Elucidating the selenium and arsenic metabolic pathways following exposure to the non-hyperaccumulating Chlorophytum comosum, spider plant

Although many studies have investigated the metabolism of selenium and arsenic in hyperaccumulating plants for phytoremediation purposes, few have explored non-hyperaccumulating plants as a model for general contaminant exposure to plants. In addition, the result of simultaneous supplementation with selenium and arsenic has not been investigated in plants. In this study, Chlorophytum comosum, commonly known as the spider plant, was used to investigate the metabolism of selenium and arsenic after single and simultaneous supplementation. Size exclusion and ion-pairing reversed phase liquid chromatography were coupled to an inductively coupled plasma mass spectrometer to obtain putative metabolic information of the selenium and arsenic species in C. comosum after a mild aqueous extraction. The chromatographic results depict that selenium and arsenic species were sequestered in the roots and generally conserved upon translocation to the leaves. The data suggest that selenium was directly absorbed by C. comosum roots when supplemented with SeVI, but a combination of passive and direct absorption occurred when supplemented with SeIV due to the partial oxidation of SeIV to SeVI in the rhizosphere. Higher molecular weight selenium species were more prevalent in the roots of plants supplemented with SeIV, but in the leaves of plants supplemented with SeVI due to an increased translocation rate. When supplemented as AsIII, arsenic is proposed to be passively absorbed as AsIII and partially oxidized to AsV in the plant root. Although total elemental analysis demonstrates a selenium and arsenic antagonism, a compound containing selenium and arsenic was not present in the general aqueous extract of the plant

Burden of childhood-onset arthritis

Juvenile arthritis comprises a variety of chronic inflammatory diseases causing erosive arthritis in children, often progressing to disability. These children experience functional impairment due to joint and back pain, heel pain, swelling of joints and morning stiffness, contractures, pain, and anterior uveitis leading to blindness. As children who have juvenile arthritis reach adulthood, they face possible continuing disease activity, medication-associated morbidity, and life-long disability and risk for emotional and social dysfunction. In this article we will review the burden of juvenile arthritis for the patient and society and focus on the following areas: patient disability; visual outcome; other medical complications; physical activity; impact on HRQOL; emotional impact; pain and coping; ambulatory visits, hospitalizations and mortality; economic impact; burden on caregivers; transition issues; educational occupational outcomes, and sexuality

ZIP8 Zinc Transporter: Indispensable Role for Both Multiple-Organ Organogenesis and Hematopoiesis In Utero

Previously this laboratory characterized Slc39a8-encoded ZIP8 as a Zn2+/(HCO3–)2 symporter; yet, the overall physiological importance of ZIP8 at the whole-organism level remains unclear. Herein we describe the phenotype of the hypomorphic Slc39a8(neo/neo) mouse which has retained the neomycin-resistance gene in intron 3, hence causing significantly decreased ZIP8 mRNA and protein levels in embryo, fetus, placenta, yolk sac, and several tissues of neonates. The Slc39a8(neo) allele is associated with diminished zinc and iron uptake in mouse fetal fibroblast and liver-derived cultures; consequently, Slc39a8(neo/neo) newborns exhibit diminished zinc and iron levels in several tissues. Slc39a8(neo/neo) homozygotes from gestational day(GD)-11.5 onward are pale, growth-stunted, and die between GD18.5 and 48 h postnatally. Defects include: severely hypoplastic spleen; hypoplasia of liver, kidney, lung, and lower limbs. Histologically, Slc39a8(neo/neo) neonates show decreased numbers of hematopoietic islands in yolk sac and liver. Low hemoglobin, hematocrit, red cell count, serum iron, and total iron-binding capacity confirmed severe anemia. Flow cytometry of fetal liver cells revealed the erythroid series strikingly affected in the hypomorph. Zinc-dependent 5-aminolevulinic acid dehydratase, required for heme synthesis, was not different between Slc39a8(+/+) and Slc39a8(neo/neo) offspring. To demonstrate further that the mouse phenotype is due to ZIP8 deficiency, we bred Slc39a8(+/neo) with BAC-transgenic BTZIP8-3 line (carrying three extra copies of the Slc39a8 allele); this cross generated viable Slc39a8(neo/neo)_BTZIP8-3(+/+) pups showing none of the above-mentioned congenital defects–proving Slc39a8(neo/neo) causes the described phenotype. Our study demonstrates that ZIP8-mediated zinc transport plays an unappreciated critical role during in utero and neonatal growth, organ morphogenesis, and hematopoiesis

Mucosal Targeting of a BoNT/A Subunit Vaccine Adjuvanted with a Mast Cell Activator Enhances Induction of BoNT/A Neutralizing Antibodies in Rabbits

