Academic Procrastination in College Students

Academic procrastination has become a prevalent issue facing students, especially college-aged students. There is a large body of research investigating the reasons behind academic procrastination and why it continues to be a growing problem for students. Researchers want to understand why procrastination affects most college students when it is associated with many long-term negative implications. Following this problem, there have been several studies conducted in hopes of finding a solution to help students procrastinate less. While there has been research about possible treatment options, there has been a lack of research specifically targeting the important predictors of procrastination. In this study, we took data from 239 students from a large, private Christian university in Virginia. We conducted bivariate correlations and a multiple regression analysis between procrastination and “self” related variables such as self-efficacy, self-esteem, self-regulation, and self-forgiveness to assess which variables have the strongest correlation with procrastination to better create treatment plans. The findings of the study indicate that self-regulation had the strongest, unique inverse relationship with procrastination which can help future researchers specifically target that variable when creating treatment plans

Effect of Carbon Supplementation on Denitrifying Bacteria in Woodchip Bioreactors

California’s agricultural sector is fundamental to the state’s economic growth and responsible for supplying a large portion of the country’s produce. An abundance of nutrient-rich irrigation is required to meet these high demands, and the resultant agricultural effluent is a source of increased nutrient content in California’s watershed and groundwater systems. This promotes eutrophication, and negatively impacts local ecosystems and human health. Effective remediation of waterways using bacteria in woodchip bioreactors can be achieved by maintaining the system within ideal conditions for productivity of the microbial populations. Bioreactor systems used wood chips to provide both substrate and a carbon source, and relied on insulated structures to maintain temperatures within the active range of the mesophilic bacteria. Corn starch was introduced to one system as a carbon supplement, as results had indicated the system was carbon-limited. A second bioreactor system acted as a control with no carbon supplement. Single pass and recirculatory experiments were conducted over a period of six weeks. More denitrification occurred in the experimental bioreactor than the control, suggesting corn starch serves as a viable carbon supplement to facilitate the metabolic processes of denitrifying bacteria

The autophagy protein Atg7 is essential for hematopoietic stem cell maintenance.

The role of autophagy, a lysosomal degradation pathway which prevents cellular damage, in the maintenance of adult mouse hematopoietic stem cells (HSCs) remains unknown. Although normal HSCs sustain life-long hematopoiesis, malignant transformation of HSCs leads to leukemia. Therefore, mechanisms protecting HSCs from cellular damage are essential to prevent hematopoietic malignancies. In this study, we crippled autophagy in HSCs by conditionally deleting the essential autophagy gene Atg7 in the hematopoietic system. This resulted in the loss of normal HSC functions, a severe myeloproliferation, and death of the mice within weeks. The hematopoietic stem and progenitor cell compartment displayed an accumulation of mitochondria and reactive oxygen species, as well as increased proliferation and DNA damage. HSCs within the Lin(-)Sca-1(+)c-Kit(+) (LSK) compartment were significantly reduced. Although the overall LSK compartment was expanded, Atg7-deficient LSK cells failed to reconstitute the hematopoietic system of lethally irradiated mice. Consistent with loss of HSC functions, the production of both lymphoid and myeloid progenitors was impaired in the absence of Atg7. Collectively, these data show that Atg7 is an essential regulator of adult HSC maintenance

Autophagy, mitochondria and oxidative stress: cross-talk and redox signalling

Reactive oxygen and nitrogen species change cellular responses through diverse mechanisms that are now being defined. At low levels, they are signalling molecules, and at high levels, they damage organelles, particularly the mitochondria. Oxidative damage and the associated mitochondrial dysfunction may result in energy depletion, accumulation of cytotoxic mediators and cell death. Understanding the interface between stress adaptation and cell death then is important for understanding redox biology and disease pathogenesis. Recent studies have found that one major sensor of redox signalling at this switch in cellular responses is autophagy. Autophagic activities are mediated by a complex molecular machinery including more than 30 Atg (AuTophaGy-related) proteins and 50 lysosomal hydrolases. Autophagosomes form membrane structures, sequester damaged, oxidized or dysfunctional intracellular components and organelles, and direct them to the lysosomes for degradation. This autophagic process is the sole known mechanism for mitochondrial turnover. It has been speculated that dysfunction of autophagy may result in abnormal mitochondrial function and oxidative or nitrative stress. Emerging investigations have provided new understanding of how autophagy of mitochondria (also known as mitophagy) is controlled, and the impact of autophagic dysfunction on cellular oxidative stress. The present review highlights recent studies on redox signalling in the regulation of autophagy, in the context of the basic mechanisms of mitophagy. Furthermore, we discuss the impact of autophagy on mitochondrial function and accumulation of reactive species. This is particularly relevant to degenerative diseases in which oxidative stress occurs over time, and dysfunction in both the mitochondrial and autophagic pathways play a role

Job loss and fetal growth restriction: identification of critical trimesters of exposure.

