bluuebunny/crossref_metadata_2025_split huggingface dataset:
Symptoms after mould exposure including Stachybotrys chartarum, and comparison with darkroom disease
Authors: Al‐Ahmad M. , Manno M. , Ng V. , Ribeiro M. , Liss G. M. , Tarlo S. M. 
Published: October 2009

To cite this article: Al‐Ahmad M, Manno M, Ng V, Ribeiro M, Liss GM, Tarlo SM. Symptoms after mould exposure including Stachybotrys chartarum, and comparison with darkroom disease. Allergy 2010; 65: 245–255.AbstractBackground:  Mould‐attributed symptoms have included features which overlap with unexplained syndromes such as sick building syndrome.Objectives:  We describe questionnaire and chart review findings in patients following exposure to moulds which include Stachybotrys and compare responses with two control groups.Methods:  Thirty‐two patients presented with symptoms attributed to mould exposures. Exposure identification for 25 patients had reported S tachybotrys chartarum as well as other mould (Aspergillus, Penicillium), 88% at work. The remaining seven had professionally visualized or self‐reported/photographic exposure evidence only. A chart review was performed and a follow‐up with a questionnaire, including questions on current health status, and nonspecific symptoms.Results:  Cough, shortness of breath and chest tightness (at presentation) were reported in 79%, 70% and 64%, respectively, and persisted >6 weeks in 91%. Skin test(s) were positive to fungal extract(s) in 30%. Seventeen returned questionnaires were obtained 3.1 (SD 0.5) years after the initial clinic assessment. Among this subgroup, persisting asthma‐like symptoms and symptoms suggestive of sick building syndrome were frequent, and similar to a group previously assessed for darkroom disease among medical radiation technologists. The mould‐exposed group more commonly reported they were bothered when walking in a room with carpets, complained of a chemical or metallic taste in their mouth, and had problems in concentration when compared with a control physiotherapist group (P < 0.005).Conclusions:  Although only a minority with health concerns from indoor mould exposure had demonstrable mould‐allergy, a significant proportion had asthma‐like symptoms. Other symptoms were also common and persistent after the initial implicated exposure.
Genetic variability in CRTH2 polymorphism increases eotaxin‐2 levels in patients with aspirin exacerbated respiratory disease
Authors: Palikhe N. S. , Kim S.‐H. , Cho B.‐Y. , Ye Y.‐M. , Choi G.‐S. , Park H.‐S. 
Published: October 2009

To cite this article: Palikhe NS, Kim S‐H, Cho B‐Y, Ye Y‐M, Choi G‐S, Park H‐S. Genetic variability in CRTH2 polymorphism increases eotaxin‐2 levels in patients with aspirin exacerbated respiratory disease. Allergy 2010; 65: 338–346.AbstractIntroduction:  CRTH2 is expressed on the surface of eosinophils and has been shown to mediate PGD2‐induced eosinophil migration in vitro. Eosinophilic infiltration in the upper and lower airways is the key feature of asthma. Considering the fact that eosinophil infiltration is prominent in the upper and lower airways of aspirin exacerbated respiratory disease (AERD) compared to aspirin‐tolerant asthma (ATA) patients, we hypothesized that activation of eosinophils via dysregulation of the CRTH2 gene may play an important role and be an important marker for AERD.Methods:  The three study groups – 107 with AERD, 115 with ATA and 133 normal healthy controls (NC) – were recruited from Ajou University Hospital, South Korea. Two polymorphisms of the CRTH2 gene at ‐466T>C and ‐129C>A were genotyped using primer extension methods.Results:  AERD patients had significantly higher serum eotaxin‐2 levels than did those with ATA (P = 0.034). A significant difference in the genotype frequencies of CRTH2 ‐466T>C was detected between AERD and ATA patients (P < 0.05). The serum eotaxin‐2 level was significantly higher in AERD patients carrying the TT genotype of CRTH2 ‐466T>C than those with the CT and CC (P < 0.05). In vitro functional study demonstrated that the ‐466T allele had lower luciferase activity (P < 0.001) and lower mRNA expression with higher production of eotaxin‐2 (P = 0.003) in human lung epithelial cells. EMSA showed that CRTH2 ‐466T produced a specific band with a higher affinity than CRTH2 ‐466C had.Conclusion:  The CRTH2 ‐466T>C polymorphism increases serum and cellular eotaxin‐2 production through lowered CRTH2 expression, leading to eosinophilic infiltration in AERD patients.
A meta‐analysis on wood dust exposure and risk of asthma
Authors: Pérez‐Ríos M. , Ruano‐Ravina A. , Etminan M. , Takkouche B. 
Published: October 2009

