bluuebunny/crossref_metadata_2025_split huggingface dataset:
Excitatory effect of thiamin on CA1 pyramidal neurones in rat hippocampal slices in vitro
Authors: Tallaksen C. M. E. , Taubøll E. 
Published: February 2003

Clinically, acute thiamin deficiency may lead to Wernicke encephalopathy and fulminant cardial beriberi. Both diseases respond to high parenteral doses of thiamin. The cofactor role of intracellular thiamin diphosphate has been thoroughly investigated, but an additional acute effect of unphosphorylated extracellular thiamin has been postulated but not elucidated.In order to investigate the role of thiamin at the membrane level in the central nervous system, a study using a well‐established in vitro rat hippocampal slice model was designed. Hippocampal slices were perfused with 0.5, 0.75 and 1 mM thiamin solutions for 30 min and the pre‐synaptic volley, field excitatory post‐synaptic potential and population spike amplitudes were recorded continuously. The results showed an acute, excitatory effect of high‐dose thiamin on hippocampal neurones by significantly increasing the number of repetitive afterdischarges. Additional experiments with low concentrations of the potassium channel blocker 4‐aminopyridine showed similar findings. The results support previous evidence of thiamin affecting membrane ion channel activity, probably involving potassium channels, although the precise mechanisms of action are still unclear.
Transcranial colour‐coded sonography for the bedside evaluation of mass effect after stroke
Authors: Bertram M. , Khoja W. , Ringleb P. , Schwab S. 
Published: February 2003

Repeated cranial computerized tomography scan examination in patients with elevated intracranial pressure is time consuming and requires patient transportation. We prospectively evaluated the diagnostic value of transcranial duplex sonography as a bedside tool for detection of the mass effect after space‐occupying ischemic stroke and brain haemorrhage and for evaluating the width and dislocation of the ventricular system and the dislocation of brain mid‐line structures.We used transcranial duplex sonography in 21 consecutive patients with space‐occupying ischemic middle cerebral artery infarction and brain haemorrhage. The transcranial duplex sonography examinations were performed within 2 h before or after corresponding follow‐up cranial computerized tomography scans. We measured the third ventricular width as a parameter for infratentorial and the mid‐line shift for supratentorial space‐occupying effect.In all patients, mid‐line structures could be identified by transcranial duplex sonography. Significant third ventricular dilation was found subsequently in most patients with infratentorial mass effect, and mid‐line shift occurred in all patients with supratentorial space‐occupying lesions, respectively. The mean difference (absolute values) between transcranial duplex sonography and cranial computerized tomography measurements was 0.8 mm for the ventricular width (standard deviation 1 mm) and 1.1 mm for the mid‐line shift (standard deviation: 1.46 mm), with a tendency for these parameters to be underestimated at higher values using transcranial duplex sonography. The linear correlation coefficients were R = 0.97 and R = 0.94, respectively.Transcranial duplex sonography appears to be a sufficiently reliable bedside method for evaluating the width and the lateral displacement of the third ventricle, as validated by cranial computerized tomography scan. Thus, it may be suitable for monitoring the space‐occupying effect of both supra‐ and infratentorial strokes during treatment on critical care and stroke units.
Hyperreflexia in a patient with motor axonal Guillain–Barré syndrome
Authors: Podnar S. , Vodušek D. B. 
Published: February 2003

We report a patient who presented after an episode of diarrhoea with ascending, symmetrical weakness without sensory loss, and without sphincter or other autonomic dysfunction. On clinical examination there were no cranial nerve deficits. Hyperreflexia of tendon jerks without other upper motor neurone signs was found. Electrophysiological examination demonstrated acute distal symmetrical motor axonal polyneuropathy. No electrophysiological signs of peripheral nerve demyelination or central nervous system involvement were found. Albuminocytologic dissociation was present in the cerebrospinal fluid. Stool culture and serological tests were inconclusive.Our patient's clinical picture was, apart from hyperreflexia of tendon jerks throughout the disease, characteristic of Guillain–Barré syndrome. This is the first such patient reported in Europe. The aetiology remained unclear. We suggest that selective axonal motor fibre affection, with possible mild pyramidal involvement, caused tendon jerk hyperreflexia.
Vogt–Koyanagi–Harada disease presenting initially as aseptic meningoencephalitis
Authors: Kamondi A. , Szegedi A. , Papp A. , Seres A. , Szirmai I. 
Published: February 2003

