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Biomedical subjects

D A Groneberg

Publications and source records attributed to D A Groneberg.

At least 37 records · Page 2Linked to original sources
PubMed2003

Severe acute respiratory syndrome: global initiatives for disease diagnosis.

We present a retrospective analysis of the available articles on severe acute respiratory syndrome (SARS) published since the outbreak of the disease. SARS is a new infectious disease caused by a novel coronavirus. Originating in Guangdong, Southern China, at the end of 2002, it has spread to regions all over the world, affecting more than 8000 people. With high morbidity and mortality, SARS is an important respiratory disease which may be encountered world-wide. The causative virus was identified by a WHO-led network of laboratories, which identified the genome sequence and developed the first molecular assays for diagnosis. For the respiratory physician, detecting SARS in its earliest stages, identifying pathways of transmission, and implementing preventive and therapeutic strategies are all important. The WHO and the CDC have published helpful definitions of 'suspected' and 'probable' cases. However, the symptoms of the disease may change, and laboratory tests and definitions are still limited. Even in a situation of no new cases of infection, SARS remains a major respiratory health hazard. As with influenza virus outbreaks, new epidemics may arise at the end of each year.

Antibodies, Viral↗
PubMed2003

Aspirin-sensitive rhinitis-associated changes in upper airway innervation.

Aspirin-sensitive rhinitis is the manifestation of aspirin intolerance in the upper respiratory tract. The disease represents a pseudoallergy against aspirin or related nonsteroidal anti-inflammatory drugs. As a major immunomodulatory role for airway innervation has been proposed in airway inflammatory diseases, the present study assessed changes in human nasal mucosa innervation in patients with aspirin-sensitive rhinitis in comparison to a control group. Immunohistochemistry for protein gene product 9.5, tachykinins, calcitonin gene-related peptide, vasoactive intestinal peptide (VIP) and neuropeptide tyrosine was performed on cryostats sections of nasal mucosa and neuropeptide containing nerves were examined independently using a score grading. In comparison to the control, the aspirin-sensitive rhinitis group had a significant increase of VIP-like immunoreactivity in mucosal nerve fibres. In contrast to constant numbers of mast cells, highly significant increases in the numbers of eosinophils were found in the group of aspirin-sensitive rhinitis patients. In summary, the present quantification of neuropeptide-immunoreactivity of mucosal nerves demonstrated differences in the human nasal mucosa innervation between nonrhinitic and aspirin-sensitive rhinitic individuals. These differences may reflect a pathophysiological role of upper airway innervation in pseudoallergic reactions.

Adolescent↗
PubMed2003

Hymenoptera sting anaphylactic reactions in the Mediterranean population of Albania.

BACKGROUND: Relatively few studies have examined the relation of different hymenoptera sting reactions. OBJECTIVE: To investigate the relation of anaphylactic reactions against stings of different hymenoptera subspecies in the Mediterranean population of Albania. MATERIALS AND METHODS: A retrospective study was conducted using the clinic files of 111 patients who were diagnosed for hymenoptera sting reactions from 1987 to 1996. Antigens used consisted of purified hymenoptera venom (bee, wasp, and paperwasp). The patients were diagnosed by intracutaneous tests in concentrations of 0.001 microgram/ml, 0.01 microgram/ml, 0.1 microgram/ml, and 1 microgram/ml. RESULTS: The median age of the patients was 27 years. 57% of stings occurred between 20 to 40 years of age. The majority of anaphylactic reactions were recorded during the months of June to October, 81% of the patients were admitted to the hospital due to Mueller grade II to III reactions. In 26% of all cases, crossreactions (bee-wasp 16%, bee-wasp-paperwasp 7%, wasp-paperwasp 2%, bee-paperwasp 1%) were found. Of all anaphylactic reactions, 64% were attributed to bees, 24% to wasps, 8% to both bees and wasps, and 2% to paperwasps. CONCLUSIONS: In contrast to industrialized countries such as the United States or Western Europe where urban populations predominate, reactions to bee venom were more prevalent in the present study population.