To cite this article: Pérez‐Ríos M, Ruano‐Ravina A, Etminan M, Takkouche B. A meta‐analysis on wood dust exposure and risk of asthma. Allergy 2010; 65: 467–473.AbstractWork‐related asthma is the most common occupational respiratory disorder in the industrialized countries. It has been postulated that wood dust exposure may increase the risk of work‐related asthma. The objective of this study was to assess, through a meta‐analysis, the risk of developing work‐related asthma associated with wood dust exposure. A systematic search of the literature was performed. Inclusion and exclusion criteria were applied and a quality scale used to measure the quality of the included studies was developed. Using standard meta‐analysis techniques, studies were pooled using both random and fixed effects models. Nineteen studies were included which consisted of three cohort studies, twelve case–control studies and four mortality studies. The pooled relative risk (RR) of asthma among workers exposed to wood dust was 1.53 (95% CI 1.25–1.87). When the analysis was restricted to studies carried out on Caucasian populations, the pooled RR was 1.59 (95% CI 1.26–2.00) while the pooled RR of studies on Asian populations was 1.15 (95% CI 0.92–1.44). Wood workers present a higher risk of asthma. Future research should include careful evaluation of ethnicity and nativity as risk modifiers.
Impact of allergic rhinitis on asthma in children: effects on bronchodilation test
Authors: Capasso M. , Varricchio A. , Ciprandi G. 
Published: October 2009

To cite this article: Capasso M, Varricchio A, Ciprandi G. Impact of allergic rhinitis on asthma in children: effects on bronchodilation test. Allergy 2010; 65: 264–268 DOI: 10.1111/j.1398‐9995.2009.02168.x.AbstractBackground:  Relevant relationship exists between upper and lower airways. Bronchial obstruction is a paramount feature of asthma and its reversibility is considered a diagnostic step for asthma diagnosis.Objective:  This study aimed at evaluating a large group of children with allergic rhinitis alone for investigating the degree of brochodilation and possible factors related to it.Methods:  Two hundred patients with allergic rhinitis and 150 normal subjects were consecutively evaluated. Clinical examination, skin prick test, spirometry, and bronchodilation test were performed in all patients.Results:  Rhinitics showed a significant FEV1 increase after bronchodilation test (P < 0.0001) in comparison both to basal values and to controls’ levels. More than 20% of rhinitics had reversibility (≥12% basal levels). Patients with reversibility had lower FEV1 levels, longer rhinitis duration, and perennial allergy.Conclusion:  This study highlights the close link between upper and lower airways and the relevance of performing bronchodilation test in patients with allergic rhinitis and these characteristics.
When is an oral food challenge positive?
Authors: Niggemann B. 
Published: October 2009

AbstractOral food challenges still remain the gold standard in the diagnosis of food related symptoms and are performed to obtain a clear ‘yes or no’ response. However, this is often difficult to achieve, and so proposals may be appropriate for criteria on when to stop oral food challenges. In daily practice it makes sense to challenge until clear objective symptoms occur without harming the patient. Clinical symptoms should be objective and/or: (a) severe or (b) reproducible or (c) persisting. A sensitive parameter for a beginning clinical reaction is a general change of mood. The sooner symptoms appear, the more likely they are to represent a ‘true’ positive reaction and the more organ systems are involved the easier it is to assess an oral food challenge as positive. In the case of subjective symptoms, the number of placebo doses should be increased. In unclear situations, the observation time until the next dose should be prolonged or the same dose repeated. Transient objective clinical symptoms usually end up in a positive challenge result. There are a number of causes for false positive and false negative challenge results, which should be considered. The aim of all oral challenge testing should be to hold the balance between two conflicting aspects: on the one hand the need to achieve clear and justified results from oral food challenges in order to avoid unnecessary diets, and on the other hand to protect patients from any harm caused by high doses of a potentially dangerous food.
Landmarks in the understanding and treatment of reflux disease
Authors: Dent John 
Published: October 2009

