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Sarcoidosis is an inflammatory disease that involves the eyes in 10–55% of cases, sometimes without systemic involvement. All eye structures can be affected, but uveitis is the most common ocular manifestation and causes vision loss. The typical ophthalmological appearance of these uveitis is granulomatous (in cases with anterior involvement), which are usually bilateral and with synechiae. Posterior involvement includes vitritis, vasculitis and choroidal lesions. Tuberculosis is a classic differential diagnosis to be wary of, especially in people who have spent time in endemic areas. The diagnosis is based on histology with the presence of non-caseating epithelioid granulomas. However, due to the technical difficulty and yield of biopsies, the diagnosis of ocular sarcoidosis is often based on clinico-radiological features. The international criteria for the diagnosis of ocular sarcoidosis have recently been revised. Corticosteroids remain the first-line treatment for sarcoidosis, but up to 30% of patients require high doses, justifying the use of corticosteroid-sparing treatments. In these cases, immunosuppressive treatments such as methotrexate may be introduced. More recent biotherapies such as anti-TNF are also very effective (as they are in other non-infectious uveitis etiologies).

Still’s disease (SD) is a heterogeneous autoinflammatory disorder for which several phenotypes have been described. We conducted a retrospective study to re-evaluate the dichotomous view of the disease, to compare the juvenile and adult forms, and to look for prognostic factors. We collected data from ten French centers, seeking patients with a diagnosis of adult-onset SD (AOSD) or systemic juvenile idiopathic arthritis (sJIA). We identified 238 patients, 152 (64%) of whom had AOSD while 86 (36%) had sJIA. The median age at SD onset was 26.6 years. In patients with identifiable patterns, the course of SD was systemic in 159 patients (74%), chronic in 55 (26%). Sore throat and myalgia were more frequent in patients with AOSD. Abnormal liver tests, serum ferritin and C-reactive protein levels were higher in AOSD group. Fever and skin rash were predictive of complete remission or recovery and high lactate dehydrogenase level was a poor prognosis factor. Symptoms such as splenomegaly, skin rash, high polymorphonuclear neutrophils count and macrophage activation syndrome were predictive of a systemic phenotype. Overall, there were no major differences between sJIA and AOSD. Our results are consistent with the “biphasic” model of an autoinflammatory disease that can progress to chronic arthritis if not treated early.

Hemophagocytic lymphohistiocytosis is a hyperinflammatory syndrome characterized by uncontrolled activation of immune cells and mediators. Two diagnostic tools are widely used in clinical practice: the HLH-2004 criteria and the Hscore. Despite their good diagnostic performance, these scores were constructed after a selection of variables based on expert consensus. We propose here a machine learning approach to build a classification model for HLH in a cohort of patients selected by glycosylated ferritin dosage in our tertiary center in Lyon, France. On a dataset of 207 adult patients with 26 variables, our model showed good overall diagnostic performances with a sensitivity of 71.4% and high specificity, and positive and negative predictive values which were 100%, 100%, and 96.9%, respectively. Although generalization is difficult on a selected population, this is the first study to date to provide a machine-learning model for HLH detection. Further studies will be required to improve the machine learning model performances with a large number of HLH cases and with appropriate controls.

