Circular ribonucleic acid circ-FADS2 promotes colorectal cancer cell proliferation and invasion by regulating miR-498/S100A16.

The aim of this study is to examine the role and functional mechanism of circ-FADS2 in colorectal cancer (CRC). The levels of expression of circ-FADS2 were detected in 48 patients with CRC and their paired normal tissue samples and cell lines (SW480, SW620, HCT116, HT29, and NCM460) using quantitative real-time polymerase chain reaction (qRT-PCR). Circ-FADS2 was then silenced in SW480 and HT29 cells using two small interfering ribonucleic acids. Themolecular mechanism of circ-FADS2 in CRC progression and migration was then examined by sponging miR-498 and promoting S100A16 expression. After this, the expression of miR-498 and S100A16 in CRC tissues was analyzed using a qRT-PCR. In results: circ-FADS2 was found to be significantly upregulated in CRC tissues, when compared with paired normal tissues. Higher circ-FADS2 expression was associated with advanced stages, lymphatic metastasis, and reduced overall survival (OS). In addition, silencing circ-FADS2 markedly inhibited the proliferation and invasion of CRC and increased the percentage of cancer cells in the G1 phase in vitro. Reducing circ-FADS2 decreased SW480 cell proliferation in vivo. By inhibiting miR-498 expression, circ-FADS2 promoted S100A16 expression leading to the activation of the AKT pathway, resulting in CRC progression. We conclude that Circ-FADS2 expression was upregulated in CRC tissues and cells and was found to be correlated with advanced cancer, metastasis, and poor OS. A study of the molecular mechanism suggests that a circ-FADS2/miR-498/S100A16/AKT signaling cascade may be a potential therapeutic target for the treatment of CRC.

Fetal growth at different gestational periods and risk of impaired childhood growth, low childhood weight and obesity: a prospective birth cohort study.

OBJECTIVE: To examine the longitudinal associations of fetal growth with adverse child growth outcomes and to assess whether maternal metabolic factors modify the associations. DESIGN: Prospective cohort study. SETTING: Born in Guangzhou Cohort Study, China. POPULATION: A total of 4818 mother-child pairs. METHODS: Fetal growth was assessed according to estimated fetal weight (EFW) from 22 weeks of gestation until birth and the measurement of the birthweight. Fetal growth Z-scores were computed from random effects in the multilevel linear spline models to represent fetal size in early pregnancy (22 weeks of gestation) and growth in mid-pregnancy (22-27 weeks of gestation), early third trimester (28-36 weeks of gestation) and late third trimester (≥37 weeks of gestation). MAIN OUTCOME MEASURES: Z-scores for childhood stunting, low weight, overweight or obesity, length/height for age (LAZ/HAZ), weight for age (WAZ) and body mass index for age (BMIZ) at the age of 3 years. Adjusted associations were examined using multiple Poisson or linear regression models. RESULTS: Increased Z-scores of fetal size in early pregnancy and growth in mid-pregnancy and early third trimester were associated with a higher risk of childhood overweight or obesity (risk ratios 1.25-1.45). Fetal growth in each period was negatively associated with stunting and low weight, with the strongest associations observed for fetal size in early pregnancy and growth in mid-pregnancy. The results for continuous outcomes (LAZ/HAZ, WAZ and BMIZ) were similar. The associations of fetal growth with overweight or obesity in childhood were stronger among mothers who were underweight and who were overweight or obese than among mothers of normal weight. CONCLUSIONS: Accelerated fetal growth before 37 weeks of gestation is associated with children who are overweight or obese, whereas the critical period for stunting and low weight occurs before 28 weeks of gestation. TWEETABLE ABSTRACT: Fetal growth during different periods is differentially associated with childhood stunting, underweight and overweight or obesity.

ZEB2-AS1 regulates the expression of TAB3 and promotes the development of colon cancer by adsorbing microRNA-188.

