The Control System of CERN Accelerators Vacuum (LS1 Activities and New Developments)

After 3 years of operation, the LHC entered its first Long Shutdown period (LS1), in February 2013 [1]. Major consolidation and maintenance works are being performed across the whole CERN’s Accelerator chain, in order to prepare the LHC to restart at higher energy, in 2015. The injector chain shall resume earlier, in mid-14. We report about the on-going vacuum-controls projects. Some of them concern the renovation of the controls of certain machines; others are associated with the consolidations of the vacuum systems of LHC and its injectors; and a few are completely new installations. ue to the wide age-span of the existing vacuum installations, there is a mix of design philosophies and of control-equipment generations. The renovations and the novel projects offer an opportunity to improve the uniformity and efficiency of vacuum controls by: reducing the number of equipment versions with similar functionality; identifying, naming, labelling, and documenting all pieces of equipment; homogenizing the control architectures, while converging to a common software framework

Monoclonal antibodies against the structural proteins of viral haemorrhagic septicaemia virus isolates

Abstract. Five VHSV isolates from different host species and Spanish geographical locations and three viral haemorrhagic septicaemia virus (VHSV) international reference serotypes (F1, F2 and 23˙75) were studied by several characterized monoclonal antibodies (MAbs) including a neutralizing MAb to four structural proteins of VHSV. We report here the lack of reaction between anti‐M1 and some of the isolates of VHSV and the homogeneity of most of the isolates with respect to the MAbs tested. The reagents obtained will improve diagnostic tests which currently use polyclonal antibodies. Copyright © 1993, Wiley Blackwell. All rights reserve

ETFAD/EADV Eczema task force 2015 position paper on diagnosis and treatment of atopic dermatitis in adult and paediatric patients.

Atopic dermatitis (AD) is a clinically defined, highly pruritic, chronic inflammatory skin disease of children and adults. The diagnosis is made using evaluated clinical criteria. Disease activity is best measured with a composite score assessing both objective signs and subjective symptoms, such as SCORAD. The management of AD must consider the clinical and pathogenic variabilities of the disease and also target flare prevention. Basic therapy includes hydrating topical treatment, as well as avoidance of specific and unspecific provocation factors. Anti-inflammatory treatment of visible skin lesions is based on topical glucocorticosteroids and the topical calcineurin inhibitors tacrolimus and pimecrolimus. Topical calcineurin inhibitors are preferred in sensitive locations. Tacrolimus and mid-potent steroids are proven for proactive therapy, which is long-term intermittent anti-inflammatory therapy of the frequently relapsing skin areas. Systemic anti-inflammatory or immunosuppressive treatment is indicated for severe refractory cases. Biologicals targeting key mechanisms of the atopic immune response are promising emerging treatment options. Microbial colonization and superinfection may induce disease exacerbation and can justify additional antimicrobial treatment. Systemic antihistamines (H1R-blockers) may diminish pruritus, but do not have sufficient effect on lesions. Adjuvant therapy includes UV irradiation, preferably UVA1 or narrow-band UVB 311 nm. Dietary recommendations should be patient specific and elimination diets should only be advised in case of proven food allergy. Allergen-specific immunotherapy to aeroallergens may be useful in selected cases. Psychosomatic counselling is recommended to address stress-induced exacerbations. 'Eczema school' educational programmes have been proven to be helpful for children and adults

ETFAD/EADV Eczema task force 2015 position paper on diagnosis and treatment of atopic dermatitis in adult and paediatric patients

Atopic dermatitis (AD) is a clinically defined, highly pruritic, chronic inflammatory skin disease of children and adults. The diagnosis is made using evaluated clinical criteria. Disease activity is best measured with a composite score assessing both objective signs and subjective symptoms, such as SCORAD. The management of AD must consider the clinical and pathogenic variabilities of the disease and also target flare prevention. Basic therapy includes hydrating topical treatment, as well as avoidance of specific and unspecific provocation factors. Anti-inflammatory treatment of visible skin lesions is based on topical glucocorticosteroids and the topical calcineurin inhibitors tacrolimus and pimecrolimus. Topical calcineurin inhibitors are preferred in sensitive locations. Tacrolimus and mid-potent steroids are proven for proactive therapy, which is long-term intermittent anti-inflammatory therapy of the frequently relapsing skin areas. Systemic anti-inflammatory or immunosuppressive treatment is indicated for severe refractory cases. Biologicals targeting key mechanisms of the atopic immune response are promising emerging treatment options. Microbial colonization and superinfection may induce disease exacerbation and can justify additional antimicrobial treatment. Systemic antihistamines (H1R-blockers) may diminish pruritus, but do not have sufficient effect on lesions. Adjuvant therapy includes UV irradiation, preferably UVA1 or narrow-band UVB 311 nm. Dietary recommendations should be patient specific and elimination diets should only be advised in case of proven food allergy. Allergen-specific immunotherapy to aeroallergens may be useful in selected cases. Psychosomatic counselling is recommended to address stress-induced exacerbations. 'Eczema school' educational programmes have been proven to be helpful for children and adults