An interpretative phenomenological analysis of the experiences of older people self-managing cancer pain at home

Cancer is predominantly an illness affecting older people, yet there is a higher risk of under-treated pain in this age group. Many older people are required to self-manage their cancer pain at home but this is currently an under-researched and poorly understood area. We explored the experiences of older adults who self-manage cancer pain at home using an Interpretative Phenomenological Analytic approach. Eight older adults (aged 72–85 years) were recruited from a hospital in the United Kingdom and interviewed using a semi-structured questionnaire. Themes which emerged from the analysis suggest the self-management of cancer pain involves a perceived loss of control followed by a temporal process of gaining control over pain. Subordinate themes reflected the physical and social restrictions caused by pain; leading to fears regarding familial burden. Participants utilized inner strengths, past experiences, and social support to cope. Successful self-management of cancer pain in late life is conceptualized utilizing a positive psychology framework.     

Smoking and the risk of first acute myocardial infarction

When analyzing risk factors for first acute myocardial infarction in the Copenhagen City Heart Study, a large prospective population study of 20,000 men and women, smoking was found to influence risk significantly in a dose-dependent manner, the risk increasing 2% to 3% for each gram of tobacco smoked daily. Risk was particularly associated with inhalation, the risk for inhalers being almost twice that of noninhalers. No difference in risk could be demonstrated between various types of tobacco (pipe, cigar/cheroots, or plain and filtered cigarettes). The risk seemed associated with current smoking only, inasmuch as the duration of the smoking habit was not important. Ex-smokers had the same risk as those who had never smoked regardless of duration of smoking and time elapsed since quitting. Relative excess risk was significantly higher in female smokers than in male smokers, and daily alcohol intake appeared to have some protective effect on the risk of first acute myocardial infarction among heavy smokers.     

Risk stratification after acute myocardial infarction by means of echocardiographic wall motion scoring and Killip classification.

In order to perform risk stratification, 195 consecutive, unselected patients with acute myocardial infarction (AMI) underwent independent echocardiographic and clinical evaluation of their left ventricular function by means of the wall motion index (WMI) and Killip classification 5 days after AMI. The patients were prospectively allocated to a low, medium or high risk class depending on WMI alone, and the 1-year mortality in these classes was 2, 34 and 37%, respectively (p < 0.0001). The 1-year mortality of the patients in Killip class I, II, or III and IV was 6, 26 and 48%, respectively (p < 0.00001). The number of patients allocated to the low risk group by means of WMI was 87, and the number of patients in Killip class I was 86. Since these groups were not identical, a total of 103 patients, i.e. 53% of the study population, could be identified as low risk patients regarding 1-year mortality 5 days after AMI, when WMI and Killip classification were used in combination. We conclude that the combination of echocardiographic and clinical evaluation of left ventricular function after AMI provides a strong and yet very simple procedure to identify low risk patients, which could be easily implemented in the routine work of coronary care units.     

Prevalence of esophageal Candida colonization in a Danish population: special reference to esophageal symptoms, benign esophageal disorders, and pulmonary disease.

A population sample selected at random after stratification for the presence of pulmonary disease was screened for benign esophageal disease; 175 subjects agreed to participate in the invasive investigation, 86 without pulmonary disease and 89 with chronic obstructive pulmonary disease (COPD). Of these, 169 underwent endoscopy of the upper gastrointestinal tract, 164 had mucosal brushings for the presence of Candida albicans in the esophagus, 169 had esophageal pressure measurements, and 113 had 12-h pH measurements. One hundred fourteen subjects with benign esophageal disease were found. The prevalence of C. albicans in the esophagus (greater than or equal to 50 colonies) in subjects with and without COPD was 12.3% and 25.1%, respectively. C. albicans occurred equally in subjects with and without esophageal symptoms. There was no relation between the presence of C. albicans and benign esophageal disease and no significant clinical correlation between esophageal plaques and colony counts of C. albicans.     

Temporal changes in colonic vascular architecture and inflammatory mediator levels in animal models of colitis

This study investigated the temporal relationship between inflammatory mediator production and colonic vascular architecture in rabbit and rat trinitrobenzene sulfonic acid (TNBS) models of colitis. In both species significant colonic damage and loss of mucosal integrity occurred over time. In the rabbit there was a significant increase in TxB₂ levels in the muscularis propria and mucosa at 1, 6, and 48 hr after TNBS, with a significant elevation in PGE₂ production in the muscularis propria at 48 hr. However, elevated mediator levels were not associated with measurable changes in vascular architecture. In contrast, significant changes in the numbers and diameters of colonic blood vessels were observed in the rat, in the absence of significant elevations in TxB₂ or PGE₂ levels. These data suggest that the role of lipid mediators in acute colitis is species-dependent and, although there are corresponding gross and microscopic changes in both models, these occur through disparate mechanisms.     

Improved recovery of heart transplants by combined use of oxygen-derived free radical scavengers and energy enhancement.

