Neurotoxicity of inhaled manganese: a reanalysis of human exposure arising from showering.
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Baths↗
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Premorbid polysomnographic signs in depressed adolescents: a reanalysis of EEG sleep after longitudinal follow-up in adulthood.
BACKGROUND: This is a report of a clinical follow-up study (10-15 years later as young adults) of adolescent major depressives and normal control subjects. Polysomnographic data were obtained during the original study period when the subjects were adolescent (time 1). With clinical follow-up (time 2) assessments in hand, our objective was to ascertain whether there were any premorbid polysomnographic signs associated with depression during adolescence. METHODS: Based upon initial (during adolescence) and follow-up clinical assessments (as adults), new subject groupings were generated: depression-free normal subjects and original normal subjects who experienced a depressive episode during the follow-up period (latent depressives). Suicidality and recurrence of depression were also examined. Multivariate analysis of covariance was used to analyze group differences in sleep measures and logistic regression for predicting three outcomes: lifetime depression, lifetime suicidality, and recurrence. RESULTS: Comparison of the depression-free normal subjects, the latent depressives, and the original major depressives revealed significant differences for sleep latency and sleep period time. Comparing all lifetime depressives (original major depressives and the latent depressives) to depression-free normal subjects revealed significantly more stages 3 and 4 combined (ST34) sleep and greater sleep period times among the depressives. An analysis involving the presence or absence of suicidality revealed no overall significant differences between the groups. Comparison of the lifetime depressives grouped by nonrecurrent and recurrent depressive course to the depression-free normal subjects revealed significant difference for sleep period time. Using logistic regression, we found that a longer sleep latency and sleep period time significantly predicted lifetime depression. Gender, ST34 sleep, and an interaction term for ST34 sleep and REM latency significantly predicted lifetime suicidality. CONCLUSIONS: There was evidence of premorbid sleep abnormalities during adolescence. A general pattern of sleep disruption around sleep onset and during the first 100 min of the sleep period and overall sleep was evident among the major and lifetime depressives, involving sleep latency (initial insomnia), sleep period time (hypersomnia), REM latency, and slow-wave sleep. This adds to the body of literature that highlights the importance of the first 100 min of the sleep period in depression.
Adolescent↗
A reanalysis of the Stanton et al. pleural sarcoma data.
An analysis of the Stanton et al. (1981, J. Natl. Cancer Inst. 67, 965-975) data reconfirms number of index particles as the primary dimensional predictor of tumor incidence. Fitting separate intercepts and/or slopes to each mineral type results in substantial significant improvement in fit, indicating the importance of mineral type. This contrasts with the "Stanton hypothesis," which states that dimensional properties alone determine carcinogenesis. Log mean aspect ratio is not as good a predictor of tumor incidence as the number of index particles; among those samples that did not have index particles, log mean aspect ratio is not a significant predictor of tumor incidence.
Air Pollutants, Occupational↗
Reanalysis of the involvement of gamma-glutamyl transpeptidase in the cell activation process.
The inhibitor of gamma-glutamyl transpeptidase (gamma-GT) acivicin modulates cellular responses including growth, myeloid maturation and apoptosis. Whether these effects result from the inhibition of gamma-GT enzyme activity remains unclear. We compared the cellular effects of acivicin against a more potent and specific inhibitor of gamma-GT (L-2-amino-4-boronobutanoic acid (L-ABBA)) in gamma-GT-negative (B lymphoblastoid Ramos) and gamma-GT-positive (myelomonocytic HL-60, gamma-GT-transfected Ramos) cell lines. Under non-oxidative stress conditions, acivicin-induced cell growth arrest, apoptosis and macrophage maturation occurred independent of gamma-GT while L-ABBA did not influence any of these processes. Acivicin triggered tyrosine phosphorylation and increased nuclear factor kappaB activity. Further insight into the role of gamma-GT in cellular processes is needed.
Apoptosis↗
Risk of leukemia in children treated with human growth hormone: review and reanalysis.
