao 대한소화기내시경학회 2019 Clinical Endoscopy Vol.52 No.4

Air embolism is a rare complication of upper endoscopy and potentially causes life-threatening events. A 67-year-old man with ahistory of surgery of cardiac carcinoma and pancreatic neuroendocrine tumor underwent painless upper endoscopy because oftarry stools. During the procedure, air embolism developed, which caused decreased pulse oxygen saturation and delayed sedationrecovery. He recovered with some weakness of the left upper limb in the intensive care unit without hyperbaric oxygen therapy. Theetiology, clinical manifestations, and treatments of air embolism are discussed based on the literature reports. Although air embolism isuncommon in endoscopic examinations, the patients’ outcomes could be improved if clinicians are alert to this potential complication,and promptly start proper diagnostic and therapeutic measures.

Effects of Dietary Acetyl-L-Carnitine on Meat Quality and Lipid Metabolism in Arbor Acres Broilers

Zhang, Yong,Ma, Qiugang,Bai, Xiumei,Zhao, Lihong,Wang, Qiang,Ji, Cheng,Liu, Laiting,Yin, Haicheng Asian Australasian Association of Animal Productio 2010 Animal Bioscience Vol.23 No.12

An experiment was conducted to evaluate the effects of dietary acetyl-L-carnitine (ALC) on growth performance, carcass characteristics, meat quality and lipid metabolism in broilers. A total of 240 one-day-old male Arbor Acres broilers were randomly allocated to 4 dietary treatments (0, 300, 600, and 900 mg/kg dietary ALC supplementation, respectively). Compared with the control treatment, addition of ALC resulted in lower (linear effect, p<0.05) ADG and AFI. Abdominal fat percentage decreased (linear effect, p<0.05) as dietary ALC was increased, but there was no effect on dressing percentage, breast muscle percentage or thigh muscle percentage. Breast muscle pH value 24 h post-mortem increased (linear effect, p<0.05), but there were no significant differences among treatments. However, thigh muscle pH value increased (linear effect, p<0.05) as dietary ALC was increased. Breast and thigh muscle $a^*$ values increased (linear effect, p<0.05), and breast and thigh muscle $b^*$ values decreased (linear effect, p<0.05) with increased ALC in the diet. In addition, breast and thigh muscle shear force value decreased (linear effect, p<0.05) as dietary ALC was increased. Total cholesterol, triglyceride, low-density lipoprotein cholesterol and lipoprotein lipase decreased (linear effect, p<0.05) and free fatty acid and lipase in serum increased (linear effect, p<0.05) with increased ALC in diets.

Expression Profiling after Induction of Demethyla-tion in MCF-7 Breast Cancer Cells Identifies Involvement of TNF-alpha Mediated Cancer Pathways

김주희,김선정,Seongeun Kang,김태우,Lihong Yin,Ran Liu 한국분자세포생물학회 2012 Molecules and cells Vol.33 No.2

Epigenetic methylation change is a major process that occurs during cancer development. Even though many tumor-related genes have been identified based on their relationship between methylation and expression, few studies have been conducted to investigate the relevant biological pathways involved in these changes. To identify essential pathways likely to be affected by methylation in breast cancer, we examined a pool of genes in which expression was upregulated after induction of demethy-lation by 5-Aza-2'-deoxycytidine (Aza) in the MCF-7 breast cancer cell line. Genome-wide demethylation was confir-med by monitoring the demethylation of a previously known gene, SULT1A1. Overall, 210 and 213 genes were found to be upregulated and downregulated (fold change > 2), respectively, in common in cells treated with 5 and 10 M of Aza. Network analysis of these 423 genes with altered expression patterns identified the involvement of a cancer related network of genes that were heavily regulated by TNF-alpha in breast tumorigenesis. Our results suggest that epigenetic dysregulation of cellular processes relevant to TNF-alpha-dependent apoptosis may be intimately involved in tumorigenesis in MCF-7 cells.

miRNA-183 Suppresses Apoptosis and Promotes Proliferation in Esophageal Cancer by Targeting PDCD4

Yang, Miao,Liu, Ran,Li, Xiajun,Liao, Juan,Pu, Yuepu,Pan, Enchun,Yin, Lihong,Wang, Yi Korean Society for Molecular and Cellular Biology 2014 Molecules and cells Vol.37 No.12