Vogt–Koyanagi–Harada (VKH) disease in a Gypsy woman was diagnosed 4 months after her initial complaints. The delay is explained by the facts that: (1) the characteristic ophthalmological symptoms, which usually herald the disease and ensure early diagnosis, developed only late during the course; and (2) only retrospective analysis of the cerebrospinal fluid (CSF) cell preparation proved the presence of melanin‐laden macrophages (MLMs), specific for the syndrome.We emphasize that VKH syndrome may initially present as aseptic meningitis, without specific ophthalmological symptoms. In suspected cases a very detailed CSF cell analysis is needed, because the presence of MLMs could confirm the diagnosis. However, VKH syndrome has a much higher incidence in Asia; cases in other races, including white people in Europe, also occur.
Prevention of allergy and asthma
Authors: Baena‐Cagnani C. E. , Serra H. , Teijeiro A. , Croce J. S. 
Published: February 2003

SummaryIn the last few decades much insight has been gained on the pathogenesis and risk factors associated with atopic diseases (asthma, rhinitis and atopic dermatitis). In addition, there are very effective drugs to manage exaceabations and to control the appearance of symptoms. The prevalence of allergic diseases, particularly in western countries (mainly English‐speaking ones), and also in Latin America and Western Europe, is very high. Even in those countries with lower prevalence (such as in Africa or Asia), this has been higher than expected. In countries where surveys have been made using the same protocol in different time periods, an upward trend in the prevalence of atopic diseases has been shown. The socio‐economic impact of atopic diseases has become a public health problem and a rise in costs can be expected in correlation with the increased prevalence. The inception of atopic diseases is the consequence of genetic and environmental interactions and some changes in environment in the last few decades could partly explain this trend. The roles of infections, allergen exposure, dietary factors, among others, are being intensively studied. Nevertheless, the reason for the increasing prevalence of atopic diseases is still unknown. The primary prevention of atopic disorders emerges as an ideal way to stop the upward trend in the prevalence of allergy and asthma and different environmental factors can be targeted to ameliorate the ‘atopic epidemic’.
Allergy: discovery of immunoglobulin E to today
Authors: Johansson S. G. O. 
Published: February 2003

SummaryKnowledge about the immunological, IgE‐mediated mechanisms of allergic rhinitis has improved our understanding of the disease and its diagnosis and treatment. Due to the very high prevalence of allergic rhinitis and allergy in general, allergy specialists must take responsibility for teaching GPs, family practitioners and other nonallergists to care for patients with allergy. For these nonallergy specialists the diagnosis is best restricted to in vitro quantitation of IgE antibodies performed by an accredited laboratory. Treatment should be limited to anti‐inflammatory drugs, allergen‐avoidance advice and patient care.
Allergic rhinitis and asthma: epidemiological evidence for the link
Authors: Katelaris C. H. 
Published: February 2003

SummaryFor years, a clinical relationship between allergic rhinoconjunctivitis (AR/C) and asthma has been observed. Recently, evidence supporting this link has been published. An important body of evidence for a real link between the two conditions has come from epidemiological studies. An increasing prevalence of both conditions is noted in the developed and developing countries. A number of studies have documented the co‐existence of AR/C and asthma, with one group reporting up to 80% of patients with asthma having AR/C. Increased bronchial hyperresponsiveness, one of the characteristic findings in asthma, is also demonstrated in those with AR/C even in the absence of clinical asthma. There are a number of common factors linking the two conditions. Atopy is a risk factor for the development of both asthma and AR/C, as is the finding of positive skin tests to common aeroallergens. There is also a well documented temporal relationship between the two conditions, with AR/C beginning soon before or simultaneously with asthma – an association noted in a number of studies examining large groups of subjects . Finally, there are a few studies that demonstrate treatment of one condition leading to an effect on the other – this has been particularly noted with the improvement in asthma control once AR/C has been adequately managed. Given the growing evidence of common factors between the two conditions and the frequent finding that they co‐exist in the same patient, management strategies must include treatment of both the upper and the lower airway rather than focusing only on the predominant complaint.
What's in a name? The allergic rhinitis–asthma connection
Authors: Simons F. E. R. 
Published: February 2003

