2024-03-29T05:43:14Zhttp://open-archive.highwire.org/handler
oai:open-archive.highwire.org:amjepid:142/7/6712015-05-11HighWireOUPamjepid:142:7
Invited Commentary on "Health Effects of Westernization and Migration among Chamorros"
Feinleib, Manning
INVITED COMMENTARY
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/671
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/6732015-05-11HighWireOUPamjepid:142:7
HEALTH EFFECTS OF WESTERNIZATION AND MIGRATION AMONG CHAMORROS
REED, DWAYNE
LABARTHE, DARWIN
STALLONES, REUEL
HISTORICAL PAPER
Reed, D. (School of Public Health, Univ. of Texas, P. O. Box 20186, Astrodome Station, Houston, Texas 77025), D. Labarthe and R. Stallones. Health effects of westernization and migration among Chamorros. <it>Amer. J. Epid., 1970, 92</it>: 94–112.—This study is an epidemiologic exploration of the relationship between disease and sociocultural discontinuity among three groups of Chamorro natives of the Mariana Islands. Although similar in genetic background, the three groups have had different sociocultural experiences by virtue of their residence on Rota, Guam and California. As a test of the hypothesis that migration and westernization are associated with an increased prevalence of a variety of diseases among adult Chamorros, we examined over 1,200 individuals. A 24-hour dietary survey was completed for a subsample in each area, and 10-year mortality data were obtained in Guam and California. The results documented the differences of the three groups in terms of migration, mobility and sociocultural orientation. The prevalence of disease characteristics was not consistent among the areas, but followed several patterns. Geographic analysis showed that the frequencies of the most specific measures of disease, except for those related to coronary heart disease, were similar in all three areas. Analysis of sociocultural and illness variables, as characteristics of individuals independent of geographic area, failed to show association of any disease variable with any measure of mobility or sociocultural orientation.
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/673
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/6922015-05-11HighWireOUPamjepid:142:7
Transferrin Saturation and Risk of Cancer
Herrinton, Lisa J.
Friedman, Gary D.
Baer, David
Selby, Joseph V.
ORIGINAL CONTRIBUTIONS
The authors examined the hypothesis that relatively high levels of transferrin saturation increase the risk of cancer. They studied a cohort of prepaid health plan members whose transferrin saturation levels were measured during the period 1969–1971 and who were followed for cancer through 1990. After the exclusion of 10 percent of the subjects who received treatment for one or more of six chronic conditions or who were pregnant when the measurement was made and persons who contributed less than 5 years of follow-up, the authors were left with 38,538 persons who were followed for an average period of 17.7 years. In women, a positive association was observed between transferrin saturation and risk of stomach carcinoma (≥34.5% compared with ≤20.3%: relative risk (RR) = 3.5, 95% confidence interval (Cl) 0.98–12). In men, transferrin saturation was inversely associated with risk of colon and rectal carcinoma (≥40.7% compared with ≤26.0%: colon, RR = 0.62, 95% Cl 0.35–1.1; rectum, RR = 0.30, 95% Cl 0.08–1.1) and with non-Hodgkin's lymphoma (32.1–40.6% compared with ≤26.0%: RR = 0.31, 95% Cl 0.11–0.88; no cases observed with transferrin saturation ≥40.7%). The authors did not find evidence that the risk of epithelial cancer (all sites combined) was related to transferrin saturation level or to iron deficiency (≤5%) or overload (≥60%). <it>Arn J Epidemiol</it> 1995; 142:692–8.
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/692
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/6992015-05-11HighWireOUPamjepid:142:7
Gamma-glutamyltransferase: Determinants and Association with Mortality from Ischemic Heart Disease and All Causes
Wannamethee, Goya
Ebrahim, Shah
Gerald Shaper, A.
