Trade-Offs Between Agricultural and Chemical Policy

In modern U.S. agriculture there are numerous tradeoffs between agricultural and chemical policies. Chemicals are major inputs in agricultural production processes (for both crops and livestock). Agricultural chemicals, however, have negative environmental side effects that are not always considered by users (Benbrook 1988). Agricultural policies primarily are designed to stabilize commodity prices and enhance farm income, which in turn changes production levels, provides incentives for different intensities of factor use, and influences the loading of chemicals. In turn, chemical policies involving taxes, use restrictions, and registration requirements change the availability and prices of chemical inputs, alter agricultural production and cost levels, and affect agricultural income

Preparation and Use of a Yeast shRNA Delivery System for Gene Silencing in Mosquito Larvae

The mosquito genome projects facilitated research in new facets of mosquito biology, including functional genetic studies in the dengue and Zika virus vector Aedes aegypti and the primary African malaria vector Anopheles gambiae. RNA interference (RNAi) has facilitated gene silencing experiments in both of these disease vector mosquito species and could one day be applied as a new method of vector control. Here, we describe a procedure for the genetic engineering of Saccharomyces cerevisiae (baker’s yeast) that express short hairpin RNA (shRNA) corresponding to mosquito target genes of interest. Following cultivation, which facilitates inexpensive propagation of shRNA, the yeast is inactivated and prepared in a ready-to-use dry tablet formulation that is fed to mosquito larvae. Ingestion of the yeast tablets results in effective larval target gene silencing. This technically straightforward and affordable technique may be applicable to a wide variety of mosquito species and potentially to other arthropods that feed on yeast

Cerebral activations related to ballistic, stepwise interrupted and gradually modulated movements in parkinson patients

Patients with Parkinson's disease (PD) experience impaired initiation and inhibition of movements such as difficulty to start/stop walking. At single-joint level this is accompanied by reduced inhibition of antagonist muscle activity. While normal basal ganglia (BG) contributions to motor control include selecting appropriate muscles by inhibiting others, it is unclear how PD-related changes in BG function cause impaired movement initiation and inhibition at single-joint level. To further elucidate these changes we studied 4 right-hand movement tasks with fMRI, by dissociating activations related to abrupt movement initiation, inhibition and gradual movement modulation. Initiation and inhibition were inferred from ballistic and stepwise interrupted movement, respectively, while smooth wrist circumduction enabled the assessment of gradually modulated movement. Task-related activations were compared between PD patients (N = 12) and healthy subjects (N = 18). In healthy subjects, movement initiation was characterized by antero-ventral striatum, substantia nigra (SN) and premotor activations while inhibition was dominated by subthalamic nucleus (STN) and pallidal activations, in line with the known role of these areas in simple movement. Gradual movement mainly involved antero-dorsal putamen and pallidum. Compared to healthy subjects, patients showed reduced striatal/SN and increased pallidal activation for initiation, whereas for inhibition STN activation was reduced and striatal-thalamo-cortical activation increased. For gradual movement patients showed reduced pallidal and increased thalamo-cortical activation. We conclude that PD-related changes during movement initiation fit the (rather static) model of alterations in direct and indirect BG pathways. Reduced STN activation and regional cortical increased activation in PD during inhibition and gradual movement modulation are better explained by a dynamic model that also takes into account enhanced responsiveness to external stimuli in this disease and the effects of hyper-fluctuating cortical inputs to the striatum and STN in particular

Engineering coherent interactions in molecular nanomagnet dimers

Proposals for systems embodying condensed matter spin qubits cover a very wide range of length scales, from atomic defects in semiconductors all the way to micron-sized lithographically defined structures. Intermediate scale molecular components exhibit advantages of both limits: like atomic defects, large numbers of identical components can be fabricated; as for lithographically defined structures, each component can be tailored to optimise properties such as quantum coherence. Here we demonstrate what is perhaps the most potent advantage of molecular spin qubits, the scalability of quantum information processing structures using bottom-up chemical self-assembly. Using Cr7Ni spin qubit building blocks, we have constructed several families of two-qubit molecular structures with a range of linking strategies. For each family, long coherence times are preserved, and we demonstrate control over the inter-qubit quantum interactions that can be used to mediate two-qubit quantum gates

At What Stage of Neural Processing Does Cocaine Act to Boost Pursuit of Rewards?