In our previous study, miRNA-183, a miRNA in the miR-96-182-183 cluster, was significantly over-expressed in esophageal squamous cell carcinoma (ESCC). In the present study, we explored the oncogenic roles of miR-183 in ESCC by gain and loss of function analysis in an esophageal cancer cell line (EC9706). Genome-wide mRNA micro-array was applied to determine the genes that were regulated directly or indirectly by miR-183. 3'UTR luciferase reporter assay, RT-PCR, and Western blot were conducted to verify the target gene of miR-183. Cell culture results showed that miR-183 inhibited apoptosis (p < 0.05), enhanced cell proliferation (p < 0.05), and accelerated G1/S transition (p < 0.05). Moreover, the inhibitory effect of miR-183 on apoptosis was rescued when miR-183 was suppressed via miR-183 inhibitor (p < 0.05). Western blot analysis showed that the expression of programmed cell death 4 (PDCD4), which was predicted as the target gene of miR-183 by microarray profiling and bioinformatics predictions, decreased when miR-183 was over-expressed. The 3'UTR luciferase reporter assay confirmed that miR-183 directly regulated PDCD4 by binding to sequences in the 3'UTR of PDCD4. Pearson correlation analysis further confirmed the significant negative correlation between miR-183 and PDCD4 in both cell lines and in ESCC patients. Our data suggest that miR-183 might play an oncogenic role in ESCC by regulating PDCD4 expression.

miRNA-183 Suppresses Apoptosis and Promotes Proliferation in Esophageal Cancer by Targeting PDCD4

Miao Yang,Ran Liu,Xiajun Li,Juan Liao,Yuepu Pu,Enchun Pan,Lihong Yin,Yi Wang 한국분자세포생물학회 2014 Molecules and cells Vol.37 No.12

In our previous study, miRNA-183, a miRNA in the miR-96-182-183 cluster, was significantly over-expressed in esophageal squamous cell carcinoma (ESCC). In the present study, we explored the oncogenic roles of miR-183 in ESCC by gain and loss of function analysis in an esophageal cancer cell line (EC9706). Genome-wide mRNA microarray was applied to determine the genes that were regulated directly or indirectly by miR-183. 3UTR luciferase reporter assay, RT-PCR, and Western blot were conducted to verify the target gene of miR-183. Cell culture results showed that miR-183 inhibited apoptosis (p < 0.05), enhanced cell proliferation (p < 0.05), and accelerated G1/S transition (p < 0.05). Moreo-ver, the inhibitory effect of miR-183 on apoptosis was rescued when miR-183 was suppressed via miR-183 inhibitor (p < 0.05). Western blot analysis showed that the expression of programmed cell death 4 (PDCD4), which was predicted as the target gene of miR-183 by microarray profiling and bioinformatics predictions, decreased when miR-183 was over-expressed. The 3'UTR luciferase reporter assay confirmed that miR-183 directly regulated PDCD4 by binding to sequences in the 3'UTR of PDCD4. Pearson correlation analysis fur-ther confirmed the significant negative correlation between miR-183 and PDCD4 in both cell lines and in ESCC patients. Our data suggest that miR-183 might play an oncogenic role in ESCC by regulating PDCD4 expression.

Caenorhabditis elegans as a useful model to assess the effect of spermiogenesis induced by three teratogens

Yunhui Li,Minhui Zhang,Xiaobo Li,Juan Zhang,Ran Liu,Geyu Liang,Yuepu Pu,Lihong Yin 대한독성 유전단백체 학회 2015 Molecular & cellular toxicology Vol.11 No.2

Caenorhabditis elegans (C. elegans), with homologous genes and conservative spermiogenesis in mammals, has a series of advantages to illuminate and study many biological processes including reproductive toxicity. So it is a very useful model to assess environmental and ecological toxicity. Here we introduce C. elegans as an animal model and three known mammalian sperm teratogens methyl methanesulfonate, mitomycin C and cyclophosphamide as experimental materials to elucidate the efficient and reliability for the assessment of chemicals altering spermiogenesis. The results showed that, with the aid of the brood size, spermatids activation, trans-activation, sperm competition as the endpoints, the adverse effects of three teratogens on C. elegans were detected. Thus, while the data of chemicals induced spermiogenesis abnormality is incomplete, we speculated that C. elegans could be a useful animal model to explore the effects on spermiogenesis of chemicals. And we propose an increased application of C. elegans that complements other model system in the reproductive toxicity.