BACKGROUND: Data have suggested that any increased incidence of leukemia in growth-hormone (GH)-treated patients was limited to those with known risk factors for leukemia. However, previous studies may have overestimated the numbers of patient-years of risk by not excluding data from "positive-risk-factor" patients. This risk was reanalyzed by using data on children in the National Cooperative Growth Study (NCGS), with correction for this possible confounding factor. METHODS: The risk of leukemia in GH-treated patients without known risk factors was determined by using patient-years of GH therapy and patient-years since first exposure to GH therapy and the values obtained were compared with values from the Surveillance, Epidemiology, and End Results program of the National Cancer Institute. RESULTS: Three cases of leukemia in patients without known risk factors were found in the NCGS database; 3.42 cases would be expected in the 119,846 patient-years in the analysis using time since GH exposure. Two of these cases of leukemia occurred during GH therapy (67,773 patient-years); 2.13 cases would be expected. CONCLUSION: Excluding data on patients with known risk factors for leukemia provides a more accurate estimate of the risks in GH-treated patients. The incidence of leukemia in these patients is comparable to that in the general population of age-matched children.
Adolescent↗
An attempt at measuring the impact of sanitation and economics on health: a reanalysis of the Colombian National Health Survey.
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Colombia↗
L and M cone input into spectral sensitivity functions: a reanalysis.
In order to better understand the nature of long-wavelength (L) and middle-wavelength (M) cone input into spectral sensitivity functions and determine the reliability with which it is possible to predict L:M cone inputs, we developed analytical methods to determine confidence intervals for L:M cone input for spectral sensitivity functions or data transformed to cone-contrast space. Spectral sensitivity functions measured by direct heterochromatic brightness matches are dominated by the L/M opponent channel over most of the spectral range. For detection of large/ long test stimuli, spectral sensitivity functions show a characteristic "notch" at the adapting wavelength, with the L/M opponent channel dominating most of the spectral range. Flicker increment threshold (FIT) spectral sensitivity functions display many of the characteristics of the luminance flicker mechanism described by Stromeyer et al. (1987). [Vision Research, 27, 1113-1137]. Previous modelling of FIT spectral sensitivity functions proposed a 2:1 L:M cone input for most of testing conditions. We show that FIT spectral sensitivity functions are dominated by L cones but show L cone suppression under bright red adapting fields. For the fitted spectral sensitivity functions or simulated data sets, we found small confidence intervals for L:M cone input into the L/M opponent channel and conclude that it is possible to reliably predict L:M cone input ratios. However, for similar data sets of additive spectral sensitivity functions, we found large confidence intervals for L:M cone input ratios and conclude that it is not possible reliably predict L:M cone input into the L/M non-opponent channel using available spectral sensitivity functions.
Adaptation, Ocular↗
Familial breast cancer: collaborative reanalysis of individual data from 52 epidemiological studies including 58,209 women with breast cancer and 101,986 women without the disease.
BACKGROUND: Women with a family history of breast cancer are at increased risk of the disease, but no study has been large enough to characterise reliably how, over women's lives, this risk is influenced by particular familial patterns of breast cancer. This report, on the relevance of breast cancer in first-degree relatives, is based on combined data from 52 epidemiological studies. METHODS: Individual data on breast cancer in first-degree relatives (mothers, sisters, and daughters) of 58209 women with breast cancer and of 101986 controls were collected, checked, and analysed centrally. Risk ratios for breast cancer were calculated by conditional logistic regression, stratified by study, age, menopausal status, number of sisters, parity, and age when the first child was born. Breast-cancer incidence and mortality rates for particular family histories were calculated by applying age-specific risk ratios to breast-cancer rates typical for more-developed countries. FINDINGS: