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Introduction Ginger root has a tradition of use as a remedy for numerous ailments that include nausea, loss of appetite, cramps, diarrhea, heartburn, migraines, colds, influenza, and arthritis.1 Ginger also contains a number of bioactive compounds with anticancer activities.2 Gingerols, which are a series of pungent phenolic homologs that differ in unbranched alkyl chain length, are important biologically active constituents of the rhizomes of ginger.3 Numerous laboratory studies attest to the anticancer activities of 6-gingerol, which has been the focus of most research.4 For example, 6-gingerol induces G1 phase cell cycle arrest and death of colorectal cancer cells, inhibits hepatocarcinoma cell motility and invasion, and the activity of metastasis-promoting matrix metalloproteinase-9.5,6 Anticancer activities have also been attributed to 10-gingerol (Figure 1), which we have recently shown to be is a potent inhibitor of breast cancer cell growth, acting via blockade of cellular proliferation and induction of programmed cell death.7 In a mouse model of triple-negative breast cancer, orthotopic tumor growth and metastasis to multiple organs is also inhibited by 10-gingerol.8 However, information regarding the biological activity of 10-gingerol in ovarian cancer cells is limited. Ovarian cancer is the leading cause of death in gynecologic cancer patients, and is in urgent need of new treatments because of its aggressive nature, high rate of recurrence, and proclivity to develop resistance to chemotherapeutic drugs.9,10 In this study, we assessed the impact of 10-gingerol on the growth of HEY, OVCAR3, and SKOV-3 ovarian cancer cell lines, as well as the mechanism of action of 10-gingerol in HEY cells. Cell growth inhibition assessment HEY, OVCAR3, or SKOV-3 cells were added to a 96-well flat-bottom microtiter plate (5 x 103 cells/well), allowed to form monolayers, and then treated with medium alone, vehicle (DMSO), or different concentrations of 10-gingerol for 24, 48, or 72 h. MTT was added (final concentration, 0.5 pg/mL) for the last 2 h of culture, after which culture supernatant was removed and 0.1 ml DMSO was added to each well to dissolve formazan crystals. Western blot analysis HEY cells were placed into 6-well plates at 2.5 x 105 cells/ well and treated with vehicle (DMSO) or 10-gingerol for 48 h. Cells were then collected and placed in ice-cold RIPA buffer (1% NP-40, 0.5% sodium deoxycholate, 0.1% SDS, 20 mM Tris-HCl, 150 mM NaCl, 1 mM ethylenediaminetetraacetic acid, and 1 mM ethylene glycol tetraacetic acid) containing a protease inhibitor cocktail (5 pg/mL leupeptin, 5 pg/mL pepstatin, 10 pg/mL aprotinin, 100 pM sodium orthovanadate, 10 mM sodium fluoride, 10 pM phenylarsine oxide, 1 mM dithiothreitol, 5 pM phenylmethyl sulphonyl fluoride) for 25 min.

Purpose: Gingerol homologs found in the rhizomes of ginger plants have the potential to benefithuman health, including the prevention and treatment of cancer. This study evaluated the effectof 10-gingerol on ovarian cancer cell (HEY, OVCAR3, and SKOV-3) growth.Methods: Cell growth was measured by MTT assays, flow cytometry was used to assess cellproliferation, cytotoxicity and cell cycle progression, and western blotting was used to measurecyclin protein expression.Results: Ovarian cancer cells that were treated with 10-gingerol experienced a time- anddose-dependent decrease in cell number, which was due to a reduction in cell proliferationrather than a cytotoxic effect. Reduced proliferation of 10-gingerol-treated ovarian cancercells was associated with an increased percentage of cells in G2 phase of the cell cycle anda corresponding reduction in the percentage of cells in G1. Ovarian cancer cells also showeddecreased cyclin A, B1, and D3 expression following exposure to 10-gingerol.Conclusion: These findings revealed that 10-gingerol caused a G2 arrest-associated suppressionof ovarian cancer cell growth, which may be exploited in the management of ovarian cancer.

