2024-03-28T22:49:33Zhttp://open-archive.highwire.org/handler
oai:open-archive.highwire.org:amjepid:146/2/1052015-05-11HighWireOUPamjepid:146:2
Insomnia in Young Men and Subsequent Depression: The Johns Hopkins Precursors Study
Chang, Patricia P.
Ford, Daniel E.
Mead, Lucy A.
Cooper-Patrick, Lisa
Klag, Michael J.
ORIGINAL CONTRIBUTIONS
The Johns Hopkins Precursors Study, a long-term prospective study, was used to study the relation between self-reported sleep disturbances and subsequent clinical depression and psychiatric distress. A total of 1,053 men provided information on sleep habits during medical school at The Johns Hopkins University (classes of 1948–1964) and have been followed since graduation. During a median follow-up period of 34 years (range 1–45), 101 men developed clinical depression (cumulative incidence at 40 years, 12.2%), including 13 suicides. In Cox proportional hazards analysis adjusted for age at graduation, class year, parental history of clinical depression, coffee drinking, and measures of temperament, the relative risk of clinical depression was greater in those who reported insomnia in medical school (relative risk (RR) 2.0, 95% confidence interval (Cl) 1.2–3.3) compared with those who did not and greater in those with difficulty sleeping under stress in medical school (RR 1.8, 95% Cl 1.2–2.7) compared with those who did not report difficulty. There were weaker associations for those who reported poor quality of sleep (RR 1.6, 95% Cl 0.9–2.9) and sleep duration of 7 hours or less (RR 1.5, 95% Cl 0.9–2.3) with development of clinical depression. Similar associations were observed between reports of sleep disturbances in medical school and psychiatric distress assessed in 1988 by the General Health Questionnaire. These findings suggest that insomnia in young men is indicative of a greater risk for subsequent clinical depression and psychiatric distress that persists for at least 30 years. <it>Am J Epidemiol</it> 1997;146:105–14.
Oxford University Press
1997-07-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/146/2/105
http://dx.doi.org/10.1093/oxfordjournals.aje.a009241
en
Copyright (C) 1997, Oxford University Press
oai:open-archive.highwire.org:amjepid:146/2/1152015-05-11HighWireOUPamjepid:146:2
Temporal Trends and Factors Associated with Survival after Pneumocystis carinii Pneumonia in California, 1983-1992
Colford, John M.
Segal, Mark
Tabnak, Farzaneh
Chen, Mi
Sun, Richard
Tager, Ira
ORIGINAL CONTRIBUTIONS
The authors investigated quarterly trends in survival after the diagnosis of <it>Pneumocystis carinii</it> pneumonia for 19,607 patients in California in the decade from January 1, 1983, through December 31, 1992. Subjects included all cases for whom <it>P. carinii</it> pneumonia was the initial (and only) acquired immunodeficiency syndrome (AIDS)-defining diagnosis as reported to the California human immunodeficiency virus/AIDS surveillance registry. There was a period of rapidly improving survival from approximately June 1986 until April 1988, coincident with the widespread Introduction of antiretroviral therapy (zidovudine) and the Institution of <it>P. carinii</it> pneumonia prophylaxis (with cotrimoxazole and pentamidine). There was no evidence, however, of meaningful improvements in survival for these patients after that period. The association of several covariates (risk transmission group, gender, race/ethnicity, certainty of <it>P. carinii</it> pneumonia diagnosis, age, region of residence, availability of CD4 count, and level of CD4 count) were also studied both by proportional hazards regression and by recursive partitioning (i.e., tree-based) survival analysis. The availability of a CD4 count (regardless of its level) was the single factor most strongly associated with survival (median survival 36 months among those with and 14 months among those without reported CD4 counts, <it>p</it> <0.05). Data from this large, population-based surveillance registry of AIDS in California suggest that, despite earlier improvements in survival after the diagnosis of <it>P. carinii</it> pneumonia, the long-term survival of these patients remains poor (39% alive 2 years after diagnosis) and that no improvement in survival has occurred since 1988. <it>Am J Epidemiol</it> 1997;146:115–27.
