107 research outputs found
Efficacy of Brassica seed meal for management of Pythium root rot in greenhouse-grown vegetables
Mustard seed meal is the material that remains after oil is extracted from the seeds of plants in the mustard (Brassica) family. When in the presence of water, this seed meal releases compounds that can suppress plant diseases and weeds. As a result, mustard seed meal was investigated as an alternative method for disease and weed control, in an effort to reduce synthetic pesticide usage. Further, few studies examined the use of mustard seed meal for application in the commercial greenhouse industry, which is a large consumer of synthetic chemicals. Instead, many researchers assessed the seed meal in an outdoor setting. This project bridged the gap in literature and evaluated mustard seed meal as an additive to the soilless potting medium commonly used in the greenhouse industry. In a laboratory setting, the seed meal was successful in killing two species of the plant pathogen Pythium, which commonly causes root-rotting diseases. In a greenhouse setting, the mustard seed meal prohibited Pythium from killing tomato and cucumber seedlings but also damaged the seedlings at higher application rates. These observations were investigated in another series of experiments to identify a maximum seed meal application rate. In these experiments, seed meal rates up to 0.4% (by volume) did not decrease or delay germination. When a sowing delay of one day was employed, there were no decreases or delays in germination for seeds grown in medium combined with seed meal at rates up to 2.4%. Increasing the duration of the sowing delay up to seven days did not yield any added benefits. These experiments' data suggest adding seed meal up to 2.4% (by volume) will not decrease or delay germination as long as there is a minimum of one day between combining the potting medium and seed meal and sowing the seeds. However, seedlings that were transplanted into the same potting medium and mustard seed meal combinations were more sensitive than seeds. Even with a one-day delay, these seedlings were damaged at 1.2% seed meal and above, and were killed at all seed meal rates when there was no planting delay
A Latent Class Analysis of Heterosexual Young Men\u27s Masculinities
Parallel bodies of research have described the diverse and complex ways that men understand and construct their masculine identities (often termed masculinities ) and, separately, how adherence to traditional notions of masculinity places men at risk for negative sexual and health outcomes. The goal of this analysis was to bring together these two streams of inquiry. Using data from a national, online sample of 555 heterosexually active young men, we employed latent class analysis (LCA) to detect patterns of masculine identities based on men\u27s endorsement of behavioral and attitudinal indicators of dominant masculinity, including sexual attitudes and behaviors. LCA identified four conceptually distinct masculine identity profiles. Two groups, termed the Normative and Normative/Male Activities groups, respectively, constituted 88Ã¥ % of the sample and were characterized by low levels of adherence to attitudes, sexual scripts, and behaviors consistent with dominant masculinity, but differed in their levels of engagement in male-oriented activities (e.g., sports teams). Only eight percent of the sample comprised a masculinity profile consistent with traditional ideas about masculinity; this group was labeled Misogynistic because of high levels of sexual assault and violence toward female partners. The remaining four percent constituted a Sex-Focused group, characterized by high numbers of sexual partners, but relatively low endorsement of other indicators of traditional masculinity. Follow-up analyses showed a small number of differences across groups on sexual and substance use health indicators. Findings have implications for sexual and behavioral health interventions and suggest that very few young men embody or endorse rigidly traditional forms of masculinity
Predicting Sexual Assault Perpetration Among Heterosexually Active Young Men
Data from an online community sample of young men were analyzed to test predictors of sexual assault perpetration. We used structural equation modeling to test the relative contributions of specific sub-types of childhood adversity to subsequent sexual aggression. Mediators included hostile masculinity, impersonal sexual behavior and attitudes, and substance use variables. Findings suggested that childhood sexual abuse had direct and mediated effects on sexual assault perpetration, but hostile masculinity was the only proximal factor significantly related to aggression. Childhood polytrauma was also associated with increased perpetration risk, suggesting that prevention efforts may be aided by increased attention to childhood maltreatment
Patterns Of Intimate Partner Violence And Sexual Risk Behavior Among Young Heterosexually Active Men