AbstractThe last 50 years have seen a transformation in the understanding and treatment of reflux disease. The development and wide use of flexible endoscopy and progressively more sophisticated approaches to measurement of pathophysiological factors have been major drivers of advances. The recognition and progressive elucidation of the mechanical events that comprise the transient lower esophageal sphincter relaxation and how they lead to reflux provide a novel and firm foundation for tailoring therapies that act directly to reduce occurrence of reflux episodes, either surgically or pharmacologically. Novel GABAB agonist drugs have been shown to inhibit transient relaxations and are currently being evaluated in clinical trials on patients with reflux disease.Better understanding has extended to recognition of the extraordinarily high prevalence of reflux disease and of the ability of proton pump inhibitor drugs to deliver major benefits to a high proportion of patients with reflux disease.The life of the Gastroenterological Society of Australia has spanned the period of these major advances. A large number of the members of the Society and their associates have contributed substantially to these advances.
Whither dyspepsia? A historical perspective of functional dyspepsia, and concepts of pathogenesis and therapy in 2009
Authors: Talley Nicholas J , Choung Rok Seon 
Published: October 2009

AbstractFunctional dyspepsia is a highly prevalent but heterogeneous disorder; multiple pathogenetic mechanisms are likely involved but the underlying causal pathways in functional dyspepsia remain obscure. The term functional dyspepsia was popularized by the famed Walter Alvarez at the Mayo Clinic early last century. Prominent Australian gastroenterologists who have contributed to our understanding of functional dyspepsia include Peter Baume, Barry Marshall, Douglas Piper, Nick Talley, John Kellow, and Gerald Holtmann. Specific dyspeptic symptoms have not generally correlated very well with any particular physiologic disturbance, although gastric disaccommodation and duodenal eosinophilia have been linked to early satiety in this condition. Genetic markers have been tentatively identified, and functional dyspepsia can follow bacterial gastroenteritis. No objective diagnostic tools for functional dyspepsia are currently agreed upon, although meal induction of symptoms appears reproducible and may have diagnostic utility. The symptomatic criteria for functional dyspepsia (Rome III criteria) are based on expert consensus and the exclusion of organic causes. Various therapeutic modalities for functional dyspepsia have been explored; however, empirical approaches are still employed for the treatment of functional dyspepsia. Better approaches for functional dyspepsia are likely to follow an improved understanding of the underlying pathophysiological abnormalities.
Family‐based screening for colorectal cancer: The Australian perspective
Authors: Leggett Barbara A 
Published: October 2009

AbstractOver the last 20 years, the rapid expansion of genetic technology has allowed much progress to be made in understanding the molecular basis of inherited bowel cancer. At the same time, improvements in endoscopic and surgical techniques have meant that very effective surveillance can be offered to subjects known to be at high risk. The genes underlying the major polyposis syndromes have been identified and the genetic basis for Lynch Syndrome (Hereditary NonPolypsis Syndrome) is well understood. In Australia, this new knowledge has been incorporated in a multidisciplinary model of care involving clinical geneticists, gastroenterologists and gastrointestinal surgeons, pathologists, and family cancer registries. Challenges for the future include identifying families which would benefit from referral to these services but also encouraging the uptake of predictive testing and appropriate surveillance by at risk members of families where the genetic mutation is known. Surprisingly high numbers of individuals for whom a predictive blood test and surveillance program is freely available fail to participate and the reasons for this choice are still poorly understood. This has implications for the utilization of new genetic knowledge in other diseases. Another major challenge for the future is identifying the genes underlying the increased risk of bowel cancer in families which do not have the syndromes described above. Australian clinicians and scientists are actively participating in the global research effort to discover these genes.
Making every colonoscopy count: Ensuring quality in endoscopy
Authors: Bourke Michael J 
Published: October 2009