Oxford University Press
1997-07-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/146/2/115
http://dx.doi.org/10.1093/oxfordjournals.aje.a009242
en
Copyright (C) 1997, Oxford University Press
oai:open-archive.highwire.org:amjepid:146/2/1282015-05-11HighWireOUPamjepid:146:2
Environmental Tobacco Smoke and Breastfeeding Duration
Horta, Bemardo Lessa
Victora, Cesar Gomes
Menezes, Ana Maria
Barros, Fernando C.
ORIGINAL CONTRIBUTIONS
The effect of smoking on breastfeeding duration was investigated in a population-based birth cohort study of 1,098 Brazilian infants. There were few losses to follow-up (3.2%) in the first 6 months. Maternal smoking was strongly associated with breastfeeding duration, even after adjustment for confounding. Compared with nonsmokers, mothers smoking 20 or more cigarettes daily presented an odds ratio of 1.94 for breastfeeding for less than 6 months. Environmental tobacco smoke was also an independent risk factor. After adjustment for maternal smoking and other confounders, households where more than 10 cigarettes were smoked daily by persons other than the mother presented an odds ratio of 1.48 compared with those without smokers. These results remained unchanged after stratification for maternal smoking. This is the first report of a possible effect of environmental tobacco smoke on breastfeeding duration. <it>Am J Epidemiol</it> 1997;146:128-33.
Oxford University Press
1997-07-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/146/2/128
http://dx.doi.org/10.1093/oxfordjournals.aje.a009243
en
Copyright (C) 1997, Oxford University Press
oai:open-archive.highwire.org:amjepid:146/2/1342015-05-11HighWireOUPamjepid:146:2
Use of Multivitamin/Mineral Prenatal Supplements: Influence on the Outcome of Pregnancy
Scholl, Theresa O.
Hediger, Mary L.
Bendich, Adrianne
Schall, Joan I.
Smith, Woollcott K.
Krueger, Paul M.
ORIGINAL CONTRIBUTIONS
The objective of this study was to examine the association of prenatal multivitamin/mineral supplement use during the first and second trimesters of pregnancy by low income, urban women in the Camden Study (1985/1995, <it>n</it> = 1,430) and preterm delivery (<37 completed weeks) and infant low birth weight (<2,500 g). Prenatal supplement use was corroborated by assay of circulating micronutrients at entry to care (no differences) and week 28 gestation (increased concentrations of folate and ferritin for supplement users). Compared with women who entered care during the first or second trimester but did not use prenatal supplements, supplement use starting in the first or second trimester was associated with approximately a twofold reduction in risk of preterrn delivery. After controlling for potential confounding variables, risk of very preterm delivery (<33 weeks' gestation) was reduced more than fourfold for first trimester users and approximately twofold when use dated from the second trimester. Infant low birth weight and very low birth weight (<1,500 g) risks were also reduced. Risk of low birth weight was reduced approximately twofold with supplement use during the first and second trimester. Diminution in risk was greater for very low birth weight infants, amounting to a sevenfold reduction in risk of very low birth weight with first trimester supplementation and a greater than sixfold reduction when supplement use started in the second trimester. Thus, in low income, urban women, use of prenatal multivitamin/mineral supplements may have the potential to diminish infant morbidity and mortality. <it>Am J Epidemiol</it> 1997;146:134-41.
Oxford University Press
1997-07-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/146/2/134
http://dx.doi.org/10.1093/oxfordjournals.aje.a009244
en
Copyright (C) 1997, Oxford University Press
oai:open-archive.highwire.org:amjepid:146/2/1422015-05-11HighWireOUPamjepid:146:2
Hostility and Increased Risk of Mortality and Acute Myocardial Infarction: The Mediating Role of Behavioral Risk Factors
Everson, Susan A.
Kauhanen, Jussi
Kaplan, George A.
Goldberg, Debbie E.
Julkunen, Juhani
Tuomilehto, Jaakko
Salonen, Jukka T.