Intimate partner violence (IPV) victimization is linked to sexual risk exposure among women. However, less is known about the intersection of IPV perpetration and sexual risk behavior among men. This study used data from a diverse, community sample of 334 heterosexually active young men, aged 18 to 25, across the United States to examine whether and how men with distinct IPV-related behavior patterns differed in sexual riskÃrelated behavior and attitudes. Participants were recruited and surveyed online, and grouped conceptually based on the types of IPV perpetration behavior(s) used in a current or recent romantic relationship. Groups were then compared on relevant sexual risk variables. Men reporting both physical abuse and sexual coercion against intimate partners reported significantly higher numbers of lifetime partners, higher rates of nonmonogamy, greater endorsement of nonmonogamy, and less frequent condom use relative to nonabusive men or those reporting controlling behavior only. This group also had higher sexually transmitted infection (STI) exposure compared to men who used controlling behavior only and men who used sexual coercion only. Findings suggest that interventions with men who use physical and sexual violence need to account for not only the physical and psychological harm of this behavior but also the sexual risk to which men may expose their partners
Histopathologic changes in the uterus, cervix and vagina of immature CD-1 mice exposed to low doses of perfluorooctanoic acid (PFOA) in a uterotrophic assay
The estrogenic and antiestrogenic potential of perfluorooctanoic acid (PFOA) was assessed using an immature mouse uterotrophic assay and by histologic evaluation of the uterus, cervix and vagina following treatment. Female offspring of CD-1 dams were weaned at 18 days old and assigned to groups of equal weight, and received 0, 0.01, 0.1, or 1 mg PFOA/kg BW/d by gavage with or without 17-β estradiol (E2, 500 μg/kg/d) from PND18-20 (n=8/treatment/block). At 24 hr after the third dose (PND 21), uteri were removed and weighed. Absolute and relative uterine weights were significantly increased in the 0.01 mg/kg PFOA only group. Characteristic estrogenic changes were present in all E2-treated mice; however, they were minimally visible in the 0.01 PFOA only mice. These data suggest that at a low dose PFOA produces minimal histopathologic changes in the reproductive tract of immature female mice, and does not antagonize the cellular effects of E2
Endemic Kaposi sarcoma in HIV-negative children and adolescents: an evaluation of overlapping and distinct clinical features in comparison with HIV-related disease
Abstract
Background
Endemic Kaposi sarcoma (KS) was first described in African children over fifty years ago, but has recently been overshadowed by HIV-related disease. We aimed to evaluate the similarities and differences between endemic HIV-negative and epidemic HIV-positive pediatric KS in a KS-associated herpesvirus-endemic region of Africa.
Methods
We describe clinical characteristics of 20 HIV-negative children with endemic KS over a six-year period and compare findings with a historical control—an HIV-related pediatric KS cohort from Lilongwe, Malawi.
Results
The HIV-negative endemic KS cohort was 70% male with a median age of 9.3 years. Lymph node involvement was present in 50%, hyperpigmented skin lesions in 45%, and woody edema in 40%. One patient (5%) presented with oral KS involvement and no patients presented initially with visceral KS. Significant anemia (hemoglobin < 8 g/dL) and thrombocytopenia (platelet count < 100 × 109/L) were found at time of original KS diagnosis in 45 and 40% respectively. In both HIV-negative and HIV-positive cohorts, lymphadenopathy was the most common presentation, prototypical skin lesions were often absent, severe cytopenias were a common clinical feature, and treatment outcomes were similar. Patients with endemic KS demonstrated less frequent oral involvement (5% versus 29%, P = 0.03) and a lower proportion of patients with visceral involvement (0% versus 16%, P = 0.06).
Conclusions
These data suggest clinical overlap between epidemiological variants. Treatment protocols for pediatric KS in sub-Saharan Africa should be devised to include both endemic HIV-negative and epidemic HIV-related disease to better define the clinical and biological comparison
Combining Asian and European genome-wide association studies of colorectal cancer improves risk prediction across racial and ethnic populations
Polygenic risk scores (PRS) have great potential to guide precision colorectal cancer (CRC) prevention by identifying those at higher risk to undertake targeted screening. However, current PRS using European ancestry data have sub-optimal performance in non-European ancestry populations, limiting their utility among these populations. Towards addressing this deficiency, we expand PRS development for CRC by incorporating Asian ancestry data (21,731 cases; 47,444 controls) into European ancestry training datasets (78,473 cases; 107,143 controls). The AUC estimates (95% CI) of PRS are 0.63(0.62-0.64), 0.59(0.57-0.61), 0.62(0.60-0.63), and 0.65(0.63-0.66) in independent datasets including 1681-3651 cases and 8696-115,105 controls of Asian, Black/African American, Latinx/Hispanic, and non-Hispanic White, respectively. They are significantly better than the European-centric PRS in all four major US racial and ethnic groups (p-values < 0.05). Further inclusion of non-European ancestry populations, especially Black/African American and Latinx/Hispanic, is needed to improve the risk prediction and enhance equity in applying PRS in clinical practice
Cumulative Burden of Colorectal Cancer-Associated Genetic Variants Is More Strongly Associated With Early-Onset vs Late-Onset Cancer.
