Suffering Matters: NEPA, Animals, and the Duty to Disclose

The National Environmental Policy Act (NEPA) requires the federal government to disclose potential environmental harms arising from agency actions. Animal suffering is an environmental harm, yet no court has ruled that its infliction triggers a reporting obligation under NEPA. This Article argues that animal suffering should be a cognizable environmental harm under NEPA, that considerations of animal suffering should factor into whether an agency must prepare an EIS--and should be discussed in the content of the EIS. Part II of this Article introduces and explains the procedural requirements of NEPA. Part III discusses animal suffering--how it is defined, how laws deal with or fail to deal with issues of animal cruelty, and outlines the ways animals suffer as a result of federal actions. Part IV offers examples of major federal actions that cause animal suffering--including federal loan guarantees for Concentrated Animal Feeding Operations (CAFOs) and wildlife management practices, such as depredation, carried out by federal Wildlife Services (WS). Part V establishes that animals are a part of the “human environment” as defined by NEPA and that the harms inflicted on animals resulting from major federal actions constitute a “significant impact,” that should trigger NEPA review and warrant discussion in an Environmental Impact Statement (EIS). Finally, we argue that even if animal suffering alone were insufficient to trigger NEPA review, that suffering in conjunction with the various other environmental impacts associated with activities that cause animal suffering should trigger NEPA review regardless

Enhanced performance of longitudinally post-tensioned long-span LVL beams

The scope of this paper is to highlight the advantages of using longitudinally post-tensioning for long-span timber beams compared to traditional glulam or LVL solutions. The analysis is limited to serviceability limit states for gravity loads. An analtycal iterative procedure which takes into account tendon elongation within beam deflecting has been implemented and validated through experimental tests carried out at the University of Canterbury.In particular, two different static configurations have been studied and different tendon profile configurations (straight and draped) internal and external to the beam section have been investigated and compared with traditional solid timber beams. The experimental results confirm the enhanced performance in terms of deflections at serviceability limit state of the longitudinally post-tensioned solutions with respect to traditional timber beams, especially if external draped tendons are adopted

GABAergic Neuron Deficit As An Idiopathic Generalized Epilepsy Mechanism: The Role Of BRD2 Haploinsufficiency In Juvenile Myoclonic Epilepsy

Idiopathic generalized epilepsy (IGE) syndromes represent about 30% of all epilepsies. They have strong, but elusive, genetic components and sex-specific seizure expression. Multiple linkage and population association studies have connected the bromodomain-containing gene BRD2 to forms of IGE. In mice, a null mutation at the homologous Brd2 locus results in embryonic lethality while heterozygous Brd2+/− mice are viable and overtly normal. However, using the flurothyl model, we now show, that compared to the Brd2+/+ littermates, Brd2+/− males have a decreased clonic, and females a decreased tonic-clonic, seizure threshold. Additionally, long-term EEG/video recordings captured spontaneous seizures in three out of five recorded Brd2+/− female mice. Anatomical analysis of specific regions of the brain further revealed significant differences in Brd2+/− vs +/+ mice. Specifically, there were decreases in the numbers of GABAergic (parvalbumin- or GAD67-immunopositive) neurons along the basal ganglia pathway, i.e., in the neocortex and striatum of Brd2+/− mice, compared to Brd2+/+ mice. There were also fewer GABAergic neurons in the substantia nigra reticulata (SNR), yet there was a minor, possibly compensatory increase in the GABA producing enzyme GAD67 in these SNR cells. Further, GAD67 expression in the superior colliculus and ventral medial thalamic nucleus, the main SNR outputs, was significantly decreased in Brd2+/− mice, further supporting GABA downregulation. Our data show that the non-channel-encoding, developmentally critical Brd2 gene is associated with i) sex-specific increases in seizure susceptibility, ii) the development of spontaneous seizures, and iii) seizure-related anatomical changes in the GABA system, supporting BRD2's involvement in human IGE

Durability of high-frequency 10-kHz spinal cord stimulation for patients with painful diabetic neuropathy refractory to conventional treatments: 12-month results from a randomized controlled trial

No abstract available

A randomized controlled trial of high frequency (10 kHz) spinal cord stimulation in painful diabetic neuropathy

