Common Environmental Factors Research Articles

Common genetic factors for uncontrolled eating mechanisms.

Reward-based eating drives are putative mechanisms of uncontrolled eating implicated in obesity and disordered eating (e.g., binge eating). Uncovering the genetic and environmental contributions to reward-related eating, and their genetic correlation with BMI, could shed light on key mechanisms underlying eating and weight-related disorders. We conducted a classical twin study to examine how much variance in uncontrolled eating phenotypes and body mass index (BMI) was explained by genetic factors, and the extent that these phenotypes shared common genetic factors. 353 monozygotic twins and 128 dizygotic twins completed the Reward-based Eating Drive 13 scale, which measures three distinct uncontrolled eating phenotypes (loss of control over eating, preoccupation with thoughts about food, and lack of satiety), and a demographic questionnaire which included height and weight for BMI calculation. We estimated additive genetic (A), common environmental (C), and unique environmental (E) factors for each phenotype, as well as their genetic correlations, with a multivariate ACE model. A common pathway model also estimated whether genetic variance in the uncontrolled eating phenotypes was better explained by a common latent uncontrolled eating factor. There were moderate genetic correlations between uncontrolled eating phenotypes and BMI (.26-.41). Variance from the uncontrolled eating phenotypes was also best explained by a common latent uncontrolled eating factor that was explained by additive genetic factors (52%). These results suggest that uncontrolled eating phenotypes are heritable traits that also share genetic variance with BMI. This has implications for understanding the cognitive mechanisms that underpin obesity and disordered eating. Our study clarifies the degree to which uncontrolled eating phenotypes and BMI are influenced by shared genetics and shows that vulnerability to uncontrolled eating traits is impacted by common genetic factors.

The Influence of Genetic and Environmental Factors on Anxiety among Chinese Adolescents: A Twin Study

This study explored the influence of genetic and environmental factors on adolescent anxiety. Ninety-eight monozygotic and dizygotic twins from Chongqing, China (aged 15–18 years) were assessed for anxiety with the Self-Rating Anxiety Scale (SAS). The Parenting Styles and Dimensions Questionnaire (PSDQ) and Strengths and Difficulties Questionnaire (SDQ) were applied to assess environmental factors. Venous blood was drawn from the twins for zygosity determination. Structural equation modeling was performed to evaluate the effects of additive genetic factors (A), common environmental factors (C), and individual-specific environmental factors (E) on adolescent anxiety. The estimates of A and E on adolescent anxiety were 0.34 (95% CI = 0.12–0.53) and 0.66 (95% CI:0.47–0.89), respectively. The environment played an important role in adolescent anxiety. Adolescent anxiety was significantly positively correlated with peer relations (r = 0.606, p < 0.05) and negatively correlated with prosocial behavior (r = 0.207, p < 0. 05). No sex differences were observed. Adolescent anxiety was influenced by both genetic and environmental factors. The individual-specific environmental factors played an important role. Consideration of these variables will facilitate the targeted and individualized implementation of specific interventions for adolescent anxiety.

Genetic and environmental influence on alcohol intent and alcohol sips among U.S. children-Effects across sex, race, and ethnicity.

Alcohol intent (the susceptibility to initiating alcohol use) and alcohol sips (the initiation of alcohol) in youth are a multifactorial puzzle with many components. This research aims to examine the connection between genetic and environmental factors across sex, race and ethnicity. Data was obtained from the twin hub of the Adolescent Brain Cognitive Development (ABCD) study at baseline (2016-2018). Variance component models were conducted to dissect the additive genetic (A), common (C) and unique environmental (E) effects on alcohol traits. The proportion of the total alcohol phenotypic variation attributable to additive genetic factors is reported as heritability (h2). The sample (n = 1,772) included an approximately equal male-female distribution. The 886 same-sex twin pairs were 60.4% dizygotic (DZ), 39.6% monozygotic (MZ), 65.4% non-Hispanic Whites, 13.9% non-Hispanic Blacks, 10.8% of Hispanics with a mean age of 121.2 months. Overall, genetic predisposition was moderate for alcohol intent (h2 = 28%, p = .006) and low for alcohol initiation (h2 = 4%, p = 0.83). Hispanics (h2 = 53%, p < .0001) and Blacks (h2 = 48%, p < .0001) demonstrated higher alcohol intent due to additive genetic factors than Whites (h2 = 34%, p < .0001). Common environmental factors explained more variation in alcohol sips in females (c2 = 63%, p = .001) than in males (c2 = 55%, p = .003). Unique environmental factors largely attributed to alcohol intent, while common environmental factors explained the substantial variation in alcohol initiation. Sex and racial/ethnic disparities in genetic and environmental risk factors for susceptibility to alcohol initiation can lead to significant health disparities. Certain populations may be at greater risk for alcohol use due to their genetic and ecological factors at an early age.

