At baseline, a 10ml venous blood specimen was collected from 1841 men and 1957 women and placed into EDTA tubes. Blood samples were stored at -70C until DNA extraction (within one year after collection). Genomic DNA was extracted for genotyping of Alu insertion/deletion (I/D) polymorphism in the ACE gene by polymerase chain reaction with forward and reverse primers (5'- AGAGAGACTCAAGCACGCCC-3' and 5'- ACCCAAGTGCCAGTGATGTT-3'). Reactions were set up in a volume of 25 ml containing 0.2 mM of each primer, 1X PCR buffer, 2 mM MgCl2, 0.2mM of each dNTP, and 0.6 U Taq polymerase (Fermentas Life Sciences). About 50 ng of DNA was used in each sample. The initial denaturation was performed at 95oC for 5 min, followed by 35 cycles of 94oC for 30 sec, 64oC for 30 sec, and 72oC for 30 sec, and a final extension at 72oC for 10 min. This method yielded amplification products of 439 bp for the D allele and 727 bp for the I allele, which were visualized in 2% agarose gels. 

The chi-square test was used to test for statistical differences between categorical variables, while student's t-test and analysis of variance were used for continuous variables between the three genotype groups. Analysis of covariance was used to adjust for confounding variables while adjusting for multiple hypothesis testing. The incidence of disease was calculated as the number without disease at baseline who developed it at follow-up. Cox regression analysis was used to examine mortality rates between the three genotype groups using a proportional hazard model.

At baseline, participants completed a questionnaire that included demographics, history of chronic disease, use of ACE inhibitors, smoking habits, physical activity level assessed using the Physical Activity Scale of the Elderly (PASE) (22), and dietary intake assessed using a food frequency questionnaire administered by an interviewer (23). Body weight was measured with subjects wearing a light gown using the Physical Balance Beam Scale (Healthometer, Bridgeview, Illinois, USA), while height was measured using the Holtain Harpenden stadiometer (Holtain Ltd., Crosswell, UK). Supine blood pressure was measured in the right arm and both ankles using a standard mercury sphygmomanometer and a handheld Doppler with an 8-MHz Doppler probe (Pocket Doppler Model 841-A, Parks Medical Electronics Inc, Aloha, Or, USA). The average reading of two measurements at each site was used. The ankle-brachial index (ABI) was calculated by dividing the blood pressure at the posterior tibial site by the brachial artery site for each side, and the lowest of the two values was used. An ABI value of <0.9 has been used as a cutoff value to indicate the presence of peripheral vascular disease (24).Also, as an indicator of atherosclerosis (25), the procedure was carried out for 1999 men and 1999 women, and the baseline results are reported elsewhere (26). During the fifth year of follow-up, participants returned, and a medical history was obtained, and ABI measurement was repeated. The Death Registry was searched. ACE gene polymorphism results were available in 1841 men and 1957 women from whom blood samples for DNA extraction had been obtained. For men, the frequencies of I/I, I/D, and D/D genotypes were 815/1841 (44.3%), 842/1841 (45.7%), and 184/1841 (9.9%), respectively. Genotype distributions in both sexes followed Hardy Weinberg equilibrium. For women, the frequencies were 46%, 43%, and 10.9%, respectively. The percentage of subjects with ABI <0.9 did not differ significantly between the three polymorphism groups. Mean ABI, the percentage of subjects with ABI <0.9, and potential confounders in the relationship between genetic factors and ABI are listed by genotype groups in Table 1a & b. In women only, participants with the D/D genotype had the greatest reduction in mean ABI value. This group also had the highest mean age. After adjusting for all potential confounding factors, the D/D group had the greatest progression of atherosclerosis (using reduction in ABI as an indicator), followed by I/I and I/D groups (Table 2). No significant variations were found across the three polymorphism groups in men or women for any of the variables listed in Table 1a & b.This text appears to be a table, but it is not properly formatted. Therefore, it is difficult to determine the exact meaning of the data. However, I can make some general observations and corrections:

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Confounding variables, including age, BMI, PASE, diabetes, heart disease, hypertension, stroke, use of ACE inhibitors, smoking, alcohol use, and dietary intake of saturated fatty acids were analyzed. The results showed no significant differences in incidence of disease between those with different ACE genotypes. However, D/D was more common among women developing hypertension or myocardial infarction. In terms of mortality, more men with the D/D genotype had died by the 5th year follow-up compared to the I/I or I/D group.