bluuebunny/crossref_metadata_2025 huggingface dataset:
Effects of a resistance training community programme in older adults
Authors: Syed-Abdul Majid Mufaqam , McClellan Chrissa L. , Parks Elizabeth J. , Ball Stephen D.
Published: January 2021

Ageing is associated with reduced muscle mass, strength, flexibility and balance, resulting in a poor quality of life (QOL). Past studies have occurred in highly controlled laboratory settings which provide strong support to determine whether similar gains can be made in community programmes. Twenty participants were enrolled in an eight-week community-based resistance training programme (mean age = 61.3 (standard error (SE) = 0.9) years); Body Mass Index = 32.0 (SE = 1.3) kg/m2). All participants completed surveys to assess outcomes associated with QOL. Given the relationship between muscle function and nerve health, nerve conduction studies (NCS) were also conducted in a separate group of participants (mean age = 64.9 (SE = 2.0) years; Body Mass Index = 32.6 (SE = 1.9) kg/m2). This community-based training programme significantly improved QOL measures in older adults (p < 0.001). Although weight loss was not the primary outcome of the study, participants reduced their body weights (p < 0.001), by primarily reducing fat mass (p = 0.007) while maintaining muscle mass. Significant improvements were observed in muscle strength (2.2%), flexibility and balance (3.2–464.2%, p ⩽ 0.05 for all). Improvements were also observed in plasma glucose (p = 0.05), haemoglobin A1C (p = 0.06) and aldolase enzyme levels (p < 0.001). Scores for surveys on memory and sleep improved (p < 0.05). Improved QOL was associated with increased lean mass (r = −0.714, p = 0.002), decreased fat mass (r = −0.702, p = 0.003) and improved flexibility and balance (r = −0.627, p = 0.008). An eight-week, community-based resistance training programme significantly improved QOL in older adults. Influence on the lipid profile and NCS still needs further investigation.
Care home residents on the move: the significance of cultural context for physical activity
Authors: Bowes Alison , Dawson Alison , Greasley-Adams Corinne , Jepson Ruth , McCabe Louise
Published: January 2021

Increased physical activity is widely promoted as beneficial for older people, but previous research indicates this may be difficult to implement in care homes, especially for people with dementia who form an increasing proportion of residents. Care home cultures can mitigate against physical activity for residents, but there is also scope for them to embed personalised physical activity. They are under-researched, but significant in terms of outcomes and quality of life for residents. This paper builds understanding of care home cultures of physical activity through qualitative, empirical research in five care homes. Key findings are that culturally framed views about physical activity, sometimes reflecting stereotypical views of dependency, can be seen in care homes. Managers, staff and residents may be invested in or resistant to physical activity and dominant managerial or societal views may be reflected or contested. The relatively closed boundaries of care homes reinforce sedentariness, and resident involvement in either chosen or enforced physical activity is varied. Interactions demonstrate potential to negotiate physical activity more or less effectively in any given care home. Rigid routines, external regulations and pressure on staffing can be negative, but management commitment has positive potential. In conclusion, the paper identifies that to increase physical activity in a sustainable manner, any intervention needs to address issues of culture change and individual needs and preferences.
Non-specific blood tests as proxies for COVID-19 hospitalisation: are there plausible associations after excluding noisy predictors?
Authors: Ishikawa G. , Argenti G. , Fadel C. B.
Published: January 2021

This study applied causal criteria in directed acyclic graphs for handling covariates in associations for prognosis of severe coronavirus disease 2019 (COVID-19) cases. To identify non-specific blood tests and risk factors as predictors of hospitalisation due to COVID-19, one has to exclude noisy predictors by comparing the concordance statistics (area under the curve − AUC) for positive and negative cases of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). Predictors with significant AUC at negative stratum should be either controlled for their confounders or eliminated (when confounders are unavailable). Models were classified according to the difference of AUC between strata. The framework was applied to an open database with 5644 patients from Hospital Israelita Albert Einstein in Brazil with SARS-CoV-2 reverse transcription – polymerase chain reaction (RT-PCR) exam. C-reactive protein (CRP) was a noisy predictor: hospitalisation could have happened due to causes other than COVID-19 even when SARS-CoV-2 RT-PCR is positive and CRP is reactive, as most cases are asymptomatic to mild. Candidates of characteristic response from moderate-to-severe inflammation of COVID-19 were: combinations of eosinophils, monocytes and neutrophils, with age as risk factor; and creatinine, as risk factor, sharpens the odds ratio of the model with monocytes, neutrophils and age.
SARS-CoV-2 viral RNA load dynamics in the nasopharynx of infected children
Authors: Kam K. Q. , Thoon K. C. , Maiwald M. , Chong C. Y. , Soong H. Y. , Loo L. H. , Tan N. W. H. , Li J. , Nadua K. D. , Yung C. F.
Published: January 2021