SummaryIn studies conducted since the epidemic of allergic disorders began, at least 40% of young patients with allergic rhinitis have been found to have concurrent asthma, and up to 100% of young patients with allergic asthma have been found to have concurrent allergic rhinitis. Many patients with occupational or nonsteroidal anti‐inflammatory drug‐induced asthma also have concurrent allergic rhinitis. In addition to being associated epidemiologically (occurring in patients with similar genetic background and triggered by similar provoking factors), allergic rhinitis and asthma are associated anatomically, physiologically, immunopathologically, and by their response to therapeutic interventions. Anatomically, both the upper and the lower airways are lined with ciliated columnar epithelium containing mucus‐secreting goblet cells. Physiologically, they are connected not only by the nasobronchial reflex, but also by the adverse effects on the lower airways produced when nasal congestion results in mouth breathing and loss of nasal air‐conditioning (warming, humidification, and filtration of inspired air). The underlying immunopathological process is similar in allergic rhinitis and asthma. It involves not only the immediate hypersensitivity (Type I) allergic response, but also persistent allergic inflammation (the Type IVa2 response in the revised Gell and Coombs classification). In addition, the systemic immunologic response to intranasal or orally‐inhaled allergens is similar in allergic rhinitis and asthma. Down‐regulation of allergic inflammation by allergen avoidance, allergen‐specific immunotherapy, and medications such as H1‐antihistamines, leukotriene modifiers, intranasal/inhaled glucocorticoids or novel immunomodulators such as anti‐IgE is the key to managing both disorders. ‘Combined allergic rhinitis/asthma syndrome’, ‘allergic rhinobronchitis’, ‘the united airways’, ‘one airway, one disease’, and other phrases in current usage lead to increased awareness that persistent allergic inflammation occurs throughout the upper and lower airways of patients with concurrent allergic rhinitis and asthma. Terms involving the words ‘allergic’ or ‘asthma’ are preferable to nonspecific terms such as ‘united airways’ or ‘one airway, one disease’. Additional studies of the immunopathophysiological processes that link the upper and lower airways are needed.
Prevention of relapsing rhino‐sinusal polyposis: efficacy of intranasal furosemide in 104 patients
Authors: Bellussi L. , Passàli F. M. , Damiani V. , Passàli G. C 
Published: February 2003

SummaryThe relapse of nasal polyps after surgical treatment remains a yet unsolved medical problem and, at the same time, a challenge for researchers. Starting from the observation that oedema, vessel dilatation and inflammatory cell infiltration are the histopathological characteristics of nasal polyps, our aim is to demonstrate the long‐term efficacy of furosemide, administered by nasal inhalation, in preventing relapses of rhino‐sinusal polyps after surgical treatment. In the study discussed in this paper, two groups of patients affected by rhino‐sinusal polyposis were enrolled: 64 patients were included in the study group and 40 in the control group. After surgical treatment, the study group started the therapy with topic intranasal furosemide; the control group received no treatment. Six years after the operation only four cases of relapse were noticed in the study group (10%), while in the control group there were 12 relapses, four slight (6.4%) and eight severe (20%). Our paper concludes that local intranasal furosemide represents a valid therapeutic aid in the prevention of naso‐sinusal polyps.
Natural history of allergic rhinitis: our experience in Italy
Authors: Passà D. , Damiani V. , Passà F. M. , Mora R. , Passà G. C. , Bellussi L. 
Published: February 2003

