High Anxiety: Forcing Medical Marijuana Patients to Choose Between Employment and Treatment

The vast majority of states recognize the potential medical benefits of marijuana in treating debilitating medical conditions. To date, thirty-six states have legalized consumption of medical marijuana and eleven have done the same for low-tetrahydrocannabinol variations of the cannabis plant. Marijuana still remains illegal under federal law, however, subjecting it to stringent regulation since the Controlled Substances Act became law in 1971. Despite this, the wave of state legalization has essentially left the federal government in the past when it comes to marijuana policy. This federal prohibition poses unique problems for medical marijuana patients seeking employment. The current status of the law leaves no federal employment protections for patients who use marijuana to treat a medical condition, even if such usage complies with applicable state law. Further, even states that have legalized medical marijuana offer little in the way of employment protections for patients. Additionally, state disability protection statutes often exclude people engaging in “illegal use of drugs”—which courts have typically interpreted to include federally illegal substances, including marijuana. The majority of courts have also declined to protect medical marijuana use under lawful activities provisions. Some states have enacted provisions protecting medical marijuana patients from employment discrimination on the basis of their marijuana use, but these are just a small minority. This Note argues that the most expedient way to bring medical marijuana patients under the umbrella of employment protections is for courts to recognize protections for medical marijuana use under the tort of wrongful discharge in violation of public policy

Sympathetic nerve-derived ATP regulates renal medullary vasa recta diameter via pericyte cells: a role for regulating medullary blood flow?

Pericyte cells are now known to be a novel locus of blood flow control, being able to regulate capillary diameter via their unique morphology and expression of contractile proteins. We have previously shown that exogenous ATP causes constriction of vasa recta via renal pericytes, acting at a variety of membrane bound P2 receptors on descending vasa recta (DVR), and therefore may be able to regulate medullary blood flow (MBF). Regulation of MBF is essential for appropriate urine concentration and providing essential oxygen and nutrients to this region of high, and variable, metabolic demand. Various sources of endogenous ATP have been proposed, including from epithelial, endothelial, and red blood cells in response to stimuli such as mechanical stimulation, local acidosis, hypoxia, and exposure to various hormones. Extensive sympathetic innervation of the nephron has previously been shown, however the innervation reported has focused around the proximal and distal tubules, and ascending loop of Henle. We hypothesize that sympathetic nerves are an additional source of ATP acting at renal pericytes and therefore regulate MBF. Using a rat live kidney slice model in combination with video imaging and confocal microscopy techniques we firstly show sympathetic nerves in close proximity to vasa recta pericytes in both the outer and inner medulla. Secondly, we demonstrate pharmacological stimulation of sympathetic nerves in situ (by tyramine) evokes pericyte-mediated vasoconstriction of vasa recta capillaries; inhibited by the application of the P2 receptor antagonist suramin. Lastly, tyramine-evoked vasoconstriction of vasa recta by pericytes is significantly less than ATP-evoked vasoconstriction. Sympathetic innervation may provide an additional level of functional regulation in the renal medulla that is highly localized. It now needs to be determined under which physiological/pathophysiological circumstances that sympathetic innervation of renal pericytes is important

Extreme stiffness tunability through the excitation of nonlinear defect modes

The incremental stiffness characterizes the variation of a material's force response to a small deformation change. In lattices with noninteracting vibrational modes, the excitation of localized states does not have any effect on material properties, such as the incremental stiffness. We report that, in nonlinear lattices, driving a defect mode introduces changes in the static force-displacement relation of the material. By varying the defect excitation frequency and amplitude, the incremental stiffness can be tuned continuously to arbitrarily large positive or negative values. Furthermore, the defect excitation parameters also determine the displacement region at which the force-displacement relation is being tuned. We demonstrate this phenomenon experimentally in a compressed array of spheres tuning its incremental stiffness from a finite positive value to zero and continuously down to negative infinity

Rearrangement of {α-P2W15} to {PW6} moieties during the assembly of transition-metal-linked polyoxometalate clusters