Investigating pedigree- and SNP-associated components of heritability in a wild population of Soay sheep

Estimates of narrow sense heritability derived from genomic data that contain related individuals may be biased due to the within-family effects such as dominance, epistasis and common environmental factors. However, for many wild populations, removal of related individuals from the data would result in small sample sizes. In 2013, Zaitlen et al. proposed a method to estimate heritability in populations that include close relatives by simultaneously fitting an identity-by-state (IBS) genomic relatedness matrix (GRM) and an identity-by-descent (IBD) GRM. The IBD GRM is identical to the IBS GRM, except relatedness estimates below a specified threshold are set to 0. We applied this method to a sample of 8557 wild Soay sheep from St. Kilda, with genotypic information for 419,281 single nucleotide polymorphisms. We aimed to see how this method would partition heritability into population-level (IBS) and family-associated (IBD) variance for a range of genetic architectures, and so we focused on a mixture of polygenic and monogenic traits. We also implemented a variant of the model in which the IBD GRM was replaced by a GRM constructed from SNPs with low minor allele frequency to examine whether any additive genetic variance is captured by rare alleles. Whilst the inclusion of the IBD GRM did not significantly improve the fit of the model for the monogenic traits, it improved the fit for some of the polygenic traits, suggesting that dominance, epistasis and/or common environment not already captured by the non-genetic random effects fitted in our models may influence these traits.

Prevalence of common mental disorders and treatment gap among patients with non-communicable diseases in the rural areas of East India.

Mental and physical non-communicable diseases (NCDs) coexist, because they share common environmental and behavioral risk factors. The treatment gap for common mental disorders, such as depression, anxiety, and substance use, is large compared to other NCDs. To determine the prevalence and treatment gap of common mental disorders among patients with non-communicable diseases. The community-based cross-sectional study was conducted in the rural parts of East India, in people aged 30years and older with NCDs. A simple random sample was chosen to select the villages and participants. Eligible participants administered with screening and diagnostic questionnaire for depression, anxiety, and substance use. Those diagnosed with mental disorders were again assessed for treatment status in the last 12months. Non-receipt of treatment was considered as treatment gap. A total of 515 participants were included in the analysis. The overall prevalence of common mental disorders among the study population was 46.4% (95% CI 42.0-50.8), and excluding substance use, the prevalence was 11.7% (95% CI 9.0-14.7). The treatment gap for common mental disorders among patients with non-communicable diseases, including and excluding substance use, was 98.3% (95% CI 95.8-99.5) and 93.3% (95% CI 83.8-98.2), respectively. The prevalence and treatment gap of common mental disorders among persons with NCDs was high. Public health interventions need to be emphasized for the integration of mental health care into NCD care.

Dietary N-carbamylglutamate (NCG) supplementation improves the survival, digestive and immunological parameters by promoting ammonia excretion in Chinese mitten crab (Eriocheir sinensis), under ammonia nitrogen stress

