AbstractBackgroundExtreme fear of contamination within obsessive compulsive disorder (OCD) is traditionally conceptualised as a physical phenomenon. More recent research has supported the notion of “mental” contamination (MC) in which people feel contaminated in the absence of physical contact. The current research sought to determine whether feelings of contact contamination (CC) and MC could be induced within a non‐clinical sample, whether the impact of MC and CC was comparable in terms of associated feelings and behaviour, and whether related psychopathology related to the impact of the tasks.MethodsUndergraduate students (n = 60) completed OCD relevant measures and were randomly assigned to either a CC condition (moving a bucket of fake vomit) or an MC condition (thinking about a bucket of vomit).ResultsBoth manipulations induced feelings of contamination. Participants in the contact condition had significantly greater urge to wash than those in the mental condition. Neutralising behaviour did not differ across conditions.ConclusionsFeelings of contamination can be induced in the absence of physical contact and for those in the MC group some aspects of OCD‐relevant psychopathology were related to the impact of the manipulation. These findings have implications for the understanding and treatment of contamination‐related fears in OCD.AbstractDisplay full sizeKey words: contact contaminationdisgust sensitivitymental contaminationOCD Funding: None.Conflict of interest: None.Funding: None.Conflict of interest: None.NotesFunding: None.Conflict of interest: None.
Small cell lung cancer (SCLC) in patients <50 years old has unique socioeconomic and clinical implications. We aimed to examine the demographics, treatment patterns, and survival of young patients with SCLC and compared them to older adults.The National Cancer Database (NCDB) was queried to identify SCLC cases diagnosed from 2004 to 2016. Patients were divided into three age groups: ≥18-<50, ≥50-<70, and ≥70 years. Patient characteristics were evaluated for survival within each age group. Kaplan-Meier and Cox regression analyses were used to assess survival.Of the 172,453 evaluated SCLC patients (median age 66 years), 8,792 were ≥18-<50 years old. Compared to the older groups, patients under 50 were more likely to be Black, uninsured or on Medicaid, have household income <$30,000, and present with stage III or IV disease (P<0.0001 for all). While young patients were more likely to receive guideline-concordant care (GCC), the hazard of death increased to 1.96 (95% CI: 1.80-2.14; P<0.0001) with receipt of nonstandard therapy. Private insurance, female gender, non-White race, Hispanic ethnicity, and higher income were associated with better survival. The youngest cohort had significantly better survival overall when compared to the older patients (P<0.0001), but the survival advantage was reduced with the advancing stage.SCLC patients under 50 years old represent a socioeconomically disadvantaged group with advanced disease at presentation. Despite having fewer comorbidities and being offered guideline-concordant treatment, younger patients with SCLC have only marginally better survival than older patients in advanced stages.
Genomic surveillance of monkeypox virus (MPXV) during the 2022 outbreak has been mainly focused on single nucleotide polymorphism (SNP) changes. DNA viruses, including MPXV, have a lower SNP mutation rate than RNA viruses due to higher fidelity replication machinery. We identified a large genomic rearrangement in a MPXV sequence from a 2022 case in the state of Minnesota (MN), USA, from an abnormal, uneven MPXV read mapping coverage profile in whole-genome sequencing (WGS) data. We further screened WGS data of 206 U.S. MPXV samples and found seven (3.4 percent) sequenced genomes contained similar abnormal read coverage profiles that suggested putative large deletions or genomic rearrangements. Here, we present three MPXV genomes containing deletions ranging from 2.3 to 15 kb and four genomes containing more complex rearrangements. Five genomic changes were each only seen in one sample, but two sequences from linked cases shared an identical 2.3 kb deletion in the 3’ terminal region. All samples were positive using VAC1 and Clade II (formerly West African)-specific MPXV diagnostic tests; however, large deletions and genomic rearrangements like the ones reported here have the potential to result in viruses in which the target of a PCR diagnostic test is deleted. The emergence of genomic rearrangements during the outbreak may have public health implications and highlight the importance of continued genomic surveillance.
Abstract We assessed mpox virus prevalence in blood, pharyngeal, and rectal specimens among persons without characteristic rash presenting for JYNNEOS vaccine. Our data indicate that the utility of risk-based screening for mpox in persons without skin lesions or rash via pharyngeal swabs, rectal swabs, and/or blood is likely limited.
T cells from systemic lupus erythematosus (SLE) patients exhibit a hyperactive phenotype with defects in homeostasis, signaling and cytokine production. We previously uncovered new roles for serine arginine-rich splicing factor 1 (SRSF1) in the control of genes involved in signaling and cytokine production in T cells. SRSF1 expression is decreased in T cells from patients with SLE and low SRSF1 levels are associated with severe disease activity. Mice with a T cell-conditional deficiency of Srsf1 exhibit T cell hyperactivity, systemic autoimmunity, and lupus-like nephritis. However, little is known about the molecular targets controlled by SRSF1 and whether they are implicated in human SLE. Our goal was to identify the molecular signatures controlled by SRSF1 and evaluation by comparative bioinformatic analysis if these genes and pathways are dysregulated in SLE. We curated publicly available gene array datasets from SLE patients and compared them with SRSF1-regulated genes in CD4 T cells from Srsf1-deficient mice. We identified 169 overlapping genes controlled by SRSF1 that are aberrantly expressed in T cells of SLE patients. Pathway analysis revealed genes enriched in interferon signaling, cytokine production, cytokine receptor interaction, cell migration and lysosomal clearance pathways. Our data reveal that SRSF1 controls genes involved in T cell homeostasis, activation, cytokine regulation/signaling and differentiation, which are altered in patients with SLE. Therefore, SRSF1 is an important regulator of T cell function and its deficiency may lead to a hyperactive T cell phenotype in SLE patients. Targeting SRSF1 and the genes controlled by this molecule to correct the aberrant T
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