OBJECTIVE: This study aimed to explore the possible role and mechanism of lncRNA ZEB2-AS1 in the pathogenesis of colon cancer (CCa). PATIENTS AND METHODS: The expression level of ZEB2-AS1 in 41 colon cancer tissue samples and 25 normal tissues was detected by qRT-PCR, and appropriate colon cancer cell lines were screened for in vitro experiments. Subcellular localization of ZEB2-AS1 was examined. After ZEB2-AS1 was transfected into colon cancer cells by liposome method, the cell proliferation, migration ability, and cell apoptosis percentage were evaluated by CCK-8 test, transwell assay, and flow cytometry, respectively. In addition, bioinformatics was applied to detect the target genes of microRNA-188. The Luciferase gene reporter assay was then performed to analyze the relative activity of Luciferase between microRNA-188 and TAB3 or ZEB2-AS1. At the same time, the control sequence, microRNA-188 mimics, microRNA-188 mimics+ ZEB2-AS1, si-TAB3, and microRNA-188 inhibitor+ si-TAB3 were respectively transfected into cells to further verify the interaction between TAB3 and microRNA-188 or ZEB2-AS1. Besides, the glucose and lactate levels were measured to explore their roles in glycolysis. RESULTS: The expression of ZEB2-AS1 in colon cancer tissues and cells was significantly higher than that in normal ones, and ZEB2-AS1 was confirmed to be mostly located in the cytoplasm. In addition, ZEB2-AS1 overexpression could enhance the cell proliferation rate and migration ability as well as reduce the cell apoptosis, which could be reversed by microRNA-188 overexpression. In addition, bioinformatics prediction and Dual-Luciferase reporter assays revealed that ZEB2-AS1 could bind to microRNA-188, which could directly target TAB3. At the same time, it was found that the overexpression of ZEB2-AS1 and low expression of microRNA-188 promoted glycolysis, while the opposite result was observed after overexpression of microRNA-188 and low expression of TAB3. CONCLUSIONS: The expression of ZEB2-AS1 is significantly increased in colon cancer tissues and cells, which can promote the proliferation, migration, and promote apoptosis of colon cancer cells. It may be involved in the development of this cancer through the process of glycolysis regulated by microRNA-188/TAB3.

AMPK regulates energy metabolism through the SIRT1 signaling pathway to improve myocardial hypertrophy.

OBJECTIVE: We investigated the correlations of adenosine monophosphate-activated protein kinase (AMPK), Silence information regulator 1 (SIRT1) and energy metabolism with myocardial hypertrophy. MATERIALS AND METHODS: Myocardial hypertrophy experimental model was established via transverse aortic constriction (TAC)-induced myocardial hypertrophy and phenylephrine (PE)-induced hypertrophic myocardial cell culture. After activation of AMPK, the messenger ribonucleic acid (mRNA) expressions in myocardial tissue- and myocardial cell hypertrophy-related genes, atrial natriuretic peptide (ANP) and ß-myosin heavy chain (ß-MHC), were detected. The production rate of 14C-labeled 14CO2 from palmitic acid was quantitatively determined to detect the fatty acid and glucose oxidation of hypertrophic myocardial tissues or cells, and the glucose uptake of myocardial cells was studied using [14C] glucose. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were performed to detect the changes in SIRT1 mRNA and protein expressions in hypertrophic myocardial tissues. Moreover, SIRT1 small interfering ribonucleic acid (siRNA) was used to interfere in SIRT1 expression to further investigate the role of SIRT1 in the effect of AMPK activation on myocardial hypertrophy. RESULTS: AMPK activation could significantly reduce the mRNA expressions of ANP and ß-MHC in vitro and in vivo. AMPK could increase the ejection fraction (EF) and decrease the protein synthesis rate in myocardial cells in mice with myocardial hypertrophy. Besides, AMPK activation could increase the fatty acid oxidation, improve the glucose uptake and reduce the glucose oxidation. After AMPK activation, both SIRT1 mRNA and protein expressions in hypertrophic myocardial tissues and myocardial cells were increased. After SIRT1 siRNA was further used to interfere in SIRT1 expression in myocardial cells, it was found that mRNA expressions and protein synthesis rates of ANP and ß-MHC were increased. CONCLUSIONS: The activation of AMPK can inhibit the myocardial hypertrophy, which may be realized through regulating the myocardial energy metabolism via SIRT1 signaling pathway.