It is important to understand the temporal trend of the paediatric severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral load to estimate the transmission potential of children in schools and communities. We determined the differences in SARS-CoV-2 viral load dynamics between nasopharyngeal samples of infected asymptomatic and symptomatic children. Serial cycle threshold values of SARS-CoV-2 from the nasopharynx of a cohort of infected children were collected for analysis. Among 17 infected children, 10 (58.8%) were symptomatic. Symptomatic children, when compared to asymptomatic children, had higher viral loads (mean cycle threshold on day 7 of illness 28.6 vs. 36.7, P = 0.02). Peak SARS-CoV-2 viral loads occurred around day 2 of illness in infected children. Although we were unable to directly demonstrate infectivity, the detection of significant amount of virus in the upper airway of asymptomatic children suggest that they have the potential to shed and transmit SARS-CoV-2. Our study highlights the importance of contact tracing and screening for SARS-CoV-2 in children with epidemiological risk factors regardless of their symptom status, in order to improve containment of the virus in the community, including educational settings.
Maltreatment timing, HPA axis functioning, multigenic risk, and depressive symptoms in African American youth: Differential associations without moderated mediation
Authors: VanZomeren Adrienne A. , Zhang Jingchen , Lee Sun-Kyung , Gunlicks-Stoessel Meredith , Piehler Timothy , Cicchetti Dante
Published: January 2021

Utilizing a large (N = 739), ancestrally homogenous sample, the current study aimed to better understand biological risk processes involved in the development of depressive symptoms in maltreated, African American children age 8-12 years. Maltreatment was independently coded from Child Protective Services records and maternal report. Self-reported depressive symptoms were attained in the context of a week-long, summer research camp. DNA was acquired from buccal cell or saliva samples and genotyped for nine polymorphisms in four hypothalamic-pituitary-adrenal (HPA)-axis-related genes: FKBP5, NR3C1, NR3C2, and CRHR1. Salivary cortisol samples were collected each morning (9 a.m.) and late afternoon (4 p.m.) throughout the week to assess HPA functioning. Results revealed that experiences of maltreatment beginning prior to age 5 were most predictive of depressive symptoms, whereas maltreatment onset after age 5 was most predictive of HPA axis dysregulation (blunted daytime cortisol patterns). Multigenic risk did not relate to HPA functioning, nor did it moderate the relationship between maltreatment and HPA activity. There was no mediation of the relationship between maltreatment and depressive symptoms by HPA dysfunction. Results are interpreted through a developmental psychopathology lens, emphasizing the principle of equifinality while carefully appraising racial differences. Implications for future research, particularly the need for longitudinal studies, and important methodological considerations are discussed.
Racial discrimination and ethnic racial identity in adolescence as modulators of HPA axis activity
Authors: Adam Emma K. , Hittner Emily F. , Thomas Sara E. , Villaume Sarah Collier , Nwafor Ednah E.
Published: January 2021

We review evidence of racial discrimination as a critical and understudied form of adversity that has the potential to impact stress biology, particularly hypothalamic–pituitary–adrenal (HPA) axis activity. We highlight ethnic racial identity (ERI) as a positive regulatory influence on HPA axis activity, as indexed by levels of salivary cortisol. In past research by our group, Black individuals with high adolescent discrimination had low adult cortisol levels (hypocortisolism). Here, we present new analyses showing that ERI, measured prospectively from ages 12 through 32 in 112 Black and white individuals, is related to better-regulated cortisol levels in adulthood, particularly for Black participants. We also describe ongoing research that explores whether the promotion of ERI during adolescence can reduce ethnic–racial disparities in stress biology and in emotional health and academic outcomes.
How developmental neuroscience can help address the problem of child poverty
Authors: Pollak Seth D. , Wolfe Barbara L.
Published: January 2021

Nearly 1 in 5 children in the United States lives in a household whose income is below the official federal poverty line, and more than 40% of children live in poor or near-poor households. Research on the effects of poverty on children's development has been a focus of study for many decades and is now increasing as we accumulate more evidence about the implications of poverty. The American Academy of Pediatrics recently added “Poverty and Child Health” to its Agenda for Children to recognize what has now been established as broad and enduring effects of poverty on child development. A recent addition to the field has been the application of neuroscience-based methods. Various techniques including neuroimaging, neuroendocrinology, cognitive psychophysiology, and epigenetics are beginning to document ways in which early experiences of living in poverty affect infant brain development. We discuss whether there are truly worthwhile reasons for adding neuroscience and related biological methods to study child poverty, and how might these perspectives help guide developmentally based and targeted interventions and policies for these children and their families.
Alpha electroencephalogram (EEG) asymmetry among toddlers in foster care
Authors: Blaisdell Kellyn N. , Barker Tyson V. , Giuliano Ryan J. , Fisher Philip A.
Published: January 2021

The majority of children living in foster care in the United States have a history of maltreatment and/or disrupted caregiving. Maltreatment in early childhood adversely affects development at many levels, including neurobiology and behavior. One neurobiological measure associated with maltreatment is alpha electroencephalogram (EEG) asymmetry. Prior research has found greater right frontal asymmetry among children with a history of maltreatment. However, little research has been extended developmentally downward to examine alpha asymmetry and its behavioral correlates among toddlers in foster care; this was the purpose of the present study. Differences in EEG asymmetry were examined between a sample of foster toddlers (mean age = 3.21 years,n= 38) and a community comparison, low-income sample without a history of foster care (mean age = 3.04 years,n= 16). The toddlers in the foster care group exhibited greater right alpha asymmetry, primarily driven by differences in parietal asymmetry. Neither frontal nor parietal asymmetry were clearly related to internalizing or externalizing behaviors, measured concurrently or at previous time points. These findings reveal differences in alpha EEG asymmetry among toddlers in foster care, and highlight the need to better understand associations between neurobiological and behavioral functioning following early adversity.
Enhancing diurnal cortisol regulation among young children adopted internationally: A randomized controlled trial of a parenting-based intervention
Authors: Raby K. Lee , Bernard Kristin , Gordon M. Kathleen , Dozier Mary
Published: January 2021