The significance of extreme hyperferritinemia and its association with certain diagnoses and prognoses are not well characterized. We performed a retrospective analysis of adult patients with at least one total serum ferritin (TSF) measurement ≥ 5000 µg/L over 2 years, in three university hospitals. Conditions associated with hyperferritinemia were collected, and patients were classified into 10 etiological groups. Intensive care unit (ICU) transfer and mortality rates were recorded. A total of 495 patients were identified, of which 56% had a TSF level between 5000 and 10,000 µg/L. There were multiple underlying causes in 81% of the patients. The most common causes were infections (38%), hemophagocytic lymphohistiocytosis (HLH, 18%), and acute hepatitis (14%). For TSF levels > 10,000 µg/L, there were no solid cancer or hematological malignancy without another cause of hyperferritinemia. Isolated iron-overload syndromes never exceeded TSF levels > 15,000 µg/L. Extreme hyperferritinemia (TSF levels > 25,000 µg/L) was associated with only four causes: HLH, infections, acute hepatitis and cytokine release syndromes. A total of 32% of patients were transferred to an ICU, and 28% died. Both ICU transfer rate and mortality were statistically associated with ferritin levels. An optimized threshold of 13,405 μg/L was the best predictor for the diagnosis of HLH, with a sensitivity of 76.4% and a specificity of 79.3%. Hyperferritinemia reflects a variety of conditions, but only four causes are associated with extreme hyperferritinemia, in which HLH and acute hepatitis are the most common. Extreme hyperferritinemia has a poor prognosis with increased mortality.

First of all, we would like to thank all of the authors for their contributions and the editorial staff who enabled the achievement of this «Diagnosis and Management of Non-infectious Uveitis: Old and New Challenges» Special Issue [...]

Glycosylated ferritin (GF) has been reported as a good diagnostic biomarker for adult-onset Still’s disease (AOSD), but only a few studies have validated its performance. We performed a retrospective study of all adult patients with at least one GF measurement over a 2-year period in one hospital laboratory. The diagnosis of AOSD was based on the expert opinion of the treating physician and validated by two independent investigators. Patients’ characteristics, disease activity, and outcome were recorded and compared. Twenty-eight AOSD and 203 controls were identified. Compared to controls, the mean GF was significantly lower (22.3% vs. 39.3, p < 0.001) in AOSD patients. GF had a high diagnostic accuracy for AOSD, independent of disease activity or total serum ferritin (AUC: 0.674 to 0.915). The GF optimal cut-off value for AOSD diagnosis was 16%, yielding a specificity of 89% and a sensitivity of 63%. We propose a modified diagnostic score for AOSD, based on Fautrel’s criteria but with a GF threshold of 16% that provides greater specificity and increases the positive predictive value by nearly 5 points. GF is useful for ruling out differential diagnoses and as an appropriate classification criterion for use in AOSD clinical trials.

Sarcoidosis is a systemic disease of unknown etiology, characterized by the presence of non-caseating granulomas in various organs, mainly the lungs, and the lymphatic system. Since the individualization of sarcoidosis-lymphoma association by Brincker et al., the relationship between sarcoidosis or granulomatous syndromes and malignancies has been clarified through observational studies worldwide. Two recent meta-analyses showed an increased risk of neoplasia in sarcoidosis. The granulomatosis can also reveal malignancy, either solid or hematological, defining paraneoplastic sarcoidosis. Recent cancer immunotherapies, including immune checkpoint inhibitors (targeting PD-1, PD-L1, or CTLA-4) and BRAF or MEK inhibitors were also reported as possible inducers of sarcoidosis-like reactions. Sarcoidosis and neoplasia, especially lymphoma, can show overlapping presentations, thus making the diagnosis and treatment harder to deal with. There are currently no formal recommendations to guide the differential diagnosis workup between the evolution of lymphoma or a solid cancer and a granulomatous reaction associated with neoplasia. Thus, in atypical presentations (e.g., deeply impaired condition, compressive lymphadenopathy, atypical localization, unexplained worsening lymphadenopathy, or splenomegaly), and treatment-resistant disease, targeted biopsies on suspect localizations with histological examination could help the clinician to differentiate neoplasia from sarcoidosis. Pathological diagnosis could sometimes be challenging since very few tumor cells may be surrounded by massive granulomatous reaction. The sensitization of currently available diagnostic tools should improve the diagnostic accuracy, such as the use of more “cancer-specific” radioactive tracers coupled with Positron Emission Tomography scan.

