Elizabeth A Streeten

University of Maryland, Baltimore, Baltimore, Maryland, United States

Are you Elizabeth A Streeten?

Claim your profile

Publications (55)508.84 Total impact

  • Elizabeth A. Streeten · Sarada Jaimungal
    [Show abstract] [Hide abstract]
    ABSTRACT: Hypercalcemia is a common problem encountered in the outpatient clinic and in hospitalized patients. Although the differential diagnosis is broad, making a correct diagnosis is generally straightforward. Identifying the mediator of hypercalcemia narrows the possible diagnoses and facilitates a diagnosis. Outpatients with asymptomatic hypercalcemia detected on routine testing are most likely to have primary hyperparathyroidism. Most patients hospitalized for symptomatic hypercalcemia have an underlying malignancy. For asymptomatic outpatients with hypercalcemia, evaluating in a stepwise manner, starting with PTH, is reasonable, only testing for other mediators when PTH is suppressed. The other mediators, PTHrP, 25(OH)D, 1,25(OH)2D, serum and urine protein immunoelectrophoresis, should be done when PTH is suppressed in outpatients and on admission in patients hospitalized for symptomatic hypercalcemia. Since PTH controls 1,25(OH)2D production, when PTH is suppressed and 1,25(OH)2D is "inappropriately normal," 1,25(OH)2D is the mediator of the hypercalcemia. The most recently discovered cause of hypercalcemia, loss-of-function mutations in CYP24A1, should be considered when 25(OH)D and/or 1,25(OH)2D are elevated in a patient with no evidence of malignancy or granulomatous disease. With a pathophysiological approach to diagnosis, the cause of hypercalcemia can be easily identified in most patients. © 2015 John P. Bilezikian, Robert Marcus, and Michael A. Levine Published by Elsevier Inc. All rights reserved..
    No preview · Chapter · Dec 2015
  • [Show abstract] [Hide abstract]
    ABSTRACT: More than 100 loci have been identified for age at menarche by genome-wide association studies; however, collectively these explain only ∼3% of the trait variance. Here we test two overlooked sources of variation in 192,974 European ancestry women: low-frequency protein-coding variants and X-chromosome variants. Five missense/nonsense variants (in ALMS1/LAMB2/TNRC6A/TACR3/PRKAG1) are associated with age at menarche (minor allele frequencies 0.08-4.6%; effect sizes 0.08-1.25 years per allele; P<5 × 10(-8)). In addition, we identify common X-chromosome loci at IGSF1 (rs762080, P=9.4 × 10(-13)) and FAAH2 (rs5914101, P=4.9 × 10(-10)). Highlighted genes implicate cellular energy homeostasis, post-transcriptional gene silencing and fatty-acid amide signalling. A frequently reported mutation in TACR3 for idiopathic hypogonatrophic hypogonadism (p.W275X) is associated with 1.25-year-later menarche (P=2.8 × 10(-11)), illustrating the utility of population studies to estimate the penetrance of reportedly pathogenic mutations. Collectively, these novel variants explain ∼0.5% variance, indicating that these overlooked sources of variation do not substantially explain the 'missing heritability' of this complex trait.
    No preview · Article · Aug 2015 · Nature Communications
  • Source
    Elizabeth A Streeten