Ammonia nitrogen is one of the most common environmental stress factors in aquaculture. The aim of this experiment was to evaluate the effects of ammonia nitrogen stress on ammonia metabolism, digestion and immune function as well as the protective effects of dietary N-carbamylglutamate (NCG) in the Chinese mitten crab (Eriocheir sinensis). Two feeds were used, namely a control feed (regular commercial feed) and an NCG feed (NCG (302.96 ± 4.07) mg/kg added). Subsequently, animals fed by these two feeds were exposed to 30 mg/L or 60 mg/L ammonia nitrogen stress (named A30 or A60) for 21 days, respectively. The rate of hemolymph ammonia excretion was significantly increased in NCG group compared to C (control) group (P < 0.05). Hemolymph ammonia levels were significantly lower in NCG A30 (NCG feed and A30) and NCG A60 (NCG feed and A60) groups compared to A30 (control feed and A30) and A60 (control feed and A60) groups (P < 0.05). Glutamate dehydrogenase and glutamine synthetase activities in the gills and hepatopancreas of NCG A60 group were significantly increased compared with the A60 group, which promoted glutamine synthesis (P < 0.05). The cumulative mortality rate of Eriocheir sinensis in NCG A30 and NCG A60 groups were effectively reduced (P < 0.05). The arginine levels of hepatopancreas were significantly increased in NCG A60 group (P < 0.05). Under ammonia nitrogen stress, NCG significantly increased the activities of trypsin, pepsin, lipase and α-Amylase in NCG feed group, and promoted feeding (P < 0.05). In hemolymph, hepatopancreas and intestine, NCG significantly increased nitric oxide synthase activity, lysozyme and phenol oxidase activities compared to the ammonia nitrogen stress group (P < 0.05). The results indicated that, NCG added in feed could decelerate the toxic effects of ammonia on Eriocheir sinensis by promoting ammonia excretion and accelerating glutamine and endogenous arginine synthesis by metabolism. Moreover, the activity of digestive enzymes and immune-related enzymes is improved.

Agronomical Performances of Gajah Mungkur Mutant Rice Varieties Under Drought Stress

The productivity of the rice plant is commonly influenced by both genotype and environmental factors. One common environmental factor that leads to harvest failure is drought, often caused by low rainfall. Therefore, the development of drought-tolerant varieties should be implemented to obtain optimum productivity under an unfavorable environment. One of the canonical approaches for achieving this is genetic manipulation, such as by gamma radiation-induced mutation. This study aimed to determine the drought tolerance and quantitative characteristics of mutant rice varieties generated from gamma radiation. The methodology used was a split-plot design with two factors, including drought as the first factor consisting of three groups namely control, mid-level, and high-level. The second factor was rice genotypes, which consisted of six genotypes comprising PMG 07/PsJ, PMG 08/ PsJ, and PMG 09/ PsJ (mutant varieties), Gajah Mungkur (parental background), Limboto (drought-tolerant), and IR 20 (drought-susceptible). The data were statistically examined using Analysis of Variance (ANOVA) and further analyzed with Duncan’s Multiple Range Test (DMRT) with a significance level of 5%. The results showed that high-level drought significantly affected plant height during both the vegetative and mature stages. Among the mutants, PMG 08/PsJ exhibited better vegetative growth under dry conditions, retaining a relatively higher height. Drought also had a negative impact on the number of tillers and productive tillers. The PMG 08/PsJ mutant had a slightly higher number of tillers under drought cultivations. On the other hand, PMG 09/PsJ was found to have a relatively more filled grain number per panicle. Leaf rolling and dryness index showed similar trends in all varieties, while drought treatments imposed a delay on the flowering and harvesting age. Although the results demonstrated no substantial improvement over the parental lines, the selected mutant lines provided several beneficial agronomical features such as maintenance of plant height, tiller number, and shorter life cycles under severe drought. These characteristics could serve as valuable genetic resources for breeding programs focused on developing drought-resistant rice varieties for challenging environments.