ORIGINAL CONTRIBUTIONS
The association of serum levels of gamma-glutamyltransferase (GGT) with cardiovascular disease risk factors, and with mortality from all causes, cardiovascular disease, and non-cardiovascular diseases, has been examined in a prospective study of 7,613 middle-aged British men followed for 11.5 years. GGT levels were strongly associated with all-cause mortality, largely due to a significant increase in deaths from ischemic heart disease and other non-cardiovascular disease causes, i.e., non-cancer deaths, in the top quintile of the GGT distribution. No association was seen with cancer mortality. However, GGT was significantly (positively) associated with alcohol intake, body mass index, smoking, preexisting ischemic heart disease, diabetes mellitus, antihypertensive medication, systolic and diastolic blood pressure, total and high density lipoprotein cholesterol, heart rate, and blood glucose, and negatively associated with physical activity and lung function (forced expiratory volume in 1 second (FEV<inf>1</inf>)). After adjustment for these personal characteristics and biologic variables, elevated GGT (highest quintile ≥24 unit/liter vs. the rest) was still associated with a significant increase in mortality from all causes (relative risk (RR) = 1.22, 95% confidence interval (Cl) 1.01–1.42; n = 818 deaths) and from ischemic heart disease (RR = 1.42, 95% Cl 1.12–1.80; <it>n</it> = 332 deaths). The increase in other non-cardiovascular disease causes was of marginal significance (RR = 1.45, 95% Cl 0.95–2.20; <it>n</it> = 127 deaths). When examined separately by the presence or absence of preexisting ischemic heart disease, the increased risk of ischemic heart disease mortality was more marked in those with evidence of ischemic heart disease at screening, particularly in those with previous myocardial infarction (RR = 1.67, 95% Cl 1.03–2.69; n = 84 deaths). The increased risk of other non-cardiovascular disease deaths was only seen in men without preexisting ischemic heart disease, largely due to an excess of hepatic cirrhosis. In summary, many factors other than alcohol intake are associated with increased levels of GGT, in particular body mass index, diabetes mellitus, and serum total cholesterol. The finding of increased risk of ischemic heart disease mortality seen in men with preexisting ischemic heart disease is related to the severity of the underlying myocardial damage. The biologic significance of raised GGT in men with preexisting ischemic heart disease merits further study. <it>Am J Epidemiol</it> 1995; 142:699–708.
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/699
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7092015-05-11HighWireOUPamjepid:142:7
A BRIEF ORIGINAL CONTRIBUTION: The AIDS Epidemic in India: A New Method for Estimating Current Human Immunodeficiency Virus (HIV) Incidence Rates
Brookmeyer, Ron
Quinn, Thomas
Shepherd, Mary
Mehendale, Sanjay
Rodrigues, Jeanette
Bollinger, Robert
ORIGINAL CONTRIBUTIONS
Human immunodeficiency virus (HIV) incidence rates in India were estimated using a new method that accounts for follow-up bias. Follow-up bias arises in epidemiologic cohort studies when the incidence rate among individuals who do and do not return for follow-up are different. The new method combines data on the prevalence of p24 antigenemia among all those initially screened together with the longitudinal follow-up data on the subset of patients who returned for follow-up. Using these methods, the current HIV incidence rate among patients attending sexually transmitted disease clinics in Pune, India, was 18.6% per year. It was found that follow-up bias can cause significant underestimation in HIV incidence rates, perhaps by as much as 60%. These incidence estimates, together with other HIV seroprevalence studies, suggest the HIV epidemic in India is growing rapidly. <it>Am J Epidemiol</it> 1995;142:709–13.
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/709
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7142015-05-11HighWireOUPamjepid:142:7
A BRIEF ORIGINAL CONTRIBUTION: Comparison of Methods of Estimating the Mother-to-Child Transmission Rate of Human Immunodeficiency Virus Type 1 (HIV-1)
Matheson, Pamela B.
Weedon, Jeremy
Cappelli, Mark
Abrams, Elaine J.
Shaffer, Nathan
Bamji, Mahrukh
Krasinski, Keith
Lambert, Genevieve
Kaul, Aditya
Grimm, Katherine
Hutson, David
Thomas, Pauline A.