Children who have been adopted internationally commonly experience institutional care and other forms of adversity prior to adoption that can alter the functioning of the hypothalamic–pituitary–adrenal (HPA) axis. In particular, internationally adopted children tend to have blunted diurnal declines compared to children raised in their birth families. The Attachment and Biobehavioral Catch-Up (ABC) intervention was developed to enhance young children's biological and behavioral regulation by promoting sensitive parenting. The current study used a randomized controlled trial to assess whether ABC improved the diurnal functioning of the HPA axis among 85 children who had been adopted internationally when they were between the ages of 4 and 33 months (M = 16.12). Prior to the intervention, there were no significant differences in diurnal cortisol production between children whose parents were randomly assigned to receive ABC and children whose parents were randomly assigned to receive a control intervention. After the intervention, children whose parents had received the ABC intervention exhibited steeper declines in cortisol levels throughout the day than children whose parents had received the control intervention. These results indicate that the ABC intervention is effective in enhancing a healthy pattern of diurnal HPA axis regulation for young children who have been adopted internationally.
Environmental determinants of physiological reactivity to stress: The interacting effects of early life deprivation, caregiving quality, and stressful life events
Authors: Wade Mark , Sheridan Margaret A. , Zeanah Charles H. , Fox Nathan A. , Nelson Charles A. , McLaughlin Katie A.
Published: January 2021

Children who spend their early lives in institutions experience profound psychosocial deprivation that is associated with altered stress response system development. Here, we used data from a longitudinal randomized controlled trial of foster care for institutionally reared children to examine whether caregiving quality and stressful life events (SLEs) in early adolescence (age 12) influence patterns of hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system (SNS) reactivity. Controlling for the effect of institutional care, higher caregiving quality at age 12 was associated with heightened cortisol and SNS reactivity. However, moderation analysis revealed that the latter effect was only observed among never-institutionalized children, whereas ever-institutionalized children demonstrated a persistently blunted SNS response regardless of recent caregiving quality. Among institutionally reared children, SLEs interacted with prior random assignment to foster care, such that those placed in foster care early in development had a SNS response that approximated never-institutionalized children when SLEs at age 12 were low. In contrast, SNS reactivity was persistently blunted among those with prolonged deprivation, regardless of recent SLEs. Early-life deprivation is associated with persistent blunting of stress response systems, but normalization may be achievable if SLEs are limited following placement into enriched family-based care.
Maternal antenatal depression and child mental health: Moderation by genomic risk for attention-deficit/hyperactivity disorder
Authors: Chen Lawrence M. , Tollenaar Marieke S. , Hari Dass Shantala A. , Bouvette-Turcot Andrée-Anne , Pokhvisneva Irina , Gaudreau Hélène , Parent Carine , Diorio Josie , McEwen Lisa M. , MacIsaac Julia L. , Kobor Michael S. , Beijers Roseriet , de Weerth Carolina , Silveira Patricia P. , Karama Sherif , Meaney Michael J. , O'Donnell Kieran J. ,   The MAVAN Study Team
Published: January 2021

Maternal antenatal depression strongly influences child mental health but with considerable inter-individual variation that is, in part, linked to genotype. The challenge is to effectively capture the genotypic influence. We outline a novel approach to describe genomic susceptibility to maternal antenatal depression focusing on child emotional/behavioral difficulties. Two cohorts provided measures of maternal depression, child genetic variation, and child mental health symptoms. We constructed a conventional polygenic risk score (PRS) for attention-deficit/hyperactivity disorder (ADHD) (PRSADHD) that significantly moderated the association between maternal antenatal depression and internalizing problems at 60 months (p = 2.94 × 10−4, R2 = .18). We then constructed an interaction PRS (xPRS) based on a subset of those single nucleotide polymorphisms from the PRSADHD that most accounted for the moderation of the association between maternal antenatal depression and child outcome. The interaction between maternal antenatal depression and this xPRS accounted for a larger proportion of the variance in child emotional/behavioral problems than models based on any PRSADHD (p = 5.50 × 10−9, R2 = .27), with similar findings in the replication cohort. The xPRS was significantly enriched for genes involved in neuronal development and synaptic function. Our study illustrates a novel approach to the study of genotypic moderation on the impact of maternal antenatal depression on child mental health and highlights the utility of the xPRS approach. These findings advance our understanding of individual differences in the developmental origins of mental health.
Prenatal maternal psychological distress and fetal developmental trajectories: associations with infant temperament
Authors: Howland Mariann A. , Sandman Curt A. , Davis Elysia Poggi , Glynn Laura M.
Published: January 2021

