Effects of dietary Enteromorpha powder supplementation on productive performance, egg quality, and antioxidant performance during the late laying period in Zi geese.

This study investigated the effects of dietary Enteromorpha powder supplementation on the productive performance, egg quality, and antioxidant performance of Zi geese during the late laying period. Three hundred twelve Zi geese (1 yr old) were randomly allocated into 2 cohorts to form a control group and an experimental group (with each cohort including 6 replicates and 21 female geese and 5 male geese in each replicate). The control group was fed a basal diet, and the experimental group was fed a diet containing 3% Enteromorpha powder. The data showed that Enteromorpha powder supplementation significantly improved egg production, laying rate, average daily egg weight (P < 0.01), and egg yolk color (P < 0.05). Supplementation decreased the ADFI and feed conversion rate (P < 0.01). Compared with the control group, glutathione peroxidase (GSH-Px) activity was significantly higher in serum and ovary tissue (P < 0.05), but GSH-Px activity was lower in liver tissue (P < 0.01). Malondialdehyde was reduced in liver and ovary tissue (P < 0.05) in the Enteromorpha powder supplementation group. Meanwhile, the expression of the CAT gene was significantly upregulated in the liver (P < 0.01) in the Enteromorpha group. These results indicate that dietary Enteromorpha powder supplementation improved productive performance and reduced the level of lipid peroxidation in Zi geese during the late laying period.

LncRNATCF7 up-regulates DNMT1 mediated by HPV-18 E6 and regulates biological behavior of cervical cancer cells by inhibiting miR-155.

OBJECTIVE: This work aimed to study the mechanism of lncRNATCF7 upregulating DNMT1 mediated by HPV-18 E6 and regulating the biological behavior of cervical cancer cells by inhibiting miR-155. PATIENTS AND METHODS: HPV-16 E6 enhanced DNMT1 expression in cervical cancer cells, which was detected by Western blotting. The expression of miR-155 in cervical cancer was detected by qPCR, the interaction between TCF-7 and miR-155 by Dual-luciferase reporter gene. The changes in invasion ability of cervical cancer cells and the effect of miR-155 on the invasion ability of cervical cancer cells after inhibiting TCF-7 were detected by the transwell invasion assay, while changes in migration ability of cervical cancer cells and the effect of miR-155 on migration ability of cervical cancer cells after inhibiting TCF-7 were observed by the scratch assay. The effect of inhibiting TCF-7 on the tumor size and volume of cervical cancer was detected by the subcutaneous tumor formation in nude mice. RESULTS: E6 expression was significantly inhibited by E6 siRNA. The knockdown of endogenous HPV-16 E6 markedly inhibited the expression of DNMT1; TCF-7 specifically bound to the 3' UTR of miR-155; inhibition of TCF-7 can inhibit invasion and migration of cervical cancer cells; enhanced miR-155 after the inhibition of TCF-7 can promote the invasion and migration of cervical cancer cells; compared with NC group, the tumor volume and weight of TCF-7-siRNA group tumor-bearing was significantly reduced. CONCLUSIONS: TCF-7 plays an important role in the development of cervical cancer. TCF-7 can target miR-155 to regulate the invasion and migration of cervical cancer cells.

Mutations in the ATP2C1 gene in Chinese patients with Hailey-Hailey disease.

Hailey-Hailey disease (HHD; MIM 16960) is a rare autosomal dominant hereditary disorder characterized by recurrent eruption of vesicles and bullae, predominantly involving the body folds. It is caused by heterozygous mutations in the ATP2C1 gene, encoding the human secretory pathway Ca2+/Mn2+-ATPase protein 1 (hSPCA1). When we studied Chinese patients with HHD, we found two different heterozygous mutations, Q506X and G353V, the former previously reported in a Hungarian patient, and the latter being a novel mutation. In a 38-year-old patient from a four-generation pedigree with a 3-year history of severe recurrent blisters, we identified a C-->T transition at nucleotide 1696, c(1696C-->T), in exon 17 of ATP2C1, resulting in a nonsenes mutation, Gln506X, which resulted in a premature termination codon. In the second patient, who represented a occurrence of sporadic Hailey-Hailey disease, a G-->T transversion of nucleotide, c(G1238T), in exon 13 of ATP2C1 was detected, which resulted in a Gly353-->Val amino acid substitution (G353V). Our molecular findings further demonstrate that the mutational events in the human ATP2C1 gene encoding the hSPCA1 pump play an important role in the pathogenesis of HHD.

The activation of human platelets mediated by two monoclonal antibodies raised against CD9.

The platelet activation induced by two anti-human platelet P24/CD9 McAbs was investigated. The results showed that: the pathway of platelet aggregation induced by the two McAbs (HI117 and SJ9A4) is not the same; HI117 and SJ9A4 induced the phosphorylation of platelet proteins (40KD and 20KD) when platelets were activated; but HI117 didn't cause a rise in intracellular Ca2+ concentration in activated platelets compared with SJ9A4; the epitope recognized by HI117 and SJ9A4 is different and this is probably the real reason why the two CD9 McAbs play different roles in platelet activation. Additionally McAbs HI117 and SJ9A4 could not promote associates of other proteins (e.g.: GPIIb/IIIa) with P24/CD9 on activated human platelets. All these results indicate that the mechanism of platelet activation induced by HI117 or SJ9A4 is different form each other. It suggests that CD9 antigen play an important and complex role in platelet activation.