Lagoons, Litter, and the Law: CAFO Regulation as Social Risk Politics

The restructuring of the animal agriculture industry in the United States, a response to globalization dynamics within the world economy, has created a new social risk profile which did not exist in this industry prior to the adoption of factory farm technology. Analysis of the CAFO [concentrated animal feeding operation] regulation debate in Kentucky illustrates the political economy genesis of social risk politics accompanying this new technology. The politics of regulatory efforts to ameliorate such risk, an increasingly frequent occurrence in the risk society era, are examined in a recent attempt to promulgate a CAFO regulatory regime in Kentucky. This case study shows how globalization processes within the U.S. agrifood system have engendered local re-regulation responses in attempts to alter the location-specific socioeconomic effects of these processes

Protein kinase A (PKA) phosphorylation of Shp2 inhibits its phosphatase activity and modulates ligand specificity.

Pathological cardiac hypertrophy (an increase in cardiac mass resulting from stress-induced cardiac myocyte growth) is a major factor underlying heart failure. Src homology 2 domain-containing phosphatase (Shp2) is critical for cardiac function as mutations resulting in loss of Shp2 catalytic activity are associated with congenital cardiac defects and hypertrophy. We have identified a novel mechanism of Shp2 inhibition that may promote cardiac hypertrophy. We demonstrate that Shp2 is a component of the A-kinase anchoring protein (AKAP)-Lbc complex. AKAP-Lbc facilitates protein kinase A (PKA) phosphorylation of Shp2, which inhibits Shp2 phosphatase activity. We have identified two key amino acids in Shp2 that are phosphorylated by PKA: Thr73 contributes a helix-cap to helix αB within the N-terminal SH2 domain of Shp2, whereas Ser189 occupies an equivalent position within the C-terminal SH2 domain. Utilizing double mutant PKA phospho-deficient (T73A/S189A) and phospho-mimetic (T73D/S189D) constructs, in vitro binding assays, and phosphatase activity assays, we demonstrate that phosphorylation of these residues disrupts Shp2 interaction with tyrosine-phosphorylated ligands and inhibits its protein tyrosine phosphatase activity. Overall, our data indicate that AKAP-Lbc integrates PKA and Shp2 signaling in the heart and that AKAP-Lbc-associated Shp2 activity is reduced in hypertrophic hearts in response to chronic β-adrenergic stimulation and PKA activation. Thus, while induction of cardiac hypertrophy is a multifaceted process, inhibition of Shp2 activity through AKAP-Lbc-anchored PKA is a previously unrecognized mechanism that may promote this compensatory response

Sample size: How many is enough?

Sample size is an element of research design that significantly affects the validity and clinical relevance of the findings identified in research studies. Factors that influence sample size include the effect size, or difference expected between groups or time points, the homogeneity of the study participants, the risk of error that investigators consider acceptable and the rate of participant attrition expected during the study. Appropriate planning in regard to each of these elements optimises the likelihood of finding an important result that is both clinically and statistically meaningful

Effects of interaction on an adiabatic quantum electron pump

We study the effects of inter-electron interactions on the charge pumped through an adiabatic quantum electron pump. The pumping is through a system of barriers, whose heights are deformed adiabatically. (Weak) interaction effects are introduced through a renormalisation group flow of the scattering matrices and the pumped charge is shown to {\it always} approach a quantised value at low temperatures or long length scales. The maximum value of the pumped charge is set by the number of barriers and is given by $Q_{\rm max} = n_b -1$. The correlation between the transmission and the charge pumped is studied by seeing how much of the transmission is enclosed by the pumping contour. The (integer) value of the pumped charge at low temperatures is determined by the number of transmission maxima enclosed by the pumping contour. The dissipation at finite temperatures leading to the non-quantised values of the pumped charge scales as a power law with the temperature ($Q-Q_{\rm int} \propto T^{2\alpha}$), or with the system size ($Q-Q_{\rm int} \propto L_s^{-2\alpha}$), where $\alpha$ is a measure of the interactions and vanishes at $T=0 ~(L_s=\infty)$. For a double barrier system, our result agrees with the quantisation of pumped charge seen in Luttinger liquids.Comment: 9 pages, 9 figures, better quality figures available on request from author