BACKGROUND & AIMS: Early-onset colorectal cancer (CRC, in persons younger than 50 years old) is increasing in incidence; yet, in the absence of a family history of CRC, this population lacks harmonized recommendations for prevention. We aimed to determine whether a polygenic risk score (PRS) developed from 95 CRC-associated common genetic risk variants was associated with risk for early-onset CRC. METHODS: We studied risk for CRC associated with a weighted PRS in 12,197 participants younger than 50 years old vs 95,865 participants 50 years or older. PRS was calculated based on single nucleotide polymorphisms associated with CRC in a large-scale genome-wide association study as of January 2019. Participants were pooled from 3 large consortia that provided clinical and genotyping data: the Colon Cancer Family Registry, the Colorectal Transdisciplinary Study, and the Genetics and Epidemiology of Colorectal Cancer Consortium and were all of genetically defined European descent. Findings were replicated in an independent cohort of 72,573 participants. RESULTS: Overall associations with CRC per standard deviation of PRS were significant for early-onset cancer, and were stronger compared with late-onset cancer (P for interaction = .01); when we compared the highest PRS quartile with the lowest, risk increased 3.7-fold for early-onset CRC (95% CI 3.28-4.24) vs 2.9-fold for late-onset CRC (95% CI 2.80-3.04). This association was strongest for participants without a first-degree family history of CRC (P for interaction = 5.61 × 10-5). When we compared the highest with the lowest quartiles in this group, risk increased 4.3-fold for early-onset CRC (95% CI 3.61-5.01) vs 2.9-fold for late-onset CRC (95% CI 2.70-3.00). Sensitivity analyses were consistent with these findings. CONCLUSIONS: In an analysis of associations with CRC per standard deviation of PRS, we found the cumulative burden of CRC-associated common genetic variants to associate with early-onset cancer, and to be more strongly associated with early-onset than late-onset cancer, particularly in the absence of CRC family history. Analyses of PRS, along with environmental and lifestyle risk factors, might identify younger individuals who would benefit from preventive measures
Deciphering colorectal cancer genetics through multi-omic analysis of 100,204 cases and 154,587 controls of European and east Asian ancestries
In the version of this article initially published, the author affiliations incorrectly listed “Candiolo Cancer Institute FPO-IRCCS, Candiolo (TO), Italy” as “Candiolo Cancer Institute, Candiolo, Italy.” The change has been made to the HTML and PDF versions of the article
Novel Common Genetic Susceptibility Loci for Colorectal Cancer
BACKGROUND: Previous genome-wide association studies (GWAS) have identified 42 loci (P < 5 × 10-8) associated with risk of colorectal cancer (CRC). Expanded consortium efforts facilitating the discovery of additional susceptibility loci may capture unexplained familial risk. METHODS: We conducted a GWAS in European descent CRC cases and control subjects using a discovery-replication design, followed by examination of novel findings in a multiethnic sample (cumulative n = 163 315). In the discovery stage (36 948 case subjects/30 864 control subjects), we identified genetic variants with a minor allele frequency of 1% or greater associated with risk of CRC using logistic regression followed by a fixed-effects inverse variance weighted meta-analysis. All novel independent variants reaching genome-wide statistical significance (two-sided P < 5 × 10-8) were tested for replication in separate European ancestry samples (12 952 case subjects/48 383 control subjects). Next, we examined the generalizability of discovered variants in East Asians, African Americans, and Hispanics (12 085 case subjects/22 083 control subjects). Finally, we examined the contributions of novel risk variants to familial relative risk and examined the prediction capabilities of a polygenic risk score. All statistical tests were two-sided. RESULTS: The discovery GWAS identified 11 variants associated with CRC at P < 5 × 10-8, of which nine (at 4q22.2/5p15.33/5p13.1/6p21.31/6p12.1/10q11.23/12q24.21/16q24.1/20q13.13) independently replicated at a P value of less than .05. Multiethnic follow-up supported the generalizability of discovery findings. These results demonstrated a 14.7% increase in familial relative risk explained by common risk alleles from 10.3% (95% confidence interval [CI] = 7.9% to 13.7%; known variants) to 11.9% (95% CI = 9.2% to 15.5%; known and novel variants). A polygenic risk score identified 4.3% of the population at an odds ratio for developing CRC of at least 2.0. CONCLUSIONS: This study provides insight into the architecture of common genetic variation contributing to CRC etiology and improves risk prediction for individualized screenin
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