P211 Impact of celiac disease on the outcome of Inflammatory Bowel Disease

Abstract Background Inflammatory bowel disease (IBD) and celiac disease (CeD) are digestive disorders that share common genetic, immunological, and environmental factors in their pathogenesis. Objective To investigate whether the concurrent diagnosis of CeD and IBD predisposes to a more aggressive phenotype of IBD. Methods A multicenter case-control study was performed including cases (celiac IBD) and controls (non-celiac IBD) (paired 1:2, matched for sex, year of diagnosis, and IBD type). CeD diagnosis was established if Marsh score was &amp;gt; 1. Disease phenotype and IBD outcomes, including mortality and neoplasm development, were ascertained from medical records. Results 66 patients with celiac IBD (39 females; 30 ulcerative colitis-UC/6 indeterminate colitis-IC/30 Crohn disease-CD; age at diagnosis 30±14 years) and 132 matched non-celiac IBD patients (85 females; 68 UC/4 IC/60 CD; age at diagnosis 32±14 years) were included. The diagnosis of CeD was confirmed by gastroscopy and duodenal biopsy in 97% of cases, and the most common histological lesion was Marsh 3. Overall, there were no significant differences in the duration of IBD (median 11±8 years vs 9±8 years; p=0.81), IBD extension (UC (E1/E2/E3): 6 (20.7%)/14 (48.3%)/9 (31%) vs 19 (29.2%)/22 (33.8%)/24 (36.9%); p=0.39); CD (L1/L2/L3/L4): 17 (56.7%)/3 (10%)/8 (26.7%)/2 (6.7%) vs 27 (45%)/6 (10%)/23 (38.3%)/4 (6.4%); p=0.71), extra-intestinal manifestations (10 (15,2%) vs 20 (12,8%); p=0.96) and other autoimmune diseases (8 (12%) vs 16 (12.1%); p=1) between celiac and non-celiac IBD, respectively. In terms of disease outcome, no differences were found either globally or by IBD subtype in terms of perianal disease, use of mesalamine, exposure to immunomodulators, receipt of biologic agents, need for IBD surgery, and development of neoplasm during follow-up (Table 1). There was no mortality in any of the cohorts. Conclusion No significant differences in disease outcome were observed in patients with a concurrent diagnosis of CeD and IBD compared with non-celiac IBD patients. In our large multicenter cohort of patients with celiac IBD and IBD controls, coexisting CeD did not show an impact on the natural history of IBD.

Trends and Age-Period-Cohort Effect on Incidence of Male Breast Cancer from 1980 to 2019 in Taiwan and the USA.

Although male breast cancer (MBC) is globally rare, its incidence significantly increased from 1990 to 2017. The aim of this study was to examine variations in the trends of MBC incidence between populations in Taiwan and the USA from 1980 to 2019. The Taiwan Cancer Registry database and the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute of the USA were used. The age-standardized incidence rate was calculated using the world standard population in 2000. The long-term trends of the age, time period, and birth cohort effect on MBC incidence rates were estimated using the SEER Age-Period-Cohort Web Tool. The results revealed that the incidence of MBC in both countries increased from 2010 to 2019 (Taiwan: average annual percentage change (AAPC) = 2.59%; USA: AAPC = 0.64%). The age and period effects on the incidence rates in both countries strengthened, but the cohort effect was only identified in Taiwan (Rate ratio: 4.03). The identified cohort effect in this study bears resemblance to that noted in a previous investigation on female breast cancer in Taiwan. This suggests the possible presence of common environmental factors influencing breast cancer incidence in both genders, such as a high fat diet and xenoestrogen.

Cutaneous Oncology: Strategies for Melanoma Prevention, Diagnosis, and Therapy.

Skin cancer comprises one-third of all diagnosed cancer cases and remains a major health concern. Genetic and environmental parameters serve as the two main risk factors associated with the development of skin cancer, with ultraviolet radiation being the most common environmental risk factor. Studies have also found fair complexion, arsenic toxicity, indoor tanning, and family history among the prevailing causes of skin cancer. Prevention and early diagnosis play a crucial role in reducing the frequency and ensuring effective management of skin cancer. Recent studies have focused on exploring minimally invasive or non-invasive diagnostic technologies along with artificial intelligence to facilitate rapid and accurate diagnosis. The treatment of skin cancer ranges from traditional surgical excision to various advanced methods such as phototherapy, radiotherapy, immunotherapy, targeted therapy, and combination therapy. Recent studies have focused on immunotherapy, with the introduction of new checkpoint inhibitors and personalized immunotherapy enhancing treatment efficacy. Advancements in multi-omics, nanotechnology, and artificial intelligence have further deepened the understanding of the mechanisms underlying tumoral growth and their interaction with therapeutic effects, which has paved the way for precision oncology. This review aims to highlight the recent advancements in the understanding and management of skin cancer, and provide an overview of existing and emerging diagnostic, prognostic, and therapeutic modalities, while highlighting areas that require further research to bridge the existing knowledge gaps.

