LEADER 04421nam 22007331c 450 001 9910454002003321 005 20200115203623.0 010 $a1-4725-6037-X 010 $a1-282-11902-8 010 $a9786612119026 010 $a1-84731-478-3 024 7 $a10.5040/9781472560377 035 $a(CKB)1000000000754910 035 $a(EBL)439016 035 $a(OCoLC)503050728 035 $a(SSID)ssj0000118948 035 $a(PQKBManifestationID)11988774 035 $a(PQKBTitleCode)TC0000118948 035 $a(PQKBWorkID)10055417 035 $a(PQKB)11232386 035 $a(MiAaPQ)EBC1772447 035 $a(MiAaPQ)EBC439016 035 $a(Au-PeEL)EBL1772447 035 $a(CaPaEBR)ebr10309154 035 $a(CaONFJC)MIL211902 035 $a(OCoLC)893332050 035 $a(UtOrBLW)bpp09256069 035 $a(Au-PeEL)EBL439016 035 $a(EXLCZ)991000000000754910 100 $a20140929d2009 uy 0 101 0 $aeng 135 $aur|n|---||||| 181 $ctxt 182 $cc 183 $acr 200 10$aCausing psychiatric and emotional harm $ereshaping the boundaries of legal liability $fHarvey Teff 205 $a1st ed. 210 1$aOxford $aPortland, Oregon $cHart Publishing $d2009. 215 $a1 online resource (228 p.) 300 $aDescription based upon print version of record. 311 $a1-84113-216-0 320 $aIncludes bibliographical references (pages [191]-200) and index 327 $aPsychiatric harm, emotional suffering and legal redress -- The development of redress for emotional harm and nervous shock -- Contemporary provision for 'accident-based' psychiatric illness -- Liability for psychiatric harm 'beyond the mainstream' -- Policy concerns -- A proposal for reform 327 $a1: Psychiatric Harm, Emotional Suffering and Legal Redress -- 2: The Development of Redress for Emotional Harm and Nervous Shock -- 3: Contemporary Provision for 'Accident-Based' Psychiatric Illness 5 -- 4: Liability for Psychiatric Harm 'Beyond the Mainstream' 9 -- 5: Policy Concerns -- 6: A Proposal For Reform 330 8 $aThough mental harm can be profoundly disabling, the law imposes strict limits on who can recover damages for it. In the absence of physical injury, compensation is not normally available for negligently caused mental suffering, however severe, unless it constitutes a 'recognisable psychiatric illness'. Claimants whose mental trauma stems from injury caused to someone else are subject to arbitrary restrictive liability rules that dispense with established legal principles and cannot be reconciled with scientific advances. The book traces the history of civil liability for mental harm up to the present day. It is argued that the reluctance to provide redress reflects an enduring suspicion of intangible injury and undue fear of proliferating claims. The scale and legal ramifications of the Hillsborough disaster; the emergence of claims arising from work-related stress, and other new categories of claims based mainly on prior relationships between the parties, have all added to a 'floodgates fear' that has intensified due to popular perceptions of a 'compensation culture'. The book contrasts the limited scope for liability under English law with developments in several other jurisdictions. It is argued that statutory reform is needed to achieve greater legal coherence and to provide a remedy that tracks the impact and severity of harm and is not confined to psychiatric disorders. A new legal framework is offered, rooted in reasonable foreseeability of mental or emotional harm, with a liability threshold of 'moderate severity'. To allay concerns about proliferating claims, modifications to the compensatory regime for personal injury are proposed 606 $aPersonal injuries 606 $2Torts / Delicts 606 $aLiability for emotional distress 606 $aNegligence$xLaw and legislation 606 $aDamages 608 $aElectronic books. 615 0$aPersonal injuries. 615 0$aLiability for emotional distress. 615 0$aNegligence$xLaw and legislation. 615 0$aDamages. 