The Impact of Poor Health on Education: New Evidence Using Genetic Markers

This paper examines the influence of health conditions on academic performance during adolescence. To account for the endogeneity of health outcomes and their interactions with risky behaviors we exploit natural variation within a set of genetic markers across individuals. We present strong evidence that these genetic markers serve as valid instruments with good statistical properties for ADHD, depression and obesity. They help to reveal a new dynamism from poor health to lower academic achievement with substantial heterogeneity in their impacts across genders. Our investigation further exposes the considerable challenges in identifying health impacts due to the prevalence of comorbid health conditions and endogenous health behaviors.health, education, genetic predisposition, obesity, ADHD, depression, instrumental variables, risky health behaviors

The Impact of Poor Health on Education: New Evidence Using Genetic Markers

This paper examines the influence of health conditions on academic performance during adolescence. To account for the endogeneity of health outcomes and their interactions with risky behaviors we exploit natural variation within a set of genetic markers across individuals. We present strong evidence that these genetic markers serve as valid instruments with good statistical properties for ADHD, depression and obesity. They help to reveal a new dynamism from poor health to lower academic achievement with substantial heterogeneity in their impacts across genders. Our investigation further exposes the considerable challenges in identifying health impacts due to the prevalence of comorbid health conditions and endogenous health behaviors.

Supporting Coastal Resiliency by Investigating Tidal Reach and Inter-Connected Factors in Coastal Georgia

The South Carolina Water Resources Conference (SCWRC) provides an integrated forum for discussion of water policies, research projects and water management in order to prepare for and meet the growing challenge of providing water resources to sustain and grow South Carolina’s economy, while preserving our natural resources

Estimating Peer Effects in Longitudinal Dyadic Data Using Instrumental Variables

The identification of causal peer effects (also known as social contagion or induction) from observational data in social networks is challenged by two distinct sources of bias: latent homophily and unobserved confounding. In this paper, we investigate how causal peer effects of traits and behaviors can be identified using genes (or other structurally isomorphic variables) as instrumental variables (IV) in a large set of data generating models with homophily and confounding. We use directed acyclic graphs to represent these models and employ multiple IV strategies and report three main identification results. First, using a single fixed gene (or allele) as an IV will generally fail to identify peer effects if the gene affects past values of the treatment. Second, multiple fixed genes/alleles, or, more promisingly, time-varying gene expression, can identify peer effects if we instrument exclusion violations as well as the focal treatment. Third, we show that IV identification of peer effects remains possible even under multiple complications often regarded as lethal for IV identification of intra-individual effects, such as pleiotropy on observables and unobservables, homophily on past phenotype, past and ongoing homophily on genotype, inter-phenotype peer effects, population stratification, gene expression that is endogenous to past phenotype and past gene expression, and others. We apply our identification results to estimating peer effects of body mass index (BMI) among friends and spouses in the Framingham Heart Study. Results suggest a positive causal peer effect of BMI between friends

Experimental validation of an electronic counting device to determine flight activity of honey bees (Apis mellifera L.)

Ein Funktionsprototyp des Bienenzählers BeeCheck sollte in dieser Arbeit auf seine Genauigkeit hin überprüft werden, um seine Tauglichkeit für den wissenschaft­lichen Einsatz zu validieren. Hierzu wurden zwei unterschiedliche Ansätze verfolgt: (i) Vergleich der elektronischen Daten des Zählgerätes durch Videoaufnahmen von Ein- und Ausflügen mit manueller Auswertung durch einen Beobachter sowie (ii) die Validierung mittels „Räubertest“ im bienendichten Zelt. Die Ergebnisse zeigten eine zu erwartende Temperatur Abhängigkeit der Flug­aktivität sowie die Fehleranfälligkeit bei gewissen Aktivitäten am Flugloch. So waren unterschiedliche Geschwindigkeiten, sich entgegenkommende oder im Flugloch verharrende Bienen, sowie sich vor- und rückwärts bewegende Bienen eine Herausforderung für den Algorithmus, der aus den gemessenen Sensordaten die Bienentransaktionen ableitet. Um diese Grenzfälle zu minimieren und die Zählgenauigkeit zu erhöhen, ist es notwendig den Algorithmus entsprechend korrektiv anzupassen. Dies soll im Folgeprojekt „Etablierung digitaler Indikatoren der Bienenvitalität in Agrarlandschaften – V-I-Bee“ angegangen werden.In this work, a functional prototype of the BeeCheck counting device was evaluated for its accuracy to validate its suitability for scientific purposes. Two different approaches were applied: (i) we manually compared electronic data of the counting device by video recordings of entry and exit events, and (ii) by using the so-called “robber’s test” in a tunnel tent. The results showed an expected temperature dependency of the general flight activity. Difficulties occurred with certain activities at the hive entrance. The various running speeds of individuals, approaching or stuck bees, and bees moving back and forth in the tube were a challenge for sensor technology and the mathematical algorithm. To minimize such mistakes and to increase the counting accuracy, it is necessary to correct the algorithm accordingly. This will be addressed in the “V-I-Bee” follow-up project and future perspectives of using an improved counting device are discussed