The New York City Perinatal HIV Transmission Collaborative Study Group,
ORIGINAL CONTRIBUTIONS
Four methods of estimating mother-to-child transmission rates of human immunodeficiency virus type 1 (HIV-1), based on the 1992 Ghent workshop, were compared in a multicenter New York City prospective cohort study in 1986–1992. Of 833 infants born to women at risk of HIV-1 infection, 388 were born HIV-1 seropositive and 445 were HIV-1 seronegative. The four methods, the Antibody Only, Indirect, Direct, and Virologic Methods, yielded transmission rate estimates of 19–25%, classifying 59–89% of the cohort. Estimation based on persistence of HIV-1 antibody and clinical assessment yielded transmission rates similar to those methods that incorporated virologic testing. <it>Am J Epidemiol</it> 1995;142:714–18.
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/714
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7192015-05-11HighWireOUPamjepid:142:7
A BREIF ORIGINAL CONTRIBUTION: Repeat Negative Human Immunodeficiency Virus (HIV) Testing in San Francisco: Magnitude and Characteristics
McFarland, William
Fischer-Ponce, Lyn
Katz, Mitchell H.
ORIGINAL CONTRIBUTIONS
The authors assessed the characteristics of repeat human immunodeficiency virus (HIV) testers at publicly funded sites in San Francisco. During 1992–1993, 31% of all HIV tests were performed on persons testing negative for the third time or more. Persons with greater numbers of prior negative tests were less likely to test HIV-positive. Repeat negative testers were more likely than first-time negative testers to be homosexual or bisexual males, homosexual or bisexual injection drug users (IDUs), or heterosexual IDUs. Repeat testers who seroconverted were more likely to be in these same transmission categories than repeat testers who remained negative. Because of the similarities in risk profile between those most likely to retest and those most likely to seroconvert, attempts to limit repeat testing must proceed cautiously. <it>Am J Epidemiol</it> 1995;142:719–23.
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/719
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7242015-05-11HighWireOUPamjepid:142:7
A BREIF ORIGINAL CONTRIBUTION: Exploration of Simple Insulin Sensitivity Measures Derived from Frequently Sampled Intravenous Glucose Tolerance (FSIGT) Tests * The Insulin Resistance Atherosclerosis Study
Anderson, Randy L.
Hamman, Richard F.
Savage, Peter J.
Saad, Mohammad F.
Laws, Ami
Kades, Wagdy W.
Evan Sands, R.
Cefalu, William
The Insulin Resistance Atherosclerosis Study,
ORIGINAL CONTRIBUTIONS
Both abnormal insulin levels and low insulin sensitivity have been implicated as risk factors for Type II diabetes mellitus and cardiovascular disease. While insulin level is relatively simple to assess, direct measurement of insulin sensitivity is much more invasive, costly, and time-consuming. The authors considered eight previously described measures or indices of insulin sensitivity derived from the frequently sampled intravenous glucose tolerance test (FSIGT). Each one was evaluated by strength and consistency of association with insulin sensitivity computed from glucose clamp (S<inf>1(clamp)</inf>), across three glucose tolerance groups, including participants with normal glucose tolerance (<it>n</it> = 11), impaired glucose tolerance (<it>n</it> = 20), and non-<it>insulin</it>-dependent diabetes <it>mellitus</it> (<it>n</it> = 24). Minimal model analysis (MINMOD S<inf>1(22)</inf>), based on the 22-sample FSIGT, performed best based on statistical criteria of strong and consistent association with S<inf>1(clamp)</inf>. An insulin sensitivity measure similar to that of Galvin et al. (<it>Diabetic Medicine</it> 1990;9:921–8), defined as glucose disappearance (10–50 minutes) divided by insulin area under the curve above baseline from 0–50 minutes, performed best based on statistical criteria and time-savings. Galvin insulin sensitivity is simple to calculate, requires only a 50–minute FSIGT, and is significantly (p ≤ 0.001) and not inconsistently (<it>p</it> = 0.12 for inconsistent association) associated with S<inf>1(clamp)</inf> over a wide range of glucose tolerance. <it>Am J Epidemiol</it> 1995;142:724–32.