Association between active and passive smoking and the clinical course of multiple sclerosis and neuromyelitis optica spectrum disorder

&lt;i&gt;Objective&lt;/i&gt;: Active and passive smoking are common environmental risk factors, but there is no definite conclusion about their effects on relapse and disability progression in multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). &lt;i&gt;Methods&lt;/i&gt;: This was a retrospective cohort study. Patients were included from four centers. Demographic and clinical data were extracted from the clinical database, while data involving environmental exposures during daily life, relapse, and disability progression were obtained through telephone follow-up interviews. Determinants of relapse were assessed by Cox proportional models, and disability progression was assessed by linear regression. Kaplan‒Meier survival was used to estimate relapse within five years after the first attack. &lt;i&gt;Results&lt;/i&gt;: A total of 130 MS patients and 318 NMOSD patients were included in this study, and females accounted for 60% and 79.6%, respectively. MS patients with an active smoking history had a higher risk of relapse, for which the association became borderline significant after accounting for covariates (aHR=1.52, 95% CI=1.00, 2.31; &lt;i&gt;p&lt;/i&gt;=0.052). The relapse risk between ever-smokers who smoked more than 10 cigarettes per day and smokers who smoked less than 10 cigarettes per day was not significantly different (aHR=0.96, 95% CI=0.63, 1.47; &lt;i&gt;p&lt;/i&gt;=0.859). However, exposure to passive smoking was associated with a reduced risk of MS relapse (aHR=0.75, 95% CI=0.56, 1.00; &lt;i&gt;p&lt;/i&gt;=0.044) compared with never-exposed patients. No associations were observed between active smoking/passive smoking and the risk of NMOSD relapse, but patients with a history of smoking were associated with a lower annual progression rate by Expanded Disability Status Scale (EDSS) (aβ=−0.20, 95% CI=−0.38, −0.01; &lt;i&gt;p&lt;/i&gt;=0.036) and Multiple Sclerosis Severity Score (MSSS) (aβ=−0.23, 95% CI=−0.44, −0.03; &lt;i&gt;p&lt;/i&gt;=0.028). &lt;i&gt;Conclusion&lt;/i&gt;: Our research shows that active smoking increases the relapse risk of MS and has a negative impact on disability progression; thus, smoking cessation should be encouraged.

EPIGENETIC AGE ACCELERATION AND IMMUNE CELL COUNT: A TWIN STUDY

Abstract Accelerated aging, as measured by epigenetic clocks, is associated with declines in immune system functioning. Investigating the causal basis of this association may provide mechanistic insight into the link between DNA methylation, on which epigenetic clocks are based, and age-related changes in immune cell composition. Using preliminary data from the Louisville Twin Study, this study examined the genetic and environmental sources of covariation between immune cell count (neutrophils, lymphocytes) and GrimAge Acceleration. GrimAge is a composite biomarker derived from 7 DNA methylation-based surrogates associated with mortality and smoking pack years. GrimAge Acceleration is the residual of GrimAge regressed onto chronological age. Participants consisted of 43 monozygotic twin pairs and 30 (18 same-sex) dizygotic twin pairs with a mean age of 54.5 years (sd = 5.27). Phenotypic analyses revealed that GrimAge Acceleration was significantly associated with neutrophil and lymphocyte count (r = 0.45 and -0.49, respectively). To examine the sources of covariation between these variables, biometric regression models were used to decompose the covariance between GrimAge Acceleration and neutrophils (and lymphocytes) into genetic and environmental components. Bivariate analyses revealed moderate, marginally significant genetic correlations between GrimAge Acceleration and immune cell count (rg = 0.32 and -0.38 for neutrophils and lymphocytes, respectively) and large, significant nonshared environmental correlations (re = .58 and -.54 for neutrophils and lymphocytes, respectively). Common genetic factors accounted for 39% of the phenotypic correlation in neutrophils and 43% in lymphocytes, whereas common nonshared environmental factors accounted for 61% and 57% of the correlation in these cell types, respectively.

The interaction effects of age, APOE and common environmental risk factors on human brain structure.

