Based on analysis of Epstein-Barr virus (EBV) BART microRNA expression profiles, we previously reported that EBV-encoded miR-BART13 is upregulated in nasopharyngeal carcinoma (NPC) plasma specimens.
Analysis of the 170 EBV genome sequences from NPC and EBV-associated gastric cancers revealed that the frequency of this SNP was associated with NPC incidence and this SNP was found to be accumulated in the BART promoter region.
Overall, our results suggested that this SNP should enhance BART promoter activity and thus, might contribute to the development of EBV-associated epithelial malignancies.
We investigated the role of the ClC-K2 Cl<sup>‒</sup> channel and its β-subunit, barttin, using barttin hypomorphic (Bsnd<sup>neo/neo</sup>) mice and found that these mice did not show low-K<sup>+</sup>-induced NCC activation and salt-sensitive hypertension.
In the present study, we quantified the plasma levels of EBV DNA/RNAs, such as LMP1, LMP2, BART and EBER1 with real-time quantitative PCR, and CTCs with a CellSpotter Analyzer in NPC patients, with or without metastasis.
In adjusted Cox models, both BART - LVH and cardiac magnetic resonance imaging- LVH were associated with mortality (hazard ratio [95% CI ], 1.88 [1.45-2.44] and 2.21 [1.74-2.81], respectively), cardiovascular disease events (hazard ratio [95% CI ], 1.46 [1.08-1.98] and 1.91 [1.46-2.51], respectively), and coronary heart disease events (hazard ratio [95% CI ], 1.72 [1.20-2.47] and 1.96 [1.41-2.73], respectively).
In adjusted Cox models, both BART - LVH and cardiac magnetic resonance imaging- LVH were associated with mortality (hazard ratio [95% CI ], 1.88 [1.45-2.44] and 2.21 [1.74-2.81], respectively), cardiovascular disease events (hazard ratio [95% CI ], 1.46 [1.08-1.98] and 1.91 [1.46-2.51], respectively), and coronary heart disease events (hazard ratio [95% CI ], 1.72 [1.20-2.47] and 1.96 [1.41-2.73], respectively).
In adjusted Cox models, both BART - LVH and cardiac magnetic resonance imaging- LVH were associated with mortality (hazard ratio [95% CI ], 1.88 [1.45-2.44] and 2.21 [1.74-2.81], respectively), cardiovascular disease events (hazard ratio [95% CI ], 1.46 [1.08-1.98] and 1.91 [1.46-2.51], respectively), and coronary heart disease events (hazard ratio [95% CI ], 1.72 [1.20-2.47] and 1.96 [1.41-2.73], respectively).
Higher levels of pain during the cold pressor task predicted less risky decisions on the BART, and participants in the Cognitive Threat with Control condition made less risky decisions.
Background We developed a new left ventricular hypertrophy ( LVH ) criterion using a machine-learning technique called Bayesian Additive Regression Trees ( BART ).
In this study, we administered tacrolimus to barttin hypomorphic (Bsnd<sup>neo/neo</sup>) mice, a murine model of type 4 BS that exhibits polyuria, hypokalemia, and metabolic alkalosis.
In adjusted Cox models, both BART - LVH and cardiac magnetic resonance imaging- LVH were associated with mortality (hazard ratio [95% CI ], 1.88 [1.45-2.44] and 2.21 [1.74-2.81], respectively), cardiovascular disease events (hazard ratio [95% CI ], 1.46 [1.08-1.98] and 1.91 [1.46-2.51], respectively), and coronary heart disease events (hazard ratio [95% CI ], 1.72 [1.20-2.47] and 1.96 [1.41-2.73], respectively).
The overlapping symptomatology of DD1 and BS, together with the homology between the proteins of the CLC family, led us to investigate whether barttin might also regulate ClC-5 transport.
We identified two novel missense mutations p.Arg8Gly and p.Thr36Asn in exon 1 of BSND gene; both mutations were described for the first time in Moroccan patients with Bartter syndrome type IV.
In the present study, we identified two novel missense mutations in BSND gene causing Bartter syndrome type IV which is a genetic disease with an autosomal recessive transmission, characterized by hypokalaemia, metabolic alkalosis, an elevation in plasma renin activity and hyperaldosteronism as well as sensorineural deafness.
In the present study, we identified two novel missense mutations in BSND gene causing Bartter syndrome type IV which is a genetic disease with an autosomal recessive transmission, characterized by hypokalaemia, metabolic alkalosis, an elevation in plasma renin activity and hyperaldosteronism as well as sensorineural deafness.
Although high expression of miR-BARTs has been detected in NPC patients, contributions of these more recently discovered viral products to the establishment of TME are still vaguely defined.