Hyphoderma paramacaronesicum sp. nov. (Meruliaceae, Polyporales, Basidiomycota), a cryptic lineage to H. macaronesicum.

This article re-evaluates the taxonomy of Hyphoderma macaronesicum based on various strategies, including the cohesion species recognition method through haplotype networks, multilocus genetic analyses using the genealogical concordance phylogenetic concept, as well as species tree reconstruction. The following loci were examined: the internal transcribed spacers of nuclear ribosomal DNA (ITS nrDNA), the intergenic spacers of nuclear ribosomal DNA (IGS nrDNA), two fragments of the protein-coding RNA polymerase II subunit 2 (RPB2), and two fragments of the translation elongation factor 1-α (EF1-α). Our results indicate that the name H. macaronesicum includes at least two separate species, one of which is newly described as Hyphoderma paramacaronesicum. The two species are readily distinguished based on the various loci analysed, namely ITS, IGS, RPB2 and EF1-α.

Propranolol inhibits the proliferation, migration and tube formation of hemangioma cells through HIF-1α dependent mechanisms

The aim of this study was to investigate the mechanism of propranolol on the regression of hemangiomas. Propranolol-treated hemangioma tissues were collected and the expression of hypoxia inducible factor-1α (HIF-1α) was examined. We also established HIF-1α overexpression and knockdown hemangioma cells, and determined the effects of HIF-1α on the hemangioma cells proliferation, apoptosis, migration and tube formation. Significantly increased HIF-1α level was found in the hemangioma tissues compared to that in normal vascular tissues, whereas propranolol treatment decreased the HIF-1α level in hemangioma tissues in a time- and dose-dependent manner. Moreover, propranolol treatment significantly decreased cell proliferation, migration and tube formation as well as promoted cell apoptosis in HIF-1α overexpression and knockdown hemangioma cells. Propranolol suppressed the cells proliferation, migration and tube formation of hemangioma cells through HIF-1α dependent mechanisms. HIF-1α could serve as a novel target in the treatment of hemangiomas.

Residue depletion of decoquinate in chicken tissues after oral administration.

A rapid, sensitive, and reliable high-performance liquid chromatography tandem mass spectrometry (LC-MS/MS) method was developed and validated for the analysis of decoquinate in chicken tissues. The compounds were extracted using acetonitrile by liquid-liquid extraction (LLE) and purified with an Oasis(™) HLB solid-phase extraction (SPE) cartridge. Chromatographic separation was performed on an XTerra C18 reversed-phase column with a mobile phase of water containing 0.1% formic acid and acetonitrile. The analyte was detected by tandem quadrupole mass spectrometry after positive electrospray ionization by multiple reaction monitoring. The detection and quantitation limits were 1 and 2.5 µg/kg, respectively. The recoveries of edible tissues ranged from 85.3% to 104.9%, with relative standard deviations (RSD) lower than 10.4%. The depletion profile of decoquinate was studied in healthy chickens after oral administration of feed containing 27.2 mg/kg decoquinate for 10 consecutive days. The residue concentrations of decoquinate in chicken muscle and liver were detected using the developed method. The highest residue concentrations were attained 0.25 day post-treatment, and decoquinate residues were still detected 5 days postmedication in the tissues examined. The developed method has been successfully applied to the depletion study of decoquinate in chicken tissues. The recommended withdrawal period with oral administration based on our research is 3 days.

Unconventional vortex states in nanoscale superconductors due to shape-induced resonances in the inhomogeneous cooper-pair condensate.

Vortex matter in mesoscopic superconductors is known to be strongly affected by the geometry of the sample. Here we show that in nanoscale superconductors with coherence length comparable to the Fermi wavelength the shape resonances of the order parameter results in an additional contribution to the quantum topological confinement-leading to unconventional vortex configurations. Our Bogoliubov-de Gennes calculations in a square geometry reveal a plethora of asymmetric, giant multivortex, and vortex-antivortex structures, stable over a wide range of parameters and which are very different from those predicted by the Ginzburg-Landau theory. These unconventional states are relevant for high-T(c) nanograins, confined Bose-Einstein condensates, and graphene flakes with proximity-induced superconductivity.