Adolescent↗
PubMed2002

Abundant expression of c-Jun in guinea pig sympathetic ganglia under basal conditions and allergen challenge.

Airway hyperresponsiveness, a keystone of allergic asthma, is mediated by the extrinsic airway innervation. As pathophysiological stimuli can induce the expression JUN proteins, which belong to the immediate early gene (IEG) family of transcription factors, the expression of c-Jun was examined under basal conditions and allergen challenge in guinea pig paravertebral and prevertebral sympathetic ganglia by quantitative double-labeling immunohistochemistry. C-Jun immunoreactivity was seen in 78.4 +/- 3.5% under normal and 82.6 +/- 4.6% under allergen-challenged conditions of protein-gene product (PGP) 9.5-positive sympathetic neurons of guinea pig superior cervical ganglia and 73.1 +/- 2.8% (normal) and 76.1 +/- 3.5% (allergen) of stellate ganglion neurons. In the coeliac-superior mesenteric ganglion, 59.5 +/- 5.0% (normal) and 57.5 +/- 4.4% (allergen) of the PGP 9.5-positive sympathetic neurons were labeled for c-Jun. The high basal levels of c-Jun expression indicate that the presence of c-Jun is not exclusively related to noxious stimulation such as allergic airway inflammation in the guinea pig.

Animals↗
PubMed2002

Expression of respiratory mucins in fatal status asthmaticus and mild asthma.

AIMS: The airways of patients with asthma are characterized by chronic inflammatory changes comprising mainly T-cells and eosinophils, and airway remodelling with goblet cell metaplasia and submucosal gland hyperplasia. Mucus hypersecretion is often a marked feature, particularly in status asthmaticus. The matrix of airway sputum consists of high molecular glycoproteins and mucins. In this study, the expression and distribution of the major gel-forming mucins MUC5AC and MUC5B were studied in fatal status asthmaticus tissues and bronchial biopsies of mild asthmatic patients. The effect of inhaled corticosteroids on the expression of these mucins was also investigated. METHODS AND RESULTS: Polyclonal antibodies specific for MUC5AC and MUC5B, and a monoclonal antibody for MUC5B were used to stain lung tissues and airway mucosal biopsies obtained from patients who died of status asthmaticus (n=5) and from mild asthmatics (n=4), respectively. Immunohistochemistry for MUC5AC revealed abundant staining of goblet cells situated in the epithelial surface lining and glandular ducts of tissues from patients with fatal asthma. MUC5B immunoreactivity was restricted to mucous cells of submucosal glands and to epithelial cells. In mild asthmatics, large amounts of MUC5B, but not MUC5AC, positive extracellular mucus was found in the airway lumen as plugs, adjacent to the epithelial lining and in the necks of glandular secretory ducts of mild asthmatics. The distribution of MUC5AC and MUC5B in bronchial biopsies of mild asthmatics was similar before and after inhaled steroid treatment. CONCLUSIONS: The expression of MUC5AC and MUC5B shares a similar distribution to normal airways in different states of asthma. The distribution is not affected by topical corticosteroid therapy.

Asthma↗
PubMed2002

Expression of MUC5AC and MUC5B mucins in normal and cystic fibrosis lung.

Hypersecretion of airway mucus is a characteristic feature of chronic airway diseases like cystic fibrosis (CF) and leads via impairment of the muco-ciliary clearance and bacterial superinfection to respiratory failure. The major components of the mucus matrix forming family of mucins in the airways are MUC5AC and MUC5B. To investigate the expression of these glycoproteins in CF, immunohistochemistry was carried out on trachea, bronchi and peripheral lung obtained from CF patients and compared to normal lung tissues. MUC5AC immunohistochemistry demonstrated signals in goblet cells of the epithelial lining. Also, goblet cells inside glandular secretory ducts revealed MUC5AC-positive staining. In comparison to those from normal subjects, CF sections were characterized by inflammatory changes and goblet cell hyperplasia, resulting in increased numbers of MUC5AC-positive cells. Immunohistochemical staining for MUC5B showed abundant staining of submucosal glands and epithelial goblet cells. Inside the glands, the immunoreactivity was restricted to glandular mucous cells. MUC5AC and MUC5B are expressed in the same histological pattern in CF compared to normal tissues with an increase of MUC5AC-positive cells due to goblet cell hyper- and metaplasia.