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/724
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7332015-05-11HighWireOUPamjepid:142:7
A BREIF ORIGINAL CONTRIBUTION: Nutrition, Latitude, and Multiple Sclerosis Mortality: An Ecologic Study
Luisa Esparza, M.
Sasaki, Satoshi
Kesteloot, Hugo
ORIGINAL CONTRIBUTIONS
An epidemiologic study has been performed on the relation between the mortality rates from multiple sclerosis for the period 1983–1989 obtained for 36 countries, dietary fat, and latitude. By stepwise multiple regression analysis, saturated fatty acids, animal fat, animal minus fish fat, and latitude correlated independently and positively with multiple sclerosis mortality (<it>p</it> ≤ 0.01–0.001 for fat consumption, and <it>p</it> ≤ 0.05–0.01 for latitude). The ratio of polyunsaturated fatty acids to saturated fatty acids (P/S ratio) and the ratio of unsaturated fatty acids (monounsaturated and polyunsaturated fatty acids) to saturated fatty acids (U/S ratio) correlated independently and negatively with multiple sclerosis mortality (<it>p</it> ≤ 0.05–0.001). These findings support the hypothesis linking dietary fat intake and latitude to multiple sclerosis mortality. <it>Am J Epidemiol</it> 1995:142:733–7.
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/733
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7382015-05-11HighWireOUPamjepid:142:7
Associations of {delta}-Aminolevulinic Acid Dehydratase Genotype with Plant, Exposure Duration, and Blood Lead and Zinc Protoporphyrin Levels in Korean Lead Workers
Schwartz, Brian S.
Lee, Byung-Kook
Stewart, Walter
Ahn, Kyu-Dong
Springer, Kathryn
Kelsey, Karl
ORIGINAL CONTRIBUTIONS
Previous studies have suggested that polymorphisms in δ-aminolevulinic acid dehydratase (ALAD), a heme synthetic enzyme, may be associated with differences in blood lead levels, perhaps due to differential binding of lead in erythrocytes. The authors examined associations of ALAD genotype with blood lead and zinc protoporphyrin (ZPP) levels, exposure duration, sex, and plant in 308 currently exposed lead workers in three lead storage battery manufacturing plants in the Republic of Korea in 1993. The overall prevalence of the variant allele, ALAD2, was 11%, but prevalence varied by plant (р = 0.02: 8.6% in plant A, 20% in plant B, and 22% in plant C). While ALAD2 was not associated with mean blood lead levels, the allele was associated with blood lead levels greater than or equal to 40 μg/dl (crude odds ratio (OR) = 2.6, 95% confidence interval (Cl) 1.1–6.3; adjusted OR = 2.3, 95% Cl 0.8–6.2, with adjustment for sex, plant, and exposure duration) and with exposure durations greater than 6 years (adjusted OR = 2.5, 95% Cl 1.2–5.4, with adjustment for blood lead, sex, and plant). Among workers in plant C, the highest exposure plant, ALAD2 was associated with lower ZPP levels when controlling for blood lead levels. These data suggest that lead toxicokinetics may be modified by ALAD genotype and that ALAD2 may be protective for the health effects of lead. ALAD genotype also appears to have been a selection factor for current lead exposure status in the studied workers. <it>Am J Epidemiol</it> 1995; 142:738–45.
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/738
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7462015-05-11HighWireOUPamjepid:142:7
Effect of Risk Factor Values on Lifetime Risk of and Age at First Coronary Event: The Adventist Health Study
Fraser, Gary E.
Lindsted, Kristian D.
Lawrence Beeson, W.