Altogether 7496 (12.9%) women with breast cancer and 7438 (7.3%) controls reported that one or more first-degree relatives had a history of breast cancer: 12% of women with breast cancer had one affected relative and 1% had two or more. Risk ratios for breast cancer increased with increasing numbers of affected first-degree relatives: compared with women who had no affected relative, the ratios were 1.80 (99% CI 1.69-1.91), 2.93 (2.36-3.64), and 3.90 (2.03-7.49), respectively, for one, two, and three or more affected first-degree relatives (p<0.0001 each). The risk ratios were greatest at young ages, and for women of a given age, were greater the younger the relative was when diagnosed. The results did not differ substantially between women reporting an affected mother (9104) or sister (6386). Other factors, such as childbearing history, did not significantly alter the risk ratios associated with a family history of breast cancer. For women in more-developed countries with zero, one, or two affected first-degree relatives, the estimated cumulative incidence of breast cancer up to age 50 was 1.7%, 3.7%, and 8.0%, respectively; corresponding estimates for incidence up to age 80 were 7.8%, 13.3%, and 21.1%. Corresponding estimates for death from breast cancer up to age 80 were 2.3%, 4.2%, and 7.6%. The age when the relative was diagnosed had only a moderate effect on these estimates. INTERPRETATION: Eight out of nine women who develop breast cancer do not have an affected mother, sister, or daughter. Although women who have first-degree relatives with a history of breast cancer are at increased risk of the disease, most will never develop breast cancer, and most who do will be aged over 50 when their cancer is diagnosed. In countries where breast cancer is common, the lifetime excess incidence of breast cancer is 5.5% for women with one affected first-degree relative and 13.3% for women with two.
Adult↗
Breast cancer and breastfeeding: collaborative reanalysis of individual data from 47 epidemiological studies in 30 countries, including 50302 women with breast cancer and 96973 women without the disease.
BACKGROUND: Although childbearing is known to protect against breast cancer, whether or not breastfeeding contributes to this protective effect is unclear. METHODS: Individual data from 47 epidemiological studies in 30 countries that included information on breastfeeding patterns and other aspects of childbearing were collected, checked, and analysed centrally, for 50302 women with invasive breast cancer and 96973 controls. Estimates of the relative risk for breast cancer associated with breastfeeding in parous women were obtained after stratification by fine divisions of age, parity, and women's ages when their first child was born, as well as by study and menopausal status. FINDINGS: Women with breast cancer had, on average, fewer births than did controls (2.2 vs 2.6). Furthermore, fewer parous women with cancer than parous controls had ever breastfed (71% vs 79%), and their average lifetime duration of breastfeeding was shorter (9.8 vs 15.6 months). The relative risk of breast cancer decreased by 4.3% (95% CI 2.9-5.8; p<0.0001) for every 12 months of breastfeeding in addition to a decrease of 7.0% (5.0-9.0; p<0.0001) for each birth. The size of the decline in the relative risk of breast cancer associated with breastfeeding did not differ significantly for women in developed and developing countries, and did not vary significantly by age, menopausal status, ethnic origin, the number of births a woman had, her age when her first child was born, or any of nine other personal characteristics examined. It is estimated that the cumulative incidence of breast cancer in developed countries would be reduced by more than half, from 6.3 to 2.7 per 100 women by age 70, if women had the average number of births and lifetime duration of breastfeeding that had been prevalent in developing countries until recently. Breastfeeding could account for almost two-thirds of this estimated reduction in breast cancer incidence. INTERPRETATION: The longer women breast feed the more they are protected against breast cancer. The lack of or short lifetime duration of breastfeeding typical of women in developed countries makes a major contribution to the high incidence of breast cancer in these countries.
Adult↗
Differences in female-male mortality after high-titre measles vaccine and association with subsequent vaccination with diphtheria-tetanus-pertussis and inactivated poliovirus: reanalysis of West African studies.
