Angioplasty and stenting to treat stenosis in the large supra-aortic vessels supplying ischemic areas of the brain

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Identifying the Service Gaps in the Management of Severe Systemic Allergic Reaction/Anaphylaxis by Paediatrics Departments of the Hospital Authority

Abstract Background: Anaphylaxis and severe systemic allergic reaction are potentially life-threatening conditions. There is a paucity of data on the management of such condition amongst Hong Kong children. Objective: This review was designed to assist health professionals to evaluate the current process of care for children admitted with anaphylaxis or severe systemic allergic reaction, to identify service gaps so that patients are appropriately investigated, treated and taught how to recognise and manage severe allergic reactions. Methods: The anaphylaxis and severe allergic reaction/angioedema for children under age of 18 were identified using ICD-9 codes 995.0, 995.1, 995.6. We performed a retrospective chart review of on

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

The interplay between habitual sleep duration and sleep need in risky decision-making

Poster Exhibition - Behaviour: P83

Growth hormone treatment of short chinese children with β-thalassaemia major without GH deficiency

Objective. Despite regular transfusion and desferrioxamine treatment, growth failure is commonly seen in adolescent children with β-thalassaemia major. The growth failure has been thought to be due to GH resistance rather than GH deficiency. We investigated the effect of GH on short non-GH deficient children with β-thalassaemia. Design. Recombinant human GH was given in a dose of 0.14 IU/kg/day subcutaneously in an open study. Patients. Fifteen prepubertal Chinese children with β-thalassaemia major (ranging from 7.16 to 14.7 years in age) with height -1.5 SD or more below the population mean for age and a growth velocity of less than 5 cm/year were treated with growth hormone for one year. All children had peak GH response >15mIU/I to insulin induced hypoglycaemia and normal thyroid function and adrenal reserve. Measurements. Anthropometric measurements were performed every 3 months. Morning urine was tested twice weekly for glycosuria. Blood count, renal and liver function tests, fasting blood glucose, IGF-I and fructosamine levels were assessed at entry and every 3 months during treatment. Pasting insulin was measured before and after 3 and 12 months of GH treatment. Skeletal maturity was assessed before and after one year of treatment. Results. Treatment was stopped in two children after 6 months because of poor growth response and noncompliance with treatment and in one child at 9 months because of bone marrow transplantation. In the 13 children, the growth velocity increased from 3.6 ± 7 cm/year to 8 ± 1.2 cm/year after one year of GH treatment (P < 0.001). IGF-I was low before treatment (10.1 ± 2.7 nmol/l), rising significantly to 15.8 ± 4.8, 18.4 ± 4.6, 19.3 ± 6.4 and 21.9 ± 7.5 nmol/l at 3, 6, 9 and 12 months of treatment (P < 0.005). The mean pretreatment bone age in the 13 children was 9.58 ± 1.41 years and increased to 10.53 ± 1.43 years after one year of treatment (ΔBA/CA 0.95 ± 0.3 years). None of the patients developed glycosuria or hypertension. There was no significant change in blood count, renal and liver function, thyroid function, fasting blood glucose or insulin concentrations during treatment. Conclusion. Growth failure in these children with normal GH reserve and low serum IGF-I concentrations would suggest GH insensitivity. Supraphysiological doses of exogenous GH can cause a significant increase in serum IGF-I levels and a significant improvement in short-term growth of short children with β-thalassaemia major.link_to_subscribed_fulltex

A cross-sectional study of growth, puberty and endocrine function in patients with thalassaemia major in Hong Kong

Methodology: A cross-sectional study of growth, puberty and endocrine function was performed on 35 girls and 33 boys with thalassaemia major. Results: Despite regular transfusion and chelation therapy, 75% of the girls and 62% of the boys over the age of 12 years were below the third percentile for height. Hypogonadotropic hypogonadism was found in a similar percentage of patients. Moderate to marked zinc deficiency secondary to chelation therapy was considered unlikely because normal serum zinc levels were found in all but three of our patients, but we could not exclude the possibility of a marginal status of zinc nutrition causing growth failure. Growth hormone deficiency and diabetes mellitus were sometimes encountered but hypothyroidism, hypoparathyroidism and adrenal Insufficiency were rare among our patients. Most of the patients with growth failure had normal growth hormone (GH) response to insulin induced hypoglycaemia. The serum insulin-like growth factor-1 (IGF-1) levels were low in our patients and no significant difference in the serum IGF-1 levels was found between prepubertal children with or without growth failure (0.4 ± 0.1 mU/mL vs 0.37 ± 0.11 mU/mL, P = 0.39). Similarly, no difference in the serum IGF-1 levels was found between pubertal children with or without growth failure (0.48 ± 0.2 U/mL vs 0.56 ± 0.14 U/mL, P = 0.26). Conclusions: Delayed sexual maturation and a possible defect in growth unrelated to the GH-IGF-1 axis may be responsible for the growth failure in adolescent children with thalassaemia major.link_to_subscribed_fulltex