    Preview · Article · Jul 2015 · Reviews in Endocrine and Metabolic Disorders
  • [Show abstract] [Hide abstract]
    ABSTRACT: A small group of Gulf War I veterans wounded in depleted uranium (DU) friendly fire incidents have been monitored in a clinical surveillance program at the Veterans Affairs Medical Center, Baltimore since 1994. An in-patient clinical surveillance protocol was performed on 35 members of the cohort, including exposure monitoring for total and isotopic uranium concentrations in urine and a comprehensive assessment of health outcomes. Although urine U concentrations continue to be elevated in this group, illustrating on-going in situ mobilization of U from embedded fragments, no consistent U-related health effects have been observed. Now more than 20 years since first exposure to DU, an aging cohort of military veterans continues to show no U-related health effects in known target organs of U toxicity. As tissue concentrations continue to accrue with exposure duration, critical tissue-specific U concentration thresholds may be reached, thus recommending on-going surveillance of this veteran cohort. Am. J. Ind. Med. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    No preview · Article · Apr 2015 · American Journal of Industrial Medicine
  • [Show abstract] [Hide abstract]
    ABSTRACT: Osteoporosis pseudoglioma syndrome (OPPG) is a rare autosomal recessive disorder of childhood osteoporosis and blindness due to inactivating mutations in LDL receptor-like protein 5 (LRP5). We and others have reported improvement in areal bone mineral density (aBMD) by DXA in OPPG on short term bisphosphonates. Long-term data on bisphosphonate use in OPPG and measures of volumetric BMD (vBMD) and cortical structure are not available. In addition, no long-term DXA data on untreated OPPG is available. The aims of this study were to: (1) record low trauma fractures and longitudinal aBMD by DXA in 5 OPPG patients on chronic bisphosphonate treatment, and in 4 OPPG patients never treated (2) to perform tibia peripheral quantitative CT (pQCT) to evaluate volumetric bone mineral density (vBMD), cortical structure and calf muscle area in 6 OPPG patients and 14unaffected first degree family members. PQCT results were converted to sex-specific Z-scores for age and adjusted for tibia length based on data in > 700 reference participants. We observed 4 fractures (3 femoral shaft) in 3 OPPG patients while on bisphosphonates, after each achieved significant improvement in aBMD. OPPG participants had significantly lower mean trabecular vBMD (-1.51 vs. 0.17, p = 0.002), cortical area (-2.36 vs. 0.37; p < 0.001) and periosteal circumference (-1.86 vs.-0.31, p = 0.001) Z-scores, compared with unaffected participants and had a trend toward lower muscle area Z-score (-0.69 vs 0.47, p = 0.12). These data demonstrate substantial bone fragility despite improvements in aBMD. The pQCT data provide insight into the fragility with substantial deficits in trabecular vBMD and cortical dimensions, consistent with OPPG effects of bone formation. Treatment that improves bone quality is needed to reduce fractures in OPPG. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Apr 2015 · Bone
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Genome mapping in animals is now one of the leading disciplines in animal sciences. It is employed for all facets in genome analysis in animals and their improvement for benefit of human beings. Mapping of genomes in farm animals, companion animals, laboratory animals, aquatic animals, insects, and primates, including humans have generated stupendous data bases to elucidate origin, evolution, phylogenetic relationship; position of genes; function, expression, regulation and sequence of genes. This information has tremendous applied value in agriculture, medicine, and environmental sciences. Paradoxically the information is mainly scattered only on the pages of journals, review papers and project/institutional reports. It is imperative now to have a comprehensive compilation of all these research findings in a single series for easy access to all levels of end users. The series Genome Mapping in Animals will fill this gap. It will provide comprehensive and up to date reviews on a large variety of selected animals systems contributed by teams of leading scientists from around the world.
    Full-text · Book · Jan 2015