Oxygen free radical injury during reperfusion of ischemically stored heart transplants may further impair the ability of the transplanted heart to reuse substrate for recovery. We compared the effects of oxygen free radical scavengers, superoxide dismutase and catalase, either alone or combined with glucose-insulin-potassium, in an improved model of the heterotopically transplanted rat heart. Group 1 hearts (n = 8) received no preservation before transplantation and were transplanted immediately. Hearts in four other groups (n = 8 for each group) underwent cold storage (4 degrees to 6 degrees C) for 3 1/2 hours before transplantation. Five minutes before reperfusion of the transplanted hearts, recipient rats received one of the following intravenous treatments: saline (group 2), glucose-insulin-potassium (group 3), superoxide dismutase/catalase (group 4), and superoxide dismutase/catalase plus glucose-insulin-potassium (group 5). Left ventricular end-diastolic pressure, rate of rise of left ventricular pressure, myocardial blood flow, coronary resistance, and tissue adenosine triphosphate content of the heart transplants were assessed during or at the end of 2 hours of reperfusion. Hearts treated with superoxide dismutase/catalase alone showed improvement of end-diastolic pressure and myocardial blood flow. The use of glucose-insulin-potassium alone did not facilitate the recovery of transplanted hearts. In contrast, the combined use of superoxide dismutase/catalase plus glucose-insulin-potassium resulted in a superior recovery of all functional and hemodynamic parameters. These results indicate that free radical scavengers in the presence of glucose-insulin-potassium significantly improve functional recovery in the setting of heart transplantation.     

Complete prevention of myocardial stunning, contracture, low-reflow, and edema after heart transplantation by blocking neutrophil adhesion molecules during reperfusion.

This study tested the hypothesis that preventing neutrophil adhesion during reperfusion, by blocking either the neutrophil membrane CD18 integrin complex or its endothelial and myocyte ligand, intercellular adhesion molecule-1 (ICAM-1), would reduce myocardial inflammation and edema and improve reflow and ventricular function after heart preservation and transplantation. After cardioplegia and insertion of a left ventricular balloon, rabbit hearts were heterotopically transplanted into recipient rabbits either immediately (immediate, n = 12) or after preservation in 4 degrees C saline (3 hours of ischemia, n = 33). Forty-five minutes before reperfusion, recipients of preserved hearts received intravenous infusions of either saline (vehicle, n = 13), anti-CD18 monoclonal antibody (Mab) R15.7 (2 mg/kg) (anti-CD18, n = 10), or anti-ICAM-1 Mab R1.1 (2 mg/kg) (anti-ICAM, n = 10). During 3 hours of reperfusion the slope of the peak-systolic pressure-volume relation and its volume-axis intercept, the exponential elastic coefficient of the end-diastolic pressure-volume relation, the unstressed ventricular volume, and the time constant of the exponential left ventricular pressure decay after dP/dtmin were serially measured. Myocardial blood flow was measured with microspheres from which coronary vascular resistance was calculated. After explanation, the degree of myocardial inflammation, estimated by tissue neutrophil sequestration (myeloperoxidase assay) and myocardial water content were determined. Within each group no significant differences in measurements made at 1, 2, and 3 hours of reperfusion were noted. Compared with the immediate transplantation group, the vehicle group demonstrated a significant increase in myeloperoxidase activity (3380 +/- 456 versus 1712 +/- 552 microU/gm, p < 0.05), coronary vascular resistance (115.5 +/- 13.4 versus 70.5 +/- 10.6 U/gm, p < 0.05), and myocardial water content (79.8% +/- 0.4% versus 75.6% +/- 1.3%, p < 0.05), a significant decrease in unstressed ventricular volume (a leftward shift in the end-diastolic pressure-volume relation) (-0.49 +/- 0.24 versus 0.28 +/- 0.21 ml, p < 0.05), and a marked prolongation in exponential left ventricular pressure delay after dP/dtmin (156.64 +/- 3.81 versus 37.25 +/- 3.34 msec, p < 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)     

Catabolism of platelet-activating factor by human colonic mucosa. Calcium dependence of the catabolizing enzymes.

The catabolism of platelet-activating factor (PAF) and lyso PAF by a supernatant fraction of human colon mucosa homogenates has been studied in vitro. PAF is initially catabolized to lyso PAF by mucosal enzymes via removal of its acetyl group. Incubates in Ca(2+)-free Tris with EDTA showed that the acetyl hydrolase was Ca2+ independent. Addition of the hydrolase inhibitor, phenyl methyl sulphonyl fluoride, significantly reduced the catabolism of PAF. Lyso PAF was further catabolized in at least two ways. An acyl group was incorporated into the sn-2 position of lyso PAF to give 1-O-alkyl-2-acyl-sn-glycero-3-phosphocholine (alkyl acyl GPC); this step was Ca2+ independent as shown by omitting Ca2+ and adding EDTA to the incubate. Formation of alkyl acyl GPC was confirmed by HPLC. Alternatively, choline was removed from the head group of lyso PAF by a calcium-dependent lyso phospholipase D. Under the experimental conditions utilized a neutral lipid product was formed but significant amounts of the intermediate lysophosphatidic acid could not be detected. A substance with a chromatographic mobility of Rf = 0.8 on TLC plates having an intact phosphorylcholine head group was also formed but has not yet been identified. It is concluded that the human colon mucosa contains enzymes that actively catabolize pro-inflammatory PAF and lyso PAF.