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oai:open-archive.highwire.org:amjepid:141/9/7972015-05-11HighWireOUPamjepid:141:9
Invited Commentary on "The Contribution of the Social Environment to Host Resistance: The Fourth Wade Hampton Frost Lecture"
Tyroler, Herman A.
ARTICLES
Oxford University Press
1995-05-01 00:00:00.0
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Copyright (C) 1995, Oxford University Press
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THE CONTRIBUTION OF THE SOCIAL ENVIRONMENT TO HOST RESISTANCE: THE FOURTH WADE HAMPTON FROST LECTURE
CASSEL, JOHN
HISTORICAL PAPER
Oxford University Press
1995-05-01 00:00:00.0
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http://aje.oxfordjournals.org/cgi/content/short/141/9/798
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Copyright (C) 1995, Oxford University Press
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Lipoprotein(a) Levels in the Japanese Population: Influence of Age and Sex, and Relation to Atherosclerotic Risk Factors: The Jichi Medical School Cohort Study
Nago, Naoki
Kayaba, Kazunori
Hiraoka, Jun
Matsuo, Hitoshi
Goto, Tadao
Kario, Kazuomi
Tsutsumi, Akizumi
Nakamura, Yosikazu
Igarashi, Masahiro
ORIGINAL CONTRIBUTIONS
The authors studied the distribution of lipoprotein(a)(Lp(a)) levels with stratification for age and sex, as well as the relation between Lp(a) and atherosclerotic risk factors in a large Japanese population between 1992 and 1993. The subjects were 1,235 males and 1,762 females over 30 years old. Lp(a) was measured by an enzyme-linked immunosorbent assay. Lp(a) levels were higher in females than in males. The increase in Lp(a) with age was statistically significant, and the proportion of subjects with Lp(a) levels <30 mg/dl also Increased with age. In the obese subjects (body mass index (BMI) (kg/m2) <26), Lp(a) levels were lower than in the non-obese subjects (BMI≥26)(р > 0.01 in males; р > 0.05 in females). Male alcohol drinkers had lower Lp(a) levels than nondrinkers (р > 0.05). Age, low density lipoprotein subtracting Lp(a) cholesterol [Lp(a) � 0.3], and fibrinogen level were all positively correlated with Lp(a) in both sexes. Alcohol consumption (g/day) and triglycerides were inversely correlated with Lp(a) in males, while total cholesterol subtracting Lp(a) cholesterol [Lp(a) � 0.3], high density lipoprotein, and factor VII were positively correlated in females. Multiple logistic regression analysis showed that triglycerides in males and BMI and fibrinogen in females were significant independent variables. The authors conclude that Lp(a) level is affected by various factors, such as alcohol drinking, BMI, sex, and age, and is not only correlated with lipid levels but also with hemostatic factors such as fibrinogen and factor VII. <it>Am J Epidemiol</it> 1995;141:815–21.
Oxford University Press
1995-05-01 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/141/9/815
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Copyright (C) 1995, Oxford University Press
oai:open-archive.highwire.org:amjepid:141/9/8222015-05-11HighWireOUPamjepid:141:9
Role of Smoking in the U-Shaped Relation of Cholesterol to Mortality in Men: The Framingham Study
D'Agostino, Ralph B.
Belanger, Albert J.
Kannel, William B.
Higgins, Millicent
ORIGINAL CONTRIBUTIONS
Elevated mortality has been reported at extremes of the serum total cholesterol distribution, with increased coronary mortality reported at high total cholesterol levels and increased cancer and non-cardiovascular/noncancer mortality at low total cholesterol levels. The authors used data collected on 1,959 males aged 35–69 years from the fourth Framingham Study examination to analyze the relations between total serum cholesterol levels and 409 coronary deaths, 325 cancer deaths, and 534 other deaths for a 32-year follow-up. Age- and risk factor-adjusted Cox regressions were computed. Nonlinear (U-shaped) relations were investigated with the use of quadratic regression and with dummy variables using the 160–199 mg/dl group as the comparison group. Subset analyses investigated the relation in smokers and men who drank ≤14 alcoholic drinks per week. All analyses were repeated removing those with existing cardiovascular disease and cancer and those who died during the first 5 years of follow-up. A significant U-shaped relation with all-cause mortality was noted, as were an inverse relation to cancer mortality and a monotonic increasing relation with coronary disease mortality. In subset analyses, the association of low serum cholesterol (>160 mg/dl) with cancer mortality was observed in men who smoked cigarettes. Compared with the 160–199 mg/dl group, the relative risk was 3.72 (р = 0.0001, 95% confidence interval 1.91–7.25). Studies of the relation of low total serum cholesterol levels, cigarette smoking, and cancer are needed. <it>Am J Epidemiol</it> 1995; 141:822–7.