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The Amish , a socially and religiously isolated population with large communities in Pennsylvania, Ohio, and Indiana, have been frequent participants in genetic studies since the 1960s. Although initial studies focused on rare, recessive diseases, others since the 1990s, largely ours, have focused on common disorders and the genetic underpinnings of their risk factors. We have shown both by simulation and practical case studies that the genetic architecture of the Old Order Amish (OOA) includes rare variants having strong phenotypic effects, some of which have reached non-negligible frequencies due to a founder effect and genetic drift . In this chapter, we review our case studies on variants in four genes: ABCG8, APOB, APOC3, and COL1A2. While traditionally medical genetics studies carried out in isolated populations have focused on individuals who are homozygous for some mutation; the four case studies that we present focus on individuals who are heterozygous carriers of a single mutation. This genetic homogeneity of the Amish and the enrichment of these variants allow us adequate statistical power to characterize the phenotypic variation resulting from a single mutation. These case studies have provided biologic insights into the relevance of these genes to human health and disease reaching beyond the OOA population.
    Full-text · Article · Jan 2015
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 x 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and gamma-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition.
    Full-text · Article · Jul 2014 · Nature
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We identified normal vs. abnormal 25-hydroxyvitamin D [25(OH)D] concentrations by examining the relation of 25(OH)D to non-bone-related measures (plasma glucose, insulin resistance, lipids, blood pressure, fitness, obesity, and regional adiposity) and asking whether there is a 25(OH)D concentration above and below which the relation between 25(OH)D and outcome changes. We examined the relation between 25(OH)D and outcome by race to see whether race-specific normal ranges are needed, and we examined the role of insulin-like growth factor-1 (IGF-1) in modulating the relation between 25(OH)D and outcome. In a cross-sectional study of 239 overweight and obese, sedentary postmenopausal women without diabetes (83 black, 156 white), outcome measures included plasma lipids, glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), IGF-1, parathyroid hormone (PTH), aerobic fitness, body composition, subcutaneous abdominal and visceral fat, and blood pressure. We identified threshold effects in the association between 25(OH)D and these variables using piecewise linear regressions. We found that 25(OH)D was inversely related to fasting glucose, fasting and 2-h insulin, HOMA-IR, visceral abdominal fat, percentage fat, PTH, and triglycerides. Evidence for a threshold effect of 25(OH)D was found for 2-h glucose, 2-h insulin, fasting insulin, and HOMA-IR. There was no evidence suggesting the need for race-specific normal 25(OH)D concentrations. IGF-1 modulated the relation between 25(OH)D and outcome but only below, and not above, a threshold 25(OH)D concentration. Our findings suggest a threshold effect of 25(OH)D on glucose-insulin metabolism such that 25(OH)D ≥ ∼26 μg/L (65.0 pmol/L) supports normal glucose homeostasis and that the same cut point defining normal 25(OH)D concentration can be used in black and white women. This study was registered at clinicaltrials.gov as NCT01798030.
    Preview · Article · Apr 2014 · Journal of Nutrition
  • Elizabeth A. Streeten · Michael A Levine
    [Show abstract] [Hide abstract]
    ABSTRACT: Since the discovery of vitamin D in 1919, great progress has been made in understanding its metabolism and the diseases resulting from mutations in related genes. Vitamin D3 is a secosteroid produced in skin in response to sunlight. Both endogenous D3 and exogenous D3 and D2 supplements are sequentially hydroxylated in the liver (25-hydroxylase) and kidneys (1α-hydroxylase), to form the active metabolite 1α,25-dihydroxyvitamin D (1α,25(OH)2D). Activation of the nuclear vitamin D receptor (VDR) by 1α,25(OH)2D leads to tissue-specific pleiotropic responses, including such different actions as increasing gastrointestinal calcium and phosphorus absorption and enhancing pancreatic insulin secretion. Hereditary disorders of vitamin D metabolism/action include the calciferol deficiency disorders vitamin D-resistant rickets (VDDR) types 1 and 2, both rare autosomal recessive disorders leading to rickets. VDDR-1 is due to mutations in CYP27B1, resulting in absent/reduced conversion of 25(OH)D into active 1α,25(OH)2D and is effectively treated with 1α,25(OH)2D (also called calcitriol). VDDR-2 is due to mutations in VDR, leading to true resistance to 1α,25(OH)2D. VDDR-2 is treated by high doses of calcium and 1α,25(OH)2D analogs. One calciferol-excess state has been described, autosomal recessive infantile hypercalcemia due to inactivating mutations in CYP24A1 (24-hydroxylase, the main catabolic enzyme) usually presenting as failure to thrive and nephrocalcinosis within the first year of life.