Mapping, expression and regulation of the TRα gene in porcine adipose tissue.

Thyroid hormone receptors (TR) are members of the nuclear receptor superfamily. There are at least two TR isoforms, TRα and TRß. The TRα isoform plays a critical role in mediating the action of thyroid hormone in adipose tissue. We mapped the porcine TRα gene to chromosome 12 p11-p13, by using the ImpRH panel. We examined tissue-localization of TRα and determined expression patterns of TRα in porcine adipose tissue with quantitative real-time PCR. TRα was expressed in all tissues, including heart, liver, spleen, stomach, pancreas, brain, small intestine, skeletal muscle, and subcutaneous adipose tissue. In the adipose tissue, the expression of TRα decreased postnatally. Compared to Yorkshire pigs, Jinhua pigs had significantly lower expression levels of TRα gene in the subcutaneous fat tissue. The expression levels of ß2-AR, HSL and ATGL were also significantly lower in Jinhua pigs than in Yorkshire pigs. However, no significant differences in PPARγ and SREBP-1C expression levels were found between Jinhua and Yorkshire pigs. Incubation of porcine adipose tissue explants with high doses of isoproterenol (100 and 1000 nM) significantly increased the expression levels of TRα. We conclude that there is considerable evidence that TRα plays an important role in fat deposition in porcine adipose tissue.

Preemptive versus prophylactic protocol to prevent cytomegalovirus infection after renal transplantation: a meta-analysis and systematic review of randomized controlled trials.

OBJECTIVE: This review was conducted to assess the efficacy of preemptive versus prophylactic protocols for the prevention and treatment of cytomegalovirus (CMV) infection and disease after renal transplantation. METHODS: PubMed, EMBASE, the Cochrane Library, SCI, the China Journal Full-text Database, the Chinese Biomedical Database, the Chinese Scientific Journals Full-text Database, and the CMA Digital Periodicals were searched to collect randomized controlled trials (RCTs) of preemptive versus prophylactic protocols for the prevention and treatment of CMV infections after renal transplantation (up to April 2010). Two reviewers independently extracted data using a designed extraction form. The quality of the included trials was evaluated according to the Cochrane Handbook. RevMan 5.0 software was used for data analysis. RESULTS: Seven RCTs, involving 560 patients, were included. The results of the meta-analysis were as follows: the prophylactic protocol was significantly more effective than the preemptive protocol in reducing CMV infections and the recurrence rates of CMV infection; both the preemptive protocol and the prophylactic protocol reduced the risk of CMV disease, with no significant differences; no significant differences were observed in the risks of mortality, acute rejection, graft loss, other infections, or neutropenia between preemptive therapy and prophylaxis. CONCLUSION: Preemptive protocols are as effective as prophylaxis in reducing the risk of CMV disease in renal transplant recipients, whereas the prophylactic protocols could more effectively reduce the CMV recurrence rates. However, the trial data were very sparse, so further observations of the long-term effects of the protocols are needed.

Effects of Ureaplasma urealyticum infection on the male reproductive system in experimental rats.

To study the effects of Ureaplasma urealyticum (Uu) infection on the male reproductive system, the mechanism of infertility induced by Uu infection was investigated in experimental rats. Male Sprague-Dowley rats were infected with Uu4 (serotype 4) through repeated natural sexual intercourse for 8 weeks to establish infection. After 8 weeks, the blood samples of the animals were collected and analysed for cytokine production, and the animals were microdissected for the analysis of the reproductive system. Morphological study showed that spermatozoa exhibited curling and breaks in the rats infected at different dosages. Of the infected rats, 27.5% had both soft and hard calculi in the urinary tract, compared with 12% in the control groups. Uu infection resulted in a decline of sperm quality, eventually leading to the death of the spermatozoa. In the infected animals, the serum interleukin 6 and interleukin 8 levels increased significantly (P < 0.05), while tumour necrosis factor-alpha and interferon-gamma showed only modest changes. Our observations showed that Uu infection has an impact on sperm morphology, leading to the death of the spermatozoa. It is plausible that the morphological alterations of spermatozoa induced by Uu infection are one of the possible factors that contribute to male infertility.