BACKGROUND: Females given high-titre measles vaccine (HTMV) have high mortality; diphtheria-tetanus-pertussis (DTP) vaccination might be associated with increased female mortality. We aimed to assess whether DTP or inactivated poliovirus (IPV) administered after HTMV was associated with increased female-male mortality ratio. METHODS: In three trials from West Africa, 2000 children were randomised to HTMV or control vaccine at 4-5 months of age; a second vaccination was given at age 9-10 months (standard measles vaccine). Children in high-titre groups were given IPV or DTP-IPV. Another 944 children received HTMV as routine vaccination in Senegal. FINDINGS: When we compared high-titre and control groups, no difference in mortality between the first and the second vaccination was noted. After the second vaccination, the female-male mortality ratio was 1.84 (95% CI 1.19-2.84) in children in the high-titre groups who received DTP-IPV or IPV, and 0.59 (0.34-1.04) in controls who received standard measles vaccine (p=0.007). Children who received HTMV but no additional DTP-IPV or IPV had a female-male mortality ratio of 0.83 (0.41-1.67). This ratio was 2.22 (1.04-4.71) for children who received DTP-IPV after routine HTMV and 1.00 (0.68-1.47) for those who did not. When we combined the results from all trials, the female-male mortality ratio was 1.93 (1.33-2.81) for those who received DTP or IPV after HTMV, and 0.96 (0.69-1.34) for those who did not (p=0.006). INTERPRETATION: A change in sequence of vaccinations, rather than HTMV itself, may have been the cause of increased female mortality in these trials.
Cause of Death↗
Breast cancer and abortion: collaborative reanalysis of data from 53 epidemiological studies, including 83?000 women with breast cancer from 16 countries.
BACKGROUND: The Collaborative Group on Hormonal Factors in Breast Cancer has brought together the worldwide epidemiological evidence on the possible relation between breast cancer and previous spontaneous and induced abortions. METHODS: Data on individual women from 53 studies undertaken in 16 countries with liberal abortion laws were checked and analysed centrally. Relative risks of breast cancer--comparing the effects of having had a pregnancy that ended as an abortion with those of never having had that pregnancy--were calculated, stratified by study, age at diagnosis, parity, and age at first birth. Because the extent of under-reporting of past induced abortions might be influenced by whether or not women had been diagnosed with breast cancer, results of the studies--including a total of 44000 women with breast cancer--that used prospective information on abortion (ie, information that had been recorded before the diagnosis of breast cancer) were considered separately from results of the studies--including 39000 women with the disease--that used retrospective information (recorded after the diagnosis of breast cancer). FINDINGS: The overall relative risk of breast cancer, comparing women with a prospective record of having had one or more pregnancies that ended as a spontaneous abortion versus women with no such record, was 0.98 (95% CI 0.92-1.04, p=0.5). The corresponding relative risk for induced abortion was 0.93 (0.89-0.96, p=0.0002). Among women with a prospective record of having had a spontaneous or an induced abortion, the risk of breast cancer did not differ significantly according to the number or timing of either type of abortion. Published results on induced abortion from the few studies with prospectively recorded information that were not available for inclusion here are consistent with these findings. Overall results for induced abortion differed substantially between studies with prospective and those with retrospective information on abortion (test for heterogeneity between relative risks: chi2(1) =33.1, p<0.0001). INTERPRETATION: Pregnancies that end as a spontaneous or induced abortion do not increase a woman's risk of developing breast cancer. Collectively, the studies of breast cancer with retrospective recording of induced abortion yielded misleading results, possibly because women who had developed breast cancer were, on average, more likely than other women to disclose previous induced abortions.
Abortion, Induced↗
Herd immunity conferred by killed oral cholera vaccines in Bangladesh: a reanalysis.
BACKGROUND: Decisions about the use of killed oral cholera vaccines, which confer moderate levels of direct protection to vaccinees, can depend on whether the vaccines also provide indirect (herd) protection when high levels of vaccine coverage are attained. We reanalysed data from a field trial in Bangladesh to ascertain whether there is evidence of indirect protection from killed oral cholera vaccines. METHODS: We analysed the first year of surveillance data from a placebo-controlled trial of B subunit-killed whole-cell and killed whole-cell-only oral cholera vaccines in children and adult women in Bangladesh. We calculated whether there was an inverse, monotonic trend for the relation between the level of vaccine coverage in a residential cluster and the incidence of cholera in individual vaccine recipients or placebo recipients residing in the cluster after controlling for potential confounding variables. FINDINGS: Vaccine coverage of the targeted population ranged from 4% to 65%. Incidence rates of cholera among placebo recipients were inversely related to levels of vaccine coverage (7.01 cases per 1000 in the lowest quintile of coverage vs 1.47 cases per 1000 in the highest quintile; p<0.0001 for trend). Receipt of vaccine by an individual and the level of vaccine coverage of the individual's cluster were independently related to a reduced risk of cholera. Moreover, after adjustment for the level of vaccine coverage of the cluster, vaccine protective efficacy remained significant (55% [95% CI 41-66], p<0.0001). INTERPRETATION: In addition to providing direct protection to vaccine recipients, killed oral cholera vaccines confer significant herd protection to neighbouring non-vaccinated individuals. Use of these vaccines could have a major effect on the burden of cholera in endemic settings.