Health status after traumatic injury

BACKGROUND: This study explored the relationships between health-related quality of life and postacute factors such as patients’ perceived access to information and support, perceptions of illness and ability to provide self-care after traumatic injury. METHODS: Adults (18 years or older) admitted to hospital for ≥24 hours for the acute treatment of trauma in two hospitals in Queensland, Australia, were enrolled in a prospective cohort study. Questionnaires completed at hospital discharge and 3 months and 6 months incorporated the following: demographic data; psychological factors (Revised Illness Perception Questionnaire, Information, Autonomy and Support Scale, and Therapeutic Self-Care Scale); and outcome data (medical short form-36). Data on injury and hospital stay were obtained from health care records and the Queensland Trauma Registry. RESULTS: One hundred ninety-four patients with a median Injury Severity Score 9 (interquartile range, 5–14) were enrolled, with 125 (64%) completing questionnaires at 6 months. More than half the cohort reported symptoms of pain, fatigue, stiff joints, sleep difficulties, and loss of strength. All subscale scores on the short form-36 were below Australian norms 6 months after injury. Predictors of poor physical health included older age, lower extremity injury, and increased perceived consequences of their injuries, whereas predictors of poor mental health included younger age, female gender, and lower perceived control over their environment. CONCLUSIONS: Patients with minor to moderate injury based on anatomic injury scoring systems have ongoing challenges with recovery including problematic symptoms and low quality of life. Interventions aimed toward assisting recovery should not be limited to trauma patients with major injury. LEVEL OF EVIDENCE: Prognostic study, level III

Environmental factors influencing the Douglas fir invasion of Nothofagus forest

Douglas fir (Pseudotsuga menziesii) was introduced to New Zealand in 1859 for timber, and in the last few decades has been recognised as an invasive species, particularly into grassland. However, its potential to invade native forests is still poorly understood. I investigated the invasion of Douglas fir into mountain beech (Nothofagus solandri var. cliffortioides) forest, particularly the factors limiting the spread, at Cora Lynn, near Arthur’s Pass. Adjacent to the beech forest is an 80 ha Douglas fir and Corsican pine (Pinus nigra) plantation, whose invasive potential started to raise concerns in the late 1980s. The study was divided into three parts. The first consisted of resampling plots established on the site in 1989 to count Douglas fir seedlings spreading into Nothofagus. In the second part, I investigated the factors limiting the establishment of Douglas fir seedlings in the beech forest. To do this I established 400 points in the native forest, and at each point I assessed the light environment (via hemispherical photography), measured altitude, and distance to the nearest seedling. Lastly, I conducted a root competition and fertiliser-addition experiment to investigate the factors limiting the growth of the Douglas fir seedlings. I selected 544 naturally regenerating seedlings (30 to 70 cm tall) in the beech forest, and applied one of four treatments: fertiliser addition, root trenching, fertiliser addition plus root trenching, and control. Light environment and altitude at each seedling were measured. The mean density of seedlings in the plots has increased 13-fold since the first measurement in 1989, from 11,267 seedlings/ha to 150,333 seedlings/ha in 2016. There is a widespread Douglas fir invasion of the mountain beech forest in progress – in only a single point out of 400 did I fail to find a seedling within a 10-m radius. Altitude had the strongest effect on the distance to the nearest seedling, with lower seedling density at higher altitudes. Although distance to the nearest seedling decreased with light, the seedlings were not restricted to light-wells or canopy gaps as generally presumed, but present throughout the native forest. Light had the strongest effect on seedling growth. At the experimental seedlings, light ranged from 3.01 to 10.29 mol m-2 d-1, that is 8.12% and 27.8% respectively of full sunlight. Altitude had a negative effect on seedling growth. Nutrient availability was second to light as a growth limiting factor. Fertiliser addition had the largest effect on seedling growth across treatments, increasing it 18.3% above that of the control. Root trenching had a small negative effect on growth, while fertilizer plus trenching had a positive effect, but still smaller than expected. I have demonstrated that Douglas fir is well able to invade Nothofagus forest, albeit slowly, and that the spread was affected by a complex relationship between light, nutrients, root competition, distance to the seed source, and altitude. In New Zealand, poor control of conifer invasions into grasslands and shrublands in the past has led to large environmental and economic impacts. The potential negative effects of the Douglas fir spread into native forest could be minimized by early control. I hope that my work will contribute to a better understanding of the Douglas fir’s invasive potential, as well as draw attention to the need for managing the spread in progress