Oxford University Press
1995-05-01 00:00:00.0
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oai:open-archive.highwire.org:amjepid:141/9/8282015-05-11HighWireOUPamjepid:141:9
Estrogen Replacement Therapy and Fatal Ovarian Cancer
Rodriguez, Carmen
Calle, Eugenia E.
Coates, Ralph J.
Miracle-McMahill, Heidi L.
Thun, Michael J.
Heath, Clark W.
ORIGINAL CONTRIBUTORS
The authors examined the relation between use of estrogen replacement therapy and ovarian cancer mortality in a large prospective mortality study of 240,073 peri- and postmenopausal women, none of whom had a prior history of cancer, hysterectomy, or ovarian surgery at enrollment in 1982. During 7 years of follow-up, 436 deaths from ovarian cancer occurred. Cox proportional hazard regression was used to adjust for other risk factors. Ever use of estrogen replacement therapy was associated with a rate ratio for fatal ovarian cancer of 1.15(95% confidence interval (Cl) 0.94–1.42). The mortality rate ratio increased with duration of use prior to entry to this study to 1.40 (95 Cl% 0.92–2.11) with 6–10 years of use and 1.71 (95% Cl 1.06–2.77) with ≤11 years of use. The increase in mortality associated with ≤6 years of use was observed in both current users (rate ratio (RR) = 1.72, 95% Cl 1.01–2.90) and former users at study entry (RR = 1.48, 95% Cl 0.99–2.22), relative to never users. Risk associated with use was not modified by any of the other risk factors. These data suggest that long-term use of estrogen replacement therapy may increase the risk of fatal ovarian cancer. <it>Am J Epidemiol</it> 1995; 141:828–35.
Oxford University Press
1995-05-01 00:00:00.0
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oai:open-archive.highwire.org:amjepid:141/9/8362015-05-11HighWireOUPamjepid:141:9
Incidence of Perforated Ulcer in Western Norway, 1935-1990: Cohart- or Period-dependent Time Trends?
Svanes, Cecilie
Terje Lie, Rolv
Kväle, Gunnar
Svanes, Knut
Sereide, Odd
ORIGINAL CONTRIBUTIONS
Previous reports have shown that peptic ulcer mortality follows birth cohorts. To the authors' knowledge, temporal variation in ulcer incidence has not been studied. Therefore, they present incidence data for a defined area of western Norway where 1,312 patients born between 1845 and 1975 were treated for ulcer perforation between 1935 and 1990. A rise and subsequent fall in incidence was observed in successive birth cohorts for both sexes, with the highest incidence observed for males bom between 1900 and 1919 and females bom between 1920 and 1929. Age-period-cohort analyses based on Poisson regression techniques were adapted to provide a statistical tool for testing specific cohort and period effects. Age-cohort models without period effects explained the variations in incidence for both sexes and all ulcer locations, suggesting cohortdependent etiology. A cohort pattern in prevalence of smoking partly explained the cohort pattern in perforation risks for both sexes. No period effects were seen that could be attributed to the increase in the sale of non-steroidal anti-inflammatory drugs, to the introduction of antibiotics around 1950, or to World War II. Susceptibility to ulcer perforation seems to follow birth cohorts, and major etiologic factors should be sought In prenatal life, in childhood, or in life-style patterns that follow birth cohorts. <it>Am J Epidemiol</it> 1995;141:836–44.
Oxford University Press
1995-05-01 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/141/9/836
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oai:open-archive.highwire.org:amjepid:141/9/8452015-05-11HighWireOUPamjepid:141:9
Adult Height and Risk of Breast Cancer among US Black Women
Palmer, Julie R.
Rosenberg, Lynn
Hartap, Susan
Strom, Brian L.
Warshauer, M. Ellen
Zauber, Ann G.
Shapiro, Samuel
ORIGINAL CONTRIBUTIONS
Adult height has been positively associated with the risk of breast cancer in a number of recent investigations. The authors assessed height in relation to breast cancer risk in a case-control study of US black women aged 25–69 years; 674 hospital patients with newly diagnosed breast cancer and 1,155 controls hospitalized for nonmalignant conditions unrelated to height were interviewed. After control for multiple confounders, the relative risk estimate for women <61 inches (<154.9 cm) tall was 0.5 (95% confidence interval (Cl) 0.3–0.7) relative to the median height of 64–65 inches (162.6–165.1 cm). Among women ≥61 inches (≥154.9 cm) tail, there was little indication of any variation in risk with increasing height. The findings suggest that short stature associated with a decreased risk of breast cancer in US black women. Am J Epidemiol 1995;141:845–9.