ORIGINAL CONTRIBUTIONS
Cynical hostility has been associated with increased cardiovascular morbidity and mortality; yet few studies have investigated this relation in population-based samples, and little is known about underlying mechanisms. This study examined the association between hostility, measured by the eight-item Cynical Distrust Scale, and risk for all-cause and cardiovascular mortality and incident myocardial infarction. Subjects were 2,125 men, ages 42–60 years, from the Kuopio lschemic Heart Disease Risk Factor Study, a longitudinal study of unestablished and traditional risk factors for ischemic heart disease, mortality, and other outcomes. There were 177 deaths (73 cardiovascular) in 9 years of follow-up. Men with hostility scores in the top quartile were at more than twice the risk of all-cause mortality (relative hazards (RH) 2.30, 95% confidence interval (Cl) 1.47–3.59) and cardiovascular mortality (RH 2.70, 95% Cl 1.27–5.76), relative to men with scores in the lowest quartile. Among 1,599 men without previous myocardial infarction or angina, high scorers also had an increased risk of myocardial infarction (RH 2.18, 95% CI 1.01–4.70). Biologic and socioeconomic risk factors, social support, and prevalent diseases had minimal impact on these associations, whereas adjustments for the behavioral risk factors of smoking, alcohol consumption, physical activity, and body mass index substantially weakened the relations. Simultaneous risk factor adjustment eliminated the observed associations. Results show that high levels of hostility are associated with increased risk of all-cause and cause-specific mortality and incident myocardial infarction and that these effects are mediated primarily through behavioral risk factors. <it>Am J Epidemiol</it> 1997;146:142-52.
Oxford University Press
1997-07-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/146/2/142
http://dx.doi.org/10.1093/oxfordjournals.aje.a009245
en
Copyright (C) 1997, Oxford University Press
oai:open-archive.highwire.org:amjepid:146/2/1532015-05-11HighWireOUPamjepid:146:2
Long-term Prognosis of Women after Myocardial Infarction
Benderly, Michal
Behar, Solomon
Reicher-Reiss, Henrietta
Boyko, Valentina
Uri Goldbourt for the SPRINT Study Group,
ORIGINAL CONTRIBUTIONS
Women sustaining myocardial infarction fare worse than men during hospitalization. Reports on long-term survival in women surviving art acute myocardial infarction are controversial. The Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) registry includes 5,839 consecutive myocardial infarction patients who were hospitalized in 13 coronary care units in Israel between 1981 and 1983. The authors examined sex differences in the long-term survival of 4,808 hospital survivors (1,120 women and 3,688 men). Women exhibited a significantly poorer long-term survival than men. After age adjustment, differences between men and women decreased, leaving a survival probability difference of 11% at the end of 12 years of follow-up. In a subgroup analysis, women exhibited poorer survival than men in a comparison of patients with and without periinfarction congestive heart failure or a history of myocardial infarction preceding the index infarction. The multivariate adjusted hazard ratios associated with female sex in diabetic and nondiabetic patients were 1.46 and 1.13, respectively. In conclusion, a cumulative survival disadvantage for women in comparison with men is still evident after 12 years of follow-up. The mortality difference is diminished but not erased after age adjustment or multivariate adjustment for confounders. The authors' results are compatible with a hypothesis that the main factor underlying the increased long-term mortality in women after myocardial infarction, besides older age, is diabetes mellitus. <it>Am J Epidemiol</it> 1997;146:153-60.
Oxford University Press
1997-07-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/146/2/153
http://dx.doi.org/10.1093/oxfordjournals.aje.a009246
en
Copyright (C) 1997, Oxford University Press
oai:open-archive.highwire.org:amjepid:146/2/1612015-05-11HighWireOUPamjepid:146:2
Breast Cancer Clusters in the Northeast United States: A Geographic Analysis
Kulldorff, Martin
Feuer, Eric J.
Miller, Barry A.
Freedma, Laurence S.
