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001) and HC (MD 2.98, 95% CI [1.99, 3.98], p<.001). The CFS group reported greater anxiety pre-task than AS (MD 14.11, 95% CI [5.57, 22.65] p<.001) and HC (MD 11.19, 95% CI [2.64, 19.75], p.=007). Parental group differences showed similar patterns to the adolescents.

Lower expectations and greater anxiety regarding exercise may reflect learning from previous difficult experiences which could impact future exercise performance. GPR agonist Further examination of pre-exercise expectations and post-exercise appraisals could improve our understanding of the mechanisms by which fatigue is maintained.

Lower expectations and greater anxiety regarding exercise may reflect learning from previous difficult experiences which could impact future exercise performance. Further examination of pre-exercise expectations and post-exercise appraisals could improve our understanding of the mechanisms by which fatigue is maintained.

Self-reported symptom questionnaires are often used for identifying individuals with functional somatic disorders (FSD) in epidemiological research. Studies on their validity in establishing clinically valid cases are, however, lacking. We aimed to compare and dissect the processes of identifying participants with FSD with symptom questionnaires and FSD diagnoses established by diagnostic interviews.

Individuals from the adult Danish population (n=1590) filled in symptom questionnaires and participated in a diagnostic research interview, performed over telephone by trained family physicians. The two methods were described and compared in different steps 1) Agreement on presence of symptoms, 2) agreement after FSD symptom pattern criteria had been applied, and 3) agreement on final FSD diagnoses.

Agreement on symptom presence was high (>82%). Using FSD symptom pattern criteria, the two methods agreed in 30-62% of cases within each category. Discrepancies were mainly due to participants fulfilling sympble as screening tools and as trans-diagnostic comparison while diagnostic interviews are necessary in establishing clinically significant FSD diagnoses.

Scar characteristics analyzed by late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) are related with ventricular arrhythmias. Current guidelines are based only on the left ventricular ejection fraction to recommend an implantable cardioverter-defibrillator (ICD) in primary prevention.

Our study aims to analyze the role of imaging to stratify arrhythmogenic risk in patients with ICD for primary prevention.

From 2006 to 2017, we included 200 patients with LGE-CMR before ICD implantation for primary prevention. The scar, border zone, core, and conducting channels (CCs) were automatically measured by a dedicated software.

The mean age was 60.9 ± 10.9 years; 81.5% (163) were men; 52% (104) had ischemic cardiomyopathy. The mean left ventricular ejection fraction was 29% ± 10.1%. After a follow-up of 4.6 ± 2 years, 46 patients (22%) reached the primary end point (appropriate ICD therapy). Scar mass (36.2 ± 19 g vs 21.7 ± 10 g; P < .001), border zone mass (26.4 ± 12.5 g vs 16.0 ± 9.5 g; P < .001), core mass (9.9 ± 8.6 g vs 5.5 ± 5.7 g; P < .001), and CC mass (3.0 ± 2.6 g vs 1.6 ± 2.3 g; P < .001) were associated with appropriate therapies. Scar mass > 10 g (25.31% vs 5.26%; hazard ratio 4.74; P = .034) and the presence of CCs (34.75% vs 8.93%; hazard ratio 4.07; P = .003) were also strongly associated with the primary end point. However, patients without channels and with scar mass < 10 g had a very low rate of appropriate therapies (2.8%).

Scar characteristics analyzed by LGE-CMR are strong predictors of appropriate therapies in patients with ICD in primary prevention. The absence of channels and scar mass < 10 g can identify patients at a very low risk of ventricular arrhythmias in this population.

Scar characteristics analyzed by LGE-CMR are strong predictors of appropriate therapies in patients with ICD in primary prevention. The absence of channels and scar mass less then 10 g can identify patients at a very low risk of ventricular arrhythmias in this population.In hosts with damaged or impaired immune systems such as those undergoing hematopoietic cell transplant (HCT) or intensive chemotherapy, breakthrough fungal infections can be fatal. Risk factors for breakthrough infections include severe neutropenia, use of corticosteroids, extended use of broad-spectrum antibiotics, and intensive care unit admission. An individual's cumulative state of immunosuppression directly contributes to the likelihood of experiencing increased infection risk. Incidence of invasive fungal infection (IFI) after HCT may be up to 5-8%. Early intervention may improve IFI outcomes, although many infections are resistant to standard therapies (voriconazole, caspofungin, micafungin, amphotericin B, posaconazole or itraconazole, as single agents or in combination). We review herein several contributing factors that may contribute to the net state of immunosuppression in recipients of HCT. We also review a new approach for IFI utilizing adjunctive therapy with sargramostim, a yeast-derived recombinant human granulocyte-macrophage colony-stimulating factor (rhu GM-CSF).The 3' repair exonuclease 1 (TREX1) gene encodes a nuclear protein with 3' exonuclease activity, and the mutations have been associated with autoimmune diseases. Herein, we performed genetic analysis for the TREX1 gene in 55 patients with systemic lupus erythematosus (SLE). We identified one SLE patient with overlapping dermatomyositis having a heterozygous p.Asp130Asn mutation in the TREX1 gene. The patient had a high level of serum interferon (IFN)-α compared with that in healthy controls and other patients with SLE. In addition, the patient expressed elevated IFN signature genes compared with healthy controls. Our molecular dynamics simulation of the TREX1 protein in a complex with double-stranded DNA revealed that the D130N mutant causes significant changes in the active site's interaction network. One of our cases exhibited a heterozygous TREX1 p.Asp130Asn mutation that contributed to the type I IFN pathway, which may lead to the development of a severe SLE phenotype.