Associations between prenatal maternal psychological distress and offspring developmental outcomes are well documented, yet relatively little research has examined links between maternal distress and development in utero, prior to postpartum influences. Fetal heart rate (FHR) parameters are established indices of central and autonomic nervous system maturation and function which demonstrate continuity with postnatal outcomes. This prospective, longitudinal study of 149 maternal–fetal pairs evaluated associations between prenatal maternal distress, FHR parameters, and dimensions of infant temperament. Women reported their symptoms of psychological distress at five prenatal visits, and FHR monitoring was conducted at the last three visits. Maternal report of infant temperament was collected at 3 and 6 months of age. Exposure to elevated prenatal maternal psychological distress was associated with higher late-gestation resting mean FHR (FHRM) among female but not male fetuses. Higher late-gestation FHRM was associated with lower infant orienting/regulation and with higher infant negative affectivity, and these associations did not differ by infant sex. A path analysis identified higher FHRM as one pathway by which elevated prenatal maternal distress was associated with lower orienting/regulation among female infants. Findings suggest that, for females, elevated maternal distress alters fetal development, with implications for postnatal function. Results also support the notion that, for both sexes, individual differences in regulation emerge prenatally and are maintained into infancy. Collectively, these findings underscore the utility of direct assessment of development in utero when examining if prenatal experiences are carried forward into postnatal life.
Elevated infant cortisol is necessary but not sufficient for transmission of environmental risk to infant social development: Cross-species evidence of mother–infant physiological social transmission
Authors: Perry Rosemarie E. , Braren Stephen H. , Opendak Maya , Brandes-Aitken Annie , Chopra Divija , Woo Joyce , Sullivan Regina , Blair Clancy ,   Family Life Project Key Investigators
Published: January 2021

Environmental adversity increases child susceptibility to disrupted developmental outcomes, but the mechanisms by which adversity can shape development remain unclear. A translational cross-species approach was used to examine stress-mediated pathways by which poverty-related adversity can influence infant social development. Findings from a longitudinal sample of low-income mother–infant dyads indicated that infant cortisol (CORT) on its own did not mediate relations between early-life scarcity-adversity exposure and later infant behavior in a mother-child interaction task. However, maternal CORT through infant CORT served as a mediating pathway, even when controlling for parenting behavior. Findings using a rodent “scarcity-adversity” model indicated that pharmacologically blocking pup corticosterone (CORT, rodent equivalent to cortisol) in the presence of a stressed mother causally prevented social transmission of scarcity-adversity effects on pup social behavior. Furthermore, pharmacologically increasing pup CORT without the mother present was not sufficient to disrupt pup social behavior. Integration of our cross-species results suggests that elevated infant CORT may be necessary, but without elevated caregiver CORT, may not be sufficient in mediating the effects of environmental adversity on development. These findings underscore the importance of considering infant stress physiology in relation to the broader social context, including caregiver stress physiology, in research and interventional efforts.
Characterizing competence among a high-risk sample of emerging adults: Prospective predictions and biological considerations
Authors: Russotti Justin , Warmingham Jennifer M. , Handley Elizabeth D. , Rogosch Fred A. , Cicchetti Dante
Published: January 2021

Few conditions epitomize severe and chronic stress to a greater extent than child maltreatment, which can derail development across multiple domains of functioning and throughout the life course. Furthermore, child maltreatment tends to co-occur with other adversities, such as poverty. Many individuals grow up under the stressful conditions of these adversities and exhibit developmental competence. The current study prospectively charted the developmental progression of economically disadvantaged maltreated and nonmaltreated children from childhood to emerging adulthood, and examined patterns of competence across multiple developmental domains of functioning central to the period of emerging adulthood. The study investigated childhood precursors to these patterns of adaptation and maladaptation, as well as the physiological cost of these patterns of adaptation (i.e., C-reactive protein; CRP). Latent class analysis revealed four distinct classes of functioning: multifaceted competence across domains (Multifaceted Competence); (multifaceted maladaptation across domains (Multi-Problem); (c) and two classes with mixed patterns of competence and maladaptation (Externalizing Problems and Work/School Impairment). Maltreated individuals were less likely than nonmaltreated individuals to demonstrate patterns of multifaceted competence and more likely to demonstrate aggregate maladaptation across domains. Additionally, Black men who demonstrated a pattern of multifaceted psychosocial competence also evidenced higher levels of low-grade inflammation (indexed by CRP), suggesting physiological distress was associated with adaptation in the context of stress among these individuals. Findings demonstrate the heterogenous patterns of functioning and diverse developmental outcomes that follow early adversity.
Immediate and longitudinal effects of maltreatment on systemic inflammation in young children
Authors: Entringer Sonja , de Punder Karin , Overfeld Judith , Karaboycheva Gergana , Dittrich Katja , Buss Claudia , Winter Sibylle Maria , Binder Elisabeth B. , Heim Christine
Published: January 2021

Exposure to child maltreatment increases the risk for psychiatric and physical diseases. Inflammation has been proposed as a mechanism through which early adverse experiences become biologically embedded. However, most studies providing evidence for the link between early adverse exposures and inflammation have been retrospective or cross-sectional in design, or did not assess inflammation immediately after maltreatment in young children. In the present study we investigated the association between childhood maltreatment and salivary C-reactive protein (CRP) concentrations in a population of N = 173 children, 3–5 years of age, who were recruited in the immediate aftermath of maltreatment and followed-up longitudinally every 6 months over a period of 2 years. We found that the association between maltreatment and CRP concentrations was significantly moderated by child sex, such that in girls, CRP concentrations were higher in the maltreated compared to the control group, and this difference was stable across the 2-year follow-up-period, while in boys, there was no association between maltreatment and CRP. Our findings suggest that the effect of maltreatment on inflammation may already emerge right after exposure at a very young age in girls and manifest over time. Our study provides important evidence for the development of personalized, early interventions strategies targeting the early-life period.
On symmetric wedge mode of an elastic solid
Authors: NAZAROV ALEXANDER , NAZAROV SERGEY , ZAVOROKHIN GERMAN
Published: January 2021