Distinguishing between macrophage activation syndrome (MAS) and a simple flare of Still’s disease (SD) may be challenging. We sought to clarify the clinical features and outcome of MAS in SD and to explore predictive factors of MAS development. Demographic and clinical data, treatments, and outcomes were recorded in a cohort of 206 SD patients. SD patients with and without MAS were compared. To explore predictive factors for the development of MAS, patients were compared at the time of SD diagnosis. Twenty (9.7%) patients experienced MAS, which was inaugural in 12 cases. Patients with MAS were more likely to have hepatomegaly (OR, 3.71; 95% CI, 1.14–11.2; p = 0.03) and neurological symptoms (OR, 4.43; 95% CI, 1.08–15.3; p = 0.04) than patients without MAS. Cytopenias, abnormal liver tests, and coagulation disorders were significantly more frequent in patients with MAS; lactate dehydrogenase and serum ferritin levels were significantly higher. An optimized threshold of 3500 μg/L for serum ferritin yielded a sensitivity (Se) of 85% and a negative predictive value (NPV) of 97% for identifying patients with/without MAS. Survival analysis showed that a high ferritin level at the time of SD diagnosis was predictive of MAS development (p < 0.001). Specific factors, including neurological symptoms, cytopenias, elevated LDH, and coagulopathy, may contribute to the early detection of MAS. Extreme hyperferritinemia at the onset of SD is a prognostic factor for the development of MAS.

Sarcoidosis is a multisystem disease characterized by the development and accumulation of granulomas, the hallmark of an inflammatory process induced by environmental and/or infectious and or genetic factors. This auto-inflammatory disease mainly affects the lungs, the gateway to environmental aggressions and viral infections. We have shown previously that genetic predisposition to sarcoidosis occurring in familial cases is related to a large spectrum of pathogenic variants with, however, a clustering around mTOR (mammalian Target Of Rapamycin)-related pathways and autophagy regulation. The context of the COVID-19 pandemic led us to evaluate whether such genetic defects may increase the risk of a severe course of SARS-CoV2 infection in patients with sarcoidosis. We extended a whole exome screening to 13 families predisposed to sarcoidosis and crossed the genes sharing mutations with the list of genes involved in the SARS-CoV2 host-pathogen protein-protein interactome. A similar analysis protocol was applied to a series of 100 healthy individuals. Using ENRICH.R, a comprehensive gene set enrichment web server, we identified the functional pathways represented in the set of genes carrying deleterious mutations and confirmed the overrepresentation of autophagy- and mitophagy-related functions in familial cases of sarcoidosis. The same protocol was applied to the set of genes common to sarcoidosis and the SARS-CoV2-host interactome and found a significant enrichment of genes related to mitochondrial factors involved in autophagy, mitophagy, and RIG-I-like (Retinoic Acid Inducible Gene 1) Receptor antiviral response signaling. From these results, we discuss the hypothesis according to which sarcoidosis is a model for studying genetic abnormalities associated with host response to viral infections as a consequence of defects in autophagy and mitophagy processes.

Sarcoidosis is a systemic granulomatous disease of unknown cause characterized by a wide variety of presentations. Its diagnosis is based on three major criteria: a clinical presentation compatible with sarcoidosis, the presence of non-necrotizing granulomatous inflammation in one or more tissue samples, and the exclusion of alternative causes of granulomatous disease. Many conditions may mimic a sarcoid-like granulomatous reaction. These conditions include infections, neoplasms, immunodeficiencies, and drug-induced diseases. Moreover, patients with sarcoidosis are at risk of developing opportunistic infections or lymphoma. Reliably confirming the diagnosis of sarcoidosis and better identifying new events are major clinical problems in daily practice. To address such issues, we present seven emblematic cases, seen in our department, over a ten-year period along with a literature review about case reports of conditions misdiagnosed as sarcoidosis.