We report the formation of two polyoxotungstates of the general formula [M6(PW6O26)(α-P2W15O56)2(H2O)2]23− (M = CoII or MnII), which contain {PW6} fragments generated from the [P2W15O56]12− precursor, which demonstrates for the first time the transformation of a Dawson lacunae into a Keggin lacunary building block. Solution analysis of the clusters has been conducted via electrospray ionisation mass spectrometry

Role Strains and Mood in Husbands of Women with Fibromyalgia Syndrome: A Test of the Stress Process Model

Spouses of patients experience role strains as a result of informal caregiving, which has been associated with mood in numerous research studies. However, most research is on female caregivers, and little is known about the experience of male spouses, or of the caregiving provided to fibromyalgia patients. The Stress Process Model was used to examine mediators and moderators of the relation between role strain and mood among 135 husbands of women with fibromyalgia. Results indicated that the more activities of daily living and instrumental activities of daily living performed by the husband, the greater the role strain. Role strain was associated with worse mood. A test of the Stress Process Model supported a partial mediation model, where social support and emotion-focused coping partially mediated the relation between role strain and mood. No evidence was found for a moderation model or for problem-focused coping as a mediator. Our research suggests significant impairment and caregiving needs among this patient population, which in turn relates to the mood of the husband who is also an informal caregiver. Our findings also support the Stress Process Model in explaining the complexity of caregiving effects. The results of the study suggest avenues for intervention for individuals strained by their partners’ illness

Role of estrogen and progesterone receptors in neonatal uterine cell proliferation in the mouse

The major endocrine regulators of the female reproductive tract are 17β-estradiol (E2) and progesterone (P4). This review discusses our recent work related to the roles of E2 and P4 and their receptors, estrogen receptor 1 (ESR1) and progesterone receptor (PR), respectively, in the neonatal uterus. Neonatal uterine cells in mice are mitogenically responsive to estrogens, but neonatal ovariectomy does not inhibit pre-weaning uterine cell proliferation, indicating that this process does not require endogenous estrogens. Neonatal uterine cell proliferation could result from ligand-independent growth factor activation of ESR1, or be independent of ESR1 neonatally despite its obligatory role in adult uterine epithelial proliferation. To determine the role of ESR1 in uterine development, we analyzed cell proliferation and uterine gland development (adenogenesis) in wild-type (WT) and Esr1 knockout (Esr1KO) mice postnatally. Our results indicate that pre-weaning uterine cell proliferation and adenogenesis are independent of ESR1, but these processes become dependent on E2/ESR1 signaling for maintenance and further proliferation and uterine growth during puberty. How pre- weaning uterine cell proliferation and adenogenesis occur independently of E2/ESR1 signaling remains unknown, but ligand-independent activation of ESR1 is not involved in this process. The synthetic glucocorticoid dexamethasone (Dex) inhibits luminal epithelial (LE) proliferation in neonatal mouse uteri, but it has been unclear whether Dex effects were mediated by glucocorticoid receptor (GR) and/or PR. We have used PR knockout (PRKO) mice to test whether PR is required for Dex inhibition of LE proliferation. Our results indicate that maximal inhibitory Dex effects on uterine LE proliferation require PR, possibly reflecting Dex crosstalk with PR. Inhibitory effects of Dex and P4 on LE proliferation may also involve GR binding, as indicated by the small but significant inhibition of LE proliferation by both Dex and P4 in PRKO mice

Matter-antimatter rearrangements using the R-matrix method

Funding The contribution of EK was supported by the Ada Lovelace Centre, UK Science and Technology Facilities Council. MP’s work made use of support by CoSeC, the Computational Science Centre for Research Communities, through Collaborative Computational Project Q and High-End-Consortium (HEC) UK-AMOR. Acknowledgments We are grateful for helpful discussions with Jonathan Tennyson and Mike Charlton. The bound-state calculations were performed using the Maxwell High Performance Computing Cluster of the University of Aberdeen IT Service.Peer reviewedPublisher PD