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Issue 183 - 26 May 2011

Articles on Gluten Free

1. The role of HLA-DQ8 ß57 polymorphism in the anti-gluten T-cell response in coeliac disease
By Hovhannisyan, Zaruhi et al.
Nature, 11/27/2008, Vol. 456 Issue 7221: p534-538
Major histocompatibility complex (MHC) class II alleles HLA-DQ8 and the mouse homologue I-Ag7 lacking a canonical aspartic acid residue at position ß57 are associated with coeliac disease and type I diabetes. However, the role of this single polymorphism in disease initiation and progression remains poorly understood. The lack of Asp 57 creates a positively charged P9 pocket, which confers a preference for negatively charged peptides. Gluten lacks such peptides, but tissue transglutaminase (TG2) introduces negatively charged residues at defined positions into gluten T-cell epitopes by deamidating specific glutamine residues on the basis of their spacing to proline residues. The commonly accepted model, proposing that HLA-DQ8 simply favours binding of negatively charged peptides, does not take into account the fact that TG2 requires inflammation for activation and that T-cell responses against native gluten peptides are found, particularly in children. Here we show that ß57 polymorphism promotes the recruitment of T-cell receptors bearing a negative signature charge in the complementary determining region 3ß (CDR3ß) during the response against native gluten peptides presented by HLA-DQ8 in coeliac disease. These T cells showed a crossreactive and heteroclitic (stronger) response to deamidated gluten peptides. Furthermore, gluten peptide deamidation extended the T-cell-receptor repertoire by relieving the requirement for a charged residue in CDR3ß. Thus, the lack of a negative charge at position ß57 in MHC class II was met by negatively charged residues in the T-cell receptor or in the peptide, the combination of which might explain the role of HLA-DQ8 in amplifying the T-cell response against dietary gluten. [ABSTRACT FROM AUTHOR]
Database: Masterfile Premier

2. Gluten intolerance possible without coeliac disease, study finds
By Amy Corderoy and Natalie Muller.
Sydney Morning Herald,  18/01/2011
Database: Australia/New Zealand Reference Centre
Doctors are not yet able to explain the condition but Kim McGlinn knows the misery gluten intolerance can inflict.

3. Pinpointing coeliac disease.
By: Anderson, Bob.
Australian Doctor, 02/10/2010, p5-7
Database: Australia/New Zealand Reference Centre
The article discusses the signs and symptoms, diagnosis, and management of patients with coeliac disease in Australia. It defines coeliac disease as an organic condition involving demonstrable injury to the small intestine. Statements from professor Bob Anderson on the significance of a definitive diagnosis of coeliac disease are also presented as well as the benefits of the gluten-free diet in managing coeliac disease.

4. Gluten-free -- just a fad?
Townsville Bulletin, 22.09.2010: p16
Database: Australia/New Zealand Reference Centre
Gluten-free is the new 'it' diet, with celebrity devotees saying it makes them feel more energetic. While for coeliacs, gluten-free food is a necessity, a growing number of people are eating it because they want to. What is gluten? The mixture of proteins found in wheat grains, which are not soluble in water and which give wheat dough its elastic texture. Gwyneth Paltrow gushes over gluten-free. Chelsea Clinton's wedding cake was baked without it. The new Old Spice guy avoids the ubiquitous protein to help stay buff. In fact, odds are good you too have tried -- or at least encountered -- a product with the gluten removed. Because gluten-free is what low-carb was a decade ago: The ``it'' diet discussed on daytime talk shows, promoted by hyper-slim actresses and adopted by masses. Grocery aisles are stocked with the likes of gluten-free pasta, crackers, cereal and beer.

5. Is Gluten Making Us Fat?
By Solan, Matthew.
Men's Health (10544836), Mar 2011, Vol. 26 Issue 2: p80-81
Database: Australia/New Zealand Reference Centre
The article discusses the fat contained in gluten. As reported, sales of gluten-free products grew about 30 percent a year from 2006 to 2010. Gluten is a protein found in wheat, barley, and rye, as well as in many common food additives and it provides elasticity to dough. Lara Field, a dietitian at the University of Chicago's celiac disease center, says gluten may even prove bad for people who don't have celiac disease. 

6. Go Gluten Free: Food. Test Your Gluten And Celiac Knowledge
By Smith, Melissa Diane.
Better Nutrition, Oct 2010, Vol. 72 Issue 10: p52-54
Database: Australia/New Zealand Reference Centre
A quiz concerning gluten and celiac disease is presented.