    No preview · Article · Dec 2013
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aiming to identify novel genetic variants and to confirm previously identified genetic variants associated with bone mineral density (BMD), we conducted a three-stage genome-wide association (GWA) meta-analysis in 26,988 study subjects. Stage 1 meta-analyzed 7 GWA samples and 11,140 subjects for BMDs at the lumbar spine, hip, and femoral neck, followed by a Stage 2 in silico replication of 33 SNPs in 9,185 subjects, and by a Stage 3 de novo validation of 3 SNPs in 6,663 subjects. Combining evidence from all the stages, we have identified 2 novel loci that have not been reported previously at the genome-wide significance (GWS, 5.0x10(-8)) level: 14q24.2 (rs227425, p-value 3.98x10(-13), SMOC1) in the combined sample of males and females and 21q22.13 (rs170183, p-value 4.15x10(-9), CLDN14) in the female specific sample. The two newly identified SNPs were also significant in the GEnetic Factors for OSteoporosis consortium (GEFOS, n=32,960) summary results. We have also independently confirmed 13 previously reported loci at the GWS level: 1p36.12 (ZBTB40), 1p31.3 (GPR177), 4p16.3 (FGFRL1), 4q22.1 (MEPE), 5q14.3 (MEF2C), 6q25.1 (C6orf97, ESR1), 7q21.3 (FLJ42280, SHFM1), 7q31.31 (FAM3C, WNT16), 8q24.12 (TNFRSF11B), 11p15.3 (SOX6), 11q13.4 (LRP5), 13q14.11 (AKAP11), and 16q24 (FOXL1). Gene expression analysis in osteogenic cells implied potential functional association of the two candidate genes (SMOC1 and CLDN14) in bone metabolism. Our findings independently confirm previously identified biological pathways underlying bone metabolism, and contribute to the discovery of novel pathways, thus providing valuable insights into the intervention and treatment of osteoporosis.
    No preview · Article · Nov 2013 · Human Molecular Genetics
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Context:Although numerous epidemiologic studies have documented associations between osteoporosis and cardiovascular disease, the mechanisms underlying this association remain to be clarified. One hypothesis is that hyperlipidemia may be a common predisposing factor to both atherosclerotic heart disease and bone fragility.Objective:To evaluate this we compared bone mineral density (BMD) between subjects with and without the R3500Q APOB mutation, the cause of familial defective apolipoprotein B-100 which has been previously shown to markedly increase low density lipoprotein cholesterol (LDL-C). We hypothesized that R3500Q carriers would have lower BMD due to lifetime, elevated LDL-C.Design:A cross-sectional study in the Old Order Amish (OOA) population.Participants:The R3500Q APOB mutation is present at a high frequency (∼6% vs. < 0.5%) in the OOA population due to a founder effect. Therefore we conducted analysis on 1097 Amish individuals of whom 125 were R3500Q carriers.Main Outcome Measure:BMD was measured by dual-energy x-ray absorptiometry.Results:After adjusting for age, age(2), sex, BMI and family structure, carriers for the Q risk allele had significantly lower BMD than non-carriers at the femoral neck (p=0.037), lumbar spine (p=0.035) and whole body (p=0.016). Adjusting for LDL-C attenuated the association between R3500Q genotype and BMD but did not completely explain the relationship. Subgroup analyses showed no significant interactions with sex, age or presence of metabolic syndrome.Conclusion:These results utilize the unique genetic architecture of the OOA population to provide a novel line of evidence supporting a causal role for elevated LDL-C in lowering BMD.
    Full-text · Article · Oct 2013 · The Journal of Clinical Endocrinology and Metabolism
  • Source
    Braxton D Mitchell · Elizabeth A Streeten
    [Show abstract] [Hide abstract]
    ABSTRACT: Osteoporotic fracture carries an enormous public health burden in terms of mortality and morbidity. Current approaches to identify individuals at high risk for fracture are based on assessment of bone mineral density and presence of other osteoporosis risk factors. Bone mineral density and susceptibility to osteoporotic fractures are highly heritable, and over 60 loci have been robustly associated with one or both traits through genome-wide association studies carried out over the past 7 years. In this review, we discuss opportunities and challenges for incorporating these genetic discoveries into strategies to prevent osteoporotic fracture and translating new insights obtained from these discoveries into development of new therapeutic targets.
    Full-text · Article · Oct 2013 · The Application of Clinical Genetics