Dopamine-containing neurons have been implicated in reward and decision making. One element of the supporting evidence is that cocaine, like other drugs that increase dopaminergic neurotransmission, powerfully potentiates reward seeking. We analyze this phenomenon from a novel perspective, introducing a new conceptual framework and new methodology for determining the stage(s) of neural processing at which drugs, lesions and physiological manipulations act to influence reward-seeking behavior. Cocaine strongly boosts the proclivity of rats to work for rewarding electrical brain stimulation. We show that the conventional conceptual framework and methods do not distinguish between three conflicting accounts of how the drug produces this effect: increased sensitivity of brain reward circuitry, increased gain, or decreased subjective reward costs. Sensitivity determines the stimulation strength required to produce a reward of a given intensity (a measure analogous to the KM of an enzyme) whereas gain determines the maximum intensity attainable (a measure analogous to the vmax of an enzyme-catalyzed reaction). To distinguish sensitivity changes from the other determinants, we measured and modeled reward seeking as a function of both stimulation strength and opportunity cost. The principal effect of cocaine was a two-fourfold increase in willingness to pay for the electrical reward, an effect consistent with increased gain or decreased subjective cost. This finding challenges the long-standing view that cocaine increases the sensitivity of brain reward circuitry. We discuss the implications of the results and the analytic approach for theories of how dopaminergic neurons and other diffuse modulatory brain systems contribute to reward pursuit, and we explore the implications of the conceptual framework for the study of natural rewards, drug reward, and mood

Elevated Plasma Von Willebrand Factor and Propeptide Levels in Malawian Children with Malaria

In children with malaria plasma VWF and propeptide levels are markedly elevated in both cerebral and mild paediatric malaria, with levels matching disease severity, and these normalize upon recovery. High levels of both markers also occur in retinopathy-negative 'cerebral malaria' cases, many of whom are thought to be suffering from diseases other than malaria, indicating that further studies of these markers will be required to determine their sensitivity and specificity

Educational Inequalities in Hospital Use Among Older Adults in England, 2004-2015.