ORIGINAL CONTRIBUTIONS
High breast cancer mortality rates have been reported in the northeastern part of the United States, with recent attention focused on Long Island, New York. In this study, the authors investigate whether the high breast cancer mortality is evenly spread over the Northeast, in the sense that any observed clusters of deaths can be explained by chance alone, or whether there are clusters of statistical significance. Demographic data and age-specific breast cancer mortality rates for women were obtained for all 244 counties in 11 northeastern states and for the District of Columbia for 1988–1992. A recently developed spatial scan statistic is used, which searches for clusters of cases without specifying their size or location ahead of time, and which tests for their statistical significance while adjusting for the multiple testing inherent in such a procedure. The basic analysis is adjusted for age, with further analyses examining how the results are affected by incorporating race, urbanicity, and parity as confounding variables. There is a statistically significant and geographically broad cluster of breast cancer deaths in the New York City-Philadelphia, Pennsylvania, metropolitan area (<it>p</it> = 0.0001), which has a 7.4% higher mortality rate than the rest of the Northeast. The cluster remains significant when race, urbanicity, and/or parity are included as confounding variables. Four smaller subclusters within this area are also significant on their own strength: Philadelphia with suburbs (<it>p</it> = 0.0001), Long Island (<it>p</it> = 0.0001), central New Jersey (<it>p</it> = 0.0001), and northeastern New Jersey (<it>p</it> = 0.0001). The elevated breast cancer mortality on Long Island might be viewed less as a unique local phenomenon and more as part of a more general situation involving large parts of the New York City-Philadelphia metropolitan area. The several known and hypothesized risk factors for which we could not adjust and that may explain the detected cluster are most notably age at first birth, age at menarche, age at menopause, breastfeeding, genetic mutations, and environmental factors. <it>Am J Epidemiol</it> 1997;146:161-70.
Oxford University Press
1997-07-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/146/2/161
http://dx.doi.org/10.1093/oxfordjournals.aje.a009247
en
Copyright (C) 1997, Oxford University Press
oai:open-archive.highwire.org:amjepid:146/2/1712015-05-11HighWireOUPamjepid:146:2
Diet and the Risk of Salivary Gland Cancer
Hom-Ross, Pamela L.
Morrow, Merrilee
Ljung, Britt-Marie
ORIGINAL CONTRIBUTIONS
Cancer of the major salivary glands is relatively rare, and little is known about its etiology. The only established risk factors are radiation exposure and a prior cancer. The role of diet in the development of salivary gland tumors has not been addressed previously. The results from a population-based case-control study conducted in the greater San Francisco-Monterey Bay area examining the association between dietary intake and salivary gland cancer risk are presented. Of 199 cases diagnosed with salivary gland tumors between 1989 and 1993, 150 (75%) were interviewed. Nine cases were subsequently excluded based on review of pathology specimens. Of 271 controls identified through random-digit dialing and the Health Care Finance Administration files, 191 (70%) were interviewed. Eight cases and seven controls who over- or underreported dietary intake were excluded from analysis. Vitamin C intake of >200 mg/day compared with ≤ 100 mg/day was associated with a 60% decrease in salivary gland cancer risk (odds ratio (OR) = 0.40, 95% confidence interval (Cl) 0.22–0.70). Inverse associations observed for carotene, vitamin E, and fiber from fruits and vegetables were diminished when adjusted for vitamin C intake. Fiber from bean sources was associated with a 51% decrease in risk after adjusting for vitamin C intake (OR = 0.49, 95% Cl 0.26–0.92 for >1.4 g/day compared with ≤0.4 g/day). Cholesterol intake was associated with elevated risk (OR = 1.67, 95% Cl 1.2–2.4 for a 10% increase in calories from cholesterol). These findings suggest that preventive strategies developed for common chronic diseases, such as increased consumption of fruits and vegetables and limiting foods high in cholesterol, also may be effective in preventing these rare tumors. <it>Am J Epidemiol</it> 1997;146:171-6.
Oxford University Press
1997-07-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/146/2/171
http://dx.doi.org/10.1093/oxfordjournals.aje.a009248
en
Copyright (C) 1997, Oxford University Press
oai:open-archive.highwire.org:amjepid:146/2/1772015-05-11HighWireOUPamjepid:146:2
Short-term Effects of Ambient Oxidant Exposure on Mortality: A Combined Analysis within the APHEA Project
Touloumi, G.