Administration, Oral↗
Clioquinol and S.M.O.N.: Reanalysis of original data.
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Clioquinol↗
Breast cancer and hormonal contraceptives: collaborative reanalysis of individual data on 53 297 women with breast cancer and 100 239 women without breast cancer from 54 epidemiological studies.
BACKGROUND The Collaborative Group on Hormonal Factors in Breast Cancer has brought together and reanalysed the worldwide epidemiological evidence on the relation between breast cancer risk and use of hormonal contraceptives. METHODS Individual data on 53 297 women with breast cancer and 100 239 women without breast cancer from 54 studies conducted in 25 countries were collected, checked, and analysed centrally. Estimates of the relative risk for breast cancer were obtained by a modification of the Mantel-Haenszel method. All analyses were stratified by study, age at diagnosis, parity, and, where appropriate, the age a woman was when her first child was born, and the age she was when her risk of conception ceased. FINDINGS The results provide strong evidence for two main conclusions. First, while women are taking combined oral contraceptives and in the 10 years after stopping there is a small increase in the relative risk of having breast cancer diagnosed (relative risk [95 percent CI] in current users 1.24 [1.15-1.33], 2p<0.00001; 1-4 years after stopping 1.16 [1.08-1.23], 2p=0.00001; 5-9 years after stopping 1.07 [1.02-1.13], 2p=0.009). Second, there is no significant excess risk of having breast cancer diagnosed 10 or more years after stopping use (relative risk 1.01 [0.96-1.05], NS). The cancers diagnosed in women who had used combined oral contraceptives were less advanced clinically than those diagnosed in women who had never used these contraceptives for ever-users compared with never-users, the relative risk for tumours that had spread beyond the breast compared with localised tumours was 0.88 (0.81-0.95; 2p=0.002). There was no pronounced variation in the results for recency of use between women with different background risks of breast cancer, including women from different countries and ethnic groups, women with different reproductive histories, and those with or without a family history of breast cancer. The studies included in this collaboration represent about 90 percent of the epidemiological information on the topic, and what is known about the other studies suggests that their omission has not materially affected the main conclusions. Other features of hormonal contraceptive use such as duration of use, age at first use, and the dose and type of hormone within the contraceptives had little additional effect on breast cancer risk, once recency of use had been taken into account. Women who began use before age 20 had higher relative risks of having breast cancer diagnosed while they were using combined oral contraceptives and in the 5 years after stopping than women who began use at older ages, but the higher relative risks apply at ages when breast cancer is rare and, for a given duration of use, earlier use does not result in more cancers being diagnosed than use beginning at older ages. Because breast cancer incidence rises steeply with age, the estimated excess number of cancers diagnosed in the period between starting use and 10 years after stopping increases with age at last use: for example, among 10 000 women from Europe or North America who used oral contraceptives from age 16 to 19, from age 20 to 24, and from age 25 to 29, respectively, the estimated excess number of cancers diagnosed up to 10 years after stopping use is 0.5 (95 percent CI 0.3-0.7), 1.5 (0.7-2.3), and 4.7 (2.7-6.7). Up to 20 years after cessation of use the difference between ever-users and never-users is not so much in the total number of cancers diagnosed, but in their clinical presentation, with the breast cancers diagnosed in ever-users being less advanced clinically than those diagnosed in never-users. The relation observed between breast cancer risk and hormone exposure is unusual, and it is not possible to infer from these data whether it is due to an earlier diagnosis of breast cancer in ever-users, the biological effects of hormonal contraceptives, or a combination of reasons...