Mounting evidence suggests considerable diversity in brain aging trajectories, primarily arising from the complex interplay between age, genetic, and environmental risk factors, leading to distinct patterns of micro- and macro-cerebral aging. The underlying mechanisms of such effects still remain unclear. We conducted a comprehensive association analysis between cerebral structural measures and prevalent risk factors, using data from 36,969 UK Biobank subjects aged 44-81. Participants were assessed for brain volume, white matter diffusivity, Apolipoprotein E (APOE) genotypes, polygenic risk scores, lifestyles, and socioeconomic status. We examined genetic and environmental effects and their interactions with age and sex, and identified 726 signals, with education, alcohol, and smoking affecting most brain regions. Our analysis revealed negative age-APOE-ε4 and positive age-APOE-ε2 interaction effects, respectively, especially in females on the volume of amygdala, positive age-sex-APOE-ε4 interaction on the cerebellar volume, positive age-excessive-alcohol interaction effect on the mean diffusivity of the splenium of the corpus callosum, positive age-healthy-diet interaction effect on the paracentral volume, and negative APOE-ε4-moderate-alcohol interaction effects on the axial diffusivity of the superior fronto-occipital fasciculus. These findings highlight the need of considering age, sex, genetic, and environmental joint effects in elucidating normal or abnormal brain aging.

Abstract A045: Adhering to a culturally responsive framework: Integrating kinship into a multilevel community-based intervention for American Indian adults with comorbid type 2 diabetes and cancer

Abstract The prolific disparities of type 2 diabetes (T2D) and cancer in tribal communities is well documented. American Indian (AI) adults living with T2D are at greater risk of not only developing cancer, but also dying from it, with cooccurrence becoming increasingly prevalent. On rural tribal reservations, common environmental diabetogenic factors (e.g., obesity, lack of physical activity, poor diet, and stress) are considered as sources of elevated risk for both T2D and cancer. Critically important in improving both diabetes and cancer-related health behaviors and outcomes, particularly for AI people, is psychosocial support from family and community ties (e.g., kinship). Despite supporting evidence, few interventions include kinship as a key factor to promote best outcomes for T2D management among AI adults with a dual diagnosis of cancer. To address this growing issue, there is an urgent need for culturally and contextually adapted interventions aiming to address the cooccurrence of T2D and cancer that are, ideally, led by tribal communities. In this session, healthcare professional Early-Stage Investigators (ESIs), some of whom also identify as AI, will present community-based participatory research (CBPR) principles used to develop a multilevel Tribally tailored intervention, with kinship as a moderating factor, for AI adults living with both T2D and cancer. The ESIs represent a unique pool of providers invested in the community within which they work by co-creating an intervention which utilizes pre-existing strong community and familial norms. The ESIs further look to break away from the common trend in research to overgeneralize interventions and findings to all AI Tribal communities by tailoring the intervention to each specific Tribal Community engaged in the research intervention. To foster innovative research methods by emphasizing important historic and socio-cultural influences relevant to understanding the holistic context of health disparities in tribal communities, the guiding framework is the NIMHD Minority Health and Health Disparities Research Framework adapted for AI and Alaska Native Nations. In this research, individuals are viewed within the context of the broader social system where they function daily, while families and community are key stakeholders and leaders in the successful management of T2D and cancer. The approach focuses on diabetes-related barriers by providing family and social units with skills for successful T2D and cancer management, healthy communication, and shared commitment. In addition to these domains of influence, involving community systems is critical for a sustainable intervention that effectively addresses health disparities for T2D and cancer. Citation Format: Sheila L. Hammer, Timian M. Godfrey. Adhering to a culturally responsive framework: Integrating kinship into a multilevel community-based intervention for American Indian adults with comorbid type 2 diabetes and cancer [abstract]. In: Proceedings of the 16th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2023 Sep 29-Oct 2;Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2023;32(12 Suppl):Abstract nr A045.