Bronchi↗
PubMed2002

Distribution and function of the peptide transporter PEPT2 in normal and cystic fibrosis human lung.

BACKGROUND: Aerosol administration of peptide based drugs has an important role in the treatment of various pulmonary and systemic diseases. The characterisation of pulmonary peptide transport pathways can lead to new strategies in aerosol drug treatment. METHODS: Immunohistochemistry and ex vivo uptake studies were established to assess the distribution and activity of the beta-lactam transporting high affinity proton coupled peptide transporter PEPT2 in normal and cystic fibrosis human airway tissue. RESULTS: PEPT2 immunoreactivity in normal human airways was localised to cells of the tracheal and bronchial epithelium and the endothelium of small vessels. In peripheral lung immunoreactivity was restricted to type II pneumocytes. In sections of cystic fibrosis lung a similar pattern of distribution was obtained with signals localised to endothelial cells, airway epithelium, and type II pneumocytes. Functional ex vivo uptake studies with fresh lung specimens led to an uptake of the fluorophore conjugated dipeptide derivative D-Ala-L-Lys-AMCA into bronchial epithelial cells and type II pneumocytes. This uptake was competitively inhibited by dipeptides and cephalosporins but not ACE inhibitors, indicating a substrate specificity as described for PEPT2. CONCLUSIONS: These findings provide evidence for the expression and function of the peptide transporter PEPT2 in the normal and cystic fibrosis human respiratory tract and suggest that PEPT2 is likely to play a role in the transport of pulmonary peptides and peptidomimetics.

Acetates↗
PubMed2001

Expression of PEPT2 peptide transporter mRNA and protein in glial cells of rat dorsal root ganglia.

The peptide-transporter PEPT2 mediates electrogenic uphill transport of di- and tripeptides, selected peptidomimetics and delta aminolevulinic acid. The transporter was cloned from rat central nervous tissue recently and its mRNA was localized to astrocytes. In the present studies the expression of PEPT2-protein and -mRNA in rat dorsal root ganglia was investigated. Immunohistochemistry revealed PEPT2-immunoreactivity in satellite glial cells surrounding the ganglionic neurons. There was no expression in neuronal cells. In-situ-hybridization studies colocalized the expression of PEPT2-mRNA to satellite cells. This is the first report on the expression of PEPT2-protein in the peripheral nervous system where PEPT2 may serve as uptake system for products of protein degradation, for removal of biologically active short-chain peptides and non-peptides such as delta aminolevulinic acid.

Animals↗
PubMed2001

Endogenous opioids as mediators of asthma.

Changes in airway innervation are believed to play a key role in the pathophysiology of asthma. A group of regulatory peptides which act as neuroregulators is resembled by the opioids. Their localization to neurons projecting into airways suggested a possible role as regulators of neurogenic inflammation, bronchoconstriction and mucus secretion. They mainly act through modification of tachykinergic and cholinergic impulses and their ability to inhibit bronchoconstriction prompted discussion of their potential value in asthma therapy. Apart from the presence of the classical opioids and their receptors in the lung and their functional role, a new group of peptides such as nociceptin and endomorphins have been characterized in the airways. Whereas at least endomorphin-1 acts via the classical OP(3) (mu) receptor, nociceptin binds to a new receptor termed opioid receptor-like-receptor (ORL(1)) and inhibits tachykinergic constriction. Contrary to these promising modulatory effects on airway smooth muscle tone, effective therapeutic strategies have not been developed yet. In conclusion, opioids resemble a group of regulatory peptides which are present within airway-innervating nerve fibres and influence a multitude of airway functions via modification of neural transmission.

Asthma↗