Study Objectives: Hypoglossal nerve stimulation (HGNS) has been widely used to treat obstructive sleep apnea in selected patients. Here we evaluate rates of revision and explant related to HGNS implantation and assess types of adverse events contributing to revision and explant. Methods: Postmarket surveillance data for HGNS implanted between January 1, 2018 and March 31, 2022, were collected. Event rates and risk were calculated using the postmarket surveillance event counts and sales volume over the same period. Indications were categorized for analysis. Descriptive statistics were reported and freedom from explant or revision curves were grouped by year of implantation. Results: Of the 20,881 HGNS implants assessed, rates of explant and revision within the first year were 0.723% and 1.542%, respectively. The most common indication for explant was infection (0.378%) and for revision was surgical correction (0.680%). Of the 5,820 devices with 3-year postimplantation data, the rate of explant was 2.680% and of revision was 3.557%. During this same interval, elective removal (1.478%) was the most common indication, and for revisions, surgical correction (1.134%). Conclusions: The efficacy of HGNS is comparable in the real world setting to published clinical trial data. Rates of explant and revision are low, supporting a satisfactory safety profile for this technology. Citation: Moroco AE, Wei Z, Byrd I, et al. Device-related outcomes following hypoglossal nerve stimulator implantation. J Clin Sleep Med . 2024;20(9):1497–1503.

To clarify what successful masculinity entailed during World War II, this thesis analyzed both the ideal male image projected through magazine fiction stories and appropriate manhood as understood by the men and women who lived through the war. This thesis argued that while significant alterations took place in the media representation of manhood from the 1930s to the end of the war, men and women did not base their own understanding of masculinity or their behavior on definitions created by propaganda. Letters written by and to servicemen, and fiction and nonfiction printed in the magazine Coronet, made up the bulk of the sources utilized for this study. Articles in Coronet clarified the ideal war-time male as depicted by propagandists, which included bravery, taciturnity, and an inability to express emotion. Women, in the letters they wrote to men serving in the military, demanded a different, more plausible, type of masculinity that focused on kindness, affection, playfulness, and involved parenting. Letters written by men to their wives, sweethearts, and families presented a distinctly different set of expectations than those of propagandists or women and allowed for a wide variety of acceptable masculine behaviors and attitudes. This thesis, by analyzing a specific time period from three different perspectives, contributed a broader understanding of the construction, interpretation, and implementation of masculinity during World War II.

Mental health professionals typically encounter patients at 1 point in patients' lives. This cross-sectional window understandably fosters focus on the current presenting diagnosis. Research programs, treatment protocols, specialist clinics, and specialist journals are oriented to presenting diagnoses, on the assumption that diagnosis informs about causes and prognosis. This study tests an alternative hypothesis: people with mental disorders experience many different kinds of disorders across diagnostic families, when followed for 4 decades. To describe mental disorder life histories across the first half of the life course. This cohort study involved participants born in New Zealand from 1972 to 1973 who were enrolled in the population-representative Dunedin Study. Participants were observed from birth to age 45 years (until April 2019). Data were analyzed from May 2019 to January 2020. Diagnosed impairing disorders were assessed 9 times from ages 11 to 45 years. Brain function was assessed through neurocognitive examinations conducted at age 3 years, neuropsychological testing during childhood and adulthood, and midlife neuroimaging-based brain age. Of 1037 original participants (535 male [51.6%]), 1013 had mental health data available. The proportions of participants meeting the criteria for a mental disorder were as follows: 35% (346 of 975) at ages 11 to 15 years, 50% (473 of 941) at age 18 years, 51% (489 of 961) at age 21 years, 48% (472 of 977) at age 26 years, 46% (444 of 969) at age 32 years, 45% (429 of 955) at age 38 years, and 44% (407 of 927) at age 45 years. The onset of the disorder occurred by adolescence for 59% of participants (600 of 1013), eventually affecting 86% of the cohort (869 of 1013) by midlife. By age 45 years, 85% of participants (737 of 869) with a disorder had accumulated comorbid diagnoses. Participants with adolescent-onset disorders subsequently presented with disorders at more past-year assessments (r = 0.71; 95% CI, 0.68 to 0.74; P < .001) and met the criteria for more diverse disorders (r = 0.64; 95% CI, 0.60 to 0.67; P < .001). Confirmatory factor analysis summarizing mental disorder life histories across 4 decades identified a general factor of psychopathology, the p-factor. Longitudinal analyses showed that high p-factor scores (indicating extensive mental disorder life histories) were antedated by poor neurocognitive functioning at age 3 years (r = -0.18; 95% CI, -0.24 to -0.12; P < .001), were accompanied by childhood-to-adulthood cognitive decline (r = -0.11; 95% CI, -0.17 to -0.04; P < .001), and were associated with older brain age at midlife (r = 0.14; 95% CI, 0.07 to 0.20; P < .001). These findings suggest that mental disorder life histories shift among different successive disorders. Data from the present study, alongside nationwide data from Danish health registers, inform a life-course perspective on mental disorders. This perspective cautions against overreliance on diagnosis-specific research and clinical protocols.