Policy Points US policymakers considering proposals to expand public health care (such as "Medicare for all") as a means of reducing inequalities in health care access and use could learn from the experiences of nations where well-funded universal health care systems are already in place. In England, which has a publicly funded universal health care system, the use of core inpatient services by adults 65 years and older is equal across groups defined by education level, after controlling for health status. However, variation among these groups in the use of outpatient and emergency department care developed between 2010 and 2015, a period of relative financial austerity. Based on England's experience, introducing universal health care in the United States seems likely to reduce, but not entirely eliminate, inequalities in health care use across different population groups. CONTEXT: Expanding access to health care is once again high on the US political agenda, as is concern about those who are being "left behind." But is universal health care that is largely free at the point of use sufficient to eliminate inequalities in health care use? To explore this question, we studied variation in the use of hospital care among education-level-defined groups of older adults in England, before and after controlling for differences in health status. In England, the National Health Service (NHS) provides health care free to all, but the growth rate for NHS funding has slowed markedly since 2010 during a widespread austerity program, potentially increasing inequalities in access and use. METHODS: Novel linkage of data from six waves (2004-2015) of the English Longitudinal Study of Ageing (ELSA) with participants' hospital records (Hospital Episode Statistics [HES]) produced longitudinal data for 7,713 older adults (65 years and older) and 25,864 observations. We divided the sample into three groups by education level: low (no formal qualifications), mid (completed compulsory education), and high (at least some higher education). Four outcomes were examined: annual outpatient appointments, elective inpatient admissions, emergency inpatient admissions, and emergency department (ED) visits. We estimated regressions for the periods 2004-2005 to 2008-2009 and 2010-2011 to 2014-2015 to examine whether potential education-related inequalities in hospital use increased after the growth rate for NHS funding slowed in 2010. FINDINGS: For the study period, our sample of ELSA respondents in the low-education group made 2.44 annual outpatient visits. In comparison, after controlling for health status, we found that participants in the high-education group made an additional 0.29 outpatient visits annually (95% confidence interval [CI], 0.11-0.47). Additional outpatient health care use in the high-education group was driven by follow-up and routine appointments. This inequality widened after 2010. Between 2010 and 2015, individuals in the high-education group made 0.48 (95% CI, 0.21-0.74) more annual outpatient visits than those in the low-education (16.9% [7.5% to 26.2%] of annual average 2.82 visits). In contrast, after 2010, the high-education group made 0.04 (95% CI, -0.075 to 0.001) fewer annual ED visits than the low-education group, which had a mean of 0.30 annual ED visits. No significant differences by education level were found for elective or emergency inpatient admissions in either period. CONCLUSIONS: After controlling for demographics and health status, there was no evidence of inequality in elective and emergency inpatient admissions among the education groups in our sample. However, a period of financial budget tightening for the NHS after 2010 was associated with the emergence of education gradients in other forms of hospital care, with respondents in the high-education group using more outpatient care and less ED care than peers in the low-education group. These estimates point to rising inequalities in the use of hospital care that, if not reversed, could exacerbate existing health inequalities in England. Although the US and UK settings differ in many ways, our results also suggest that a universal health care system would likely reduce inequality in US health care use

Microstructural Abnormalities in Subcortical Reward Circuitry of Subjects with Major Depressive Disorder

Previous studies of major depressive disorder (MDD) have focused on abnormalities in the prefrontal cortex and medial temporal regions. There has been little investigation in MDD of midbrain and subcortical regions central to reward/aversion function, such as the ventral tegmental area/substantia nigra (VTA/SN), and medial forebrain bundle (MFB).We investigated the microstructural integrity of this circuitry using diffusion tensor imaging (DTI) in 22 MDD subjects and compared them with 22 matched healthy control subjects. Fractional anisotropy (FA) values were increased in the right VT and reduced in dorsolateral prefrontal white matter in MDD subjects. Follow-up analysis suggested two distinct subgroups of MDD patients, which exhibited non-overlapping abnormalities in reward/aversion circuitry. The MDD subgroup with abnormal FA values in VT exhibited significantly greater trait anxiety than the subgroup with normal FA values in VT, but the subgroups did not differ in levels of anhedonia, sadness, or overall depression severity.These findings suggest that MDD may be associated with abnormal microstructure in brain reward/aversion regions, and that there may be at least two subtypes of microstructural abnormalities which each impact core symptoms of depression

Self-Compassion, emotion regulation and stress among australian psychologists: Testing an emotion regulation model of self-compassion using structural equation modeling

Psychologists tend to report high levels of occupational stress, with serious implications for themselves, their clients, and the discipline as a whole. Recent research suggests that selfcompassion is a promising construct for psychologists in terms of its ability to promote psychological wellbeing and resilience to stress; however, the potential benefits of self-compassion are yet to be thoroughly explored amongst this occupational group. Additionally, while a growing body of research supports self-compassion as a key predictor of psychopathology, understanding of the processes by which self-compassion exerts effects on mental health outcomes is limited. Structural equation modelling (SEM) was used to test an emotion regulation model of self-compassion and stress among psychologists, including postgraduate trainees undertaking clinical work (n = 198). Self-compassion significantly negatively predicted emotion regulation difficulties and stress symptoms. Support was also found for our preliminary explanatory model of self-compassion, which demonstrates the mediating role of emotion regulation difficulties in the self-compassion-stress relationship. The final self-compassion model accounted for 26.2% of variance in stress symptoms. Implications of the findings and limitations of the study are discussed