239 research outputs found

    Surf and turf: predation by egg-eating snakes has led to the evolution of parental care in a terrestrial lizard

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    Animals display a great diversity of parental care tactics that ultimately enhance offspring survival, but how such behaviors evolve remains unknown for most systems. Here, we studied the evolution of maternal care, in the form of nest guarding, in a single population of long-tailed sun skink (Eutropis longicaudata) living on Orchid Island (Taiwan). This species typically does not provide protection to its offspring. Using a common garden experiment, we show that maternal care is genetically determined in this population. Through field manipulations, we demonstrate that care provides a significant increase in egg survival on Orchid Island by reducing predation from egg-eating snakes (Oligodon formosanus); this predator is not abundant in other populations of the lizard, which do not display parental care. Finally, using extensive field surveys, we show that the seasonal availability of green sea turtle (Chelonia mydas) nests is the cause for the high abundance of snake predators on Orchid Island, with the snakes consuming lizard eggs when green turtle eggs are not available. Together, these lines of evidence provide the first full demonstration of how predation can trigger the evolution of parental care in a species derived from a non-caring ancestor

    Increased Risk for Entamoeba histolytica Infection and Invasive Amebiasis in HIV Seropositive Men Who Have Sex with Men in Taiwan

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    Entamoeba histolytica, morphologically identical to but genetically different from E. dispar and E. moshkovskii, is the causative agent of amebiasis. Recently there have been reports of increased risk for amebiasis among men who have sex with men (MSM) due to oral-anal sexual contact in several developed countries. In this longitudinal follow-up study, the incidence of amebiasis was determined among HIV-infected patients using serological and specific amebic antigen assays. DNA extracted from stool samples containing E. histolytica were analyzed by PCR, sequenced, and compared. Clinical manifestations and treatment response of invasive amebiasis in HIV-infected patients were reviewed. The results demonstrated that HIV-infected MSM were at significantly higher risk of amebiasis than patients from other risk groups. Clustering of E. histolytica isolates by sequencing analyses from geographically unrelated patients suggested person-to-person transmission. Despite immunosuppression, amebic liver abscesses and colitis responded favorably to metronidazole therapy. It is important to investigate in areas of high incidence of both amebiasis and HIV (sub-Saharan Africa) how generalizable these findings are

    Using nomogram of the Barcelona Clinic Liver Cancer system for treatment selection in patients with stage C hepatocellular carcinoma

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    Abstract Background The nomogram of the Barcelona Clinic Liver Cancer (BCLC) for hepatocellular carcinoma (HCC) has been used for outcome prediction. Patients with BCLC stage C HCC often undergo anti-cancer therapy against current treatment guidelines in real world practice. We aimed to use the nomogram to provide guidance on treatment selection for BCLC stage C patients. Methods A total of 1317 patients with stage C HCC were retrospectively analyzed and divided into four groups by nomogram points. One-to-one matched pairs between patients receiving different treatments were generated by the propensity score with matching model within these groups. Survival analysis was performed by Kaplan-Meier method with log-rank test. Results Patients with higher nomogram points were more often treated with targeted or supportive therapies (p  15, there was no significant difference in survival between patients receiving two different treatment strategies. Conclusions The nomogram of BCLC system is a feasible tool to help stage C HCC patients to select primary anti-cancer treatment in pursuance of better overall survival.https://deepblue.lib.umich.edu/bitstream/2027.42/142787/1/12885_2018_Article_4202.pd

    Stent implantation for a totally occluded right coronary artery in a six-year-old boy after Kawasaki disease: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>Coronary stenting has previously been considered to be less feasible in children under 12 years old due to the limitation of vascular access. We report the case of a six-year-old boy who successfully underwent stent implantation for his totally occluded right coronary artery.</p> <p>Case presentation</p> <p>A Taiwanese boy aged six years and nine months old was found to have giant aneurysms after an acute episode of Kawasaki disease. An angiography revealed that his middle right coronary artery was totally occluded. A 0.014-inch guidewire was advanced to cross the totally occluded site. After pre-dilating the middle portion of his right coronary artery with a 1.5 mm balloon, stenting of his right coronary artery was accomplished using a 2.5 × 28 mm and a 2.5 × 18 mm bare metal stent. A final angiography demonstrated no residual stenosis or dissection.</p> <p>Conclusion</p> <p>Coronary stenting could be a therapeutic option for children as young as six years old. Close follow-up is mandatory because the long-term outcome is still unclear, especially in a small child.</p

