Review of hydrologic and hydraulic studies and unsteady flow routing of the 1993 flood in the Upper Mississippi River system

"December 1997.""A division of the Illinois Department of Natural Resources.

A double ITCZ phenomenology of wind errors in the equatorial Atlantic in seasonal forecasts with ECMWF models

Modern coupled general circulation models produce systematic biases in the tropical Atlantic that hamper the reliability of long-range predictions. This study focuses on a common springtime westerly wind bias in the equatorial Atlantic in seasonal hindcasts from two coupled models – ECMWF System 4 and EC-Earth v2.3 – and in hindcasts also based on System 4, but with prescribed sea-surface temperatures. The development of the equatorial westerly bias in early April is marked by a rapid transition from a wintertime easterly, cold tongue bias to a springtime westerly bias regime that displays a marked double intertropical convergence zone (ITCZ). The transition is a seasonal feature of the model climatology (independent of initialisation date) and is associated with a seasonal increase in rainfall where a second branch of the ITCZ is produced south of the Equator. Excess off-equatorial convergence redirects the trade winds away from the Equator. Based on arguments of temporal coincidence, the results of our analysis contrast with those from previous work, and alleged causes hereto identified as the likely cause of the equatorial westerly bias in other models must be discarded. Quite in general, we find no evidence of remote influences on the development of the springtime equatorial bias in the Atlantic in the IFS-based models. Limited evidence however is presented that supports the hypothesis of an incorrect representation of the meridional equatorward flow in the marine boundary layer of the southern Atlantic as a contributing factor. Erroneous dynamical constraints on the flow upstream of the Equator may generate convergence and associated rainfall south of the Equator. This directs attention to the representation of the properties of the subtropical boundary layer as a potential source for the double ITCZ bias

Potential toxicity of Chlorpheniramine plus chloroquine for the treatment of childhood malaria

Objectives: To compare the adverse effects of two regimens of chlorpheniramine plus chloroquine (CP+CQ) in childrenwho live in a countrywhere chloroquine resistantmalaria is endemic. Methods: 99 children with acute uncomplicated malaria were randomised into two treatment groups. Group I received high dose chlorpheniramine (6mg +12mg/day for 7days in children = 5years; 8mg + 18mg/day for 7days in those >5years) plus chloroquine 10mg/kg daily for 3 days. Group II received a 50% higher dose of chlorpheniramine plus chloroquine 10mg/kg daily for 3 days. Outcome measures were vital signs, clinical response and parasite clearance on days 0-7 and day 14. Results: Parasite clearance, fever clearance and cure rate were comparable for the two groups. Drowsiness occurred in 66.7% of high dose and 86.3% of higher dose CP+CQ subjects (p = 0.05). Compared to children treated with high dose, those treated with higher dose CP+CQhad significantly lower respiratory rates on day 2 (p = 0.001), day 6 (p = 0.015), and on day 14 (p = 0.003). Conclusion: The higher rates of drowsiness and lower respiratory rates in children treated with higher dose CP+CQ calls for caution in the clinical application of the higher dose combination. The higher dose has no additional benefit andmay in fact be dangerous.Keywords: Chloroquine resistant malaria, chlorpheniramine-chloroquine, treatment, adverse effects, drowsiness, respiratory depressio

A parsimonious explanation for intersecting perinatal mortality curves: understanding the effects of race and of maternal smoking

BACKGROUND: Neonatal mortality rates among black infants are lower than neonatal mortality rates among white infants at birth weights <3000 g, whereas white infants have a survival advantage at higher birth weights. This finding is also observed when birth weight-specific neonatal mortality rates are compared between infants of smokers and non-smokers. We provide a parsimonious explanation for this paradoxical phenomenon. METHODS: We used data on births in the United States in 1997 after excluding those with a birth weight <500 g or a gestational age <22 weeks. Birth weight- and gestational age-specific perinatal mortality rates were calculated per convention (using total live births at each birth weight/gestational age as the denominator) and also using the fetuses at risk of death at each gestational age. RESULTS: Perinatal mortality rates (calculated per convention) were lower among blacks than whites at lower birth weights and at preterm gestational ages, while blacks had higher mortality rates at higher birth weights and later gestational ages. With the fetuses-at-risk approach, mortality curves did not intersect; blacks had higher mortality rates at all gestational ages. Increases in birth rates and (especially) growth-restriction rates presaged gestational age-dependent increases in perinatal mortality. Similar findings were obtained in comparisons of smokers versus nonsmokers. CONCLUSIONS: Formulating perinatal risk based on the fetuses-at-risk approach solves the intersecting perinatal mortality curves paradox; blacks have higher perinatal mortality rates than whites and smokers have higher perinatal mortality rates than nonsmokers at all gestational ages and birth weights