Research on Positioning Accuracy of Mobile Robot in Indoor Environment Based on Improved RTABMAP Algorithm

Visual simultaneous localization and mapping is a widely used technology for mobile robots to carry out precise positioning in the environment of GNSS technology failure. However, as the robot moves around indoors, its position accuracy will gradually decrease over time due to common and unavoidable environmental factors. In this paper, we propose an improved method called RTABMAP-VIWO, which is based on RTABMAP. The basic idea is to use an Extended Kalman Filter (EKF) framework for fusion attitude estimates from the wheel odometry and IMU, and provide new prediction values. This helps to reduce the local cumulative error of RTABMAP and make it more accurate. We compare and evaluate three kinds of SLAM methods using both public datasets and real indoor scenes. In the dataset experiments, our proposed method reduces the Root-Mean-Square Error (RMSE) coefficient by 48.1% compared to the RTABMAP, and the coefficient is also reduced by at least 29.4% in the real environment experiments. The results demonstrate that the improved method is feasible. By incorporating the IMU into the RTABMAP method, the trajectory and posture errors of the mobile robot are significantly improved.

Genetic and environmental influences on early-age susceptibility and initiation of nicotine-containing product use: A twin-pairs study.

Nicotine-containing products (NCPs) such as electronic nicotine delivery systems (ENDS) are increasingly common throughout the landscape of youth use of nicotine-containing products (NCP), and have overtaken traditional cigarette smoking modalities. This study seeks to examine the genetic and environmental influences on liability for susceptibility and initiation of ENDS and other NCPs among US children. Data were drawn from 886 monozygotic (MZ) and dizygotic (DZ) twin pairs aged 9-10 years in the Adolescent Brain & Cognitive Development (ABCD) study at the baseline during 2016-2018. Heritability (h2) measured the proportion of the total phenotypic variation attributable to genes. Variance component models were utilized to analyze influences from the common environment (c2) and unique environmental factors (e2), taking into account correlations within twin pairs. The national sample included 50% females, 69.5% of non-Hispanic Whites, 12.8% of non-Hispanic Blacks, and 11.6% of Hispanics, with a mean age of 121.5 months. The twin sets were 60% DZ and 40% MZ. Heritability was low for NCP susceptibility (h2=0) and moderate for NCP initiation (h2=39%, p=0.02). The variance associated with NCP susceptibility was primarily influenced by environmental factors, especially one's unique factors (c2=37%, p<0.0001 vs e2=63%, p<0.0001). In contrast, the variance associated with NCP initiation was split across common and unique environmental factors (c2=32%, p=0.02 vs e2=29%, p=0.02). In the era with ENDS use surging among youth, NCP initiation remains to be a heritable trait with joint influence from the environment. NCP susceptibility is largely influenced by environmental factors, especially unique environments. Continued assessment of gene × environment interaction can better inform future youth NCP interventions.

SYNCHRONOUS DIAGNOSIS OF TESTICULAR AND THYROID CANCER IN A YOUNG MALE.

Testicular cancer is the most common neoplasm in young males. The early diagnosis and the appropriate treatment make it a curable malignancy in over 90% of the patients, but 6% of the patients with testicular cancer develop a second, mostly treatment-related, malignancy in another primary site many years after the first diagnosis. The simultaneous appearance of a testicular tumor with another primary neoplasm is rarely described in the literature. Here is presented an interesting case of a coexisting non-seminomatous germ cell testicular tumor with a papillary thyroid carcinoma, which was detected early during post-treatment restaging of the testicular tumor. The synchronous presence of these two neoplasms might indicate a probable common pathogenetic background. As treatment-related oncogenesis is highly improbable in this case and the common environmental factors are not known yet, the interest is focused on genetic predisposition. Recent discoveries in molecular genetics show that the two neoplasms share common genetic alterations in the RAS and BRAF genes, which affect the significant signaling pathways. Interestingly, BRAF-V600E was positive in both primary malignancies in our individual.

Brain network integration underpins differential susceptibility of adolescent anxiety.

Parenting is a common and potent environmental factor influencing adolescent anxiety. Yet, the underlying neurobiological susceptibility signatures remain elusive. Here, we used a longitudinal twin neuroimaging study to investigate the brain network integration and its heritable relation to underpin the neural differential susceptibility of adolescent anxiety to parenting environments. 216 twins from the Beijing Twin Study completed the parenting and anxiety assessments and fMRI scanning. We first identified the brain network integration involved in the influences of parenting at age 12 on anxiety symptoms at age 15. We then estimated to what extent heritable sensitive factors are responsible for the susceptibility of brain network integration. Consistent with the differential susceptibility theory, the results showed that hypo-connectivity within the central executive network amplified the impact of maternal hostility on anxiety symptoms. A high anti-correlation between the anterior salience and default mode networks played a similar modulatory role in the susceptibility of adolescent anxiety to paternal hostility. Genetic influences (21.18%) were observed for the connectivity pattern in the central executive network. Brain network integration served as a promising neurobiological signature of the differential susceptibility to adolescent anxiety. Our findings deepen the understanding of the neural sensitivity in the developing brain and can inform early identification and personalized interventions for adolescents at risk of anxiety disorders.