AbstractThe last few years have seen a burgeoning interest in the measurement of clinical performance and its impact on quality standards. The advent of the National Bowel Cancer Screening Program has highlighted the many deficiencies that exist in the provision of colonoscopy services in Australia. These include the absence of an agreed tool to measure the quality of colonoscopy on either an individual, departmental or regional basis and the absence of an endoscopic or colonoscopy training curriculum or an agreed standard for colonoscopy trainers. This review will discuss the current status and shortfalls of measuring quality in colonoscopy, highlight some recent initiatives by the Gastroenterological Society of Australia and articulate a direction for the future.
New insights into alcoholic pancreatitis and pancreatic cancer
Authors: Apte Minoti , Pirola Romano , Wilson Jeremy 
Published: October 2009

AbstractPancreatitis and pancreatic cancer represent two major diseases of the exocrine pancreas. Pancreatitis exhibits both acute and chronic manifestations. The commonest causes of acute pancreatitis are gallstones and alcohol abuse; the latter is also the predominant cause of chronic pancreatitis. Recent evidence indicates that endotoxinemia, which occurs in alcoholics due to increased gut permeability, may trigger overt necroinflammation of the pancreas in alcoholics and one that may also play a critical role in progression to chronic pancreatitis (acinar atrophy and fibrosis) via activation of pancreatic stellate cells (PSCs). Chronic pancreatitis is a major risk factor for the development of pancreatic cancer, which is the fourth leading cause of cancer‐related deaths in humans. Increasing attention has been paid in recent years to the role of the stroma in pancreatic cancer progression. It is now well established that PSCs play a key role in the production of cancer stroma and that they interact closely with cancer cells to create a tumor facilitatory environment that stimulates local tumor growth and distant metastasis. This review summarizes recent advances in our understanding of the pathogenesis of alcoholic pancreatitis and pancreatic cancer, with particular reference to the central role played by PSCs in both diseases. An improved knowledge of PSC biology has the potential to provide an insight into pathways that may be therapeutically targeted to inhibit PSC activation, thereby inhibiting the development of fibrosis in chronic pancreatitis and interrupting stellate cell–cancer cell interactions so as to retard cancer progression.
New and emerging therapies for inflammatory bowel diseases
Authors: Grimm Michael C 
Published: October 2009

AbstractThe inflammatory bowel diseases have undergone an explosion of discovery in the last 10 years. The overwhelming focus of this has been in genetics and immune mechanisms of disease. While the former has provided critical information on predisposing factors, the latter has resulted in a panoply of novel immune‐based therapies and technologies. These range from an improved approach to the use of conventional immunomodulators, such as azathioprine and 6‐mercaptopurine, to commonplace availability of anti‐tumor necrosis factor agents such as infliximab and adalimumab, through to small molecule inhibition of immune mediators. Unusual treatments, such as helminth infestation, stem cell transplantation, and leucocytapheresis, all derive from the burgeoning understanding of pathogenesis. Most important to our successful use of these therapies will be a fundamental understanding of the patient phenotypes and genotypes that will dictate particular treatment approaches in the future.
Fifty years of Australian pediatric gastroenterology
Authors: Cameron Don 
Published: October 2009

AbstractWhen the Gastroenterological Society of Australia (GESA) began 50 years ago there were very few pediatric gastroenterologists in the world. The ‘Mother’ of Paediatric Gastroenterology was Australian Charlotte (‘Charlo’) Anderson who established one of the world's first pediatric gastroenterology units in Melbourne in the early 1960s. Her earlier work in Birmingham had identified gluten as the component of wheat responsible for celiac disease and helped separate maldigestion (cystic fibrosis) and mucosal malabsorption. The first comprehensive textbook of Paediatric Gastroenterology was edited by Charlotte Anderson and Valerie Burke in 1975. Rudge Townley succeeded Charlotte Anderson in Melbourne and went on to further develop small bowel biopsy techniques making it a safe, simple, and quick procedure that led to much greater understanding of small bowel disease and ultimately the discovery of Rotavirus by Ruth Bishop et al. and subsequently to Rotavirus immunization. Australian Paediatric Gastroenterology subsequently developed rapidly with units being established in all mainland capital cities by the end of the 1970s. The Australian Society of Paediatric Gastroenterology Hepatology and Nutrition (AuSPGHAN) was established in the 1980s. Australians have contributed significantly in many areas of gastroenterology in infants, children, and adolescents including celiac disease, cystic fibrosis, liver disease, transplantation, gastrointestinal infection, allergy, indigenous health, inflammatory bowel disease, gastrointestinal motility, and the development of novel tests of gastrointestinal function and basic science. There have also been major contributions to nutrition in cystic fibrosis, end‐stage liver disease, and intestinal failure. The future of Australian Paediatric Gastroenterology is in good hands.
Intestinal failure: A new era in clinical management
Authors: Bines Julie E 
Published: October 2009