The existence of a symmetric mode in an elastic solid wedge for all admissible values of the Poisson ratio and arbitrary interior angles close to π has been proven.
Variation in outcomes of the Melbourne Infant, Feeding, Activity and Nutrition Trial (INFANT) according to maternal education and age 2 and 3·5 years post-intervention
Authors: Delisle Nyström Christine , Cameron Adrian J , Campbell Karen J , Hesketh Kylie D
Published: January 2021

Objective:

This study aimed to assess whether the long-term effectiveness of the Melbourne Infant, Feeding, Activity and Nutrition Trial (INFANT) at 2 and 3·5 years post-intervention varied according to maternal education and age.

Design:

Two and 3·5 years post-intervention follow-up of the INFANT cluster-randomised controlled trial. Outcomes at both follow-ups included children’s BMI z-scores, physical activity (ActiGraph), television viewing (parental report) and dietary intake (3 × 24-h dietary recalls). Dichotomous moderator variables included maternal education (university v. no university) and age (< 32 v. ≥ 32 years).

Setting:

Population based.

Participants:

Families completing the 15-month programme (n 492) were invited to participate in the follow-ups when their child was 3·6 and 5 years old.

Results:

At the 2-year follow-up, the intervention effects on vegetable (positive) and sweet snack (negative) intake were greater in children with higher educated mothers, whereas water consumption (positive) was greater in children with lower educated mothers. At the 2-year follow-up, the intervention was more effective in increasing water consumption in children with younger mothers and decreasing sweet snack intake in children with older mothers (opposite result observed at the 3·5-year follow-up). At the 3·5-year follow-up, children with younger and older mothers increased and decreased their consumption of savoury snacks, respectively.

Conclusions:

Moderation by maternal education and age were observed for some outcomes; however, clear patterns were not evident at both follow-ups, with little consistency across outcomes. This indicates that INFANT was more-or-less equally effective in children irrespective of their mother’s education level or age, which is important in community-based interventions.
A systematic review of interventions to increase breakfast consumption: a socio-cognitive perspective
Authors: Harris Jessica A , Carins Julia E , Rundle-Thiele Sharyn
Published: January 2021

Objective:

Regular breakfast skipping is related to unhealthy dietary behaviours, such as consuming an overall poorer quality diet and lower rates of physical activity, both of which are linked to a higher BMI. Adolescent breakfast skippers struggle with mental focus, sleep issues and lower grades. Solutions that can be implemented to overcome breakfast skipping are needed.

Design:

A systematic literature review was undertaken to identify programmes that aimed to increase breakfast eating. Following the PRISMA framework, studies were sourced to examine details of behaviour change, evidence of theory use and other important programme learnings and outcomes.

Setting:

Breakfast consumption empirical studies published from 2000 onwards.

Participants:

Nineteen empirical studies that aimed to improve breakfast eating behaviour.

Results:

Out of the nineteen studies examined, ten studies reported an increase in breakfast consumption frequency for the entire study group or subgroups. Seven studies found no change, one was inconclusive and one observed a decrease in breakfast frequency. Positive changes to the dietary quality of breakfast were observed in five of the studies that did not observe increased frequency of breakfast consumption. Only six studies reported using theory in the intervention.

Conclusions:

This evidence review points needed to extend theory application to establish a reliable evidence base that can be followed by practitioners seeking to increase breakfast eating rates in their target population.
Effects of salinity stress on proline content and expression ofΔ1-pyrroline-5-carboxylate synthaseandvacuolar-type H+subunit Egenes in wheat
Authors: Goharrizi Kiarash Jamshidi , Baghizadeh Amin , Afroushteh Malihe , Amirmahani Farzane , Kermani Sepideh Ghotbzadeh
Published: January 2021

To evaluate the responses of some important agronomic traits of 14 bread wheat cultivars, a split plot experiment was conducted based on a randomized complete block design under non-stress, moderate and severe salinity stress conditions. In this study, Backcross and Roshan were identified as the most salinity-tolerant cultivars, while Mihan and Shirudi were considered as the most salinity-sensitive cultivars. The proline content, as well asΔ1-pyrroline-5-carboxylate synthase(P5CS) andvacuolar-type H+-ATPase subunit E(W36) gene expression levels, were examined in these cultivars under normal, moderate and high salinity stress conditions. The proline content andP5CSgene expression level increased with a rise in NaCl concentration. Further, a direct relationship was observed between the proline content andP5CSgene expression in all samples. Our results showed thatW36gene expression in Backcross and Roshan cultivars, as the most resistant ones, strongly increased with elevation of the NaCl concentrations. On the other hand, in the sensitive cultivars such as Mihan and Shirudi, small changes were observed in the gene expression levels with rising salinity levels. Additionally, Backcross and Roshan cultivars had the highest proline content as well asP5CSandW36genes expression levels under moderate and high salinity stress levels.
Validation of Morality as Cooperation Questionnaire in Turkey, and	Its Relation to Prosociality, Ideology, and Resource Scarcity
Authors: Yilmaz Onurcan , Harma Mehmet , Doğruyol Burak
Published: January 2021