Katsouyanni, K.
Zmirou, D.
Schwartz, J.
Spix, C.
Ponce de Leon, A.
Tobias, A.
Quennel, P.
Rabczenko, D.
Bacharova, L.
Bisanti, L.
Vonk, J. M.
Ponka, A.
ORIGINAL CONTRIBUTIONS
The Air Pollution and Health: a European Approach (APHEA) project is a coordinated study of the short-term effects of air pollution on mortality and hospital admissions using data from 15 European cities, with a wide range of geographic, sociodemographic, climatic, and air quality patterns. The objective of this paper is to summarize the results of the short-term effects of ambient oxidants on daily deaths from all causes (excluding accidents). Within the APHEA project, six cities spanning Central and Western Europe provided data on daily deaths and NO<inf>2</inf> and/or O<inf>3</inf> levels. The data were analyzed by each center separately following a standardized methodology to ensure comparability of results. Poisson autoregressive models allowing for overdispersion were fitted. Fixed effects models were used to pool the individual regression coefficients when there was no evidence of heterogeneity among the cities and random effects models otherwise. Factors possibly correlated with heterogeneity were also investigated. Significant positive associations were found between daily deaths and both NO<inf>2</inf> and O<inf>3</inf>. Increases of 50 μg/m3 in NO<inf>2</inf> (1-hour maximum) or O<inf>3</inf> (1-hour maximum) were associated with a 1.3% (95% confidence interval 0.9–1.8) and 2.9% (95% confidence interval 1.0–4.9) increase in the daily number of deaths, respectively. Stratified analysis of NO<inf>2</inf> effects by low and high levels of black smoke or O<inf>3</inf> showed no significant evidence for an interaction within each city. However, there was a tendency for larger effects of NO<inf>2</inf> in cities with higher levels of black smoke. The pooled estimate for the O<inf>3</inf> effect was only slightly reduced, whereas the one for NO<inf>2</inf> was almost halved (although it remained significant) when two pollutant models including black smoke were applied. The internal validity (consistency across cities) as well as the external validity (similarities with other published studies) of our results on the O<inf>3</inf> effect support the hypothesis of a causal relation between O<inf>3</inf> and all cause daily mortality. However, the short-term effects of NO<inf>2</inf> on mortality may be confounded by other vehicle-derived pollutants. Thus, the issue of independent NO<inf>2</inf> effects requires additional investigation. <it>Am J Epidemiol</it> 1997;146:177-85.
Oxford University Press
1997-07-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/146/2/177
http://dx.doi.org/10.1093/oxfordjournals.aje.a009249
en
Copyright (C) 1997, Oxford University Press
oai:open-archive.highwire.org:amjepid:146/2/1862015-05-11HighWireOUPamjepid:146:2
Cohort Mortality Study of Pulp and Paper Mill Workers in British Columbia, Canada
Band, Pierre R.
Le, Nhu D.
Fang, Raymond
Threlfall, William J.
Astrakianakis, George
Anderson, Judith T. L.
Keefe, Anya
Krewski, Daniel
ORIGINAL CONTRIBUTIONS
The authors studied a cohort of 30,157 male pulp and paper workers in British Columbia, Canada. Of these, 20,373 worked in kraft mills only, 5,249 in sulfite mills only, and 4,535 in both kraft and sulfite mills. All workers with at least 1 year of employment on January 1, 1950, or thereafter until December 31, 1992, were studied. Standardized mortality ratios (SMRs) were used to compare the mortality rates of the cohort with those of the Canadian male population. Ninety percent confidence intervals (Cls) for the SMRs were obtained. Cancer risks significantly associated with work duration and time from first employment of 15 years or more were observed: 1) total cohort: pleura (SMR = 3.61, 90% Cl 1.42–7.58); kidney (SMR = 1.69, 90% Cl 1.13–2.43); brain (SMR = 1.51, 90% Cl 1.03–2.16); 2) workers in kraft mills only: kidney(SMR = 1.92, 90% Cl 1.04–3.26); 3) workers in sulfite mills only: Hodgkin's disease (SMR = 4.79, 90% Cl 1.29–12.37); 4) workers ever employed in both kraft and sulfite mills: esophagus (SMR = 1.91, 90% Cl 1.00–3.33). These malignancies have been associated with the following known or suspected carcinogens to which pulp and paper workers may have been exposed: asbestos (pleura), biocides (kidney), formaldehyde (kidney, brain, Hodgkin's disease), hypochlorite (esophagus). A nested case-control study with detailed exposure assessment is under way to help determine whether excess risks for specific cancers reflect exposure among subsets of workers. <it>Am J Epidemiol</it> 1997;146:186–94.
