Over 90% of breast cancer is cured; yet there remain highly aggressive breast cancers that develop rapidly and are extremely difficult to treat, much less prevent. Breast cancers that rapidly develop between breast image screening are called “interval cancers.” The efforts of our team focus on identifying multiscale integrated strategies to identify biologically aggressive precancerous breast lesions. Our goal is to identify spatiotemporal changes that occur prior to development of interval breast cancers. To accomplish this requires integration of new technology. Our team has the ability to perform single cell in situ transcriptional profiling, noncontrast biological imaging, mathematical analysis, and nanoscale evaluation of receptor organization and signaling. These technological innovations allow us to start to identify multidimensional spatial and temporal relationships that drive the transition from biologically aggressive precancer to biologically aggressive interval breast cancer. This article is categorized under Cancer > Computational Models Cancer > Molecular and Cellular Physiology Cancer > Genetics/Genomics/Epigenetics.

Intravenous iloprost improves Raynaud’s phenomenon (RP) and promotes healing of digital ulcers in systemic sclerosis (SSc; scleroderma). D-Galactose order Despite a short half-life, its clinical efficacy lasts weeks. Endothelial adherens junctions, which are formed by VE-cadherin clustering between endothelial cells (ECs), regulate endothelial properties including barrier function, endothelial-to-mesenchymal transition (EndoMT), and angiogenesis. We undertook this study to investigate the hypothesis that junctional disruption contributes to vascular dysfunction in SSc, and that the protective effect of iloprost is mediated by strengthening of those junctions.

Dermal ECs from SSc patients and healthy controls were isolated. The effect of iloprost on ECs was examined using immunofluorescence, permeability assays, Matrigel tube formation, and quantitative polymerase chain reaction.

Adherens junctions in SSc were disrupted compared to normal ECs, as indicated by reduced levels of VE-cadherin and increased permeability in SScsis and barrier function and reduced EndoMT. These findings provide a mechanistic basis for the use of iloprost in treating SSc patients with RP and digital ulcers.

Traumatic Antecedents Questionnaire (TAQ) is a traumatic experience scale that measures exposure to traumatic events across four age periods. Although the TAQ has good convergent validity with other traumatic scales, the classification of the domains and the psychometric properties of the scale has not been verified.

A total of 290 young adults completed the TAQ, and 156 participated in the retest. The number of trauma domains was determined using principal component analysis. Rasch model was used for verifying the items that each domain might represent in one common measurement.

When scores were transformed as binary a code 0 and 1 from the original 4 categories, 8 domains were established consisting of Domestic violence, Sexual/other rare trauma, Incompetence, Caring family, Accidents to close person, Unstable caring environment, Safe environment, and Lack of sexual/extreme trauma. Most domains had acceptable psychometric properties with a mean-square fit value within the range of 0.7-1.3. The Bland and Altman analysis suggest 98.7% of difference scores between test and retest were within ±2 standard deviations from the mean. TAQ severity showed a significant relationship with the multiplicity score of the Maltreatment and Abuse Chronology of Exposure scale (r=0.677).

The newly proposed scoring system and 8 domains for the TAQ demonstrated excellent internal consistency, test-retest reliability, and validity. Further studies are needed to develop new items in domains with less than 5 items to improve the psychometric properties of the scale and to create a maltreatment domain that includes bullying items.

The newly proposed scoring system and 8 domains for the TAQ demonstrated excellent internal consistency, test-retest reliability, and validity. Further studies are needed to develop new items in domains with less than 5 items to improve the psychometric properties of the scale and to create a maltreatment domain that includes bullying items.

This study aimed to quantitatively examine the association between gestational weight gain (GWG) and risk of autism spectrum disorder (ASD) in offspring.

Electronic databases were searched for studies of excessive or inadequate GWG, as compared with recommended GWG, in relation to the risk of ASD in offspring. Measures of the association from primary studies were pooled using a meta-analytic approach and expressed as weighted odds ratios (ORs) with 95% CIs.

Nine studies were identified, including 323,253 participants with 4,135 cases of ASD from five cohort studies and 1,462 cases and 3,265 controls from four case-control studies. Evidence from cohort studies indicates that both excessive and inadequate GWG was significantly associated with a higher risk for ASD in offspring. The pooled OR of ASD was 1.10 (95% CI 1.02-1.18) for excessive GWG and 1.13 (95% CI 1.04-1.24) for inadequate GWG using recommended GWG as the reference. Evidence from case-control studies suggests that excessive GWG (1.38 [95% CI 1.19-1.62]) but not inadequate GWG (0.87 [95% CI 0.72-1.04]) was significantly associated with a higher risk for ASD.

The accumulated evidence has supported that gaining weight outside the recommended GWG is associated with a higher risk for ASD in offspring.

The accumulated evidence has supported that gaining weight outside the recommended GWG is associated with a higher risk for ASD in offspring.

This study was designed to investigate the effects of a novel carcinogenetic molecule, p130cas (breast cancer antiestrogen resistance protein 1 or BCAR1) on proliferation and cell growth in lung adenocarcinoma. The study also aimed to identify the possible underlying signal networks of BCAR1.

First, we evaluated proliferation, cell colony formation, apoptosis, and cell cycle after BCAR1 was knocked out (KO) using CRISPR-Cas9 technology in H1975 and H1299 human lung adenocarcinoma cells. Subsequently, BCAR1 was upregulated in 293T cells and immunoprecipitation-mass spectrometry (IP-MS) was used with bioinformatics analysis to screen for potential networks of BCAR1 interacting proteins. Ultimately, we validated the correlated expressions of BCAR1 and a selected hub gene, RNA polymerase II subunit A (POLR2A), in 54 lung adenocarcinoma tissues, as well as in H1975 and H1299 cells.

Cell proliferation of H1975 and H1299 was significantly inhibited following BCAR1-KO. Colony formation of H1975 cells was also significantly decreased following BCAR1-KO.