Antiretroviral Therapy outcomes among adolescents and youth in rural Zimbabwe

Around 2 million adolescents and 3 million youth are estimated to be living with HIV worldwide. Antiretroviral outcomes for this group appear to be worse compared to adults. We report antiretroviral therapy outcomes from a rural setting in Zimbabwe among patients aged 10-30 years who were initiated on ART between 2005 and 2008. The cohort was stratified into four age groups: 10-15 (young adolescents) 15.1-19 years (adolescents), 19.1-24 years (young adults) and 24.1-29.9 years (older adults). Survival analysis was used to estimate rates of deaths and loss to follow-up stratified by age group. Endpoints were time from ART initiation to death or loss to follow-up. Follow-up of patients on continuous therapy was censored at date of transfer, or study end (31 December 2008). Sex-adjusted Cox proportional hazards models were used to estimate hazard ratios for different age groups. 898 patients were included in the analysis; median duration on ART was 468 days. The risk of death were highest in adults compared to young adolescents (aHR 2.25, 95%CI 1.17-4.35). Young adults and adolescents had a 2-3 times higher risk of loss to follow-up compared to young adolescents. When estimating the risk of attrition combining loss to follow-up and death, young adults had the highest risk (aHR 2.70, 95%CI 1.62-4.52). This study highlights the need for adapted adherence support and service delivery models for both adolescents and young adults

A genome-wide association study for blood lipid phenotypes in the Framingham Heart Study

<p>Abstract</p> <p>Background</p> <p>Blood lipid levels including low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) are highly heritable. Genome-wide association is a promising approach to map genetic loci related to these heritable phenotypes.</p> <p>Methods</p> <p>In 1087 Framingham Heart Study Offspring cohort participants (mean age 47 years, 52% women), we conducted genome-wide analyses (Affymetrix 100K GeneChip) for fasting blood lipid traits. Total cholesterol, HDL-C, and TG were measured by standard enzymatic methods and LDL-C was calculated using the Friedewald formula. The long-term averages of up to seven measurements of LDL-C, HDL-C, and TG over a ~30 year span were the primary phenotypes. We used generalized estimating equations (GEE), family-based association tests (FBAT) and variance components linkage to investigate the relationships between SNPs (on autosomes, with minor allele frequency ≥10%, genotypic call rate ≥80%, and Hardy-Weinberg equilibrium p ≥ 0.001) and multivariable-adjusted residuals. We pursued a three-stage replication strategy of the GEE association results with 287 SNPs (P < 0.001 in Stage I) tested in Stage II (n ~1450 individuals) and 40 SNPs (P < 0.001 in joint analysis of Stages I and II) tested in Stage III (n~6650 individuals).</p> <p>Results</p> <p>Long-term averages of LDL-C, HDL-C, and TG were highly heritable (h²= 0.66, 0.69, 0.58, respectively; each P < 0.0001). Of 70,987 tests for each of the phenotypes, two SNPs had p < 10^-5in GEE results for LDL-C, four for HDL-C, and one for TG. For each multivariable-adjusted phenotype, the number of SNPs with association p < 10^-4ranged from 13 to 18 and with p < 10^-3, from 94 to 149. Some results confirmed previously reported associations with candidate genes including variation in the lipoprotein lipase gene (<it>LPL</it>) and HDL-C and TG (rs7007797; P = 0.0005 for HDL-C and 0.002 for TG). The full set of GEE, FBAT and linkage results are posted at the <b>d</b>ata<b>b</b>ase of <b>G</b>enotype <b>a</b>nd <b>P</b>henotype (dbGaP). After three stages of replication, there was no convincing statistical evidence for association (i.e., combined P < 10^-5across all three stages) between any of the tested SNPs and lipid phenotypes.</p> <p>Conclusion</p> <p>Using a 100K genome-wide scan, we have generated a set of putative associations for common sequence variants and lipid phenotypes. Validation of selected hypotheses in additional samples did not identify any new loci underlying variability in blood lipids. Lack of replication may be due to inadequate statistical power to detect modest quantitative trait locus effects (i.e., <1% of trait variance explained) or reduced genomic coverage of the 100K array. GWAS in FHS using a denser genome-wide genotyping platform and a better-powered replication strategy may identify novel loci underlying blood lipids.</p