ORIGINAL CONTRIBUTIONS
The effect of traditional coronary heart disease risk factors on lifetime risk, age at onset, and survival free of coronary disease has not been extensively studied. The authors have used the cohort data from 27,321 California Seventh-day Adventists who had no known heart disease in 1976 to investigate these questions. Multiple decrement life tables incorporating non-parametric estimates of conditional probabilities for both coronary disease and all other competing endpoints were used to estimate these survival outcomes. Variance estimators are provided in an appendix. Persons characterized by being either past smokers, diabetic, hypertensive, physically inactive, non-vegetarian, or infrequent consumers of nuts often showed substantial differences in these survival outcomes. Statistically significant results include earlier age at onset of coronary disease at between 4 and 10 years, reduced life expectancy free of the disease between 5 and 9 years, and increased lifetime risk between 8% and 16%, when comparing groups with and without adverse values for different risk factors. The presence of adverse levels of two risk factors predicted even greater differences in these endpoints. These important effects are easily understood by the layman or non-epidemiologist professional, which is often not true of a relative risk. This should increase the effectiveness of such results when promoting behavioral change. Am J Epidemiol 1995;142:746–58.
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/746
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7592015-05-11HighWireOUPamjepid:142:7
Impaired Immune Response to Natural Infection as a Correlate of Vaccine Failure in a Field Trial of Killed Oral Cholera Vaccines
Clemens, J.
Rao, M.
Sack, D.
Ahmed, F.
Khan, M. R.
Chakraborty, J.
Kay, B.
Huda, S.
Yunus, M.
van Loon, F.
Svennerholm, A. M.
Holmgren, J.
ORIGINAL CONTRIBUTIONS
In a field trial carried out in 1985 in Matlab, Bangladesh, the authors evaluated whether subjects who developed <it>Vibrio cholerae</it> 01 infections during the first year after earlier receipt of B subunit-killed whole cell (BS-WC) or killed whole cell-only (WC) oral cholera vaccines exhibited deficient serum vibriocidal immune responses to these infections. After severe <it>V. cholerae</it> 01 infections (<it>n</it> = 70) in subjects < 5 years of age, the age group in which both vaccines were efficacious, a 6.5 geometric mean-fold rise of serum vibriocidal antibodies was observed among vaccinees, compared with an 18.6 geometric mean-fold rise in placeborecipients (<it>p</it> > 0.01). Depressions of serum vibriocidal responses among vaccinees were even more marked after asymptomatic infections (<it>n</it> = 30): a 1.1 geometric mean-fold rise in vaccinees versus a 5.9 geometric mean-fold rise in placebo-recipients (<it>p</it> < 0.01). The authors conclude that subjects who failed to be protected by BS-WC and WC, despite being in the age group for which these vaccines were protective, exhibited poor immune responses even to the vigorous stimulus of natural infection. These findings raise the possibility that immune hyporesponsiveness may limit the potential efficacy attainable by cholera vaccines in populations with endemic cholera. <it>Am J Epidemiol</it> 1995;142:759–64.
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/759
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7652015-05-11HighWireOUPamjepid:142:7
Use of Multiple Reporting Sources for Perinatal Hepatitis B Surveillance and Follow-up
Ikeda, Robin M.
Birkhead, Guthrie S.
Flynn, Michael K.
Thompson, Sharon F.
Morse, Dale L.
ORIGINAL CONTRIBUTIONS
The New York State Perinatal Hepatitis B Prevention Program was implemented in New York State (excluding New York City) as a surveillance and control program in 1988. This report describes and evaluates the program and provides data from 1991 regarding hepatitis B surface antigen (HBsAg)-positive mothers and their infants' subsequent hepatitis B vaccination. The program was created using multiple existing surveillance and data collection systems. Completeness of case-ascertainment was estimated by means of the Chandra Sekar-Deming method (<it>J Am Stat Assoc</it> 1949;44:101–15). An audit of hospital medical records and follow-up by local health departments were used to validate reporting accuracy. Of 158,273 live births in 1991, 363 (0.2%) were born to confirmed HBsAg-positive mothers. Estimated completeness of case-ascertainment was 96%. Thirty-five percent of HBsAg-positive mothers did not report risk factors for hepatitis B, confirming the need for universal testing. Of the infants, 83% received hepatitis B immune globulin and three doses of vaccine within one year of birth. By using existing data collection systems, the program was established quickly, and start-up funding and training requirements were simplified. Multiple reporting increased case-ascertainment to almost 100%. The program effectively identifies and ensures prompt vaccination of infants born to HBsAgpositive mothers. <it>Am J Epidemiol</it> 1995;142:765–70.