NEIL1 excises 3′ end proximal oxidative DNA lesions resistant to cleavage by NTH1 and OGG1

Base excision repair is the major pathway for the repair of oxidative DNA damage in human cells that is initiated by a damage-specific DNA glycosylase. In human cells, the major DNA glycosylases for the excision of oxidative base damage are OGG1 and NTH1 that excise 8-oxoguanine and oxidative pyrimidines, respectively. We find that both enzymes have limited activity on DNA lesions located in the vicinity of the 3′ end of a DNA single-strand break, suggesting that other enzymes are involved in the processing of such lesions. In this study, we identify and characterize NEIL1 as a major DNA glycosylase that excises oxidative base damage located in close proximity to the 3′ end of a DNA single-strand break

Telomere length and telomerase activity in malignant lymphomas at diagnosis and relapse

Telomere length maintenance, in the vast majority of cases executed by telomerase, is a prerequisite for long-term proliferation. Most malignant tumours, including lymphomas, are telomerase-positive and this activity is a potential target for future therapeutic interventions since inhibition of telomerase has been shown to result in telomere shortening and cell death in vitro. One prerequisite for the suitability of anti-telomerase drugs in treating cancer is that tumours exhibit shortened telomeres compared to telomerase-positive stem cells. A scenario is envisioned where the tumour burden is reduced using conventional therapy whereafter remaining tumour cells are treated with telomerase inhibitors. In evaluating the realism of such an approach it is essential to know the effects on telomere status by traditional therapeutic regimens. We have studied the telomere lengths in 47 diagnostic lymphomas and a significant telomere shortening was observed compared to benign lymphoid tissues. In addition, telomere length and telomerase activity were studied in consecutive samples from patients with relapsing non-Hodgkin's lymphomas. Shortened, unchanged and elongated telomere lengths were observed in the relapse samples. The telomere length alterations found in the relapsing lymphomas appeared to be independent of telomerase and rather represented clonal selection random at the telomere length level. These data indicate that anti-telomerase therapy would be suitable in only a fraction of malignant lymphomas. © 2000 Cancer Research Campaig

Exome sequencing followed by large-scale genotyping suggests a limited role for moderately rare risk factors of strong effect in schizophrenia.

Schizophrenia is a severe psychiatric disorder with strong heritability and marked heterogeneity in symptoms, course, and treatment response. There is strong interest in identifying genetic risk factors that can help to elucidate the pathophysiology and that might result in the development of improved treatments. Linkage and genome-wide association studies (GWASs) suggest that the genetic basis of schizophrenia is heterogeneous. However, it remains unclear whether the underlying genetic variants are mostly moderately rare and can be identified by the genotyping of variants observed in sequenced cases in large follow-up cohorts or whether they will typically be much rarer and therefore more effectively identified by gene-based methods that seek to combine candidate variants. Here, we consider 166 persons who have schizophrenia or schizoaffective disorder and who have had either their genomes or their exomes sequenced to high coverage. From these data, we selected 5,155 variants that were further evaluated in an independent cohort of 2,617 cases and 1,800 controls. No single variant showed a study-wide significant association in the initial or follow-up cohorts. However, we identified a number of case-specific variants, some of which might be real risk factors for schizophrenia, and these can be readily interrogated in other data sets. Our results indicate that schizophrenia risk is unlikely to be predominantly influenced by variants just outside the range detectable by GWASs. Rather, multiple rarer genetic variants must contribute substantially to the predisposition to schizophrenia, suggesting that both very large sample sizes and gene-based association tests will be required for securely identifying genetic risk factors. © 2012 The American Society of Human Genetics