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Background: Children with maltreatment histories demonstrate weaker reading abilities compared to their peers. However, the differential processes driving this effect remain unclear. Prior studies focused on social and behavioral factors explaining this effect, yet reading research has shown that one's ability to comprehend written text is driven by a set of underlying dynamic and interactive cognitive abilities., Objective: This systematic review sought to understand what theoretical or conceptual frameworks researchers cited as guiding their studies, what reading processes and abilities were studied as outcomes, how reading processes or abilities were measured, and what constructs were included to help understand the relationship between maltreatment and reading., Method: Three databases were searched for empirical peer-reviewed journal articles. Articles retained using inclusion and exclusion criteria were coded based on their sample characteristics, reference to theoretical or conceptual frameworks, reading processes and abilities measured, and included predictors of reading. Procedures were documented using the reporting items for systematic reviews and meta-analyses (PRISMA) statement (Moher et al., 2009)., Results: Twenty-seven studies were included in the final systematic review. Those that discussed theoretical or conceptual frameworks focused on the social and behavioral predictors of reading. Many studies (51.9 %) examined effects of maltreatment on reading achievement, rather than specific reading processes or abilities. Most studies (92.6 %) used at least one standardized reading measure. However, only four studies included cognitive abilities as potential predictor variables., Conclusions: Future research could benefit from investigating specific cognitive and reading-related processes, using measures to examine specific reading processes leading to breakdowns in reading achievement, and incorporation of reading theories to drive research questions and methods., Competing Interests: Declaration of competing interest None., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Type 2 diabetes (T2D) is a challenging health concern worldwide. A lifestyle intervention to treat T2D is difficult to adhere, and the effectiveness of approved medications such as metformin, thiazolidinediones (TZDs), and sulfonylureas are suboptimal. On the other hand, bariatric procedures such as Roux-en-Y gastric bypass (RYGB) are being recognized for their remarkable ability to achieve diabetes remission, although the underlying mechanism is not clear. Recent evidence points to branched-chain amino acids (BCAAs) as a potential contributor to glucose impairment and insulin resistance. RYGB has been shown to effectively lower plasma BCAAs in insulin-resistant or T2D patients that may help improve glycemic control, but the underlying mechanism for BCAA reduction is not understood. Hence, we attempted to explore the mechanism by which RYGB reduces BCAAs. To this end, we randomized diet-induced obese (DIO) mice into three groups that underwent either sham or RYGB surgery or food restriction to match the weight of RYGB mice. We also included regular chow-diet-fed healthy mice as an additional control group. Here, we show that compared to sham surgery, RYGB in DIO mice markedly lowered serum BCAAs most likely by rescuing BCAA breakdown in both liver and white adipose tissues. Importantly, the restored BCAA metabolism following RYGB was independent of caloric intake. Fasting insulin and HOMA-IR were decreased as expected, and serum valine was strongly associated with insulin resistance. While gut hormones such as glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) are postulated to mediate various surgery-induced metabolic benefits, mice lacking these hormonal signals (GLP-1R/Y2R double KO) were still able to effectively lower plasma BCAAs and improve glucose tolerance, similar to mice with intact GLP-1 and PYY signaling. On the other hand, mice deficient in fibroblast growth factor 21 (FGF21), another candidate hormone implicated in enhanced glucoregulatory action following RYGB, failed to decrease plasma BCAAs and normalize hepatic BCAA degradation following surgery. This is the first study using an animal model to successfully recapitulate the RYGB-led reduction of circulating BCAAs observed in humans. Our findings unmasked a critical role of FGF21 in mediating the rescue of BCAA metabolism following surgery. It would be interesting to explore the possibility of whether RYGB-induced improvement in glucose homeostasis is partly through decreased BCAAs.