Abstract. The theory of morality as cooperation (MAC) argues that there are seven distinct and evolved universal moral foundations. Curry, Chesters, and Van Lissa (2019) developed a scale to test this theoretical approach and showed that the Relevance subscale of the MAC questionnaire (MAC-Q) fits data well, unlike the Judgment and full-form. However, an independent test of the validity of this questionnaire has not been hitherto conducted, and its relation with ideology is unknown. In the first study, we attempted to validate the Turkish form of MAC-Q and then examined the relationship with prosociality and political ideology. The results showed that the fit indices of MAC-Q Relevance are above the standard criteria, unlike the Judgment and full form ( n = 445), and significant relationships with prosociality and political ideology provided additional evidence for the validity. We used the MAC-Q Relevance in Study 2 ( n = 576, Turkey) and Study 3 ( n = 921, US), and investigated whether manipulating resource scarcity influences the endorsement of MAC. Although there was no effect of the manipulation, correlational findings provided some support for the predictive validity of MAC-Q. Overall, MAC-Q Relevance performs well in representing the lay notions of morality in both Turkey and the US, unlike full-form.
Freshened Groundwater in the Sub-seafloor
Authors: Micallef Aaron
Published: January 2021

Scientists are using a variety of geochemical, geophysical, and numerical methods to study offshore freshened groundwater and better understand its role in the global water cycle.
Metabolic activities affect femur and lumbar vertebrae remodeling, and anti-resorptive risedronate disturbs femoral cortical bone remodeling
Authors: Kim Mi Yeong , Lee Kyunghee , Shin Hong-In , Lee Kyung-Jae , Jeong Daewon
Published: January 2021

Metabolic activities are closely correlated with bone remodeling and long-term anti-resorptive bisphosphonate treatment frequently causes atypical femoral fractures through unclear mechanisms. To explore whether metabolic alterations affect bone remodeling in femurs and lumbar vertebrae and whether anti-osteoporotic bisphosphonates perturb their reconstruction, we studied three mouse strains with different fat and lean body masses (BALB/c, C57BL6, and C3H mice). These mice displayed variable physical activity, food and drink intake, energy expenditure, and respiratory quotients. Following intraperitoneal calcein injection, double calcein labeling of the femoral diaphysis, as well as serum levels of the bone-formation marker procollagen type-I N-terminal propeptide and the bone-resorption marker C-terminal telopeptide of type-I collagen, revealed increased bone turnover in mice in the following order: C3H > BALB/c ≥ C57BL6 mice. In addition, bone reconstitution in femurs was distinct from that in lumbar vertebrae in both healthy control and estrogen-deficient osteoporotic mice with metabolic perturbation, particularly in terms of femoral trabecular and cortical bone remodeling in CH3 mice. Interestingly, subcutaneous administration of bisphosphonate risedronate to C3H mice with normal femoral bone density led to enlarged femoral cortical bones with a low bone mineral density, resulting in bone fragility; however, this phenomenon was not observed in mice with ovariectomy-induced femoral cortical bone loss. Together, these results suggest that diverse metabolic activities support various forms of bone remodeling and that femur remodeling differs from lumbar vertebra remodeling. Moreover, our findings imply that the adverse effect of bisphosphonate agents on femoral cortical bone remodeling should be considered when prescribing them to osteoporotic patients.
Role of FMRP in rapid antidepressant effects and synapse regulation
Authors: Heaney Chelcie F. , Namjoshi Sanjeev V. , Uneri Ayse , Bach Eva C. , Weiner Jeffrey L. , Raab-Graham Kimberly F.
Published: January 2021

Rapid antidepressants are novel treatments for major depressive disorder (MDD) and work by blocking N-methyl-D-aspartate receptors (NMDARs), which, in turn, activate the protein synthesis pathway regulated by mechanistic/mammalian target of rapamycin complex 1 (mTORC1). Our recent work demonstrates that the RNA-binding protein Fragile X Mental Retardation Protein (FMRP) is downregulated in dendrites upon treatment with a rapid antidepressant. Here, we show that the behavioral effects of the rapid antidepressant Ro-25-6981 require FMRP expression, and treatment promotes differential mRNA binding to FMRP in an mTORC1-dependent manner. Further, these mRNAs are identified to regulate transsynaptic signaling. Using a novel technique, we show that synapse formation underlying the behavioral effects of Ro-25-6981 requires GABABR-mediated mTORC1 activity in WT animals. Finally, we demonstrate that in an animal model that lacks FMRP expression and has clinical relevance for Fragile X Syndrome (FXS), GABABR activity is detrimental to the effects of Ro-25-6981. These effects are rescued with the combined therapy of blocking GABABRs and NMDARs, indicating that rapid antidepressants alone may not be an effective treatment for people with comorbid FXS and MDD.
Involvement of the nuclear factor-κB transcriptional complex in prefrontal cortex immune activation in bipolar disorder
Authors: Roman Kaitlyn M. , Jenkins Aaron K. , Lewis David A. , Volk David W.
Published: January 2021