    Revealing the Anti-Tumor Effect of Artificial miRNA p-27-5p on Human Breast Carcinoma Cell Line T-47D

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    microRNAs (miRNAs) cause mRNA degradation or translation suppression of their target genes. Previous studies have found direct involvement of miRNAs in cancer initiation and progression. Artificial miRNAs, designed to target single or multiple genes of interest, provide a new therapeutic strategy for cancer. This study investigates the anti-tumor effect of a novel artificial miRNA, miR P-27-5p, on breast cancer. In this study, we reveal that miR P-27-5p downregulates the differential gene expressions associated with the protein modification process and regulation of cell cycle in T-47D cells. Introduction of this novel artificial miRNA, miR P-27-5p, into breast cell lines inhibits cell proliferation and induces the first “gap” phase (G1) cell cycle arrest in cancer cell lines but does not affect normal breast cells. We further show that miR P-27-5p targets the 3′-untranslated mRNA region (3′-UTR) of cyclin-dependent kinase 4 (CDK4) and reduces both the mRNA and protein level of CDK4, which in turn, interferes with phosphorylation of the retinoblastoma protein (RB1). Overall, our data suggest that the effects of miR p-27-5p on cell proliferation and G1 cell cycle arrest are through the downregulation of CDK4 and the suppression of RB1 phosphorylation. This study opens avenues for future therapies targeting breast cancer

    Hepatitis B Virus-Encoded X Protein Downregulates EGFR Expression via Inducing MicroRNA-7 in Hepatocellular Carcinoma Cells

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    Hepatitis B virus (HBV) infection accounts for over a half of cases of hepatocellular carcinoma (HCC), the most frequent malignant tumor of the liver. HBV-encoded X (HBx) plays critical roles in HBV-associated hepatocarcinogenesis. However, it is unclear whether and how HBx regulates the expression of epidermal growth factor receptor (EGFR), an important gene for cell growth. Therefore, the study aimed to investigate the association between HBx and EGFR expression. In this study, we found that HBx upregulates miR-7 expression to target 3′UTR of EGFR mRNA, which in turn results in the reduction of EGFR protein expression in HCC cells. HBx-mediated EGFR suppression renders HCC cells a slow-growth behavior. Deprivation of HBx or miR-7 expression or restoration of EGFR expression can increase the growth rate of HCC cells. Our data showed the miR-7-dependent EGFR suppression by HBx, supporting an inhibitory role of HBx in the cell growth of HCC. These findings not only identify miR-7 as a novel regulatory target of HBx, but also suggest HBx-miR-7-EGFR as a critical signaling in controlling the growth rate of HCC cells

    Elevated BCRP/ABCG2 Expression Confers Acquired Resistance to Gefitinib in Wild-Type EGFR-Expressing Cells

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    The sensitivity of non-small cell lung cancer (NSCLC) patients to EGFR tyrosine kinase inhibitors (TKIs) is strongly associated with activating EGFR mutations. Although not as sensitive as patients harboring these mutations, some patients with wild-type EGFR (wtEGFR) remain responsive to EGFR TKIs, suggesting that the existence of unexplored mechanisms renders most of wtEGFR-expressing cancer cells insensitive.Here, we show that acquired resistance of wtEGFR-expressing cancer cells to an EGFR TKI, gefitinib, is associated with elevated expression of breast cancer resistance protein (BCRP/ABCG2), which in turn leads to gefitinib efflux from cells. In addition, BCRP/ABCG2 expression correlates with poor response to gefitinib in both cancer cell lines and lung cancer patients with wtEGFR. Co-treatment with BCRP/ABCG2 inhibitors enhanced the anti-tumor activity of gefitinib.Thus, BCRP/ABCG2 expression may be a predictor for poor efficacy of gefitinib treatment, and targeting BCRP/ABCG2 may broaden the use of gefitinib in patients with wtEGFR
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