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Background: Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with multi organ involvement. One of the most common manifestations is pulmonary disease with a reported prevalence between 5%–90%. Purpose: Given this wide range of prevalence, there is a need to more closely define types of pulmonary disease in SLE and associated risk factors. Research Design: We sought to characterize the presentation of pulmonary manifestations in an established SLE cohort using electronic health record data. Study Sample: All patients were >18 years of age and had confirmed SLE by a rheumatologist using SLICC or 2019 ACR/EULAR classification criteria. 220 patients with imaging were included in this study; average age was 42.5 years, 86.7% identified as female, 60.5% identified as white, 37.3% as Black, and 1.82% as Asian. Analysis: Generalized estimating equations were utilized to analyze the data, accounting for its repeated measured nature. Results: We found an association between smoking (present/prior smoker) and radiologist reported disease on computerized tomography (CT) scan, as well as an association between smoking (present/prior smoker), older age, and male sex with having pulmonary disease identified on chest X-ray. The most common findings on CT and X-ray were increased lung density (24%, 12%) and atelectasis (18%, 10%). The most common disease found on CT was pleural effusion (24%) and mediastinal/axillary lymphadenopathy (16%). Conclusion: While our study is limited by the retrospective nature, our results show that certain factors, namely smoking, older age, or male sex should prompt clinicians to have a higher suspicion for lung disease in SLE patients. [ABSTRACT FROM AUTHOR]

Hidradenitis suppurativa (HS) is a debilitating chronic inflammatory skin condition affecting hair follicles in flexural sites. Obesity is considered to be a risk factor for HS occurrence and thought to be associated with increased severity of HS symptoms. Here, we review the literature examining the impact of dietary factors on HS. Moreover, we propose potential mechanistic links between dietary factors and HS pathogenesis, incorporating evidence from both clinical and basic science studies. [ABSTRACT FROM AUTHOR]

This article explores the relationship between food insecurity and inflammatory-mediated dermatological diseases. The study found that food insecurity may be more prevalent in individuals with certain skin conditions, such as alopecia and atopic dermatitis. Inflammatory skin diseases have been associated with processed foods, additives, and low nutrient levels. The study suggests that individuals experiencing food insecurity may be at an increased risk of developing inflammatory skin conditions or experiencing a higher burden of their disease. However, the study is limited by a small sample size and predominantly female participation. Further research is needed to investigate the influence of food insecurity on dermatological diseases. [Extracted from the article]

Background: Anorexia nervosa (AN) is a psychiatric disorder with complex etiology, with a significant portion of disease risk imparted by genetics. Traditional genome-wide association studies (GWAS) produce principal evidence for the association of genetic variants with disease. Transcriptomic imputation (TI) allows for the translation of those variants into regulatory mechanisms, which can then be used to assess the functional outcome of genetically regulated gene expression (GReX) in a broader setting through the use of phenome-wide association studies (pheWASs) in large and diverse clinical biobank populations with electronic health record phenotypes. Methods: Here, we applied TI using S-PrediXcan to translate the most recent PGC-ED AN GWAS findings into AN-GReX. For significant genes, we imputed AN-GReX in the Mount Sinai Bio Me ™ Biobank and performed pheWASs on over 2000 outcomes to test the clinical consequences of aberrant expression of these genes. We performed a secondary analysis to assess the impact of body mass index (BMI) and sex on AN-GReX clinical associations. Results: Our S-PrediXcan analysis identified 53 genes associated with AN, including what is, to our knowledge, the first-genetic association of AN with the major histocompatibility complex. AN-GReX was associated with autoimmune, metabolic, and gastrointestinal diagnoses in our biobank cohort, as well as measures of cholesterol, medications, substance use, and pain. Additionally, our analyses showed moderation of AN-GReX associations with measures of cholesterol and substance use by BMI, and moderation of AN-GReX associations with celiac disease by sex. Conclusions: Our BMI-stratified results provide potential avenues of functional mechanism for AN-genes to investigate further. [ABSTRACT FROM AUTHOR]

The Nimrud Rescue Project is a collaborative project to recover fragments of Neo-Assyrian sculptures bombed by the Islamic State of Iraq and Syria (ISIS) in 2015–2016, and to develop a long-term plan for the preservation and use of the site and its architectural remains through capacity-building and support of Iraqi heritage professionals. The Smithsonian Institution has been working with colleagues from the Nineveh Provincial Office of the Iraqi State Board of Antiquities and Heritage (SBAH) since early 2017. The project is one of many managed through a partnership with the Iraqi Institute for the Conservation of Antiquities and Heritage (IICAH) in Erbil, Iraq. The Smithsonian has approached recovery and preservation of the site in partnership with Iraqi stewards. Together with the SBAH Nineveh Directorate, the Smithsonian worked to define site needs and develop the skills required by the cadre of local archaeologists (called the 'Nimrud Rescue Team', or NRT) to recover and protect stone sculpture fragments scattered across the site. A purpose-built storage facility has been completed and the NRT has begun the process of recovery using the 'First Aid to Cultural Heritage in Times of Crisis' (FAC) methodology developed by ICCROM and others for organized recovery of cultural heritage objects after a disaster. [ABSTRACT FROM AUTHOR]

One of the duties of conservators at the National Museum of the American Indian (NMAI) is to serve as conservation liaison to exhibit projects. The role of the conservation liaison is to ensure that preservation and conservation issues are considered throughout the exhibit development and production, and to ensure that the conservation treatment process incorporates the concerns of other museum staff and Native community members who are involved in the project. This paper uses a recent exhibit Listening to our Ancestors to illustrate how the conservation liaison ensures collaboration both with other NMAI staff and contractors and with Native people who work with the museum to produce exhibits and to involve conservation staff at all stages. [ABSTRACT FROM AUTHOR]

