MATERIALS AND METHODS: This is prospective controlled trial. Peripheral venous blood sample is obtained from 20 patients with AAA and 36 normal control subjects. MMP-9 concentration levels were determined by an enzyme-linked immunosorbent assay and compared with subjects abdominal ultrasonography or computed tomography of abdomen.
RESULTS: Mean (± SE) MMP-9 was 23.94 ± 0.60 ng/mL in normal control subjects and 21.39 ± 1.03 ng/mL in patients with AAAs (p ← 0.05 versus normal control subjects). MMP-9 correlate significantly with AAA (p=0.004). There was no correlation of MMP-9 levels with age, gender, or other risk factors. The cutoff point is 12.54 for aorta size <3.0 cm. The sensitivity and specificity of MMP-9 were 60% and 64% respectively.
CONCLUSIONS: MMP-9 levels correlate significantly with AAA with a cutoff point of 12.54. However, the utility of MMP-9 as a diagnostic test is limited due to low sensitivity and specificity. An elevated MMP-9 has limited use to predict the presence of AAA (positive predictive value: 60%) and a normal MMP-9 level was insufficient to determine the absence of AAA (negative predictive value: 36.1%).
AIMS: We assessed outcomes of a pilot long-term stroke care clinic which combined secondary prevention and rehabilitation at community level.
SETTINGS AND DESIGN: A prospective observational study of stroke patients treated between 2008 and 2010 at a primary care teaching facility.
SUBJECTS AND METHODS: Analysis of patients was done at initial contact and at 1-year post treatment. Clinical outcomes included stroke risk factor(s) control, depression according to Patient Health Questionnaire (PHQ9), and level of independence using Barthel Index (BI).
STATISTICAL ANALYSIS USED: Differences in means between baseline and post treatment were compared using paired t-tests or Wilcoxon-signed rank test. Significance level was set at 0.05.
RESULTS: Ninety-one patients were analyzed. Their mean age was 62.9 [standard deviation (SD) 10.9] years, mean stroke episodes were 1.30 (SD 0.5). The median interval between acute stroke and first contact with the clinic 4.0 (interquartile range 9.0) months. Mean systolic blood pressure decreased by 9.7 mmHg (t = 2.79, P = 0.007), while mean diastolic blood pressure remained unchanged at 80mmHg (z = 1.87, P = 0.06). Neurorehabilitation treatment was given to 84.6% of the patients. Median BI increased from 81 (range: 2-100) to 90.5 (range: 27-100) (Z = 2.34, P = 0.01). Median PHQ9 scores decreased from 4.0 (range: 0-22) to 3.0 (range: 0-19) though the change was not significant (Z= -0.744, P = 0.457).
CONCLUSIONS: Primary care-driven long-term stroke care services yield favorable outcomes for blood pressure control and functional level.
MATERIALS AND METHODS: A multicentre prospective cohort study was conducted among employees from 2 different public universities in Malaysia. Interventions include at least 2 sessions of behavioural therapy combined with free nicotine replacement therapy (NRT) for 8 weeks. Participants were followed up for 6 months. Independent variables assessed were on sociodemographic and environmental tobacco smoke. Their quit status were determined at 1 week, 3 months and 6 months.
RESULTS: One hundred and eighty- five smokers volunteered to participate. Among the participants, 15% and 13% sustained quit at 3 months and 6 months respectively. Multivariate analysis revealed that at 6 months, attending all 3 behavioural sessions predicted success. None of the environmental tobacco exposure variables were predictive of sustained cessation.
CONCLUSION: Individual predictors of success in intra-workplace smoking cessation programmes do not differ from the conventional clinic-based smoking cessation. Furthermore, environmental tobacco exposure in low intensity smoke-free workplaces has limited influence on smokers who succeeded in maintaining 6 months quitting.
METHODS: This study was conducted within the European Prospective Investigation into Nutrition and Cancer cohort, comprising male and female participants from 10 European countries. Between 1992 and 2000, there were 477,312 participants without cancer who completed a dietary questionnaire and were followed up to determine pancreatic cancer incidence. Coffee and tea intake was calibrated with a 24-hour dietary recall. Adjusted hazard ratios (HRs) were computed using multivariable Cox regression.
RESULTS: During a mean follow-up period of 11.6 y, 865 first incidences of pancreatic cancers were reported. When divided into fourths, neither total intake of coffee (HR, 1.03; 95% confidence interval [CI], 0.83-1.27; high vs low intake), decaffeinated coffee (HR, 1.12; 95% CI, 0.76-1.63; high vs low intake), nor tea were associated with risk of pancreatic cancer (HR, 1.22, 95% CI, 0.95-1.56; high vs low intake). Moderately low intake of caffeinated coffee was associated with an increased risk of pancreatic cancer (HR, 1.33; 95% CI, 1.02-1.74), compared with low intake. However, no graded dose response was observed, and the association attenuated after restriction to histologically confirmed pancreatic cancers.
CONCLUSIONS: Based on an analysis of data from the European Prospective Investigation into Nutrition and Cancer cohort, total coffee, decaffeinated coffee, and tea consumption are not related to the risk of pancreatic cancer.