Oxford University Press
1995-05-01 00:00:00.0
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oai:open-archive.highwire.org:amjepid:141/9/8502015-05-11HighWireOUPamjepid:141:9
Public Drinking Water Contamination and Birth Outcomes
Bove, Frank J.
Fulcomer, Mark C.
Klotz, Judith B.
Esmart, Jorge
Dufficy, Ellen M.
Savrin, Jonathan E.
ORIGINAL CONTRIBUTIONS
The effects of public drinking water contamination on birth outcomes were evaluated in an area of northern New Jersey. After excluding plural births and chromosomal defects, 80,938 live births and 594 fetal deaths that occurred during the period 1985–1988 were studied. Information on birth outcome status and maternal risk factors was obtained from vital records and the New Jersey Birth Defects Registry. Monthly exposures during pregnancy were estimated for all births using tap water sample data. Odds ratios of ≥1.50 were found for the following: total trihalomethanes with small for gestational age, central nervous system defects, oral cleft defects, and major cardiac defects; carbon tetrachloride with term low birth weight, small for gestational age, very low birth weight, total surveillance birth defects, central nervous system defects, neural tube defects, and oral cleft defects; trichloroethylene with central nervous system defects, neural tube defects, and oral cleft defects; tetrachloroethylene with oral cleft defects; total dichloroethylenes with central nervous system defects and oral cleft defects; benzene with neural tube defects and major cardiac defects; and 1,2-dichloroethane with major cardiac defects. Total trihalomethane levels >100 ppb reduced birth weight among term births by 70.4 g. By itself, this study cannot resolve whether the drinking water contaminants caused the adverse birth outcomes; therefore, these findings should be followed up utilizing available drinking water contamination databases. <it>Am J Epidemiol</it> 1995;141:850–62.
Oxford University Press
1995-05-01 00:00:00.0
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oai:open-archive.highwire.org:amjepid:141/9/8632015-05-11HighWireOUPamjepid:141:9
How Accurate is Self-Reported Family History of Colorectal Cancer?
Aitken, Joanne
Bain, Christopher
Ward, Michael
Siskind, Victor
MacLennan, Robert
ORIGINAL CONTRIBUTIONS
Much of the evidence that supports a relation between a positive family history of and increased risk for colorectal cancer is based on information obtained exclusively from patients. There have been few assessments of the accuracy of such data. The validity of self-reported family history of colorectal cancer was assessed in the course of a case-control study of colorectal adenomas conducted among patients aged 20–75 years who underwent colonoscopy in Brisbane, Australia between 1980 and 1985. Family histories reported by a subsample of 237 colonoscopy patients (74 cases and 163 controls) were compared with relatives' medical records and death certificates. Patients' reports of colorectal cancer in 90 relatives were confirmed for 70 (77.8%; 95% confidence interval (Cl) 67.8–85.9). Among 124 reports by patients of relatives who had other abdominal cancer or bowel conditions, 114 (91.9%; 95% Cl 85.7–96.1) were confirmed to be correct, while 10 (8.1%) were found to be colorectal cancer. Finally, 105 (99.1%; 95% Cl 94.9–100.0) of a random sample of 106 completely negative reports by patients were confirmed to be correct. Overall, 77% of positive family histories (any positive relatives) were confirmed, and it was estimated that 98% of negative family histories (no positive relatives) were correct. Cases were slightly more accurate than controls in reporting both positive and negative histories among their relatives. By extrapolation of these results to the total sample of 1,244 patients in the larger case-control study, sensitivity of self-reported positive family history was estimated to be 0.87 among cases and 0.82 among controls, and specificity was estimated to be 0.97 in both groups. <it>Am J Epidemiol</it> 1995:141:863–71.
Oxford University Press
1995-05-01 00:00:00.0
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oai:open-archive.highwire.org:amjepid:141/9/8722015-05-11HighWireOUPamjepid:141:9
Validity of Mother's Report of Father's Occupation in a Study of Paternal Occupation and Congenital Malformations
Schnitzer, Patricia G.
Olshan, Andrew F.
Savitz, David A.
Erickson, J. David
ORIGINAL CONTRIBUTIONS
Agreement between the mother's and father's report of the father's occupation was assessed in a case-control study of paternal occupation and birth defects. Cases were identified from births registered with the Metropolitan Atlanta Congenital Defects Program between 1968 and 1980; controls were selected from livebom infants without defects. Both parents were sought for interview, and each parent was asked about the father's job history for 2 years prior to the infant's birth. This concordance analysis is based on 3,739 case infants and 2,279 control infants for whom both parents were interviewed. The authors considered the father's report of his occupation as correct, and they assessed the ability of the mother to report the same occupation(s) during a 7-month period around conception. The exact agreement between mother's and father's report of the father's occupation was 59%. Agreement improved slightly with increasing family income and when fathers were college graduates. Female partners were not accurate proxy respondents in this study of paternal occupation and birth defects, which suggests that investigators should interview both parents in studies of paternal exposures and reproductive outcomes, i.e., mothers for pregnancy history and maternal confounders and fathers for occupational history and paternal confounders. <it>Am J Epidemiol</it> 1995; 141:872–7.