7. Gluten-Sensitive Enteropathy (Celiac Disease): Controversies in Diagnosis and Classification
By Ensari, Arzu. Archives of Pathology & Laboratory Medicine, Jun 2010, Vol. 134 Issue 6: p826-836
Database: Nursing and Allied Health
Celiac disease, or gluten-sensitive enteropathy, is a chronic inflammatory disorder of the small intestine characterized by malabsorption after ingestion of gluten in individuals with a certain genetic background. Clinical presentation can vary from full-blown malabsorption to subtle and atypical symptoms. Diagnosis currently relies on clinicopathologic studies including mucosal biopsy, serologic tests, and the effects of a diet free of gluten on the symptoms. Mucosal pathologic features are also variable, ranging from mild abnormalities, including intraepithelial lymphocytosis, to completely flat mucosa. Since patients with minimal histologic lesion of intraepithelial lymphocytosis often present with normal serologic findings, biopsy diagnosis becomes more important for identifying such individuals. Classification of mucosal pathology in gluten-sensitive enteropathy has been a subject of controversy among pathologists and needs to be revised according to the current understanding of the disease.
Objectives.--To highlight the variations in clinical and pathologic presentation of gluten-sensitive enteropathy, to emphasize the importance of small-intestinal biopsy evaluation in the diagnosis, and to propose a new classification of mucosal pathology in gluten-sensitive enteropathy, in an effort to overcome the problems related to the classification systems currently available. Data Sources.--A review of the literature on clinicopathologic features and the morphologic spectrum of gluten-sensitive enteropathy is presented.
Conclusions.--Considering that there are many entities in the differential diagnosis of gluten-sensitive enteropathy, because of the varied clinicopathologic spectrum of the disease, diagnosis depends on good clinicopathologic communication. The classification that is presented in this review is a simple and practical approach to improve clinicopathologic correlation in gluten-sensitive enteropathy. [ABSTRACT FROM AUTHOR].

8. The effect of biopsy-positive silent coeliac disease and treatment with a gluten-free diet on growth and glycaemic control in children with Type 1 diabetes
By Sun, S. et al.
Diabetic Medicine, Dec 2009, Vol. 26 Issue 12: p1250-1254
Database: Nursing and Allied Health
Abstract: Objective
To determine the effect of coeliac disease and treatment with a gluten-free diet on growth and glycaemic control in asymptomatic children with Type 1 diabetes. Methods Data were compared in children with coeliac disease diagnosed by annual antibody screening and jejunal biopsy and treated with a gluten-free diet ( n = 49) against individuals who were antibody negative ( n = 49) matched for age, sex and duration of diabetes.
Results: No differences in growth were observed. In the years prior to diagnosis of coeliac disease, mean glycated haemoglobin (HbA1c) was lower in cases compared with control subjects [8.3 ± 1.1% vs. 8.7 ± 0.9%, P = 0.02 (mean ± sd)]. In cases, HbA1c deteriorated 12 months from the start of a gluten-free diet to levels similar to control subjects (8.9 ± 1.5% vs. 8.8 ± 1.5%, P-value for analysis of variance = 0.9). In regression analysis, the diagnosis of coeliac disease and start of a gluten-free diet was associated with a rise in HbA1c in the first year of treatment [odds ratio 1.56 (95% confidence intervals 1.16–2.10), P = 0.003] after adjusting for insulin dose and regimen and other variables. Conclusions In children with Type 1 diabetes, lower HbA1c prior to diagnosis of silent coeliac disease rises following treatment with a gluten-free diet to levels similar to those without coeliac disease. Although unproven, these observations may relate to abnormalities at the small bowel mucosa before the appearance of circulating coeliac antibodies. [ABSTRACT FROM AUTHOR].

9. Metabolic osteopathy in celiac disease: importance of a gluten-free diet.
By Capriles, Vanessa D. et al. Nutrition Reviews, Oct 2009, Vol. 67 Issue 10: p599-606
Reduced bone mineral density (BMD) is frequently found in individuals with untreated celiac disease (CD), possibly due to calcium and vitamin D malabsorption, release of pro-inflammatory cytokines, and misbalanced bone remodeling. A gluten-free diet (GFD) promotes a rapid increase in BMD that leads to complete recovery of bone mineralization in children. Children may attain normal peak bone mass if the diagnosis is made and treatment is given before puberty, thereby preventing osteoporosis in later life. A GFD improves, but rarely normalizes, BMD in patients diagnosed with CD in adulthood. In some cases, nutritional supplementation may be necessary. More information on therapeutic alternatives is needed. [ABSTRACT FROM AUTHOR].