Plants activate distinct defense responses depending on the lifestyle of the attacker encountered. In these responses, salicylic acid (SA) and jasmonic acid (JA) play important signaling roles. SA induces defense against biotrophic pathogens that feed and reproduce on live host cells, whereas JA activates defense against necrotrophic pathogens that kill host cells for nutrition and reproduction. Cross-talk between these defense signaling pathways has been shown to optimize the response against a single attacker. However, its role in defense against multiple pathogens with distinct lifestyles is unknown. Here we show that infection with biotrophic Pseudomonas syringae. which induces SA-mediated defense, rendered plants more susceptible to the necrotrophic pathogen Alternaria brassicicola by suppression of the JA signaling pathway. This process was partly dependent on the cross-talk modulator NPR1. Surprisingly, this tradeoff was restricted to tissues adjacent to the site of initial infection; A. brassicicola infection in systemic tissue was not affected. Even more surprisingly, tradeoff occurred only with the virulent Pseudomonas strain. Avirulent strains that induced programmed cell death (PCD), an effective plant-resistance mechanism against biotrophs, did not cause suppression of JA-dependent defense. This result might be advantageous to the plant by preventing necrotrophic pathogen growth in tissues undergoing PCD. Our findings show that plants tightly control cross-talk between SA- and JA-dependent defenses in a previously unrecognized spatial and pathogen type-specific fashion. This process allows them to prevent unfavorable signal interactions and maximize their ability to concomitantly fend off multiple pathogens. [ABSTRACT FROM AUTHOR]

Various organic polymers have been used in the field for preserving the morphological structure of bone. Archaeologists and conservators have separately devised techniques and materials using these polymers to give structural support to deteriorating, fragile bone. Historical examination of the methods and materials used by archaeologists helps to identify materials found on collections stored in museums that may be needed for analysis, identifies types of materials used successfully in the past, and points out differences in the approaches of conservation and archaeology towards the preservation of archaeological materials. The decision to apply a polymer to bone should be carefully considered, based on an understanding of the physical and chemical interactions between the bone and consolidation system, and the effects one's choice may have on long-term preservation and future research needs. [ABSTRACT FROM AUTHOR]

Genetic studies of schizophrenia have implicated numerous risk loci including several copy number variants (CNVs) of large effect and hundreds of loci of small effect. In only a few cases has a specific gene been clearly identified. Rare CNVs affecting a single gene offer a potential avenue to discovering schizophrenia risk genes. CNVs were generated from exome sequencing of 4913 schizophrenia cases and 6188 control subjects from Sweden. We integrated two CNV calling methods (XHMM and ExomeDepth) to expand our set of single-gene CNVs and leveraged two different approaches for validating these variants (quantitative polymerase chain reaction and NanoString). We found a significant excess of all rare CNVs (deletions: p =.0004, duplications: p =.0006) and single-gene CNVs (deletions: p =.04, duplications: p =.03) in schizophrenia cases compared with control subjects. An expanded set of CNVs generated from integrating multiple approaches showed a significant burden of deletions in 11 of 21 gene sets previously implicated in schizophrenia and across all genes in those sets (p =.008), although no tests survived correction. We performed an extensive validation of all deletions in the significant set of voltage-gated calcium channels among CNVs called from both exome sequencing and genotyping arrays. In total, 4 exonic, single-gene deletions were validated in schizophrenia cases and none in control subjects (p =.039), of which all were identified by exome sequencing. These results point to the potential contribution of single-gene CNVs to schizophrenia, indicate that the utility of exome sequencing for CNV calling has yet to be maximized, and note that single-gene CNVs should be included in gene-focused studies using other classes of variation. [ABSTRACT FROM AUTHOR]

Inherited alleles account for most of the genetic risk for schizophrenia. However, new (de novo) mutations, in the form of large chromosomal copy number changes, occur in a small fraction of cases and disproportionally disrupt genes encoding postsynaptic proteins. Here we show that small de novo mutations, affecting one or a few nucleotides, are overrepresented among glutamatergic postsynaptic proteins comprising activity-regulated cytoskeleton-associated protein (ARC) and N-methyl-d-aspartate receptor (NMDAR) complexes. Mutations are additionally enriched in proteins that interact with these complexes to modulate synaptic strength, namely proteins regulating actin filament dynamics and those whose messenger RNAs are targets of fragile X mental retardation protein (FMRP). Genes affected by mutations in schizophrenia overlap those mutated in autism and intellectual disability, as do mutation-enriched synaptic pathways. Aligning our findings with a parallel case-control study, we demonstrate reproducible insights into aetiological mechanisms for schizophrenia and reveal pathophysiology shared with other neurodevelopmental disorders. [ABSTRACT FROM AUTHOR]

B Background: b Rare deleterious coding variants can have large effects on gene dosage potentially increasing risk for disease. B Methods: b Genome-sequencing quality control (QC) followed GATK best practices using Variant Quality Score Recalibration (VQSR) tool along with additional filtering steps. We analyzed the data from 394 samples of European descent in the Common Mind Consortium, where all samples had both genome-sequencing and RNA-sequencing of the dorsal lateral prefrontal cortex (DLPFC), anterior cingulate cortex (ACC) or both. [Extracted from the article]