SummaryTo date, several aspects of allergic rhinitis remain controversial. In particular, data concerning its epidemiological evolution are extremely contradictory and vary between negation and assertion of an increased prevalence within the last decade. In the study discussed in this paper, our aim was to follow the evolution of allergic rhinitis in three different territorial areas of Central Italy in the last 20 years and to analyse the long‐term efficacy of treatment. Between 1980 and 1981, 1620 children, attending seven state schools (four elementary and three lower secondary), were screened for allergic rhinitis. All children underwent a skin test on the inner forearm. Positive‐skin‐test children were examined to specify the exact nasal allergy. Between 1998 and 1999, positive‐skin‐test patients were contacted and re‐examined. The results revealed that elementary school children showed lower degrees of skin positivity, a better nasal patency, a more efficient nasal clearance and less frequent anomalous radiological findings. Seventy‐three children were positive to skin tests (4.5%). Forty‐six positive‐skin‐test subjects were re‐examined: 21 recovered, 12 were unchanged, 10 developed complications, three become asthmatics. Twenty‐one subjects had not received any treatment, 15 were treated with symptomatic drugs, and 10 with immunotherapy. Our study showed an increased prevalence of allergic rhinitis in the last 20 years of the 20th century, with a jump from 4.5 to 10–20%; moreover, it showed that immunotherapy guarantees remission of local symptoms and valid protection against localized and bronchial complications. Symptomatic treatment with antihistamines and/or corticosteroids, although not always resolutive, represents a valid alternative.
The bone marrow and airway inflammation: evidence for allergy as a systemic disease
Authors: Denburg J. A. 
Published: February 2003

SummaryRhinitis and asthma are linked closely epidemiologically, as has been known for quite some time and emphasized in recent surveys (ISAAC study). Patients with seasonal allergic rhinitis without asthma symptoms can, as a group, be shown to have increased bronchial hyperresponsiveness. During the course of seasonal allergen exposure, patients with allergic rhinitis can be shown to have increased numbers of inflammatory cells (eosinophils and mast cells) in the lower airways, even without symptoms of lower airway disease. Long‐standing observations from our laboratory have indicated fluctuations of eosinophil/basophil (Eo‐B) progenitors in the peripheral blood in patients with seasonal allergic rhinitis, paralleling changes that are recognized in mature eosinophils and basophils in circulation. The finding of Eo‐B progenitor decreases during the height of seasonal allergen exposure led us to hypothesize the concept of ‘in situ haemopoiesis’ to explain a process of systemic activation of haemopoietic mechanisms, in which communication among bone marrow peripheral blood and airway tissue compartments contributed to the allergic inflammatory process at a systemic level. Indeed, allergen challenge to the lower airways in atopic asthmatics elicits an immediate rise in Eo‐B progenitors, especially in subjects with late phase responses. These original observations have been buttressed by a series of investigations demonstrating conclusively that exacerbations of asthma are attended by increases in peripheral blood Eo‐B progenitors; that allergen challenge to dogs or mice with allergic airways inflammation elicits bone marrow progenitor responses, with trafficking of bone marrow cells to the airway either in pure upper or lower airway disease; and that allergen challenge to atopic asthmatics up‐regulates the high affinity receptor for IL‐5 on bone marrow progenitors (IL‐5Rα), beginning a process of eosinophil differentiation that is probably driven by the release of a serum haemopoietic factor – as we have found in the canine model – which acts on the bone marrow and initiates a series of systemic events.
Nose and lung cross‐talk in allergic airways disease
Authors: Braunstahl G. J. , Prins J. B. , KleinJan A. , Overbeek S. E. , Hoogsteden H. C. , Fokkens W. J. 
Published: February 2003

SummaryAllergic rhinitis and asthma are two manifestations of the atopic syndrome. Allergic rhinitis often coexists with, and may even precede, allergic asthma. Both diseases are characterized by a similar inflammatory process in which mast cells and eosinophils are major effector cells. To date, however, interaction between the upper and lower airways' inflammatory processes has not been demonstrated. Allergen provocation studies provide a good model to analyse the aspects of naso‐bronchial cross‐talk. We performed segmental bronchial provocation (SBP) and nasal provocation (NP) in seasonal allergic rhinitis patients without asthma. In allergic rhinitis patients, SBP as well as NP induced allergic inflammation in both nasal and bronchial mucosa. Furthermore, allergen provocation resulted in an increase in circulating inflammatory cells and mediators. Although the clinical response was more severe after SBP, allergic rhinitis patients developed pulmonary symptoms and decreased airway function after NP as well. These studies demonstrate that allergic rhinitis is not a local disease, but that the entire respiratory tract is involved even in the absence of clinical asthma. The systemic pathway, involving bloodstream and bone marrow, contributes to the cross‐talk between upper and lower airways.
Global Resources in Allergy (GLORIA): allergic rhinitis and allergic conjunctivitis
Authors: Van Cauwenberge P. , De Belder T. , Vermeiren J. , Kaplan A. 
Published: February 2003

