Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Angiotensin II (Ang II) signaling has been implicated in cardiac arrhythmogenesis, which involves induction of reactive oxygen species (ROS). It was shown that Ang II can activate Ca/Calmodulin kinase II (CaMKII) by oxidation via a NADPH oxidase 2 (NOX2)-dependent pathway leading to increased arrhythmic afterdepolarizations. Interestingly, cAMP-dependent protein kinase A (PKA) which regulates similar targets as CaMKII has recently been shown to be redox-sensitive as well.', 'This study aims to investigate the distinct molecular mechanisms underlying Ang II-related cardiac arrhythmias with an emphasis on the individual contribution of PKA vs. CaMKII.', 'Isolated ventricular cardiac myocytes from rats and mice were used. Ang II exposure resulted in increased NOX2-dependent ROS generation assessed by expression of redox-sensitive GFP and in myocytes loaded with ROS indicator MitoSOX. Whole cell patch clamp measurements showed that Ang II significantly increased peak Ca and Na current (ICa and INa) possibly by enhancing steady-state activation of ICa and INa. These effects were absent in myocytes lacking functional NOX2 (gp91phox(-/-)). In parallel experiments using PKA inhibitor H89, the Ang II effects on peak INa and ICa were also absent. In contrast, genetic knockout of CaMKIIδ (CaMKIIδ(-/-)) did not influence the Ang II-dependent increase in peak ICa and INa. On the other hand, Ang II enhanced INa inactivation, increased late INa and induced diastolic SR (sarcoplasmic reticulum) Ca leak (confocal Ca spark measurements) in a CaMKIIδ-, but not PKA-dependent manner. Surprisingly, only the increase in diastolic SR Ca leak was absent in gp91phox(-/-)myocytes suggesting that Ang II regulates INa inactivation in a manner dependent on CaMKII- but not on NOX2. Finally, we show that Ang II increased the propensity for cellular arrhythmias, for which PKA and CaMKII contribute, both dependent on NOX2.
Does nADPH oxidase 2 mediate angiotensin II-dependent cellular arrhythmias via PKA and CaMKII?

Intellectual disability (ID) features in numerous heritable medical conditions that result from ATRX mutations. Alpha-thalassemia mental retardation syndrome (ATR-X syndrome) is the most notable manifestation of ATRX dysfunction. In addition to ID, genitourinary and craniofacial abnormalities are regularly observed with or without alpha-thalassemia.', 'The study sought to characterize two cases of ATR-X in a Yemeni family clinically and molecularly.', 'PCR amplification and Sanger sequencing were used to study the ATRX gene in a Yemeni family. Also, methylation-sensitive PCR was used to perform X-inactivation studies. CADD, SNAP2 and PolyPhen-2 helped to predict the functional consequences of the variant.', 'Molecular testing revealed a novel hemizygous missense mutation (c.5666T>G) in the ATRX gene in the two Yemeni brothers. This mutation was found in a heterozygous state in the mother, with the chromosome harboring the mutated allele being under strongly skewed X-inactivation.
Does a novel missense mutation in ATRX uncovered in a Yemeni family lead to alpha-thalassemia/mental retardation syndrome without alpha-thalassemia?

It is suggested that maternal obesity perpetuates offspring obesity to future generations.', 'To determine whether location of neonate fat mass (FM: central vs. peripheral) is related to total neonate FM and whether maternal obesity influences this relationship.', 'Neonate body composition and skin-fold thicknesses were assessed in healthy neonates (n\u2009=\u2009371; 1-3 days old). Linear regression models examined the relationship between total FM and location of FM (central vs. peripheral). Location of FM was calculated by skin-folds: peripheral was the sum of (biceps and triceps)/2 and central was represented by the subscapular skin-fold.', 'A significant interaction was found for location of FM and maternal obesity. Holding all predictors constant, in offspring born to non-obese mothers, a 0.5\u2009mm increase in central FM predicted a 15\u2009g greater total FM, whereas a 0.5\u2009mm increase in peripheral FM predicted a 66\u2009g greater total FM. However, in offspring born to obese mothers, a 0.5\u2009mm increase in central FM predicted a 56\u2009g total FM, whereas a 0.5\u2009mm increase in peripheral FM predicted a 14\u2009g greater total FM.

Does maternal obesity influence the relationship between location of neonate fat mass and total fat mass?