In-hospital cardiac arrests: Effect of amended Australian Resuscitation Council 2006 guidelines

Objective: To evaluate cardiac arrest outcomes following the introduction of the Australian Resuscitation Council (ARC) 2006 amended guidelines for basic and advanced life support. Methods: A retrospective study of all consecutive cardiac arrests during a 3-year phase pre-implementation (2004–06) and a 3-year phase post-implementation (2007–09) of the ARC 2006 guidelines was conducted at a tertiary referral hospital in Brisbane, Australia. Results: Over the 6-year study phase 690 cardiac arrests were reported. Resuscitation was attempted in 248 patients pre-implementation and 271 patients post-implementation of the ARC 2006 guidelines. After adjusting for significant prognostic factors we found no significant change in return of spontaneous circulation (ROSC) (odds ratio 1.21, 95% confidence interval 0.80–1.85, P = 0.37) or survival to discharge (odds ratio 1.49, 95% confidence interval 0.94–2.37, P = 0.09) after the implementation of the ARC 2006 guidelines. Factors that remained significant in the final model for both outcomes included having an initial shockable rhythm, a shorter length of time from collapse to arrival of cardiac arrest team, location of the patient in a critical-care area, shorter length of resuscitation and a day-time arrest (0700–2259 hours). In addition the arrest being witnessed was significant for ROSC and younger age was significant for survival to discharge. Conclusions: There are multiple factors that influence clinical outcomes following an in-hospital cardiac arrest and further research to refine these significant variables will assist in the future management of cardiac arrests. What is known about this topic?: The evaluation of outcomes from in-hospital cardiac arrests focuses on immediate survival expressed as ROSC and survival to hospital discharge. These clinical outcomes have not improved substantially over the last two decades. What does this paper add?: This paper identifies the factors that are related to ROSC and survival to discharge following the implementation of the ARC 2006 guidelines, which included a refocus on providing quality cardiopulmonary resuscitation with minimal interruptions. What are the implications for practitioners?: Given that multiple factors can influence clinical outcomes following an in-hospital cardiac arrest, focusing on maximising a range of factors surrounding cardiopulmonary resuscitation is essential to improve outcomes

BDNF Val 66 Met genotype is associated with drug‐seeking phenotypes in heroin‐dependent individuals: a pilot study

Brain‐derived neurotrophic factor (BDNF) Val 66 Met genotype has been associated with neurobehavioral deficits. To examine its relevance for addiction, we examined BDNF genotype differences in drug‐seeking behavior. Heroin‐dependent volunteers ( n  = 128) completed an interview that assessed past‐month naturalistic drug‐seeking/use behaviors. In African Americans ( n  = 74), the Met allele was uncommon (carrier frequency 6.8%); thus, analyses focused on European Americans ( n  = 54), in whom the Met allele was common (carrier frequency 37.0%). In their natural setting, Met carriers ( n  = 20) reported more time‐ and cost‐intensive heroin‐seeking and more cigarette use than Val homozygotes ( n  = 34). BDNF Val 66 Met genotype predicted 18.4% of variance in ‘weekly heroin investment’ (purchasing time × amount × frequency). These data suggest that the BDNF Met allele may confer a ‘preferred drug‐invested’ phenotype, resistant to moderating effects of higher drug prices and non‐drug reinforcement. These preliminary hypothesis‐generating findings require replication, but are consistent with pre‐clinical data that demonstrate neurotrophic influence in drug reinforcement. Whether this genotype is relevant to other abused substances besides opioids or nicotine, or treatment response, remains to be determined.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/99593/1/adb431.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/99593/2/adb431_sm_fig_s1.pd