Adolescent↗
The efficacy of imipramine and psychotherapy in early-onset chronic depression: a reanalysis of the National Institute of Mental health Treatment of Depression Collaborative Research Program.
The authors compared the effectiveness of Cognitive Behavioral Therapy (CBT), Interpersonal Psychotherapy (IPT), Imipramine Clinical Management (ICM) to Placebo Clinical Management (PCM) for outpatients with early-onset chronic depression (N = 65) in the National Institute of Mental Health (NIMH) Treatment of Depression Collaborative Research Program (TDRP). The post-treatment depression scores of the CBT. IPT, and ICM groups were not significantly different from the PCM group. We did not find a relationship between the duration of Major Depression and response to a specific treatment. Studies are needed to determine if combining psychotherapy with medication improves social functioning and enhances the quality of life for patients with chronic depression.
Adult↗
Reanalysis of surveillance data regarding health care worker risk of nosocomial acquisition of HIV.
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Acquired Immunodeficiency Syndrome↗
A quality-adjusted reanalysis of a Phase III trial comparing once-daily thoracic radiation vs. twice-daily thoracic radiation in patients with limited-stage small-cell lung cancer(1).
PURPOSE: We undertook an analysis of quality-adjusted survival using the Q-TWiST (Quality Time Without Symptoms or Toxicity) methodology and developed a new graphic representation called a quality-adjusted life-years plot, which presents a complete and concise Q-TWiST analysis on a single plot. METHODS AND MATERIALS: The Q-TWiST plot incorporates the time without symptoms or toxicity and several combinations of utility coefficients for toxicity and relapse days into the same plot. In addition, the plot includes threshold lines, to judge whether a particular combination of utility coefficients reaches a significance level. RESULTS: The differential in toxicity incidence and severity between the two thoracic radiation treatment arms was inconsequential. Sensitivity analyses were run using Q-TWiST plots. For all combinations of the various toxicity definitions and utility coefficients, the median Q-TWiST was greater for the once-daily thoracic radiation treatment arm than for the twice-daily treatment arm, without achieved significance. CONCLUSION: This work refines the results previously reported for this Phase III clinical trial in patients with limited-stage small-cell cancer, and there was no significant difference in survival after adjusting for toxicity and progression. Furthermore, the new methods developed for this trial allow for a more detailed and parsimonious presentation of survival and toxicity data for all oncology clinical trials.
Algorithms↗
A reanalysis of the Collaborative Ocular Melanoma Study Medium Tumor Trial eye plaque dosimetry.
PURPOSE: To recalculate the radiation doses delivered to structures of interest within the eye, i.e., the lens, tumor apex, 5-mm point, optic disk, and macula for patients treated with eye plaque radiotherapy on the Collaborative Ocular Melanoma Study (COMS) Medium Tumor Trial, using updated dosimetric data. METHODS AND MATERIALS: Using the Plaque Simulator planning system, doses were recalculated for a sampling of COMS patients for each plaque size. Dosimetry parameters incorporated into the recalculation were line source approximation, a 90% Silastic transmission factor, and a 0% gold transmission factor. Generic solutions were generated from the dose recalculations for each plaque size and structures of interest combination. Doses for the remainder of the patient population were recalculated using the generic solutions and compared with the originally reported COMS doses. RESULTS: Doses to all structures of interest were reduced 7%-21%, depending on the plaque size and structure combination. The reduction in dose for the macula, optic disc, lens, tumor apex, and 5-mm point was on average 10%, 18%, 8%, 11%, and 12%, respectively. The closer the macula and optic disk were to the plaque rim, the greater the dose reduction. Incorporation of the Silastic transmission factor accounted for a large part of the dose reduction. CONCLUSIONS: Incorporating anisotropy, line source approximation, and Silastic and gold shield attenuation into dose recalculations resulted in a significant and consistent reduction of doses to structures of interest within the eyes.
Algorithms↗