Search PubMed⌕ Search

Biomedical subjects

W Roche

Publications and source records attributed to W Roche.

8 recordsLinked to original sources
PubMed1994

Expression of integrin adhesion molecules in endometrium and endometriosis.

OBJECTIVE: To compare the expression of cell adhesion molecules by endometrium and endometriosis. DESIGN: A comparative study of integrin expression, determined immunohistochemically, in eutopic and ectopic endometrium biopsied synchronously from patients with endometriosis diagnosed at laparoscopy or laparotomy. SETTING: University Departments of Obstetrics and Gynaecology, and Pathology, Southampton; Department of Obstetrics and Gynaecology, Newcastle upon Tyne. SAMPLES: Eighteen paired samples of endometria and endometriosis. RESULTS: A wide distribution of collagen-laminin receptor proteins was demonstrated. alpha 1 integrin expression was limited to secretory endometrium. beta 3 expression was only demonstrated on proliferative endometrium. CONCLUSIONS: Expressions of the integrin proteins differed between the various elements of the endometrium. Cyclical changes in integrin expression also were demonstrated. No difference in cell adhesion molecule expression was seen when comparing endometrial and endometriosis samples.

Cell Adhesion Molecules↗
PubMed1993

Pathology of asthma and its clinical implications.

Although detailed histopathologic studies have described the inflammatory processes present in fatal asthma, until recently the pathology of less severe forms of the disease has been less well understood. Now a series of important studies has extended our understanding of the pathophysiology of mild asthma. Studies that examine sputum or fluid obtained by bronchoalveolar lavage from mildly asthmatic subjects revealed findings consistent with an active inflammatory process within the airways. The histopathologic examination of endobronchial biopsy specimens from stable asthmatic patients has shown that inflammatory cell infiltration of the mucosa is a distinctive feature of mildly asthmatic subjects requiring only intermittent inhaled beta-agonist therapy. These studies have also shown that marked tissue disruption may occur early in the natural history of mild asthma. These investigations have demonstrated that asthma is a disease characterized by acute and chronic inflammatory changes within the airways and that in many respects the histopathologic features of mild allergic asthma are similar to those observed in fatal asthma. The therapeutic implications of these findings are that management of mild asthma should be directed toward resolving this inflammatory process. There is now sufficient evidence to suggest that anti-inflammatory drugs such as cromolyn sodium, inhaled corticosteroids, and nedocromil sodium be used earlier in the course of the disease and that the use of these therapeutic agents should not be limited to patients with severe forms of asthma. This may be particularly important in view of the increasing awareness of the potential problems associated with the overreliance on beta-agonist therapy in patients with asthma.

Asthma↗
PubMed1991

Allergic inflammation and its pharmacological modulation in asthma.

While most asthma occurs in association with atopy, the relationship of this to clinical expression of the disease is not clearly understood. Allergen provocation causes an immediate bronchoconstriction (early asthmatic reaction) due to the release of mast-cell-derived histamine, prostaglandin D2 and leukotriene C4. The late reaction and attendent increase in bronchial responsiveness are associated with eosinophil influx, activation and mediator secretion, resulting in mucosal swelling in addition to smooth muscle contraction. Endobronchial biopsy and broncho-alveolar lavage have provided compelling evidence that both mast cells and eosinophils contribute to disordered airway function in 'clinical' asthma and that these cells are under the control of T lymphocytes. Topical corticosteroids which produce beneficial clinical effects probably do so by inhibiting those factors that maintain mast cell and eosinophil populations and their enhanced activation. The most likely contenders for these regulatory functions are the cytokines, particularly interleukin-3, -4 and -5.

Adrenal Cortex Hormones↗
PubMed1991

The need for a pathological classification of asthma.

Historically, asthma has been described in functional terms as reversible airways obstruction and bronchial hyperresponsiveness. Whilst there is no agreed definition of asthma, studies involving bronchoalveolar lavage and endobronchial biopsy are highlighting inflammatory processes as an essential component of the disorder. With the success already achieved in quantifying mast cells, neutrophils, eosinophils, T-cells, monocytes and fibroblasts in the bronchial mucosa it should be possible to investigate the cellular basis of asthma, both in relation to clinical patterns of disease and their response to treatment. With such information it may well be possible that a definition of asthma could be arrived at based on pathology rather than function alone.

Asthma↗
PubMed1989

Inflammatory processes in bronchial asthma.

Bronchial asthma is an inflammatory disease. The characteristic pathological features of epithelial cell loss, goblet cell hyperplasia, increased deposition of collagen beneath the basement membrane, mast cell degranulation, and inflammatory cell infiltration of the mucosa are not limited to fatal asthma. Similar inflammatory events have been observed in subjects who would be considered to have clinically stable asthma. These observations would suggest that pharmacological treatment directed against the underlying inflammatory processes in asthma should not be limited to those patients with severe forms of the disease.

Animals↗