  • No preview · Article · May 2013
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Forearm fractures affect 1.7 million individuals worldwide each year and most occur earlier in life than hip fractures. While the heritability of forearm bone mineral density (BMD) and fracture is high, their genetic determinants are largely unknown. Aim To identify genetic variants associated with forearm BMD and forearm fractures. Methods BMD at distal radius, measured by dual-energy x-ray absorptiometry, was tested for association with common genetic variants. We conducted a meta-analysis of genome-wide association studies for BMD in 5866 subjects of European descent and then selected the variants for replication in 715 Mexican American samples. Gene-based association was carried out to supplement the single-nucleotide polymorphism (SNP) association test. We then tested the BMD-associated SNPs for association with forearm fracture in 2023 cases and 3740 controls. Results We found that five SNPs in the introns of MEF2C were associated with forearm BMD at a genome-wide significance level (p<5×10–8) in meta-analysis (lead SNP, rs11951031[T] −0.20 SDs per allele, p=9.01×10–9). The gene-based association test suggested an association between MEF2C and forearm BMD (p=0.003). The association between MEF2C variants and risk of fracture did not achieve statistical significance (SNP rs12521522[A]: OR=1.14 (95% CI 0.92 to 1.35), p=0.14). Meta-analysis also revealed two genome-wide suggestive loci at CTNNA2 and 6q23.2. Conclusions These findings demonstrate that variants at MEF2C were associated with forearm BMD, implicating this gene in the determination of BMD at forearm.
    Preview · Article · Apr 2013 · Journal of Medical Genetics
  • Elizabeth A Streeten