The quality factor of a passive, linear, small acoustic radiator is fundamentally limited by its volume normalized to the emitted wavelength, imposing severe constraints on the bandwidth and efficiency of compact acoustic sources and ofmetamaterials composed of arrangements of small acoustic resonators. We demonstrate that these bounds can be overcome by loading a piezoelectric transducer with a non-Foster active circuit, showing that its radiation bandwidth and efficiency can be largely extended beyond what is possible in passive radiators, fundamentally limited only by stability considerations. Based on these principles, we experimentally observe a threefold bandwidth enhancement compared to its passive counterpart, paving the way toward non-Foster acoustic radiation and more broadly active metamaterials that overcome the bandwidth constraints hindering passive systems.

Biological aging is the gradual, progressive decline in system integrity that occurs with advancing chronological age, causing morbidity and disability. Measurements of the pace of aging are needed as surrogate endpoints in trials of therapies designed to prevent disease by slowing biological aging. We report a blood-DNA-methylation measure that is sensitive to variation in pace of biological aging among individuals born the same year. We first modeled change-over-time in 18 biomarkers tracking organ-system integrity across 12 years of follow-up in n = 954 members of the Dunedin Study born in 1972–1973. Rates of change in each biomarker over ages 26–38 years were composited to form a measure of aging-related decline, termed Pace-of-Aging. Elastic-net regression was used to develop a DNA-methylation predictor of Pace-of-Aging, called DunedinPoAm for Dunedin(P)ace(o)f(A)ging(m)ethylation. Validation analysis in cohort studies and the CALERIE trial provide proof-of-principle for DunedinPoAm as a single-time-point measure of a person’s pace of biological aging. People’s bodies age at different rates. Age-related biological changes that increase the risk of disease and disability progress rapidly in some people. In others, these processes occur at a slower pace, allowing those individuals to live longer, healthier lives. This observation has led scientists to try to develop therapies that slow aging. The hope is that such treatments could prevent or delay diseases like heart disease or dementia, for which older age is the leading risk factor. Studies in animals have identified treatments that extend the creatures’ lives and slow age-related disease. But testing these treatments in humans is challenging. Our lives are much longer than the worms, flies or mice used in the experiments. Scientists would have to follow human study participants for decades to detect delays in disease onset or an extension of their lives. An alternative approach is to try to develop a test that measures the pace of aging, or essentially “a speedometer for aging”. This would allow scientists to more quickly determine if treatments slow the aging process. Now, Belsky et al. show a blood test designed to measure the pace of aging predicts which people are at increased risk of poor health, chronic disease and an earlier death. First, data about chemical changes to an individual’s DNA, called DNA methylation, were analyzed from white blood cell samples collected from 954 people in a long-term health study known as “The Dunedin Study”. Using the data, Belsky et al. then developed an algorithm – named “DunedinPoAm” – that identified people with an accelerated or slowed pace of aging based on a single blood test. Next, they used the algorithm on samples from participants in three other long-term studies. This verified that those people the algorithm identified as aging faster had a greater risk of poor health, developing chronic diseases or dying earlier. Similarly, those identified as aging more slowly performed better on tests of balance, strength, walking speed and mental ability, and they also looked younger to trained raters. Additionally, Belsky et al. used the test on participants in a randomized trial testing whether restricting calories had potential to extend healthy lifespan. The results suggested that the calorie restriction could counter the effects of an accelerated pace of aging. The test developed by Belsky et al. may provide an alternate way of measuring whether age-slowing treatments work. This would allow faster testing of treatments that can extend the healthy lifespan of humans. The test may also help identify individuals with accelerated aging. This might help public health officials test whether policies or programs can help people lead longer, healthier lives.