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/765
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7712015-05-11HighWireOUPamjepid:142:7
Contraceptive Methods and the Risk of Chlamydia trachomatis Infection in Young Women
Park, Byung Joo
Stergachis, Andy
Scholes, Delia
Heidrich, Fred E.
Holmes, King K.
Stamm, Walter E.
ORIGINAL CONTRIBUTIONS
To evaluate the relation between contraceptive methods and cervical <it>Chlamydia trachomatis</it> infection, the authors studied a population-based sample of 1,779 nonpregnant women aged 15–34 years who underwent cell culture diagnostic testing for the detection of <it>C. trachomatis</it> at a health maintenance organization. Barrier contraceptive method users were classified as those who reported using one of the following methods at time of testing: condom, diaphragm, cervical cap, spermicidal sponge, foam, or vaginal spermicidal suppositories. Barrier methods were associated with a reduction in the risk of chlamydial infection in women aged 25 years or older when compared with all other women in the same age category (adjusted prevalence odds ratio = 0.15, 95% confidence interval (Cl) 0.04–0.66). When compared with only noncontracepting women, the adjusted prevalence odds ratio was 0.34 (95% Cl 0.06–1.99). The protective effect of barrier methods was not evident in women younger than age 25 years. Oral contraceptive use was not associated with the risk of C. trachomatis infection using either referent group; the adjusted prevalence odds ratio was 0.99 (95% Cl 0.57–1.73) compared with all other women, and 0.88 (95% Cl 0.44–1.79) compared with noncontracepting women. These findings suggest that present patterns of use of barrier methods differ by age and afford only selective protection against cervical <it>C. trachomatis</it> infections. <it>Am J Epidemiol</it> 1995;142:771–8.
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/771
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7792015-05-11HighWireOUPamjepid:142:7
RE: "POINT/COUNTERPOINT: META-ANALYSIS OF OBSERVATIONAL STUDIES"
Longnecker, Matthew P.
LETTERS TO THE EDITOR
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/779
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7802015-05-11HighWireOUPamjepid:142:7
DR. SHAPIRO REPLIES
Shapiro, Samuel
LETTERS TO THE EDITOR
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/780
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7812015-05-11HighWireOUPamjepid:142:7
DR. GREENLAND REPLIES
Greenland, Sander
LETTERS TO THE EDITOR
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/781
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7822015-05-11HighWireOUPamjepid:142:7
RE: "WHEN WILL NONDIFFERENTIAL MISCLASSIFICATION OF AN EXPOSURE PRESERVE THE DIRECTION OF A TREND?'
Thomas, Duncan C.
LETTERS TO THE EDITOR
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/782
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7832015-05-11HighWireOUPamjepid:142:7
RE: "WHEN WILL NONDIFFERENTIAL MISCLASSIFICATION OF AN EXPOSURE PRESERVE THE DIRECTION OF A TREND?'
Birkett, Nicholas J.
LETTERS TO THE EDITOR
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/783
en
Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:142/7/7842015-05-11HighWireOUPamjepid:142:7
WEINBERG ET AL REPLY
Weinberg, Clarice R.
Umbach, David M.
Greenland, Sander
LETTERS TO THE EDITOR
Oxford University Press
1995-10-01 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/142/7/784
en
Copyright (C) 1995, Oxford University Press