Leigh P Brody,1,* Meliz Sahuri-Arisoylu,1,* James R Parkinson,1 Harry G Parkes,2 Po Wah So,3 Nabil Hajji,4 E Louise Thomas,1 Gary S Frost,5 Andrew D Miller,6,* Jimmy D Bell1,* 1Department of Life Sciences, Faculty of Science and Technology, University of Westminster, 2CR-UK Clinical MR Research Group, Institute of Cancer Research, Sutton, Surrey, 3Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, 4Department of Medicine, Division of Experimental Medicine, Centre for Pharmacology & Therapeutics, Toxicology Unit, Imperial College London, 5Faculty of Medicine, Nutrition and Dietetic Research Group, Division of Diabetes, Endocrinology and Metabolism, Department of Investigative Medicine, Imperial College London, Hammersmith Hospital, 6Institute of Pharmaceutical Science, King’s College London, London, UK *These authors contributed equally to this work Abstract: Metabolic reengineering using nanoparticle delivery represents an innovative therapeutic approach to normalizing the deregulation of cellular metabolism underlying many diseases, including cancer. Here, we demonstrated a unique and novel application to the treatment of malignancy using a short-chain fatty acid (SCFA)-encapsulated lipid-based delivery system – liposome-encapsulated acetate nanoparticles for cancer applications (LITA-CAN). We assessed chronic in vivo administration of our nanoparticle in three separate murine models of colorectal cancer. We demonstrated a substantial reduction in tumor growth in the xenograft model of colorectal cancer cell lines HT-29, HCT-116 p53+/+ and HCT-116 p53-/-. Nanoparticle-induced reductions in histone deacetylase gene expression indicated a potential mechanism for these anti-proliferative effects. Together, these results indicated that LITA-CAN could be used as an effective direct or adjunct therapy to treat malignant transformation in vivo. Keywords: lipid-based nanoparticles, liposomes, cancer, short-chain fatty acids, epigenetics

Sarcoidosis is a multi-system disease of unknown etiology characterized by the formation of granulomas in various organs. It affects people of all ethnic backgrounds and occurs at any time of life but is more frequent in African Americans and Scandinavians and in adults between 30 and 50 years of age. Sarcoidosis can affect any organ with a frequency varying according to ethnicity, sex and age. Intrathoracic involvement occurs in 90% of patients with symmetrical bilateral hilar adenopathy and/or diffuse lung micronodules, mainly along the lymphatic structures which are the most affected system. Among extrapulmonary manifestations, skin lesions, uveitis, liver or splenic involvement, peripheral and abdominal lymphadenopathy and peripheral arthritis are the most frequent with a prevalence of 25–50%. Finally, cardiac and neurological manifestations which can be the initial manifestation of sarcoidosis, as can be bilateral parotitis, nasosinusal or laryngeal signs, hypercalcemia and renal dysfunction, affect less than 10% of patients. The diagnosis is not standardized but is based on three major criteria: a compatible clinical and/or radiological presentation, the histological evidence of non-necrotizing granulomatous inflammation in one or more tissues and the exclusion of alternative causes of granulomatous disease. Certain clinical features are considered to be highly specific of the disease (e.g., Löfgren’s syndrome, lupus pernio, Heerfordt’s syndrome) and do not require histological confirmation. New diagnostic guidelines were recently published. Specific clinical criteria have been developed for the diagnosis of cardiac, neurological and ocular sarcoidosis. This article focuses on the clinical presentation and the common differentials that need to be considered when appropriate.

Spondyloarthritis (Spa), Behçet’s disease (BD) and sarcoidosis are major systemic inflammatory diseases worldwide. They are all multisystem pathologies and share a possible ocular involvement, especially uveitis. We hereby describe selected cases who were referred by ophthalmologists to our internal medicine department for unexplained uveitis. Physical examination and/or the use of laboratory and imaging investigations allowed to make a diagnosis of a systemic inflammatory disease in a large proportion of patients. In our tertiary referral center, 75 patients have been diagnosed with Spa (n = 20), BD (n = 9), or sarcoidosis (n = 46) in the last two years. There was a significant delay in the diagnosis of Spa-associated uveitis. Screening strategies using Human Leukocyte Antigen (HLA)-B27 determination and sacroiliac magnetic resonance imaging in patients suffering from chronic low back pain and/or psoriasis helped in the diagnosis. BD’s uveitis affects young people from both sexes and all origins and usually presents with panuveitis and retinal vasculitis. The high proportion of sarcoidosis in our population is explained by the use of chest computed tomography (CT) and 18F-fluorodeoxyglucose positron emission tomography CT that helped to identify smaller hilar or mediastinal involvement and allowed to further investigate those patients, especially in the elderly. Our results confirm how in these sight- and potentially life-threatening diseases a prompt diagnosis is mandatory and benefits from a multidisciplinary approach.

