300 research outputs found
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Determination of biomembrane bending moduli in fully atomistic simulations.
The bilayer bending modulus (Kc) is one of the most important physical constants characterizing lipid membranes, but precisely measuring it is a challenge, both experimentally and computationally. Experimental measurements on chemically identical bilayers often differ depending upon the techniques employed, and robust simulation results have previously been limited to coarse-grained models (at varying levels of resolution). This Communication demonstrates the extraction of Kc from fully atomistic molecular dynamics simulations for three different single-component lipid bilayers (DPPC, DOPC, and DOPE). The results agree quantitatively with experiments that measure thermal shape fluctuations in giant unilamellar vesicles. Lipid tilt, twist, and compression moduli are also reported
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Does linguistic input play the same role in language learning for children with and without early brain injury?
Children with unilateral pre- or perinatal brain injury (BI) show remarkable plasticity for language
learning. Previous work highlights the important role that lesion characteristics play in explaining
individual variation in plasticity in the language development of children with BI. The current study
examines whether the linguistic input that children with BI receive from their caregivers also contributes
to this early plasticity, and whether linguistic input plays a similar role in children with BI as it does in
typically developing (TD) children. Growth in vocabulary and syntactic production is modeled for 80
children (53 TD, 27 BI) between 14 and 46 months. Findings indicate that caregiver input is an equally
potent predictor of vocabulary growth in children with BI and in TD children. In contrast, input is a more
potent predictor of syntactic growth for children with BI than for TD children. Controlling for input,
lesion characteristics (lesion size, type, seizure history) also affect the language trajectories of children
with BI. Thus, findings illustrate how both variability in the environment (linguistic input) and variability
in the organism (lesion characteristics) work together to contribute to plasticity in language learning
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Genetic Variation in the Base Excision Repair Pathway, Environmental Risk Factors, and Colorectal Adenoma Risk
Cigarette smoking, high alcohol intake, and low dietary folate levels are risk factors for colorectal adenomas. Oxidative damage caused by these three factors can be repaired through the base excision repair pathway (BER). We hypothesized that genetic variation in BER might modify colorectal adenoma risk. In a sigmoidoscopy-based study, we examined associations between 182 haplotype tagging SNPs in 14 BER genes, and colorectal adenoma risk, and examined their potential role as modifiers of the effect cigarette smoking, alcohol intake, and dietary folate levels. Among all individuals, no statistically significant associations between BER SNPs and adenoma risk persisted after correction for multiple comparisons. However, among Asian-Pacific Islanders we observed two SNPs in FEN1 and one in NTHL1, and among African-Americans one SNP in APEX1 that were associated with colorectal adenoma risk. Significant associations were also observed between SNPs in the NEIL2 gene and rectal adenoma risk. Three SNPS modified the effect of smoking (MUTYH interaction p = 0.002; OGG1 interaction p = 0.013); FEN1 interaction p = 0.013)), one SNP in LIG3 modified the effect of alcohol consumption (interaction p = 0.024) and two SNPs in LIG3 modified the effect of dietary folate (interaction p = 0.001 and p = 0.08) on colorectal adenoma risk. These findings support a role for genetic variants in the BER pathway as potential modifiers of colorectal adenoma risk. Our findings strengthen the role of oxidative damage induced by key lifestyle and dietary risk factors in colorectal adenoma formation
Clinical application of three-dimensional echocardiographic laser stereolithography: Effect of leaflet funnel geometry on the coefficient of orifice contraction, pressure loss and the Gorlin formula in aortic stenosis
International audienc
Does linguistic input play the same role in language learning for children with and without early brain injury?
Clinicopathologic Risk Factor Distributions for MLH1 Promoter Region Methylation in CIMP-Positive Tumors
The CpG Island Methylator Phenotype (CIMP) is a major molecular pathway in colorectal cancer (CRC). Approximately 25% to 60% of CIMP tumors are microsatellite unstable (MSI-H) due to DNA hypermethylation of the MLH1 gene promoter. Our aim was to determine if the distributions of clinicopathologic factors in CIMP-positive tumors with MLH1 DNA methylation differed from those in CIMP-positive tumors without DNA methylation of MLH1
The USNO-B Catalog
USNO-B is an all-sky catalog that presents positions, proper motions,
magnitudes in various optical passbands, and star/galaxy estimators for
1,042,618,261 objects derived from 3,643,201,733 separate observations. The
data were obtained from scans of 7,435 Schmidt plates taken for the various sky
surveys during the last 50 years. USNO-B1.0 is believed to provide all-sky
coverage, completeness down to V = 21, 0.2 arcsecond astrometric accuracy at
J2000, 0.3 magnitude photometric accuracy in up to five colors, and 85%
accuracy for distinguishing stars from non-stellar objects. A brief discussion
of various issues is given here, but the actual data are available from
http://www.nofs.navy.mil and other sites.Comment: Accepted by Astronomical Journa
BRCA2 polymorphic stop codon K3326X and the risk of breast, prostate, and ovarian cancers
Background: The K3326X variant in BRCA2 (BRCA2*c.9976A>T; p.Lys3326*; rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormone-related cancers.
Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76 637 cancer case patients and 83 796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided.
Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9x10- 6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8x10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor–negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4x10-5 and ORw = 1.50, 95% CI = 1.28 to 1.76, P = 4.1x10-5, respectively). For BRCA1 mutation carriers, there was a statistically significant inverse association of the K3326X variant with risk of ovarian cancer (HR = 0.43, 95% CI = 0.22 to 0.84, P = .013) but no association with breast cancer. No association with prostate cancer was observed.
Conclusions: Our study provides evidence that the K3326X variant is associated with risk of developing breast and ovarian cancers independent of other pathogenic variants in BRCA2. Further studies are needed to determine the biological mechanism of action responsible for these associations
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