Plasma Intercellular Adhesion Molecule-1 and von Willebrand Factor in Primary Graft Dysfunction After Lung Transplantation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75029/1/j.1600-6143.2007.01981.x.pd

Associations of Hair Dye and Relaxer Use with Breast Tumor Clinicopathologic Features: Findings from the Women’s Circle of Health Study

Background Building upon our earlier findings of significant associations between hair dye and relaxer use with increased breast cancer risk, we evaluated associations of select characteristics of use with breast tumor clinicopathology. Methods Using multivariable-adjusted models we examined the associations of interest in a case-only study of 2998 women with breast cancer, overall and stratified by race and estrogen receptor (ER) status, addressing multiple comparisons using Bonferroni correction. Results Compared to salon application of permanent hair dye, home kit and combination application (both salon and home kit application) were associated with increased odds of poorly differentiated tumors in the overall sample. This association was consistent among Black (home kit: OR 2.22, 95 % CI: 1.21–5.00; combination: OR 2.46, 95 % CI: 1.21–5.00), but not White women, and among ER+ (home kit: OR 1.47, 95 % CI: 0.82–2.63; combination: OR 2.98, 95 % CI: 1.62–5.49) but not ER-cases. Combination application of relaxers was associated with increased odds of tumors \u3e2.0 cm vs. \u3c1.0 cm (OR = 1.82, 95 % CI: 1.23–2.69). Longer duration and earlier use of relaxers and combination application of permanent hair dyes and relaxers were associated with breast tumor features including higher tumor grade and larger tumor size, which often denote more aggressive phenotypes, although the findings did not maintain significance with Bonferroni correction. Conclusions These novel data support reported associations between hair dye and relaxer use with breast cancer, showing for the first time, associations with breast tumor clinicopathologic features. Improved hair product exposure measurement is essential for fully understanding the impact of these environmental exposure with breast cancer and to guide risk reduction strategies in the future

Offspring's leukocyte telomere length, paternal age, and telomere elongation in sperm.

PublishedJournal ArticleResearch Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov'tThis is the final version of the article. Available from Public Library of Science via the DOI in this record.Leukocyte telomere length (LTL) is a complex genetic trait. It shortens with age and is associated with a host of aging-related disorders. Recent studies have observed that offspring of older fathers have longer LTLs. We explored the relation between paternal age and offspring's LTLs in 4 different cohorts. Moreover, we examined the potential cause of the paternal age on offspring's LTL by delineating telomere parameters in sperm donors. We measured LTL by Southern blots in Caucasian men and women (n=3365), aged 18-94 years, from the Offspring of the Framingham Heart Study (Framingham Offspring), the NHLBI Family Heart Study (NHLBI-Heart), the Longitudinal Study of Aging Danish Twins (Danish Twins), and the UK Adult Twin Registry (UK Twins). Using Southern blots, Q-FISH, and flow-FISH, we also measured telomere parameters in sperm from 46 young (50 years) donors. Paternal age had an independent effect, expressed by a longer LTL in males of the Framingham Offspring and Danish Twins, males and females of the NHLBI-Heart, and females of UK Twins. For every additional year of paternal age, LTL in offspring increased at a magnitude ranging from half to more than twice of the annual attrition in LTL with age. Moreover, sperm telomere length analyses were compatible with the emergence in older men of a subset of sperm with elongated telomeres. Paternal age exerts a considerable effect on the offspring's LTL, a phenomenon which might relate to telomere elongation in sperm from older men. The implications of this effect deserve detailed study.Supported by NIH grants R01-AG021593, R01-AG020132, and P01-AG0876. Support was also provided by NIH contract NOHC25195, the NHLBI cooperative agreement grants U01 HL 67893, U01 HL67894, U01 HL67895, U01 HL67896, U01 HL67897, U01 HL67898, U01 HL67899, U01 HL67900, U01 HL67901, U01 HL67902, U01 HL56563, U01 HL56564, U01 HL56565, U01 HL56566, U01 HL56567, U01 HL56568, and U01 HL56569. Also funded in part by the Wellcome Trust grant (ref 074951)