This article uses interviews of long-standing neighborhood residents' sentiments of university expansion into their community. These data provide persuasive empirical evidence for the need of urban anchor institutions to include as an integral component of their campus reopening efforts, intentional plans for reducing the disruption of housing patterns of permanent residents. The term "COVID exposure" has come to signify not only the potential to succumb to the virus, but it also implies the revealing of inequities in systems that impact the effects of the crisis within Black and Brown communities. Every sector of U.S. society has been impacted by COVID-19, and it has required a paradigm shift in our interactions with one another. Academic institutions are enacting robust de-densification efforts which will stimulate dramatic shifts in the off-campus housing needs for students, but they stand the chance of displacing or further disadvantaging the long-standing residents who reside outside of their campus border. Universities must use reopening plans as an instrument to change the trajectory of relationships they hope to cultivate with their long-standing neighbors, through renewed engagement efforts that integrate lessons from the past and that seek to build stronger neighborhoods by challenging housing inequity and housing inequality.

This phenomenological case study examined the emergence of critical scholar identities among five urban youth who participated in a 2-year critical research fellows program. The program was grounded on the theoretical framework of Social Justice Youth Development, which included the development of self, social/community, and global awareness leading to critical consciousness and social action. Findings depict the personal and programmatic components of nurturing urban youth's critical scholar identities and contribute to the growing body of literature in critical youth studies and scholar identity development with marginalized urban youth.

Educational researchers and practitioners have cited the need for new directions in youth leadership studies as it relates to globalization. Globalization is considered one of the most important economic, cultural, and social trends of the last century, yet there is much debate about the educational curricula that best support the development of global leadership in youth. Most existing global-focused programs (i.e. IB/AP) engender grave inequities in access and opportunities, particularly for urban youth, and do not often allow youth to critically interrogate the myriad injustices that plague the world. There is, however, a burgeoning body of scholarship centered on critical youth studies as a transformative process for youth development. This phenomenological case study shares the findings from the Urban Youth Scholars program, an after-school program focused on cultivating the global leadership development of five youth in the program. This study utilized a Social Justice Youth Development framework to explore the development of the youth's self, social/community, and global awareness through critical consciousness building and critical social analysis. Findings depict youth perceptions of global leadership development and include implications for scholars and practitioners for centering youth-led justice-oriented research as a tool for global leadership development.

Objectives To analyse genetic mechanisms triggering familial sarcoidosis, whole exome screening of a family of six persons with four cases of sarcoidosis and two healthy controls was performed integrating progressive and spontaneous remission cases and evaluating involved genetic alterations that could potentially determine the individual course of the disease. Methods Clinical diagnostic criteria in patients of the selected sarcoidosis family were according to American Thoracic Society/European Respiratory Society/World Association of Sarcoidosis and other Granulomatous Disorders guidelines. Exome screening of four patients and the two intrafamilial healthy relatives was performed by paired-end (2 × 100 bp) sequencing. We then selected the gene variants considered pathogenic on the basis of a series of prediction software applications and presence only in members of the family affected by sarcoidosis, after subtracting the common variations observed in healthy subjects. Results Four persons out of six family members were affected by sarcoidosis. Fifty genes with uncommon in silico pathogenic variants could be identified that differentiated affected and healthy family members. One patient with sarcoidosis showed spontaneous remission whereas the remaining three patients required immunosuppressive treatment. Subtraction analysis revealed 18 genes that distinguished the three progressive cases from the patient with spontaneous remission. Conclusion The genetic analysis of these cases with familial sarcoidosis identified several involved genes and functional pathways that could help in understanding the basic mechanisms that determine the development of the disease and that discriminate spontaneously regressive and progressive forms. [ABSTRACT FROM AUTHOR]

