Profiles of Alexandrium catenella cysts in Puget Sound sediments and the relationship to paralytic shellfish poisoning events

The magnitude of paralytic shellfish poisoning (PSP) toxins in shellfish and the geographical scope of shellfish closures in Puget Sound have increased in recent decades. PSP, monitored by the Washington Department of Health, has spread from Sequim Bay in the 1950s into central Puget Sound in the 1970s and throughout Puget Sound by the 1990s. Alexandrium catenella, the species responsible for PSP toxins, produces a benthic resting cyst that, upon germinating, can seed blooms. This study examined whether there is a relationship between profiles of cysts in the sediment and temporal variation in PSP in shellfish and if the history of the toxin's southward expansion through Puget Sound can be seen in the cyst record. To address this question, sediment cores were collected from three Puget Sound basins, Sequim Bay, Penn Cove, and Carr Inlet, and cyst profiles were determined. Activities of ²¹⁰Pb were fitted to a depth-dependent diagenetic model to date the sediment cores and determine mixing and sediment-accumulation rates. In order to compare historical variation in PSP with cyst profiles that have been altered by bioturbation, a depth and time-dependent diagenetic model was then used to predict vertical profiles of cysts that would occur under the assumption that cyst deposition rates are proportional to PSP concentration in shellfish measured over several decades at each site. The cyst profiles predicted by the model were compared to measured cyst profiles. These comparisons suggested that Alexandrium blooms and resulting PSP concentration in shellfish are more closely linked to cyst germination and deposition at some stations than at others. Sequim Bay had relatively large numbers of cysts and it is likely that the persistent toxicity here is the result of recurrent seeding from the cyst bed. Penn Cove and Carr Inlet had few cysts despite occasional blooms, suggesting that blooms are transported into those areas, perhaps from other sites of cyst germination. Sequim Bay and Penn Cove had cysts from top to bottom of the cores so it was not possible to determine the date when cysts were first introduced into these bays, but it is likely that A. catenella has been in Penn Cove since at least 1955 or for about two decades before the WDOH PSP toxicity data would indicate. The cyst profile in Carr Inlet suggested a first appearance date of 1985 that is consistent with the first appearance of PSP in shellfish in 1988.     

EPA,not DHA,prevents fibrosis in pressure overload-induced heart failure: potential role of free fatty acid receptor 4

Heart failure with preserved ejection fraction (HFpEF) is half of all HF, but standard HF therapies are ineffective. Diastolic dysfunction, often secondary to interstitial fibrosis, is common in HFpEF. Previously, we found that supra-physiologic levels of ω3-PUFAs produced by 12 weeks of ω3-dietary supplementation prevented fibrosis and contractile dysfunction following pressure overload [transverse aortic constriction (TAC)], a model that resembles aspects of remodeling in HFpEF. This raised several questions regarding ω3-concentration-dependent cardioprotection, the specific role of EPA and DHA, and the relationship between prevention of fibrosis and contractile dysfunction. To achieve more clinically relevant ω3-levels and test individual ω3-PUFAs, we shortened the ω3-diet regimen and used EPA- and DHA-specific diets to examine remodeling following TAC. The shorter diet regimen produced ω3-PUFA levels closer to Western clinics. Further, EPA, but not DHA, prevented fibrosis following TAC. However, neither ω3-PUFA prevented contractile dysfunction, perhaps due to reduced uptake of ω3-PUFA. Interestingly, EPA did not accumulate in cardiac fibroblasts. However, FFA receptor 4, a G protein-coupled receptor for ω3-PUFAs, was sufficient and required to block transforming growth factor β1-fibrotic signaling in cultured cardiac fibroblasts, suggesting a novel mechanism for EPA. In summary, EPA-mediated prevention of fibrosis could represent a novel therapy for HFpEF.     

Enhanced reactivity to pain in patients with rheumatoid arthritis

Introduction  

Maladaptive physiological responses to stress appear to play a role in chronic inflammatory diseases such as rheumatoid arthritis (RA). However, relatively little stress research in RA patients has involved the study of pain, the most commonly reported and most impairing stressor in RA. In the present study, we compared psychophysical and physiological responses to standardized noxious stimulation in 19 RA patients and 21 healthy controls.     

The Revised Fibromyalgia Impact Questionnaire (FIQR): validation and psychometric properties

Introduction  

The Fibromyalgia Impact Questionnaire (FIQ) is a commonly used instrument in the evaluation of fibromyalgia (FM) patients. Over the last 18 years, since the publication of the original FIQ, several deficiencies have become apparent and the cumbersome scoring algorithm has been a barrier to widespread clinical use. The aim of this paper is to describe and validate a revised version of the FIQ: the FIQR.     

Psychological correlates of self-reported functional limitation in patients with ankylosing spondylitis

Introduction  

Functional status is an integral component of health-related quality of life in patients with ankylosing spondylitis (AS). The purpose of this study was to investigate the role of psychological variables in self-reported functional limitation in patients with AS, while controlling for demographic and medical variables.     

Genome‐wide analysis of TNF‐alpha response in pigs challenged with porcine circovirus 2b

Tumor necrosis factor alpha (TNF‐α) is a pro‐inflammatory cytokine with a role in activating adaptive immunity to viral infections. By inhibiting the capacity of plasmacytoid dendritic cells to produce interferon‐α and TNF‐α, porcine circovirus 2 (PCV2) limits the maturation of myeloid dendritic cells and impairs their ability to recognize viral and bacterial antigens. Previously, we reported QTL for viremia and immune response in PCV2‐infected pigs. In this study, we analyzed phenotypic and genetic relationships between TNF‐α protein levels, a potential indicator of predisposition to PCV2 co‐infection, and PCV2 susceptibility. Following experimental challenge with PCV2b, TNF‐α reached the peak at 21 days post‐infection (dpi), at which time a difference was observed between pigs that expressed extreme variation in viremia and growth (P < 0.10). A genome‐wide association study (n = 297) revealed that genotypes of 56 433 SNPs explained 73.9% of the variation in TNF‐α at 21 dpi. Major SNPs were identified on SSC8, SSC10 and SSC14. Haplotypes based on SNPs from a SSC8 (9 Mb) 1‐Mb window were associated with variation in TNF‐α (P < 0.02), IgG (P = 0.05) and IgM (P < 0.13) levels at 21 dpi. Potential overlap of regulatory mechanisms was supported by the correlations between genomic prediction values of TNF‐α and PCV2 antibodies (21 dpi, r > 0.22), viremia (14–21 dpi, P > 0.29) and viral load (r = 0.31, P < 0.0001). Characterization of the QTL regions uncovered genes that could influence variation in TNF‐α levels as well as T‐ and B‐cell development, which can affect disease susceptibility.