Alzheimer's disease (AD) is an irreversible neurodegenerative disorder with a complex pathophysiology. Type 2 diabetes (T2D) is a strong risk factor for AD that shares similar abnormal features including metabolic dysregulation and brain pathology such as amyloid and/or Tau deposits. Emerging evidence suggests that circulating branched-chain amino acids (BCAAs) are associated with T2D. While excess BCAAs are shown to be harmful to neurons, its connection to AD is poorly understood. Here we show that individuals with AD have elevated circulating BCAAs and their metabolites compared to healthy individuals, and that a BCAA metabolite is correlated with the severity of dementia. APP Swe mouse model of AD also displayed higher plasma BCAAs compared to controls. In pursuit of understanding a potential causality, BCAA supplementation to HT-22 neurons was found to reduce genes critical for neuronal health while increasing phosphorylated Tau. Moreover, restricting BCAAs from diet delayed cognitive decline and lowered AD-related pathology in the cortex and hippocampus in APP/PS1 mice. BCAA restriction for two months was sufficient to correct glycemic control and increased/restored dopamine that were severely reduced in APP/PS1 controls. Treating 5xFAD mice that show early brain pathology with a BCAA-lowering compound recapitulated the beneficial effects of BCAA restriction on brain pathology and neurotransmitters including norepinephrine and serotonin. Collectively, this study reveals a positive association between circulating BCAAs and AD. Our findings suggest that BCAAs impair neuronal functions whereas BCAA-lowering alleviates AD-related pathology and cognitive decline, thus establishing a potential causal link between BCAAs and AD progression.

Background: Students who experience maltreatment tend to underperform academically relative to their peers, requiring an understanding of academically-related mechanisms that are potential intervention targets. Academic engagement, a multidimensional construct that is influential in students' investment in learning and the school context, is one such mechanism that has been associated with positive academic outcomes and develops through interactions between students and their environment., Objective: The purpose of this study was to examine how maltreatment experiences and trauma symptoms were indirectly associated with academic achievement in adolescence through academic engagement., Participants and Setting: The study was conducting on a subsample of 583 youths from the National Study of Child and Adolescent Wellbeing II (NSCAW II) cohort., Methods: Structural equation modeling was used to examine the indirect effect engagement on the relationship between maltreatment and trauma symptomology and academic achievement., Results: Academic engagement significantly mediated trauma symptoms and later standardized reading (β = -0.02; 95 % CI [-0.04, -0.0004]) and math (β = -0.02; 95 % CI [-0.05, -0.0003]) achievement test scores. However, similar mediating effects were not found for engagement on maltreatment and later standardized reading (β = -0.01; 95 % CI [-0.03, 0.01]) and math (β = -0.01; 95 % CI [-0.03, 0.01]) achievement test scores., Conclusions: These findings suggest that variability in academic outcomes was indirectly associated with engagement but only for students who exhibited trauma symptoms rather than experiencing maltreatment alone. The findings suggest future researchers should consider engagement should as an academically-related mechanism to help students who were maltreated succeed academically., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Obesity prevalence is increasing at an unprecedented rate throughout the world, and is a strong risk factor for metabolic, cardiovascular, and neurological/neurodegenerative disorders. While low-grade systemic inflammation triggered primarily by adipose tissue dysfunction is closely linked to obesity, inflammation is also observed in the brain or the central nervous system (CNS). Considering that the hypothalamus, a classical homeostatic center, and other higher cortical areas (e.g. prefrontal cortex, dorsal striatum, hippocampus, etc.) also actively participate in regulating energy homeostasis by engaging in inhibitory control, reward calculation, and memory retrieval, understanding the role of CNS oxidative stress and inflammation in obesity and their underlying mechanisms would greatly help develop novel therapeutic interventions to correct obesity and related comorbidities. Here we review accumulating evidence for the association between ER stress and mitochondrial dysfunction, the main culprits responsible for oxidative stress and inflammation in various brain regions, and energy imbalance that leads to the development of obesity. Potential beneficial effects of natural antioxidant and anti-inflammatory compounds on CNS health and obesity are also discussed.

A large health care system developed standard data sets for business and clinical modules using clinical content experts from across the organization. Vendor software to control facility edits was employed. The organizational structure and decision making methodology for managing change requests, challenges encountered and solutions developed are described. More than 1000 change requests have been handled in the nursing and clinical ancillary modules during the 1st year of the process.

We have reported a case of lactic acidosis induced by ingestion of sustained-release nicotinic acid. Prompt recovery followed treatment with glucose-containing fluids and discontinuation of nicotinic acid therapy.