Single crystals of YbAlB4 were grown in excess Al flux. Plate- and needle-shaped crystals were found. The plates are found to be ß-YbAlB4, which crystallizes with the ThMoB4 structure type in space group Cmmm (No. 65), Z = 4, with lattice parameters of a = 7.3080(4), b = 9.3150(5), and c = 3.4980(2) Å. The needle-shaped crystals were identified as the first form of YbAlB4 which crystallizes with the YCrB4 structure type in space group Pbam (No. 55), Z = 4, with lattice parameters of a = 5.9220(2), b = 11.4730(3), and c = 3.5060(5) Å. While both compounds have heavy fermion ground states with Isinglike magnetic anisotropy, the electronic specific heat coefficients (γ) differ. The ß-phase has a γ value near 300 mJ mol -1 K-2, more than twice that of the α-phase, γ = 130 mJ mol-1 K-2. A comparison of the structures and physical properties of both polymorphs is presented. © 2007 American Chemical Society.

The crystal structures of three new intermetallic ternary compounds in the LnNiSb 3 (Ln=Pr, Nd and Sm) family have been characterized by single crystal X-ray diffraction. PrNiSb 3, NdNiSb 3 and SmNiSb 3 all crystallize in an orthorhombic space group, Pbcm (No. 57), Z=12, with a=12.5700(2)Å, b=6.2010(4)Å, c=18.670(6)Å, and V=1431.64(11)Å3; a=12.5090(2)Å, b=6.1940(3)Å, c=18.3350(6)Å, and V=1420.61(9)Å3; and a=12.3900(1)Å, b=6.1760(3)Å, c=18.2650(6)Å, and V=1397.65(8)Å3, for Ln=Pr, Nd and Sm, respectively. These compounds consist of rare-earth atoms located above and below layers of nearly square, buckled Sb nets, along with layers of highly distorted edge- and face-sharing NiSb 6 octahedra. Resistivity data indicate metallic behavior for all three compounds. Magnetization measurements show antiferromagnetic behavior with TN=4.5K (PrNiSb 3), 4.6 K (NdNiSb 3), and 2.9 K (SmNiSb 3). Effective moments of 3.62 μ B, 3.90 μ B and 0.80 μ B are found for PrNiSb 3, NdNiSb 3 and SmNiSb 3, respectively, and are consistent with Pr 3+ (f 2), Nd 3+ (f 3), and Sm 3+ (f 4). Structure of PrNiSb 3 viewed down the b-axis containing Pr atoms (gray circles) located between layers of nearly square Sb nets and highly distorted Ni-centered octahedra. © 2004 Elsevier Inc. All rights reserved.

Abstract Steroid-induced neuropsychiatric sequelae are common, and pose significant risks to people usually receiving glucocorticoids in the context of physical illness. Steroid-induced mania and hypomania are the most common of the acute complications, yet despite great progress in understandings in neurophysiology there are no recent studies which review the factors which might predict who will experience this severe complication, nor are there consensus guidelines on management. We report the unusual case of a woman in her 50s admitted to a psychiatric unit with steroid-induced mania despite compliance with two mood stabilisers, several days after the administration of a Dexamethasone and Docetaxel chemotherapy regime adjunctive to lumpectomy for breast cancer. She had previously been diagnosed with an organic affective disorder (with classical bipolar 1 pattern) following severe ventriculitis related to ventricular drain insertion for obstructive hydrocephalus secondary to a colloid cyst. She had no psychiatric illness before this brain injury, but has a maternal history of idiopathic bipolar 1 affective disorder. Her episode of steroid-induced mania resolved following use of sedative medications, continuation of her existing mood stabilisers, and reductions of the steroid dosing in collaboration with her oncology team, which also protected her from further manic relapses during continued chemotherapy. Established mental illness, a family history, and acquired brain injury may reflect risk factors for steroid-induced mania through currently unclear pathways. Future epidemiological studies could better confirm these observations, and basic neuroscience may look to further explore the role of extrinsic glucocorticoids in the pathophysiology of affective disorders.