676 $a346.4203 700 $aTeff$b Harvey$0249550 801 0$bUtOrBLW 801 1$bUtOrBLW 801 2$bUkLoBP 906 $aBOOK 912 $a9910454002003321 996 $aCausing psychiatric and emotional harm$92459687 997 $aUNINA LEADER 04524nam 2200421z- 450 001 9910136816903321 005 20210212 035 $a(CKB)3710000000631045 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/60913 035 $a(oapen)doab60913 035 $a(EXLCZ)993710000000631045 100 $a20202102d2015 |y 0 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 00$aThymic stromal alterations and genetic disorders of immune system 210 $cFrontiers Media SA$d2015 215 $a1 online resource (81 p.) 225 1 $aFrontiers Research Topics 311 08$a2-88919-717-4 330 $aThe pathogenic mechanisms underlying primary T-cell disorders are mainly related to molecular alterations of genes whose expression is intrinsic to hematopoietic cells. However, since the differentiation process requires a crosstalk among thymocytes and the thymic microenvironment, molecular alterations of genes, involved in the differentiation and functionality of the stromal component of the thymus, may lead to a severe T-cell defect or failure of central tolerance, as well. The first example of severe combined immunodeficiency (SCID) not related to an intrinsic alteration of the hematopoietic cell but rather of the thymic epithelial component is the Nude/SCID phenotype, inherited as an autosomal recessive disorder, whose hallmarks are the T-cell defect and the absence of the thymus. The clinical and immunological phenotype is the human equivalent of the murine Nude/SCID syndrome, which represents the first spontaneous SCID identified in nude mice in 1966. For over 3 decades studies of immune system in these mice enormously contributed to the overall knowledge of cell mediated immunity, in the assumption that the athymia of these mice was solely responsible for the T-cell immunological defect. This syndrome is due to mutations of the transcription factor FOXN1, belonging to the forkhead-box gene family, which is mainly expressed in the thymus and skin epithelial cells, where it plays a critical role in differentiation and survival. An alteration of the thymic structure is also a feature of the DiGeorge syndrome (DGS), which has been long considered the human counterpart of the nude mice phenotype. This syndrome is frequently associated to a deletion of the 22q11 region, which contains approximately 30 genes, including the TBX1 gene, which is responsible for most of the clinical features of DGS in humans and mice. In this syndrome common manifestations are cardiac malformations, speech delay, hypoparathyrodism and immunodeficiency, even though the immunological hallmarks of the T-cell defect in DiGeorge syndrome are profoundly different from those reported in human Nude/SCID. The divergence of the phenotype among these 2 entities raised the possibility that the FOXN1 transcription factor represents the real key stromal molecule implicated in directing the hematopoietic stem cell toward a proper T-cell fate. Thymic stromal component of the primary lymphoid organ is also required to negatively select the autoreactive clones, a process driven by the expression of tissue specific antigens (TSA) by medullary thymic epithelial cells (mTECs). The expression of genes encoding TSA antigens is mediated by autoimmune regulator (AIRE) gene, encoding a transcription factor expressed in mTECs. Molecular alterations of this gene are associated to autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED), a rare autosomal disorder, which may be considered the prototype of an autoimmune disease due to the failure of central tolerance homeostasis. All these "experiments of nature" led to unravel novel pathogenic mechanisms underlying inherited disorders of immune system and, of note, to clarify the pivotal role of epithelial cells in the maturation and education process of T-cell precursors. 606 $aMedicine and Nursing$2bicssc 610 $aAPECED 610 $aCentral Tolerance 610 $aCombined immunodeficiency 610 $aDiGeorge Syndrome 610 $aFoxn1 610 $amedullary thymic epithelial cells 610 $aRag defects 615 7$aMedicine and Nursing 700 $aClaudio Pignata$4auth$01296297 702 $aAna E. Sousa$4auth 906 $aBOOK 912 $a9910136816903321 996 $aThymic stromal alterations and genetic disorders of immune system$93023971 997 $aUNINA