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Differential Risk (differential + risk)
Selected AbstractsDifferential risks to males and females for congenital malformations among 2.5 million California births, 1989,1997BIRTH DEFECTS RESEARCH, Issue 12 2003Gary M. Shaw Abstract BACKGROUND Although many studies have observed variations in the prevalence of specific malformations by sex, there is a lack of population-based data on potential malformation prevalence differences by sex at birth. METHODS Our objective was to explore differences in the prevalence of structural congenital malformation phenotypes between sexes in a California population of 2.5 million live- and stillbirths, using data from a population-based active surveillance system. Ascertainment was performed among offspring of California women who delivered in nonmilitary hospitals during the period of 1989,1997. Malformations were grouped according to the four-digit malformation codes of the British Pediatric Association. RESULTS Overall, 32,619 males and 21,835 females were considered to have structural congenital malformations, with prevalences of 2.52% and 1.76%, respectively. Thus, males demonstrated a malformation prevalence that was 22% higher than that in females. Using a criterion of a 40% increase or decrease in the relative risk for males, increased risks for 15 and decreased risks for 17 specific malformation categories were observed. Increased risks were associated with most organ systems, with the notable exception of the nervous system (increased risks for nervous system malformations were observed among female births). Risks were not substantially influenced by adjusting for maternal age, race/ethnicity, parity, or education. CONCLUSIONS Our observations extend the relatively few studies that have investigated differential prevalences of a large number of specific structural malformations between male and female births. Birth Defects Research (Part A) 67:000,000, 2003. © 2003 Wiley-Liss, Inc. [source] The impact of developmental speech and language impairments on the acquisition of literacy skillsDEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 3 2004C. Melanie Schuele Abstract Children with developmental speech/language impairments are at higher risk for reading disability than typical peers with no history of speech/language impairment. This article reviews the literacy outcomes of children with speech/language impairments, clarifying the differential risk for three groups of children: speech production impairments alone, oral language impairments alone, and speech production and oral language impairments. Children at greatest risk for reading and writing disabilities are children with language impairments alone and children with comorbid speech impairments and language impairments. For children with speech impairments alone, there is limited risk for literacy difficulties. However, even when reading skills are within the average range, children with speech impairments may have difficulties in spelling. Children with language impairments are likely to display reading deficits in word decoding and reading comprehension. It is not clear what role early literacy interventions play in the amelioration of reading difficulties in these populations. © 2004 Wiley-Liss, Inc. MRDD Research Reviews 2004;10:176,183. [source] Relevance of the genes for bone mass variation to susceptibility to osteoporotic fractures and its implications to gene search for complex human diseasesGENETIC EPIDEMIOLOGY, Issue 1 2002Hong-Wen Deng Abstract We investigate the relevance of the genetic determination of bone mineral density (BMD) variation to that of differential risk to osteoporotic fractures (OF). The high heritability (h2) of BMD and the significant phenotypic correlations between high BMD and low risk to OF are well known. Little is reported on h2 for OF. Extensive molecular genetic studies aimed at uncovering genes for differential risks to OF have focussed on BMD as a surrogate phenotype. However, the relevance of the genetic determination of BMD to that of OF is unknown. This relevance can be characterized by genetic correlation between BMD and OF. For 50 Caucasian pedigrees, we estimated that h2 at the hip is 0.65 (P < 0.0001) for BMD and 0.53 (P < 0.05) for OF; however, the genetic correlation between BMD and OF is nonsignificant (P > 0.45) and less than 1% of additive genetic variance is shared between them. Hence, most genes found important for BMD may not be relevant to OF at the hip. The phenotypic correlation between high BMD and low risk to OF at the hip (approximately ,0.30) is largely due to an environmental correlation (,E = ,0.73, P < 0.0001). The search for genes for OF should start with a significant h2 for OF and should include risk factors (besides BMD) that are genetically correlated with OF. All genes found important for various risk factors must be tested for their relevance to OF. Ideally, employing OF per se as a direct phenotype for gene hunting and testing can ensure the importance and direct relevance of the genes found for the risk of OF. This study may have significant implications for the common practice of gene search for complex diseases through underlying risk factors (usually quantitative traits). Genet. Epidemiol. 