Neurodevelopment among children exposed to HIV and uninfected in sub-Saharan Africa.

The population of 16 million children exposed to HIV and uninfected (CHEU) under 15 years of age continues to expand rapidly, and the estimated prevalence of CHEU exceeds 20% in several countries in sub-Saharan Africa with high HIV prevalence. Some evidence suggests that CHEU experience suboptimal neurodevelopmental outcomes compared to children born to women without HIV. In this commentary, we discuss the latest research on biologic and socio-behavioural factors associated with neurodevelopmental outcomes among CHEU. Some but not all studies have noted that CHEU are at risk of poorer neurodevelopment across multiple cognitive domains, most notably in language and motor skills, in diverse settings, ages and using varied assessment tools. Foetal HIV exposure can adversely influence infant immune function, structural brain integrity and growth trajectories. Foetal exposure to antiretrovirals may also influence outcomes. Moreover, general, non-CHEU-specific risk factors for poor neurodevelopment, such as preterm birth, food insecurity, growth faltering and household violence, are amplified among CHEU; addressing these factors will require multi-factorial solutions. There is a need for rigorous harmonised approaches to identify children at the highest risk of delay. In high-burden HIV settings, existing maternal child health programmes serving the general population could adopt structured early child development programmes that educate healthcare workers on CHEU-specific risk factors and train them to conduct rapid neurodevelopmental screening tests. Community-based interventions targeting parent knowledge of optimal caregiving practices have shown to be successful in improving neurodevelopmental outcomes in children and should be adapted for CHEU. CHEU in sub-Saharan Africa have biologic and socio-behavioural factors that may influence their neurodevelopment, brain maturation, immune system and overall health and wellbeing. Multidisciplinary research is needed to disentangle complex interactions between contributing factors. Common environmental and social risk factors for suboptimal neurodevelopment in the general population are disproportionately magnified within the CHEU population, and it is, therefore, important to draw on existing knowledge when considering the socio-behavioural pathways through which HIV exposure could impact CHEU neurodevelopment. Approaches to identify children at greatest risk for poor outcomes and multisectoral interventions are needed to ensure optimal outcomes for CHEU in sub-Saharan Africa.

Cancer Incidence and Mortality Estimates in Arab Countries in 2018: A GLOBOCAN Data Analysis.

Arab countries are projecting increase in cancer incidence and mortality; however, there are limited studies that compare the epidemiology of cancer in Arab countries compared with other parts of the world. We used the 2018 Global Cancer Observatory data to compare the age-standardized incidence and mortality estimates in Arab-speaking countries to the rest of the world. Rates for incidence and mortality for all cancers in Arab countries were lower than the world's rates but the incidence rates of non-Hodgkin and Hodgkin lymphoma, bladder, breast, and liver cancers were higher. Arab countries generally had higher mortality-to-incidence ratio than the world's ratio. Incidence rates, even in age-specific groups, varied between subregions of Arab countries (the Levant, Arabian Gulf, and Arab African subregions), and Iraq and Egypt, suggesting some common and unique environmental factors and possible ethnic or genetic heritages. There are essential scopes for improvements in Arab countries including better treatments to reduce the high mortality-to-incidence ratio, and supporting vaccination programs and antiviral treatments that would prevent the prevalent viral infection-related cancers. The high incidence of several cancers in younger Arabs suggests genetic factors and underlines the importance of genetic epidemiology studies. This study is an essential reference to evaluate and monitor the progress of national cancer initiatives in Arab countries for surveillance and prevention programs and improving clinical management. The study also provides a comprehensive snapshot of cancers in a unique region that could shed light on the interplay of environmental, lifestyle, and genetic risk factors.