Oxford University Press
1997-07-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/146/2/186
http://dx.doi.org/10.1093/oxfordjournals.aje.a009250
en
Copyright (C) 1997, Oxford University Press
oai:open-archive.highwire.org:amjepid:146/2/1952015-05-11HighWireOUPamjepid:146:2
Logistic Regression When the Outcome Is Measured with Uncertainty
Magder, Laurence S.
Hughes, James P.
ORIGINAL CONTRIBUTIONS
In epidemiologic research, logistic regression is often used to estimate the odds of some outcome of interest as a function of predictors. However, in some datasets, the outcome of interest is measured with imperfect sensitivity and specificity. It is well known that the misclassification induced by such an imperfect diagnostic test will lead to biased estimates of the odds ratios and their variances. In this paper, the authors show that when the sensitivity and specificity of a diagnostic test are known, it is straightforward to incorporate this information into the fitting of logistic regression models. An EM algorithm that produces unbiased estimates of the odds ratios and their variances is described. The resulting odds ratio estimates tend to be farther from the null but have greater variance than estimates found by ignoring the imperfections of the test. The method can be extended to the situation where the sensitivity and specificity differ for different study subjects, i.e., nondifferential misclassification. The method is useful even when the sensitivity and specificity are not known, as a way to see the degree to which various assumptions about sensitivity and specificity affect one's estimates. The method can also be used to estimate sensitivity and specificity under certain assump tions or when a validation subsample is available. Several examples are provided to compare the results of this method with those obtained by standard logistic regression. A SAS macro that implements the method is available on the World Wide Web at <inter-ref locator="http://som1.ab.umd.edu/Epidemiology/software" locator-type="url">http://som1.ab.umd.edu/Epidemiology/software.</inter-ref>html <it>Am J Epidemiol</it> 1997;146:195–203.
Oxford University Press
1997-07-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/146/2/195
http://dx.doi.org/10.1093/oxfordjournals.aje.a009251
en
Copyright (C) 1997, Oxford University Press
oai:open-archive.highwire.org:amjepid:146/2/2042015-05-11HighWireOUPamjepid:146:2
BOOK REVIEWS
Trichopoulos, Dimitrios
BOOK REVIEWS
Oxford University Press
1997-07-15 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/146/2/204
http://dx.doi.org/10.1093/oxfordjournals.aje.a009252
en
Copyright (C) 1997, Oxford University Press
oai:open-archive.highwire.org:amjepid:146/2/2052015-05-11HighWireOUPamjepid:146:2
BOOK REVIEWS
Armenian, Haroutune K.
BOOK REVIEWS
Oxford University Press
1997-07-15 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/146/2/205
http://dx.doi.org/10.1093/oxfordjournals.aje.a009253
en
Copyright (C) 1997, Oxford University Press
oai:open-archive.highwire.org:amjepid:146/2/2062015-05-11HighWireOUPamjepid:146:2
BOOK REVIEWS
Prentice, Ross L.
BOOK REVIEWS
Oxford University Press
1997-07-15 00:00:00.0
TEXT
text/html
http://aje.oxfordjournals.org/cgi/content/short/146/2/206
http://dx.doi.org/10.1093/oxfordjournals.aje.a009254
en
Copyright (C) 1997, Oxford University Press