PURPOSE: Previous research suggests that job loss in a household during pregnancy may perturb fetal growth. However, this work often cannot rule out unmeasured confounding due to selection into job loss. Recent work using data on exogenous job loss (due to a plant closure) finds that a fathers unexpected job loss during his spouses pregnancy increases the risk of a low weight birth. Using a unique set of linked registries in Denmark, we build on this work and examine whether associations between a fathers unexpected job loss and low birthweight differ by trimester of in utero exposure. We additionally examine trimester-specific associations of job loss with small-for-gestational-age, a proxy for restricted fetal growth, which may cause low birthweight. METHODS: We apply a sibling control design to over 1.4 million live births in Denmark, 1980 to 2017, to examine whether this plausibly exogenous form of job loss corresponds with increased risk of low weight or small-for-gestational-age births, depending on the timing of displacement in the first, second, or third trimester. RESULTS: Results indicate an elevated risk of low birthweight (OR = 1.80, 95% CI: 1.24, 2.62) and small-for-gestational-age (OR = 1.40, 95% CI: 1.02, 1.93) among gestations exposed to job loss in the second trimester of pregnancy. Sensitivity analyses using continuous outcome measures (e.g., birthweight in grams, birthweight for gestational age percentile) and maternal fixed effects analyses produce substantively similar inference. CONCLUSIONS: Findings support the notion that unexpected job loss may affect fetal growth and that the second trimester in particular appears sensitive to this external stressor

Birth outcomes following unexpected job loss:A matched-sibling design

BACKGROUND: Research documents social and economic antecedents of adverse birth outcomes, which may include involuntary job loss. Previous work on job loss and adverse birth outcomes, however, lacks high-quality individual data on, and variation in, plausibly exogenous job loss during pregnancy and therefore cannot rule out strong confounding. METHODS: We analysed unique linked registries in Denmark, from 1980 to 2017, to examine whether a father’s involuntary job loss during his spouse’s pregnancy increases the risk of a low-weight (i.e. <2500 grams) and/or preterm (i.e. <37 weeks of gestational age) birth. We applied a matched-sibling design to 743 574 sibling pairs. RESULTS: Results indicate an increased risk of a low-weight birth among infants exposed in utero to fathers’ unexpected job loss [odds ratio (OR) = 1.37, 95% confidence interval (CI): 1.07, 1.75]. Sex-specific analyses show that this result holds for males (OR = 1.70, 95% CI: 1.14, 2.53) but not females (OR = 1.24, 95% CI: 0.80, 1.91). We find no relation with preterm birth. CONCLUSIONS: Findings support the inference that a father’s unexpected job loss adversely affects the course of pregnancy, especially among males exposed in utero

Psychiatric disorders with postpartum onset: Possible early manifestations of bipolar affective disorders

Context: Childbirth has an important influence on the onset and course of bipolar affective disorder, and it is well established that there may be a delay of many years before receiving a diagnosis of bipolar disorder following an initial episode of psychiatric illness. Objective: To study to what extent psychiatric disorders with postpartum onset are early manifestations of an underlying bipolar affective disorder. Design: Survival analyses were performed in a register-based cohort study linking information from the Danish Civil Registration System and the Danish Psychiatric Central Register. Setting: Denmark. Participants: A total of 120 378 women with a first-time psychiatric inpatient or outpatient contact with any type of mental disorder excluding bipolar affective disorder. Main Outcome Measures: Each woman was followed up individually from the day of discharge, with the outcome of interest being an inpatient or outpatient contact during the follow-up period with a first-time diagnosis of bipolar affective disorder. Results: A total of 3062 women were readmitted or had an outpatient contact with bipolar affective disorder diagnoses. A postpartum onset of symptoms within 0 to 14 days after delivery predicted subsequent conversion to bipolar disorder (relative risk = 4.26; 95% CI =3.11-5.85). Approximately 14% of women with first-time psychiatric contacts during the first postpartum month converted to a bipolar diagnosis within the 15-year follow-up period compared with 4% of women with a first psychiatric contact not related to childbirth. Postpartum inpatient admissions were also associated with higher conversion rates to bipolar disorder than outpatient contacts (relative risk = 2.16; 95% CI = 1.27-3.66). Conclusions: A psychiatric episode in the immediate postpartum period significantly predicted conversion to bipolar affective disorder during the follow-up period. Results indicate that the presentation of mental illness in the early postpartum period is a marker of possible underlying bipolarity