22:12,25, 2002. © 2002 Wiley-Liss, Inc. [source] Heterogeneous Regional Endocardial Repolarization is Associated with Increased Risk for Ischemia-Dependent Ventricular Fibrillation after Myocardial InfarctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2003Michael H. Swann M.SC. Introduction: The aim of this study was to investigate whether the characteristics of endocardial ventricular repolarization are associated with differential risk for sudden death. Prolonged surface QT interval is associated with increased arrhythmic risk after myocardial infarction (MI), but the underlying mechanism of QT prolongation and its relation to lethal arrhythmias are unclear. Methods and Results: Ventricular fibrillation (VF) risk was assessed in 12 dogs 1 month after anterior MI during an exercise test coupled with brief circumflex coronary occlusion. Susceptible dogs (n = 5) developed VF during the brief ischemic episode, whereas resistant dogs did not (n = 7). Surface QT interval was measured at rest. Endocardial electroanatomic catheter maps of left ventricular repolarization were obtained in four unique regions identified by echocardiography and compared between groups. Compared to resistant dogs, susceptible dogs were characterized by prolonged surface QT intervals (240 ± 10 msec vs 222 ± 7 msec, P = 0.04). In addition, they had lower baroreflex sensitivity (9.7 ± 1.5 msec/mmHg vs 28 ± 9.8 msec/mmHg, P < 0.01) and a tachycardic response to acute ischemia suggesting higher propensity for stronger sympathetic reflexes. Surface QT interval prolongation in susceptible dogs was due to a marked heterogeneity of endocardial left ventricular repolarization (239 ± 42 msec, basal anterior wall vs 197 ± 35, lateral wall; P < 0.001). Resistant animals had no regional differences in endocardial repolarization. Conclusion: Sympathetic activation following MI not only produces adverse structural remodeling but also contributes to adverse electrophysiologic remodeling resulting in heterogeneous ventricular repolarization and in a myocardial substrate conducive to lethal reentrant arrhythmias. (J Cardiovasc Electrophysiol, Vol. 14, pp. 873-879, August 2003) [source] Aminoglycoside dosing in diabetesJOURNAL OF CLINICAL PHARMACY & THERAPEUTICS, Issue 2 2000Axworthy Studies have evaluated the comparative efficacy, toxicity and costs associated with extended-interval vs. standard multiple daily dosing of aminoglycosides. In this case, an elderly man with diabetes and good renal function at baseline was switched from standard to extended-interval dosing. During the course of therapy there was evidence of decreased renal function. Pertinent literature was searched for, uncovered and critically evaluated to determine if and what evidence supports using extended dosing of aminoglycosides in this population. No data were found specifically evaluating the different dosing strategies in diabetic patients. However, there were many trials and several meta-analysis located that compared the two dosing strategies, most suggesting at least a cost advantage and possibly less toxicity with extended-interval dosing. Further information is needed to determine whether there is a differential risk for toxicity between these dosing regimens in patient with diabetes. [source] Association of CASP8 D302H polymorphism with reduced risk of aggressive prostate carcinomaTHE PROSTATE, Issue 6 2010Jessica Lubahn Abstract BACKGROUND Because of the dramatically different clinical course of aggressive and indolent prostate carcinoma (PCa), markers that distinguish between these phenotypes are of critical importance. Apoptosis is an important protective mechanism for unrestrained cellular growth and metastasis. Therefore, dysfunction in this pathway is a key step in cancer progression. As such, genetic variants in apoptosis genes are potential markers of aggressive PCa. Recent work in breast carcinoma has implicated the histidine variant of CASP8 D302H (rs1045485) as a protective risk allele. METHODS We tested the hypothesis that the H variant was protective for aggressive PCa in a pooled analysis of 796 aggressive cases and 2,060 controls. RESULTS The H allele was associated with a reduced risk of aggressive PCa (ORper allele,= 0.67, 95% CI: 0.54,0.83, Ptrend,=,0.0003). The results were similar for European-Americans (ORper allele,=,0.68; 95% CI: 0.54,0.86) and African-Americans (ORper allele,=,0.61; 95% CI: 0.34,1.10). We further determined from the full series of 1,160 cases and 1,166 controls in the Prostate, Lung, Colorectal, Ovarian (PLCO) population that the protective effect of the H allele tended to be limited to high-grade and advanced PCa (all cases ORper allele,=,0.94; 95% CI: 0.79,1.11; localized, low-grade disease ORper allele,=,0.98; 95% CI: 0.79,1.23; and aggressive disease ORper allele,=,0.73; 95% CI: 0.50,1.07). CONCLUSION These results suggest that histidine variant of CASP8 D302H is a protective allele for aggressive PCa with potential utility for identification of patients at differential risk for this clinically significant phenotype. Prostate 70: 646,653, 2010. © 2009 Wiley-Liss, Inc. [source] Relevance of the genes for bone mass variation to susceptibility to osteoporotic fractures and its implications to gene search for complex human diseasesGENETIC EPIDEMIOLOGY, Issue 1 2002Hong-Wen Deng Abstract We investigate the relevance of the genetic determination of bone mineral density (BMD) variation to that of differential risk to osteoporotic fractures (OF). The high heritability (h2) of BMD and the significant phenotypic correlations between high BMD and low risk to OF are well known. Little is reported on h2 for OF. Extensive molecular genetic studies aimed at uncovering genes for differential risks to OF have focussed on BMD as a surrogate phenotype. However, the relevance of the genetic determination of BMD to that of OF is unknown. This relevance can be characterized by genetic correlation between BMD and OF. For 50 Caucasian pedigrees, we estimated that h2 at the hip is 0.65 (P < 0.0001) for BMD and 0.53 (P < 0.05) for OF; however, the genetic correlation between BMD and OF is nonsignificant (P > 0.45) and less than 1% of additive genetic variance is shared between them. Hence, most genes found important for BMD may not be relevant to OF at the hip. The phenotypic correlation between high BMD and low risk to OF at the hip (approximately ,0.30) is largely due to an environmental correlation (,E = ,0.73, P < 0.0001). The search for genes for OF should start with a significant h2 for OF and should include risk factors (besides BMD) that are genetically correlated with OF. All genes found important for various risk factors must be tested for their relevance to OF. Ideally, employing OF per se as a direct phenotype for gene hunting and testing can ensure the importance and direct relevance of the genes found for the risk of OF. This study may have significant implications for the common practice of gene search for complex diseases through underlying risk factors (usually quantitative traits). Genet. Epidemiol. 22:12,25, 2002. © 2002 Wiley-Liss, Inc. [source] | |||||||||||||