10. Gluten-free diets: Are you prepared?
By Alicea, Ronni.
Long-Term Living: For the Continuing Care Professional, Dec 2008, Vol. 57 Issue 12: p22-24
The article offers information on a gluten-free diet and its significance on celiac disease. Gluten is a protein complex found in wheat, barley and rye; on the other hand, celiac disease is an autoimmune response to gluten. Managing gluten-free diets, like other food allergies, depends on facility-wide awareness..

Journals - Table of Contents

11. From Journal of Infection Prevention, May 2011
11A. Pathfinder shows the way
11B. IPS & RCN Position Statement: Equity and excellence: Liberating the NHS Securing continuing infection prevention support for NHS England
11C. Norovirus: changing epidemiology, changing virology. The challenges for infection control
11D. Norovirus - a serious threat to business continuity for hospitals
11E. A major outbreak of Norovirus in an acute NHS hospital in 2010: a practical management approach
11F. Rapid molecular screening for meticillin-sensitive Staphylococcus aureus (MSSA) carriage: an economic evaluation 11G. An outbreak of group A streptococcal infection

12. From International Nursing Review, Volume 58, Number 2, June 2011
12A. Nurses must influence governments and policy
12B. Openness and clarity are essential in research reporting
12C. Music intervention and preoperative anxiety: an integrative review
12D. Emotional distress and health risk behaviours of mothers of United States marines
12E. A qualitative content analysis of nurse-patient communication in Iranian nursing
12F. Nursing students' immunisation status and knowledge about viral hepatitis in Turkey: a multi-centre cross-sectional study
12G. Commentary: the importance of education and vaccination in reducing the risk of hepatitis infection among nursing students
12H. Intercultural education of nurses and health professionals in Europe (IENE)
12I. A framework to develop a clinical learning culture in health facilities: ideas from the literature
12J. The effect of a peer-mentoring strategy on student nurse stress reduction in clinical practice
12K. Perceptions of nursing students' parents regarding the profession and their college
12L. 21st century nursing practice in Ghana: challenges and opportunities
12M. New Zealand general practice nurses' roles in mental health care
12N. Nursing personnel's perceptions of the organizational climate in public and private hospitals in Spain
12O. Conflict management in public hospitals: the Cyprus case
12P. The relationship between management safety commitment and patient safety culture
12Q. Hospital nurses' work environment, quality of care provided and career plans
12R. Making it real: a hands-on approach to teaching research


13. NZNO AGM and Conference
Closing the gaps increasing access and equity
Wednesday, 24 August, 2011 - Thursday, 25 August, 2011
Venue: Duxton Hotel
Registrations: Closing Friday 10th June 2011
More information: Ph 0800 28 38 48

14. The 2011 Conference for General Practice
Playing the Advantage

Just before the Rugby World Cup kicks off, we are co-hosting the 2011 Conference for General Practice proudly brought to you by the Royal New Zealand College of General Practitioners and General Practice New Zealand
Health Informatics New Zealand (HINZ) has already put their hand up to be part of our team and will facilitate an 'information as an enable' stream throughout the conference.
Date: 1-4 September 2011
Venue: The Langham, Auckland
More information:

15. Innovative Strategies for Engaging and Supporting Net Generation Students
30 September - 30 September 2011
Venue: Darling Harbour, NSW, Australia
Seminar Aims
- Showcase successful planning, strategy and educational development initiatives that have demonstrated improvements in student engagement and support
- Share information about what works and doesn't work to improve student engagement and support
- Network with like minded leaders to develop innovative solutions to student engagement challenges

News International

16. CDC Expert Commentary
Preventing Norovirus Transmission: New Guidelines Released
Tara MacCannell, PhD
Posted: 05/09/2011

17. Norovirus in Healthcare Settings
Noroviruses are a group of viruses that cause gastroenteritis [gas-tro-en-ter-i-tis] in people. Gastroenteritis is an inflammation of the lining of the stomach and intestines, causing an acute onset of severe vomiting and diarrhea. Norovirus illness is usually brief in people who are otherwise healthy. Young children, the elderly, and people with other medical illnesses are most at risk for more severe or prolonged infection

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