AbstractOnly 50 years ago intestinal failure was considered incompatible with life. Since then, developments in parenteral nutrition, and, more recently, small intestinal transplantation, have provided new therapeutic options with the potential to offer long‐term survival with a good quality of life. Current medical and surgical strategies are aimed at enhancing intestinal adaptation, improving absorption to achieve nutritional independence, and minimizing the complications of parenteral nutrition therapy. An integrated, multidisciplinary approach to the management of patients with intestinal failure, closely linked to a transplantation program to facilitate early referral, is recognized as a key factor in optimizing patient outcomes.
Overview: Liver disease and transplantation
Authors: Powell Lawrie W 
Published: October 2009

AbstractAustralia has had a proud and enviable record of seminal contributions to hepatology, with many contributors. Thus, any attempt to summarize these contributions ab initio in a brief review article is a significant challenge, primarily because it is so easy to overlook or underestimate particular aspects. In this article, I have confined my comments primarily to the areas where the contributions have had a significant global impact and have clearly been recognized internationally. This means that many worthwhile Australian additions will be omitted if there was less apparent international impact. The first significant interest in liver disease in Australia was from the Melbourne group at the Walter and Eliza Hall Institute (WEHI) and Royal Melbourne Hospital, leading to seminal contributions to the description, diagnosis, aetiopathogenesis and therapy of autoimmune hepatitis and primary biliary cirrhosis. Others from Royal Prince Alfred Hospital in Sydney contributed substantially to the effects of immunosuppression of autoimmune hepatitis and to early descriptions of primary sclerosing cholangitis. Other areas where Australians have contributed significantly include steatohepatitis, iron metabolism (and in particular hemochromatosis), viral hepatitis (both at the molecular and clinical level), portal hypertension, and transplant immunology. The remarkable contribution of Professor Dame Sheila Sherlock to Australian hepatology is also summarized.
The liver and the waistline: Fifty years of growth
Authors: Farrell Geoffrey C 
Published: October 2009

AbstractFifty years of the Gastroenterological Society of Australia have witnessed the changing appearance of Australians. Asian immigration has transformed the dominant urban culture from European to Eurasian, with some unique Australian attributes. Meanwhile, global conditions have altered body shape, and our sports‐proud country is now fat! Thus, as in North America, Europe, China, and affluent Asia–Pacific countries, prosperity and lifestyle, cheap processed foods coupled with reduced physical activity have created an epidemic of over‐nutrition resulting in overweight/obesity. Additional genetic factors are at the core of the apple shape (central obesity) that typifies over‐nourished persons with metabolic syndrome. Indigenous Australians, once the leanest and fittest humans, now have exceedingly high rates of obesity and type 2 diabetes, contributing to shorter life expectancy; Asian Australians are also at higher risk. Like non‐steroidal anti‐inflammatory drugs (NSAIDs) and cigarette smoking, obesity now contributes much to gastrointestinal morbidity and mortality (gastroesophageal reflux disease, cancers, gallstones, endoscopy complications). This review focuses on Australian research about fatty liver, particularly roles of central obesity/insulin resistance in non‐alcoholic fatty liver disease/steatohepatitis (NAFLD/NASH). The outputs include many highly cited original articles and reviews and the first book on NAFLD. Studies have identified community prevalence, clinical outcomes, association with insulin resistance, metabolic syndrome and hypoadiponectinemia, developed and explored animal models for mechanisms of inflammation and fibrosis, conceptualized etiopathogenesis, and demonstrated that NASH can be reversed by lowering body weight and increasing physical activity. The findings have led to development of regional guidelines on NAFLD, the first internationally, and should now inform daily practice of gastroenterologists.