Importance: Many patients with diabetic peripheral neuropathy experience chronic pain and inadequate relief despite best available medical treatments. Objective: To determine whether 10-kHz spinal cord stimulation (SCS) improves outcomes for patients with refractory painful diabetic neuropathy (PDN). Design, Setting, and Participants: The prospective, multicenter, open-label SENZA-PDN randomized clinical trial compared conventional medical management (CMM) with 10-kHz SCS plus CMM. Participants with PDN for 1 year or more refractory to gabapentinoids and at least 1 other analgesic class, lower limb pain intensity of 5 cm or more on a 10-cm visual analogue scale (VAS), body mass index (calculated as weight in kilograms divided by height in meters squared) of 45 or less, hemoglobin A1c (HbA1c) of 10% or less, daily morphine equivalents of 120 mg or less, and medically appropriate for the procedure were recruited from clinic patient populations and digital advertising. Participants were enrolled from multiple sites across the US, including academic centers and community pain clinics, between August 2017 and August 2019 with 6-month follow-up and optional crossover at 6 months. Screening 430 patients resulted in 214 who were excluded or declined participation and 216 who were randomized. At 6-month follow-up, 187 patients were evaluated. Interventions: Implanted medical device delivering 10-kHz SCS. Main Outcomes and Measures: The prespecified primary end point was percentage of participants with 50% pain relief or more on VAS without worsening of baseline neurological deficits at 3 months. Secondary end points were tested hierarchically, as prespecified in the analysis plan. Measures included pain VAS, neurological examination, health-related quality of life (EuroQol Five-Dimension questionnaire), and HbA1c over 6 months. Results: Of 216 randomized patients, 136 (63.0%) were male, and the mean (SD) age was 60.8 (10.7) years. Additionally, the median (interquartile range) duration of diabetes and peripheral neuropathy were 10.9 (6.3-16.4) years and 5.6 (3.0-10.1) years, respectively. The primary end point assessed in the intention-to-treat population was met by 5 of 94 patients in the CMM group (5%) and 75 of 95 patients in the 10-kHz SCS plus CMM group (79%; difference, 73.6%; 95% CI, 64.2-83.0; P < .001). Infections requiring device explant occurred in 2 patients in the 10-kHz SCS plus CMM group (2%). For the CMM group, the mean pain VAS score was 7.0 cm (95% CI, 6.7-7.3) at baseline and 6.9 cm (95% CI, 6.5-7.3) at 6 months. For the 10-kHz SCS plus CMM group, the mean pain VAS score was 7.6 cm (95% CI, 7.3-7.9) at baseline and 1.7 cm (95% CI, 1.3-2.1) at 6 months. Investigators observed neurological examination improvements for 3 of 92 patients in the CMM group (3%) and 52 of 84 in the 10-kHz SCS plus CMM group (62%) at 6 months (difference, 58.6%; 95% CI, 47.6-69.6; P < .001). Conclusions and Relevance: Substantial pain relief and improved health-related quality of life sustained over 6 months demonstrates 10-kHz SCS can safely and effectively treat patients with refractory PDN. Trial Registration: ClincalTrials.gov Identifier: NCT0322842

26th Annual Computational Neuroscience Meeting (CNS*2017): Part 3 - Meeting Abstracts - Antwerp, Belgium. 15–20 July 2017

This work was produced as part of the activities of FAPESP Research,\ud Disseminations and Innovation Center for Neuromathematics (grant\ud 2013/07699-0, S. Paulo Research Foundation). NLK is supported by a\ud FAPESP postdoctoral fellowship (grant 2016/03855-5). ACR is partially\ud supported by a CNPq fellowship (grant 306251/2014-0)

Sharp regularity for evolutionary obstacle problems, interpolative geometries and removable sets

In this paper we prove, by showing that solutions have exactly the same degree of regularity as the obstacle, optimal regularity results for obstacle problems involving evolutionary p-Laplace type operators. A main ingredient, of independent interest, is a new intrinsic interpolative geometry allowing for optimal linearization principles via blow-up analysis at contact points. This also opens the way to the proof of a removability theorem for solutions to evolutionary p-Laplace type equations. A basic feature of the paper is that no differentiability in time is assumed on the obstacle; this is in line with the corresponding linear results

Thyroxine targets different pathways of internalization of type II iodothyronine 5\u27-deiodinase in astrocytes

In the brain, thyroid hormone dynamically regulates levels of the short-lived plasma membrane protein, type II iodothyronine 5\u27-deiodinase. In cultured astrocytes, thyroxine modulates deiodinase levels by activating cytoskeletal-plasma membrane interactions that increase the rate of inactivation of the enzyme. Here we characterized the effects of these thyroxine-dependent cytoskeletal interactions upon the route of internalization of the deiodinase by following the intracellular transit of the affinity-labeled substrate-binding subunit of the deiodinase (p29). Thyroxine rapidly induced the inactivation of the deiodinase and initiated the binding of p29 to F-actin. By 40 min, \u3e 75% of the p29 had been transported to an endosomal pool, which was followed by dissociation of the F-actin-p29 complex. There was no significant accumulation of p29 in the dense lysosomes seen in the presence of thyroxine. In the absence of thyroxine, p29 was internalized and transported to the dense lysosomes at a rate parallel to the inactivation rate of the deiodinase (t1/2 0.75 and 0.64 h, respectively) without involvement with the microfilaments. These data demonstrate that thyroxine targets type II iodothyronine 5\u27-deiodinase to an endosomal pool by activating specific protein-F-actin interactions involved in microfilament-mediated intracellular protein trafficking