Oxford University Press
1995-05-01 00:00:00.0
TEXT
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oai:open-archive.highwire.org:amjepid:141/9/8782015-05-11HighWireOUPamjepid:141:9
Injury Mortality among Iowa Farmers, 1980-1988: Comparison of PMR and SMR Approaches
Zwerling, Craig
Burmeister, Leon F.
Jensen, Christine M.
ORIGINAL CONTRIBUTIONS
State and provincial proportional mortality studies in the United States and Canada have found increased ratios of overall injury mortality among farmers, including occupational injuries and other unintentional injuries, such as those from motor vehicle crashes and fires, as well as suicides. In contrast, Scandinavian standardized mortality (morbidity) studies have found no increase in the injury fatality or morbidity ratios of farmers in comparison with the rest of the population. This study reviews the injury mortality of Iowa farmers for the years 1980–1988. Among white male farmers, we found an increased proportional mortality ratio for all injuries of 1.26 (95% confidence interval (Cl) 1.21–1.31). In part, this was a result of the increased proportional mortality ratio for at-work injuries of 3.77 (95% Cl 3.35–4.24), but there were also elevated proportional mortality ratios for such nonoccupational injuries as suicides, 1.20 (95% Cl 1.09–1.32), motor vehicle crashes, 1.23 (95% Cl 1.12–1.34), and electrocutions, 1.78 (95% Cl 1.08–2.95). For younger farmers aged 20–64 years, we calculated standardized mortality ratios as well. The standardized mortality ratios were generally within 10% of the proportional mortality ratios, which suggests that the differences between North America and Scandinavia are not the result of methodological differences, but are more likely related to differences in environmental exposures and safety practices. <it>Am J Epidemiol</it> 1995; 141:878–82.
Oxford University Press
1995-05-01 00:00:00.0
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THE AUTHORS REPLY
Wingren, Gun
Axelson, Olav
Hatschek, Thomas
LETTERS TO THE EDITOR
Oxford University Press
1995-05-01 00:00:00.0
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http://aje.oxfordjournals.org/cgi/content/short/141/9/883-a
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Copyright (C) 1995, Oxford University Press
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RE: "DETERMINANTS OF PAPILLARY CANCER OF THE THYROID"
Stenström, Birgitta
Holm, Lars-Erik
LETTERS TO THE EDITOR
Oxford University Press
1995-05-01 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/141/9/883
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DR. PRESTON-MARTIN COMMENTS
Preston-Martin, Susan
LETTERS TO THE EDITOR
Oxford University Press
1995-05-01 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/141/9/884
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RE: "SUICIDAL BEHAVIORS IN YOUNG ADOLESCENTS" AND "MAJOR DEPRESSIVE DISORDER AND DYSTHYMIA IN YOUNG ADOLESCENTS"
Garrison, Carol Z.
Jackson, Kirby L.
Addy, Cheryl L.
McKeown, Robert E.
Waller, Jennifer L.
LETTERS TO THE EDITOR
Oxford University Press
1995-05-01 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/141/9/885
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oai:open-archive.highwire.org:amjepid:141/9/8862015-05-11HighWireOUPamjepid:141:9
ERRATUM
ERRATUM
Dr. S. D. Walter has informed the <it>Journal</it> that Prof. Knut Laake of the University of Oxford has brought to his attention two typographic errors that appeared in Dr. Walter's article, “Calendar Effects in the Analysis of Seasonal Data” (<it>Am J Epidemiol</it> 1994;140:649–57). Dr. Walter explains that on p. 656, in the Appendix, the third displayed equation should read <fd>$$T=8N({S}^{2}+{C}^{2})/{W}^{2},$$</fd> and that, also on p. 656, in the text immediately following the equation, the sentence that begins “Alternatively” should read: “Alternatively, <it>T</it> = 8<it>Nd</it>2, where <it>d</it> is the distance of <it>C</it> from <it>O</it>.” Dr. Walter notes that equivalent forms of these basic equations are stated correctly in the text of his article as equation 1 at the bottom of p. 650 and in the second line of text on p. 651. He says that the correct equations were used to calculate the numerical results of the paper, which are thus unaffected by the above corrections.
Oxford University Press
1995-05-01 00:00:00.0
TEXT
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http://aje.oxfordjournals.org/cgi/content/short/141/9/886
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Copyright (C) 1995, Oxford University Press