SummaryAllergic rhinitis is a common disease, affecting 25–35% of the population. Allergic rhinitis is still increasing in prevalence. It is characterized by rhinorrhoea, itching, sneezing and nasal obstruction. Allergic rhinitis is classically classified into three groups: seasonal (intermittent), perennial (persistent) and occupational allergic rhinitis. In the ARIA document allergic rhinitis is classified into intermittent and persistent. There is a known relationship between allergic rhinitis and asthma, sinusitis, otitis media with effusion, nasal polyposis and upper respiratory tract infections. Allergic rhinitis results from IgE‐mediated allergy, associated with cellular inflammation of the nasal mucosa. The diagnosis of allergic rhinitis is confirmed by a clinical history of typical allergic symptoms and in vivo or in vitro tests for detection of free or cell‐bound IgE. Treatment of allergic rhinitis comprises avoidance of the allergens, oral/nasal antihistamines, decongestants, chromones, ipratropium bromide and intranasal/oral corticosteroids. It is advised to follow the international guidelines, ‘a stepwise approach’. Allergic conjunctivitis is the most common ocular allergic disorder, affecting 5–22% of the population. Ocular allergy involves typical symptoms (itching, watery, stringy or ropey discharge and redness), recurrent/intermittent/persistent episodes, a strong personal and/or family history of atopy and an early age of onset. Treatment of allergic conjunctivitis includes oral/intraocular antihistamines, cromones or topical corticosteroids.
Allergic Rhinitis and its Impact on Asthma (ARIA)
Authors: Bousquet J. 
Published: February 2003

SummaryAllergic rhinitis is a worldwide health problem and prevalence of the disease is increasing, with economic and social consequences. An initiative from ARIA (Allergic Rhinitis and its Impact on Asthma), an NGO working with the World Health Organization, has forwarded three main developments in the management of allergic rhinitis. Firstly, ARIA has provided new evidence‐based guidelines for the treatment of rhinitis that can be used worldwide, including in developing countries. The guidelines were designed to be used by the specialist as well as by the primary caregiver. Secondly, ARIA proposes a new subdivision of allergic rhinitis and suggests evidence‐based management of the disease using a stepwise approach. Thirdly, ARIA notes that asthma and rhinitis are common comorbidities and proposes that allergic patients are treated globally to combine treatment of upper and lower airway disease.
Functional relationships between allergic rhinitis and asthma
Authors: Togias A. 
Published: February 2003

SummaryAllergic rhinitis and asthma should be considered manifestations of one syndrome in two parts of the respiratory tract. In addition, the notion that these entities affect each other should be strongly entertained. The pathophysiology of allergic rhinitis is very similar to that of allergic asthma and their responses to pharmacological and immunological interventions are very comparable, as well. Epidemiological data attest to the strong link; 85% or more of allergic asthmatics have rhinitis and, in cross‐sectional population studies, rhinitis is a major risk factor for asthma. Adults with allergic rhinitis have a threefold higher probability of developing asthma, compared with those without rhinitis. A model has been developed to describe the relationships between allergic rhinitis and asthma. According to the model, the two conditions are linked in a horizontal and a vertical fashion. When both conditions are present, their clinical activity tracks in parallel; however, rhinitis appears as a lone condition in the mildest forms of the syndrome. The vertical relationship reflects the fact that experimentally‐induced allergic reactions in the nose can induce changes in the lower airways and the fact that local treatment of rhinitis can have beneficial effects in patients with asthma. Various mechanisms have been proposed to explain the vertical relationship. Investigation into these mechanisms can offer major insights into the physiological and immunological basis of all allergic conditions.