ABSTRACT
AIM: To summarise the diagnosis and management of IgE-mediated food allergy (FA) in New Zealand children. METHOD: A review of the scientific literature and subsequent consensus development. RESULTS: FA is a common problem in New Zealand children with management necessitating accurate diagnosis, appropriate risk management, and reassessment over time. CONCLUSION: This paper highlights the importance of a structured approach to diagnosis and management of FA in New Zealand children, guided by appropriately skilled health professionals.
Subject(s)
Food Hypersensitivity/diagnosis , Food Hypersensitivity/immunology , Food Hypersensitivity/therapy , Immunoglobulin E/immunology , Child , Food Hypersensitivity/epidemiology , Humans , New Zealand/epidemiology , Referral and Consultation , Skin TestsABSTRACT
(2S)-2-{[(3,5-Diflurophenyl)acetyl]amino}-N-[(3S)-1-methyl-2-oxo-5-phenyl-2,3-dihydro-1H-1,4-benzodiazepin-3-yl]propanamide (compound E) is a gamma-secretase inhibitor capable of reducing amyloid beta-peptide (1-40) and amyloid beta-peptide (1-42) levels. In this study we investigated the effect of in vivo administration of compound E on guinea-pig plasma, CSF and cortical amyloid beta-peptide (1-40) concentration. Using repeated sampling of CSF, compound E (30 mg/kg p.o.) was shown to cause a time-dependent decrease in CSF amyloid beta-peptide (1-40) levels, which was maximal at 3 h (70% inhibition), compared to baseline controls. After 3 h administration, compound E (3, 10 and 30 mg/kg p.o.), reduced plasma, CSF and DEA-extracted cortical amyloid beta-peptide (1-40) levels by 95, 97 and 99%; 26, 48 and 78%; 32, 33, and 47%, respectively, compared to vehicle control values. In the same animals, compound E (3, 10 and 30 mg/kg p.o.) inhibited cortical gamma-secretase activity, determined ex vivo using the recombinant substrate C100Flag, by 40, 71 and 79% of controls, respectively. These data demonstrate the value of determining not only the extent by which systemic administration of a gamma-secretase inhibitor reduces amyloid beta-peptide, but also the inhibition of brain gamma-secretase activity, as a more direct estimate of enzyme occupancy.
Subject(s)
Aspartic Acid Endopeptidases/metabolism , Cerebral Cortex/drug effects , Cerebral Cortex/enzymology , Protease Inhibitors/administration & dosage , Administration, Oral , Amyloid Precursor Protein Secretases , Amyloid beta-Peptides/metabolism , Animals , Arsenicals/administration & dosage , Bisbenzimidazole/administration & dosage , Bisbenzimidazole/analogs & derivatives , Dose-Response Relationship, Drug , Endopeptidases , Enzyme Activation/drug effects , Enzyme Activation/physiology , Guinea Pigs , Male , Peptide Fragments/metabolismABSTRACT
A careful check on the Westminster Hospital's telephone system showed that, among other things, the hospital was being charged for extensions which did not exist. Eventually the Post Office made a rebate of nearly 15,000 pounds. D. V. Hodgson, telephone supervisor, and T. J. Townend, district residences manager, tell how this was achieved and what steps have been taken to see the hospital is not over-charged in the future.