    No preview · Article · Mar 2013 · Endocrine Practice
  • Sruti Chandrasekaran · Nicoleta Ionica · Elizabeth A Streeten

    No preview · Article · Mar 2013 · Endocrine Practice
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Obesity is associated with vitamin D deficiency, and both are areas of active public health concern. We explored the causality and direction of the relationship between body mass index (BMI) and 25-hydroxyvitamin D [25(OH) D] using genetic markers as instrumental variables (IVs) in bi-directional Mendelian randomization (MR) analysis. Methods and Findings: We used information from 21 adult cohorts (up to 42,024 participants) with 12 BMI-related SNPs (combined in an allelic score) to produce an instrument for BMI and four SNPs associated with 25(OH) D (combined in two allelic scores, separately for genes encoding its synthesis or metabolism) as an instrument for vitamin D. Regression estimates for the IVs (allele scores) were generated within-study and pooled by meta-analysis to generate summary effects. Associations between vitamin D scores and BMI were confirmed in the Genetic Investigation of Anthropometric Traits (GIANT) consortium (n = 123,864). Each 1 kg/m(2) higher BMI was associated with 1.15% lower 25(OH) D (p = 6.52x10(-27)). The BMI allele score was associated both with BMI (p = 6.30x10(-62)) and 25(OH) D (20.06% [95% CI -0.10 to -0.02], p = 0.004) in the cohorts that underwent meta-analysis. The two vitamin D allele scores were strongly associated with 25(OH) D (p = 0.57 for both vitamin D scores). Conclusions: On the basis of a bi-directional genetic approach that limits confounding, our study suggests that a higher BMI leads to lower 25(OH) D, while any effects of lower 25(OH) D increasing BMI are likely to be small. Population level interventions to reduce BMI are expected to decrease the prevalence of vitamin D deficiency.
    Full-text · Article · Feb 2013 · PLoS Medicine
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: Distinguishing sHPT from eucalcemic primary hyperparathyroidism (EC-pHPT) is important. The objective of this study was to measure PTH-stimulated production of 1,25(OH)2D in early postmenopausal patients with idiopathic sHPT, who also fit the criteria for EC-pHPT, compared to age-matched controls.Methods: In this pilot case-control study, postmenopausal women aged 44-55 with normal serum calcium (Ca), glomerular filtration rate (GFR) ≥65 ml/min, 25(OH)D ≥ 75 nmol/L (30 ng/ml) were given an 8 hour infusion of PTH(1-34), 12 pmol/kg/hr. Patients (n=5) had elevated PTH, normal 1,25(OH)2D and no hypercalciuria. Controls (n=5) had normal PTH. At baseline, 4 and 8 hours serum Ca, creatinine (Cr), phosphorus (P), 1,25(OH)2D, FGF23, 24,25(OH)2D; urine Ca, P, Cr and cAMP/GFR were measured; FeCa, TMP/GFR were calculated.Results: Patients had lower 1,25(OH)2D levels (±SD) than controls at 4 (39.8±6.9 vs 58.8±6.7, p=0.002) and 8 hours (56.4±9.2 vs 105±2.3, p=0.003) of PTH infusion, attenuated after adjusting for higher BMI in patients (p=0.05, 0.04). 24,25(OH)2D levels were lower in patients than controls (1.9±0.6 vs 3.4±0.6, p=0.007). No differences were seen in: serum Ca, P; urine cAMP/GFR, TRP/GFR, FeCa, PTH suppression at 8 hours (patients 50%, controls 64%).Conclusions: Vitamin D sufficient patients who fit the criteria for EC-pHPT, had reduced PTH-stimulated 1,25(OH)2D compared to controls, partially attributable to their higher BMI. Other causes of reduced 1,25(OH)2D production ruled out were excessive catabolism of vitamin D metabolites, elevated FGF23 and CYP27B1 mutation. Elevated BMI and idiopathic reduced PTH-stimulated 1,25(OH)2D production should be considered in the differential of sHPT.
    No preview · Article · Nov 2012 · Endocrine Practice
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We aimed to identify genetic variants associated with cortical bone thickness (CBT) and bone mineral density (BMD) by performing two separate genome-wide association study (GWAS) meta-analyses for CBT in 3 cohorts comprising 5,878 European subjects and for BMD in 5 cohorts comprising 5,672 individuals. We then assessed selected single-nucleotide polymorphisms (SNPs) for osteoporotic fracture in 2,023 cases and 3,740 controls. Association with CBT and forearm BMD was tested for ∼2.5 million SNPs in each cohort separately, and results were meta-analyzed using fixed effect meta-analysis. We identified a missense SNP (Thr>Ile; rs2707466) located in the WNT16 gene (7q31), associated with CBT (effect size of -0.11 standard deviations [SD] per C allele, P = 6.2 × 10(-9)). This SNP, as well as another nonsynonymous SNP rs2908004 (Gly>Arg), also had genome-wide significant association with forearm BMD (-0.14 SD per C allele, P = 2.3 × 10(-12), and -0.16 SD per G allele, P = 1.2 × 10(-15), respectively). Four genome-wide significant SNPs arising from BMD meta-analysis were tested for association with forearm fracture. SNP rs7776725 in FAM3C, a gene adjacent to WNT16, was associated with a genome-wide significant increased risk of forearm fracture (OR = 1.33, P = 7.3 × 10(-9)), with genome-wide suggestive signals from the two missense variants in WNT16 (rs2908004: OR = 1.22, P = 4.9 × 10(-6) and rs2707466: OR = 1.22, P = 7.2 × 10(-6)). We next generated a homozygous mouse with targeted disruption of Wnt16. Female Wnt16(-/-) mice had 27% (P<0.001) thinner cortical bones at the femur midshaft, and bone strength measures were reduced between 43%-61% (6.5 × 10(-13)<P<5.9 × 10(-4)) at both femur and tibia, compared with their wild-type littermates. Natural variation in humans and targeted disruption in mice demonstrate that WNT16 is an important determinant of CBT, BMD, bone strength, and risk of fracture.
    Full-text · Article · Jul 2012 · PLoS Genetics

Publication Stats

2k Citations
508.84 Total Impact Points

Institutions

  • 2002-2015
    • University of Maryland, Baltimore
      • • Division of Endocrinology, Diabetes and Nutrition
      • • Department of Medicine
      Baltimore, Maryland, United States
  • 2013
    • University of Maryland Medical Center
      Baltimore, Maryland, United States
  • 2001
    • Johns Hopkins Medicine
      Baltimore, Maryland, United States