Contesting the psychiatric framing of ME / CFS

ME/CFS is a medically contested illness and its understanding, framing and treatment has been the subject of heated debate. This paper examines why framing the condition as a psychiatric issue—what we refer to as ‘psychiatrisation’—has been so heavily contested by patients and activists. We argue that this contestation is not simply about stigmatising mental health conditions, as some have suggested, but relates to how people diagnosed with mental illness are treated in society, psychiatry and the law. We highlight the potentially harmful consequences of psychiatrisation which can lead to people’s experiential knowledge being discredited. This stems, in part, from a psychiatric-specific form of ‘epistemic injustice’ which can result in unhelpful, unwanted and forced treatments. This understanding helps explain why the psychiatrisation of ME/CFS has become the focus of such bitter debate and why psychiatry itself has become such a significant field of contention, for both ME/CFS patients and mental health service users/survivors. Notwithstanding important differences, both reject the way psychiatry denies patient explanations and understandings, and therefore share a collective struggle for justice and legitimation. Reasons why this shared struggle has not resulted in alliances between ME and mental health activists are noted

The Mannich base NC1153 promotes long-term allograft survival and spares the recipient from multiple toxicities

JAK3 is a cytoplasmic tyrosine kinase with limited tissue expression but is readily found in activated T cells. Patients lacking JAK3 are immune compromised, suggesting that JAK3 represents a therapeutic target for immunosuppression. Herein, we show that a Mannich base, NC1153, blocked IL-2-induced activation of JAK3 and its downstream substrates STAT5a/b more effectively than activation of the closely related prolactin-induced JAK2 or TNF-alpha-driven NF-kappa B. In addition, NC1153 failed to inhibit several other enzymes, including growth factor receptor tyrosine kinases, Src family members, and serine/threonine protein kinases. Although NC1153 inhibited proliferation of normal human T cells challenged with IL-2, IL-4, or IL-7, it did not block T cells void of JAK3. In vivo, a 14-day oral therapy with NC1153 significantly extended survival of MHC/non-MHC mismatched rat kidney allografts, whereas a 90-day therapy induced transplantation tolerance (> 200 days). Although NC1153 acted synergistically with cyclosporin A (CsA) to prolong allograft survival, it was not nephrotoxic, myelotoxic, or lipotoxic and did not increase CsA-induced nephrotoxicity. In contrast to CsA, NC1153 was not metabolized by cytochrome P450 3A4. Thus, NC1153 prolongs allograft survival without several toxic effects associated with current inummosuppressive drugs

QTL analysis of pasta quality using a composite microsatellite and SNP map of durum wheat

Bright yellow color, firmness and low cooking loss are important factors for the production of good-quality pasta products. However, the genetic factors underlying those traits are still poorly understood. To fill this gap we developed a population of 93 recombinant inbred lines (RIL) from the cross between experimental line UC1113 (intermediate pasta quality) with the cultivar Kofa (excellent pasta quality). A total of 269 markers, including 23 SNP markers, were arranged on 14 linkage groups covering a total length of 2,140 cM. Samples from each RIL from five different environments were used for complete pasta quality testing and the results from each year were used for QTL analyses. The combined effect of different loci, environment and their interactions were analyzed using factorial ANOVAs for each trait. We identified major QTLs for pasta color on chromosomes 1B, 4B, 6A, 7A and 7B. The 4B QTL was linked to a polymorphic deletion in the Lpx-B1.1 lipoxygenase locus, suggesting that it was associated with pigment degradation during pasta processing. The 7B QTL for pasta color was linked to the Phytoene synthase 1 (Psy-B1) locus suggesting difference in pigment biosynthesis. QTLs affecting pasta firmness and cooking loss were detected on chromosomes 5A and 7B, and in both cases they were overlapping with QTL for grain protein content and wet gluten content. These last two parameters were highly correlated with pasta firmness (R > 0.71) and inversely correlated to cooking loss (R < -0.37). The location and effect of other QTLs affecting grain size and weight, gluten strength, mixing properties, and ash content are also discussed.Fil: Zhang, W.. University of California; Estados UnidosFil: Chao, S.. United States Department of Agriculture. Agricultural Research Service; Estados UnidosFil: Manthey, F.. North Dakota State University. Department of Plant Sciences; Estados UnidosFil: Chicaiza, O.. University of California; Estados UnidosFil: Brevis, J. C.. University of California; Estados UnidosFil: Echenique, Carmen Viviana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Centro de Recursos Naturales Renovables de la Zona Semiárida. Universidad Nacional del Sur. Centro de Recursos Naturales Renovables de la Zona Semiárida; ArgentinaFil: Dubcovsky, J.. University of California; Estados Unido