Bipolar disorder and schizophrenia have multiple clinical and genetic features in common, including shared risk associated with overlapping susceptibility loci in immune-related genes. Higher activity of the nuclear factor-κB (NF-κB) transcription factor complex, which regulates the transcription of multiple immune markers, has been reported to contribute to immune activation in the prefrontal cortex in schizophrenia. These findings suggest the hypothesis that elevated NF-κB activity is present in the prefrontal cortex in bipolar disorder in a manner similar to that seen in schizophrenia. Therefore, we quantified levels of NF-κB-related mRNAs in the prefrontal cortex of 35 matched pairs of bipolar disorder and unaffected comparison subjects using quantitative PCR. We found that transcript levels were higher in the prefrontal cortex of bipolar disorder subjects for several NF-κB family members, NF-κB activation receptors, and NF-κB-regulated mRNAs, and were lower for an NF-κB inhibitor. Transcript levels for NF-κB family members, NF-κB activation receptors, and NF-κB-regulated mRNAs levels were also highly correlated with each other. This pattern of elevated transcript levels for NF-κB-related markers in bipolar disorder is similar to that previously reported in schizophrenia, suggesting that cortical immune activation is a shared pathophysiological feature between the two disorders.
Sensory over-responsivity is related to GABAergic inhibition in thalamocortical circuits
Authors: Wood Emily T. , Cummings Kaitlin K. , Jung Jiwon , Patterson Genevieve , Okada Nana , Guo Jia , O’Neill Joseph , Dapretto Mirella , Bookheimer Susan Y. , Green Shulamite A.
Published: January 2021

Sensory over-responsivity (SOR), extreme sensitivity to or avoidance of sensory stimuli (e.g., scratchy fabrics, loud sounds), is a highly prevalent and impairing feature of neurodevelopmental disorders such as autism spectrum disorders (ASD), anxiety, and ADHD. Previous studies have found overactive brain responses and reduced modulation of thalamocortical connectivity in response to mildly aversive sensory stimulation in ASD. These findings suggest altered thalamic sensory gating which could be associated with an excitatory/inhibitory neurochemical imbalance, but such thalamic neurochemistry has never been examined in relation to SOR. Here we utilized magnetic resonance spectroscopy and resting-state functional magnetic resonance imaging to examine the relationship between thalamic and somatosensory cortex inhibitory (gamma-aminobutyric acid, GABA) and excitatory (glutamate) neurochemicals with the intrinsic functional connectivity of those regions in 35 ASD and 35 typically developing pediatric subjects. Although there were no diagnostic group differences in neurochemical concentrations in either region, within the ASD group, SOR severity correlated negatively with thalamic GABA (r = −0.48, p < 0.05) and positively with somatosensory glutamate (r = 0.68, p < 0.01). Further, in the ASD group, thalamic GABA concentration predicted altered connectivity with regions previously implicated in SOR. These variations in GABA and associated network connectivity in the ASD group highlight the potential role of GABA as a mechanism underlying individual differences in SOR, a major source of phenotypic heterogeneity in ASD. In ASD, abnormalities of the thalamic neurochemical balance could interfere with the thalamic role in integrating, relaying, and inhibiting attention to sensory information. These results have implications for future research and GABA-modulating pharmacologic interventions.
Structure, function, and pathology of protein O-glucosyltransferases
Authors: Mehboob Muhammad Zubair , Lang Minglin
Published: January 2021

Protein O-glucosylation is a crucial form of O-glycosylation, which involves glucose (Glc) addition to a serine residue within a consensus sequence of epidermal growth factor epidermal growth factor (EGF)-like repeats found in several proteins, including Notch. Glc provides stability to EGF-like repeats, is required for S2 cleavage of Notch, and serves to regulate the trafficking of Notch, crumbs2, and Eyes shut proteins to the cell surface. Genetic and biochemical studies have shown a link between aberrant protein O-glucosylation and human diseases. The main players of protein O-glucosylation, protein O-glucosyltransferases (POGLUTs), use uridine diphosphate (UDP)-Glc as a substrate to modify EGF repeats and reside in the endoplasmic reticulum via C-terminal KDEL-like signals. In addition to O-glucosylation activity, POGLUTs can also perform protein O-xylosylation function, i.e., adding xylose (Xyl) from UDP-Xyl; however, both activities rely on residues of EGF repeats, active-site conformations of POGLUTs and sugar substrate concentrations in the ER. Impaired expression of POGLUTs has been associated with initiation and progression of human diseases such as limb-girdle muscular dystrophy, Dowling–Degos disease 4, acute myeloid leukemia, and hepatocytes and pancreatic dysfunction. POGLUTs have been found to alter the expression of cyclin-dependent kinase inhibitors (CDKIs), by affecting Notch or transforming growth factor-β1 signaling, and cause cell proliferation inhibition or induction depending on the particular cell types, which characterizes POGLUT’s cell-dependent dual role. Except for a few downstream elements, the precise mechanisms whereby aberrant protein O-glucosylation causes diseases are largely unknown, leaving behind many questions that need to be addressed. This systemic review comprehensively covers literature to understand the O-glucosyltransferases with a focus on POGLUT1 structure and function, and their role in health and diseases. Moreover, this study also raises unanswered issues for future research in cancer biology, cell communications, muscular diseases, etc.
DHA/AA alleviates LPS-induced Kupffer cells pyroptosis via GPR120 interaction with NLRP3 to inhibit inflammasome complexes assembly
Authors: Fan Guoqiang , Li Yanfei , Chen Jinglong , Zong Yibo , Yang Xiaojing
Published: January 2021