When applied in large scale to electronic medical record data, the PheWAS approach replicates GWAS associations and reveals potentially new pleiotropic associations. Candidate gene and genome-wide association studies (GWAS) have identified genetic variants that modulate risk for human disease; many of these associations require further study to replicate the results. Here we report the first large-scale application of the phenome-wide association study (PheWAS) paradigm within electronic medical records (EMRs), an unbiased approach to replication and discovery that interrogates relationships between targeted genotypes and multiple phenotypes. We scanned for associations between 3,144 single-nucleotide polymorphisms (previously implicated by GWAS as mediators of human traits) and 1,358 EMR-derived phenotypes in 13,835 individuals of European ancestry. This PheWAS replicated 66% (51/77) of sufficiently powered prior GWAS associations and revealed 63 potentially pleiotropic associations with P < 4.6 × 10 −6 (false discovery rate < 0.1); the strongest of these novel associations were replicated in an independent cohort ( n = 7,406). These findings validate PheWAS as a tool to allow unbiased interrogation across multiple phenotypes in EMR-based cohorts and to enhance analysis of the genomic basis of human disease.

Children from lower-income households are at increased risk for poor health, educational failure, and behavioral problems. This social gradient is one of the most reproduced findings in health and social science. How people view their position in social hierarchies also signals poor health. However, when adolescents’ views of their social position begin to independently relate to well-being is currently unknown. A cotwin design was leveraged to test whether adolescents with identical family backgrounds, but who viewed their family’s social status as higher than their same-aged and sex sibling, experienced better well-being in early and late adolescence. Participants were members of the Environmental Risk Longitudinal Twin Study, a representative cohort of British twins (n = 2,232) followed across the first 2 decades of life. By late adolescence, perceptions of subjective family social status (SFSS) robustly correlated with multiple indicators of health and well-being, including depression; anxiety; conduct problems; marijuana use; optimism; not in education, employment, or training (NEET) status; and crime. Findings held controlling for objective socioeconomic status both statistically and by cotwin design after accounting for measures of childhood intelligence (IQ), negative affect, and prior mental health risk and when self-report, informant report, and administrative data were used. Little support was found for the biological embedding of adolescents’ perceptions of familial social status as indexed by inflammatory biomarkers or cognitive tests in late adolescence or for SFSS in early adolescence as a robust correlate of well-being or predictor of future problems. Future experimental studies are required to test whether altering adolescents’ subjective social status will lead to improved well-being and social mobility.

A collection of 112 winter barley varieties (Hordeum vulgare L.) was grown in the field for two years (2008/09 and 2009/10) in northern Italy and grain and straw yields recorded. In the first year of the trial, a severe attack of barley yellow mosaic virus (BaYMV) strongly influenced final performances with an average reduction of ~ 50% for grain and straw harvested in comparison to the second year. The genetic determination (GD) for grain yield was 0.49 and 0.70, for the two years respectively, and for straw yield GD was low in 2009 (0.09) and higher in 2010 (0.29). Cell wall polymers in culms were quantified by means of the monoclonal antibodies LM6, LM11, JIM13 and BS-400-3 and the carbohydrate-binding module CBM3a using the high-throughput CoMPP technique. Of these, LM6, which detects arabinan components, showed a relatively high GD in both years and a significantly negative correlation with grain yield (GYLD). Overall, heritability (H2) was calculated for GYLD, LM6 and JIM and resulted to be 0.42, 0.32 and 0.20, respectively. A total of 4,976 SNPs from the 9K iSelect array were used in the study for the analysis of population structure, linkage disequilibrium (LD) and genome-wide association study (GWAS). Marker-trait associations (MTA) were analyzed for grain yield and cell wall determination by LM6 and JIM13 as these were the traits showing significant correlations between the years. A single QTL for GYLD containing three MTAs was found on chromosome 3H located close to the Hv-eIF4E gene, which is known to regulate resistance to BaYMV. Subsequently the QTL was shown to be tightly linked to rym4, a locus for resistance to the virus. GWAs on arabinans quantified by LM6 resulted in the identification of major QTLs closely located on 3H and hypotheses regarding putative candidate genes were formulated through the study of gene expression levels based on bioinformatics tools.