Search PubMed⌕ Search

Biomedical subjects

S F Moss

Publications and source records attributed to S F Moss.

80 records · Page 5Linked to original sources
PubMed1991

Time course of recovery of lung function in sulphasalazine-induced alveolitis.

Interstitial lung disease has long been recognized as one of the side effects of sulphonamide drugs (1) but we have found only 13 case reports of alveolitis in association with sulphasalazine (2-8). Although the clinical picture and radiological changes are known to be reversible, there is little information regarding the lung function abnormalities and no description of the time course of its recovery. We describe a patient with very severe impairment of gas exchange secondary to sulphasalazine which completely recovered after the drug was stopped.

Aged↗
PubMed1989

Abnormal lung lymphatics and respiratory failure.

A 65 year old man presented with respiratory failure, pleural effusions, fine reticulonodular shadowing on a chest radiograph, and severe impairment of carbon monoxide diffusing capacity (transfer factor). Open lung biopsy showed only dilated pleural and subpleural lymphatic channels. Hypoplastic deep pulmonary lymphatics may have led to respiratory failure.

Aged↗
PubMed1976

Relationship between central and autonomic nervous system activity: correlates of psychomotor performance in elderly men.

The relationship between heart rate deceleration (HRD) and the contingent negative variation (CNV) was evaluated in 12 healthy, elderly men during performance of a signaled reaction time task. While amplitude of the CNV and HRD did parallel RT, CNV alone was found to be predictive of individual differences in speed of response indicating that phasic concordance of these physiological responses is probably not an important factor in age changes in RT. The results indicate the probable importance of central physiological indices such as the CNV over peripheral events such as HRD in the evaluation of RT performance in elderly individuals.

Aged↗
PubMedDate not supplied

Modulation of abnormal colonic epithelial cell proliferation and differentiation by low-fat dairy foods: a randomized controlled trial.

CONTEXT: Before the development of human colonic neoplasms, colonic epithelial cells showed altered growth and differentiation. These alterations characterized mucosa at risk for cancer formation and were termed intermediate biomarkers of risk. Modifications of the mucosa toward more normal features by nutrients or drugs are putative approaches to chemoprevention of colon cancer. OBJECTIVE: To determine whether increasing calcium intake via dairy products alters colonic biomarkers toward normal. DESIGN: Randomized, single-blind, controlled study. SETTING: Outpatient clinic. PARTICIPANTS: Seventy subjects with a history of polypectomy for colonic adenomatous polyps. INTERVENTION: Low-fat dairy products containing up to 1200 mg/d of calcium. Subjects were randomized to 4 strata by diet (control vs higher calcium) and age (<60 vs > or = 60 years). MAIN OUTCOME MEASURES: Changes in total colonic epithelial cells and number and position of thymidine-labeled epithelial cells and changes in the ratio of sulfomucins (predominantly secreted by distal colorectal epithelial cells) to sialomucins and expression of cytokeratin AE1, 2 markers of colonic cell differentiation. RESULTS: During 6 and 12 months of treatment, reduction of colonic epithelial cell proliferative activity (P<.05), reduction in size of the proliferative compartment (P<.05), and restoration of acidic mucin (P<.02), cytokeratin AE1 distribution (P<.05), and nuclear size (P<.05) toward that of normal cells occurred. Control subjects showed no differences from baseline proliferative values at 6 and 12 months (P>.05). CONCLUSION: Increasing the daily intake of calcium by up to 1200 mg via low-fat dairy food in subjects at risk for colonic neoplasia reduces proliferative activity of colonic epithelial cells and restores markers of normal cellular differentiation.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

Helicobacter pylori and apoptosis.

In an attempt to understand the diverse effects of infection with Helicobacter pylori on epithelial mucosal mass and consequent clinical outcome, the relationship between H. pylori infection and gastric epithelial cellular turnover has been investigated. Our results indicate that H. pylori increases epithelial cell proliferation and apoptosis in vivo, but that infection with bacteria of the cagA genotype leads to relatively more proliferation than apoptosis. This review explores the causes of the induction of apoptosis in gastric epithelial cells by H. pylori and the consequences of alterations in apoptosis to the maintenance of gastric mucosal homeostasis.

Antigens, Bacterial↗