We previously reported that the immunogenicity of Hcβtre, a botulinum neurotoxin A (BoNT/A) immunogen, was enhanced by fusion to an epithelial cell binding domain, Ad2F, when nasally delivered to mice with cholera toxin (CT). This study was performed to determine if Ad2F would enhance the nasal immunogenicity of Hcβtre in rabbits, an animal model with a nasal cavity anatomy similar to humans. Since CT is not safe for human use, we also tested the adjuvant activity of compound 48/80 (C48/80), a mast cell activating compound previously determined to safely exhibit nasal adjuvant activity in mice.New Zealand White or Dutch Belted rabbits were nasally immunized with Hcβtre or Hcβtre-Ad2F alone or combined with CT or C48/80, and serum samples were tested for the presence of Hcβtre-specific binding (ELISA) or BoNT/A neutralizing antibodies.Hcβtre-Ad2F nasally administered with CT induced serum anti-Hcβtre IgG ELISA and BoNT/A neutralizing antibody titers greater than those induced by Hcβtre + CT. C48/80 provided significant nasal adjuvant activity and induced BoNT/A-neutralizing antibodies similar to those induced by CT.Ad2F enhanced the nasal immunogenicity of Hcβtre, and the mast cell activator C48/80 was an effective adjuvant for nasal immunization in rabbits, an animal model with a nasal cavity anatomy similar to that in humans

Associations Between Pain, Current Tobacco Smoking, Depression, and Fibromyalgia Status Among Treatment‐Seeking Chronic Pain Patients

ObjectiveAs smoking impacts physiological pathways in the central nervous system, it is important to consider the association between smoking and fibromyalgia, a pain condition caused predominantly by central nervous system dysfunction. The objectives were to assess the prevalence of current smoking among treatment‐seeking chronic pain patients with (FM+) and without (FM−) a fibromyalgia‐like phenotype; test the individual and combined influence of smoking and fibromyalgia on pain severity and interference; and examine depression as a mediator of these processes.MethodsQuestionnaire data from 1566 patients evaluated for a range of conditions at an outpatient pain clinic were used. The 2011 Survey Criteria for Fibromyalgia were used to assess the presence of symptoms associated with fibromyalgia.ResultsCurrent smoking was reported by 38.7% of FM+ patients compared to 24.7% of FM− patients. FM+ smokers reported higher pain and greater interference compared to FM+ nonsmokers, FM− smokers, and FM− nonsmokers. There was no interaction between smoking and fibromyalgia. Significant indirect effects of fibromyalgia and smoking via greater depression were observed for pain severity and interference.ConclusionsCurrent smoking and positive fibromyalgia status were associated with greater pain and impairment among chronic pain patients, possibly as a function of depression. Although FM+ smokers report the most negative clinical symptomatology (i.e., high pain, greater interference) smoking does not appear to have a unique association with pain or functioning in FM+ patients, rather the effect is additive. The 38.7% smoking rate in FM+ patients is high, suggesting FM+ smokers present a significant clinical challenge.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/112206/1/pme12747.pd

Sleep and mood in older adults: coinciding changes in insomnia and depression symptoms

The aim of this analysis was to test if changes in insomnia symptoms and global sleep quality are associated with coinciding changes in depressed mood among older adults. We report on results yielded from secondary analysis of longitudinal data from a clinical trial of older adults (N = 49) aged 55 to 80 years who reported at least moderate levels of sleep problems. All measures were collected at baseline and after the trial ten weeks later. We computed change scores for two separate measures of disturbed sleep, the Athens Insomnia Scale (AIS) and the Pittsburgh Sleep Quality Index (PSQI), and tested their association with change in depressed mood (Beck Depression Inventory-II; BDI-II) in two separate linear regression models adjusted for biological covariates related to sleep (sex, age, body mass index, and NF-κB as a biological marker previously correlated with insomnia and depression). Change in AIS scores was associated with change in BDI-II scores (β = 0.38, p < 0.01). Change in PSQI scores was not significantly associated with change in BDI-II scores (β = 0.17, p = 0.26). Our findings suggest that improvements over ten weeks in insomnia symptoms rather than global sleep quality coincide with improvement in depressed mood among older adults

Sleep and mood in older adults: coinciding changes in insomnia and depression symptoms

The aim of this analysis was to test if changes in insomnia symptoms and global sleep quality are associated with coinciding changes in depressed mood among older adults. We report on results yielded from secondary analysis of longitudinal data from a clinical trial of older adults (N = 49) aged 55 to 80 years who reported at least moderate levels of sleep problems. All measures were collected at baseline and after the trial ten weeks later. We computed change scores for two separate measures of disturbed sleep, the Athens Insomnia Scale (AIS) and the Pittsburgh Sleep Quality Index (PSQI), and tested their association with change in depressed mood (Beck Depression Inventory-II; BDI-II) in two separate linear regression models adjusted for biological covariates related to sleep (sex, age, body mass index, and NF-κB as a biological marker previously correlated with insomnia and depression). Change in AIS scores was associated with change in BDI-II scores (β = 0.38, p < 0.01). Change in PSQI scores was not significantly associated with change in BDI-II scores (β = 0.17, p = 0.26). Our findings suggest that improvements over ten weeks in insomnia symptoms rather than global sleep quality coincide with improvement in depressed mood among older adults