Abstract Tissue characterisation using T1 mapping has become an established magnetic resonance imaging (MRI) technique to detect myocardial diseases. This retrospective study aimed to determine the influence of left bundle branch block (LBBB) on T1 mapping at 1.5 T. Datasets of 36 patients with LBBB and 27 healthy controls with T1 mapping (Modified Look-Locker inversion-recovery (MOLLI), 5(3)3 sampling) were included. T1 relaxation times were determined on mid-cavity short-axis images. R2 maps were generated as a pixel-wise indicator for the goodness of the fit of T1 maps. R2 values were significantly lower in patients with LBBB than in healthy controls (whole myocardium/septum, 0.997, IQR, 0.00 vs. 0.998, IQR, 0.00; p = 0.008/0.998, IQR, 0.00 vs. 0.999, IQR, 0.00; p = 0.027). Manual correction of semi-automated evaluation tended to improve R2 values but not significantly. Strain analysis was performed and the systolic dyssynchrony index (SDIglobal) was calculated as a measure for left ventricular dyssynchrony. While MRI is generally prone to artefacts, lower goodness of the fit in LBBB may be mainly attributable to asynchronous contraction. Therefore, careful checking of the source data and, if necessary, manual post-processing is important. New techniques might improve the goodness of the fit of T1 mapping by reducing sampling in the motion prone diastole of LBBB patients.

We, the QUARTET Collaboration, propose an experiment to measure the nuclear charge radii of light elements with up to 20 times higher accuracy. These are essential both for understanding nuclear physics at low energies, and for experimental and theoretical applications in simple atomic systems. Such comparisons advance the understanding of bound-state quantum electrodynamics and are useful for searching for new physics beyond the Standard Model. The energy levels of muonic atoms are highly susceptible to nuclear structure, especially to the mean square charge radius. The radii of the lightest nuclei (with the atomic number, Z=1,2) have been determined with high accuracy using laser spectroscopy in muonic atoms, while those of medium mass and above were determined using X-ray spectroscopy with semiconductor detectors. In this communication, we present a new experiment, aiming to obtain precision measurements of the radii of light nuclei 3≤Z≤10 using single-photon energy measurements with cryogenic microcalorimeters; a quantum-sensing technology capable of high efficiency with outstanding resolution for low-energy X-rays.

Abstract Soldiers may be exposed to traumatic stress during combat deployment and thus are at risk for developing posttraumatic stress disorder (PTSD). Genetic and epigenetic evidence suggests that PTSD is linked to forming stress-related memories. In the current study, we investigated post-deployment associations of PTSD symptoms with differential DNA methylation in a sample of Burundian soldiers returning from the African Union Mission in Somalia’s war zone. We used a matched longitudinal study design to explore epigenetic changes associated with PTSD symptoms in N = 191 participants. PTSD symptoms and saliva samples were collected at 1–3 (t1) and 9–14 months (t2) after the return of the soldiers to their home base. Individuals with either worsening or improving PTSD symptoms were matched for age, stressful, traumatic and self-perpetrated events prior to the post-assessment, traumatic and violent experiences between the post- and the follow-up assessment, and violence experienced during childhood. A mixed model analysis was conducted to identify top nominally significantly differentially methylated genes, which were then used to perform a gene enrichment analysis. The linoleic acid metabolism pathway was significantly associated with post-deployment PTSD symptoms, after accounting for multiple comparisons. Linoleic acid has been linked to memory and immune related processes in previous research. Our findings suggest that differential methylation of linoleic acid pathway genes is associated with PTSD and thus may merit closer inspection as a possible mediator of resilience.