Pyroptosis is a novel type of programmed cell death associated with the pathogenesis of many inflammatory diseases. Docosahexaenoic acid (DHA) and Arachidonic acid (AA) is widely involved in inflammatory pathological processes. However, the effect and mechanism of DHA and AA on pyroptosis in Kupffer cells are poorly understood. The present study demonstrated that DHA and AA ameliorated lipopolysaccharide (LPS)-induced Kupffer cells pyroptosis by reversing the increased expression of NLRP3 inflammasome complex, GSDMD, IL-1β, IL-18, and PI-stained positive rate. Next, the study revealed that GPR120 silencing eliminated the anti-pyroptosis of DHA and AA in LPS-induced Kupffer cells, suggesting that DHA and AA exerted their effect through GPR120 signaling. Importantly, GPR120 endocytose and binds to NLRP3 under LPS stimulation. Furthermore, co-immunoprecipitation showed that DHA and AA promoted the interaction between GPR120 and NLRP3 in LPS-exposed Kupffer cells, thus inhibiting the self-assembly of NLRP3 inflammasome complex. Finally, the study verified that DHA and AA alleviated hepatic injury through inhibiting Kupffer cells pyroptosis in vivo. The findings indicated that DHA and AA alleviated LPS-induced Kupffer cells pyroptosis via GPR120 interaction with NLRP3, it might become a potential therapeutic approach hepatic injury.
SRPS associated protein WDR60 regulates the multipolar-to-bipolar transition of migrating neurons during cortical development
Authors: Li Cui , Zheng Yu , Zheng Yufang , Xu Zhiheng
Published: January 2021

Mutations of WD40 repeat domain 60 (WDR60) have been identified in short-rib polydactyly syndromes (SRPS I–V), a group of lethal congenital disorders characterized by short ribs, polydactyly, and a range of extraskeletal phenotypes. However, the underlying mechanism is still unclear. Here, we report that WDR60 is essential for embryonic development and plays a critical role in the multipolar-bipolar transition and migration of newborn neurons during brain development. Mechanically, we found that WDR60 was located at the microtubule-organizing center to control microtubule organization and possibly, the trafficking of cellular components. Importantly, the migration defect caused by Wdr60 knockdown could be rescued by the stable form of α-Tubulin, α-TubulinK40Q (an acetylation-mimicking mutant). These findings identified a non-cilia function of WDR60 and provided insight into its biological function, as well as the pathogenesis of WDR60 deficiency associated with SRPS.
SIRT6 promotes angiogenesis and hemorrhage of carotid plaque via regulating HIF-1α and reactive oxygen species
Authors: Yang Zhou , Huang Yijun , Zhu Lei , Yang Kai , Liang Kun , Tan Jinyun , Yu Bo
Published: January 2021

As a member of Sirtuins family, SIRT6 participates in the physiological and pathological progress of DNA repair, anti-aging, metabolism, and so on. Several studies have demonstrated that knockdown of SIRT6 inhibited the development of atherosclerosis (AS), indicated SIRT6 as a protective factor for AS. However, we confirmed SIRT6 was significantly overexpressed in human unstable carotid plaques compared with stable carotid plaques. This result indicated a more complex role of SIRT6 in AS. Furthermore, we constructed mice model with unstable carotid plaque and injected them with SIRT6 overexpressed adeno-associated virus (AAV-SIRT6). AAV-SIRT6 significantly promoted angiogenesis as well as hemorrhage in plaques. In vitro, we demonstrated overexpression of SIRT6 prevented HIF-1α from degradation by deubiquitination at K37 and K532 of HIF-1α, thus promoted the expression of HIF-1α under both normoxia and hypoxia in human umbilical vein endothelial cells (HUVECs). Through regulating HIF-1α, overexpression of SIRT6 promoted invasion, migration, proliferation, as well as tube formation ability of HUVECs. Interestingly, under different conditions, SIRT6 played different roles in the function of HUVECs. Under oxidative stress, another important pathological environment for AS, SIRT6 bound to the promoter of Catalase, a main reactive oxygen species scavenger, and depleted H3K56 acetylation, thus inhibited expression and activity of Catalase at the transcriptional level. Subsequently, inhibited Catalase promoted reactive oxygen species (ROS) under oxidative stress. Accumulated ROS further aggravated oxidative stress injury of HUVECs. On one hand, SIRT6 promoted angiogenesis in plaque via HIF-1α under hypoxia. On the other hand, SIRT6 promoted injury of neovascular via ROS under oxidative stress. It is this process of continuous growth and damage that leads to hemorrhage in carotid plaque. In conclusion, we innovatively confirmed SIRT6 promoted the angiogenesis and IPH via promoting HIF-1α and ROS in different environments, thus disclosed the unknowing danger of SIRT6.