Impact of chart reminders on smoking cessation practices of pulmonary physicians.

Cigarette smoking remains one of the most preventable causes of premature death in our society, yet only a third to a half of smokers visiting a physician are counseled to quit. In the primary care setting, chart reminders can increase physician smoking cessation counseling rates. It is unclear, however, whether pulmonary physicians require prompting to discuss smoking cessation with patients. We hypothesized that chart reminders would improve the smoking cessation counseling and referral practices in our pulmonary clinic. Chart reviews were performed for two 1-mo periods and documentation of smoking status, counseling, and referrals to smoking cessation clinic were recorded. After the implementation of chart reminders, charts were reviewed at 1, 3, and 8 mo. Chart reminders increased documentation of smoking status from 33 to 83% (p = 0.0001). The proportion of all patients counseled increased from 6.0 to 13.2% (p = 0.01). The improvement in counseling to quit occurred primarily by increasing the identification of active smokers. Pulmonary physicians counseled 70% of smokers to quit once patients were identified as smokers. Chart reminders, an inexpensive and easily implemented smoking cessation intervention, increased the overall number and proportion of patients counseled to stop smoking by increasing the number of identified smokers. This simple intervention can improve counseling in populations at high risk for smoking related lung disease.

Recovery of Pseudomonas aeruginosa in respiratory specimens from HIV positive patients being evaluated for Pneumocystis carinii pneumonia.

BACKGROUND: Despite the immune suppression, frequent hospital admissions, and many intercurrent illnesses associated with HIV infection, Pseudomonas aeruginosa has been cited relatively infrequently as a respiratory pathogen in HIV positive patients. METHODS: The microbiological isolates, medical records, radiographic reports, and laboratory data from 224 patients undergoing sputum induction and/or bronchoalveolar lavage for evaluation of respiratory symptoms suspicious for Pneumocystis carinii pneumonia (PCP) from 1989 to 1992 were reviewed retrospectively. RESULTS: An increasing number of respiratory isolates with Pseudomonas aeruginosa was found over this time period. Eighteen of the 224 patients were identified in whom P aeruginosa was recovered on at least one occasion. These patients were more likely to have a history of smoking and prior PCP than those in whom Pseudomonas was not recovered. Mean CD4 counts were also significantly lower in these patients. CONCLUSIONS: Pseudomonas aeruginosa may be recovered from a substantial number of respiratory isolates from HIV positive patients suspected of having PCP. The prevalence of this phenomenon may be increasing.

Endothelial cell hypoxia associated proteins are cell and stress specific.

Vascular endothelial cells (EC) are one of the initial cells exposed to decreases in blood oxygen tension. Bovine EC respond not only by altering secretion of vasoactive, mitogenic, and thrombogenic substances, but also by developing adaptive mechanisms in order to survive acute and chronic hypoxic exposures. EC exposed to hypoxia in vitro upregulate a unique set of stress proteins of Mr 34, 36, 39, 47, and 56 kD. Previous studies have shown that these proteins are cell associated, upregulated in a time and oxygen-concentration dependent manner, and are distinct from heat shock (HSPs) and glucose-regulated proteins (GRPs). To further characterize these hypoxia-associated proteins (HAPs), we investigated their upregulation in human EC from various vascular beds and compared this to possible HAP upregulation in other cell types. Human aortic, pulmonary artery, and microvascular EC upregulated the same set of proteins in response to hypoxia. In comparison, neither lung fibroblasts, pulmonary artery smooth muscle cells, pulmonary alveolar type II cells, nor renal tubular epithelial cells upregulated proteins of these Mr. Instead, most of these cell types induced synthesis of proteins of Mrs corresponding to either HSPs, GRPs, or both. Further studies demonstrated that exposure of EC to related stresses such as cyanide, 2-deoxyglucose, hydrogen peroxide, dithiothreitol, and glucose deprivation did not cause upregulation of HAPs. Evaluation of cellular damage during hypoxia using phase-contrast microscopy, trypan blue exclusion, chromium release, and adherent cell counts showed that EC survived longer with less damage than any of the above cell types. The induction of HAPs, and the lack of induction of HSPs or GRPs, by EC in response to hypoxia may be related to their unique ability to tolerate hypoxia for prolonged periods.

Hypoxia induces a specific set of stress proteins in cultured endothelial cells.

Vascular endothelial cells (EC) are the initial cells within the vascular wall exposed to decreases in blood ambient oxygen concentration. The mechanisms by which they tolerate low levels of oxygen are unknown, but may parallel the response to other cellular stresses, such as heat shock. After 4-8 h of hypoxia, we found a decrease in total protein synthesis in both cultured bovine aortic and pulmonary arterial EC. SDS-PAGE and autoradiographic analysis of [35S]methionine-labeled proteins demonstrated the concomitant induction of a specific set of proteins (Mr 34, 36, 47, and 56 kD) in both cell types. These hypoxia-associated proteins (HAPs) were cell-associated and up-regulated in a time- and oxygen concentration-dependent manner. Comparison of these proteins with heat shock proteins (HSPs) demonstrated that HAPs were distinct from HSPs. EC maintained chronically in 3% O2 continued to synthesize elevated levels of HAPs, yet further up-regulated these proteins when exposed to 0% O2. The presence of five times the normal media glucose concentration did not alter the appearance of HAPs. Hypoxia sensitive renal tubular epithelial cells up-regulated no proteins corresponding to HAPs and were irreversibly damaged within 8 h of exposure to 0% O2. In vitro translation experiments demonstrated that the steady-state level of several mRNAs was higher in the anoxic EC than in normoxic EC and encoded for proteins of Mr 32, 35, 37, 40, and 48 kD that were different from proteins encoded by HSP mRNAs. The induction of HAPs during acute hypoxia and their continued synthesis in chronic hypoxia suggest that HAPs may be important in the maintenance of endothelial cell integrity under conditions of decreased ambient oxygen.