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ContextDespite the recognition of attention deficit hyperactivity disorder (ADHD) as a multifaceted neurodevelopmental disorder, its core causes are still ambiguous. The objective of this study was to explore if the traits of circulating immune cells contribute causally to susceptibility to ADHD.MethodsBy employing a unified GWAS summary data covering 731 immune traits from the GWAS Catalog (accession numbers from GCST0001391 to GCST0002121), our analysis focused on the flow cytometry of lymphocyte clusters, encompassing 3,757 Sardinians, to identify genetically expected immune cells. Furthermore, we obtained summarized GWAS statistics from the Psychiatric Genomics Consortium to evaluate the genetic forecasting of ADHD. The studies employed ADHD2019 (20,183 cases and 35,191 controls from the 2019 GWAS ADHD dataset) and ADHD2022 (38,691 cases and 275,986 controls from the 2022 GWAS ADHD dataset). Through the examination of genome-wide association signals, we identified shared genetic variances between circulating immune cells and ADHD, employing the comprehensive ADHD2022 dataset. We primarily utilized inverse variance weighted (IVW) and weighted median methods in our Mendelian randomization research and sensitivity assessments to evaluate diversity and pleiotropy.ResultsAfter adjusting for false discovery rate (FDR), three distinct immunophenotypes were identified as associated with the risk of ADHD: CD33 in Im MDSC (OR=1.03, CI: 1.01~1.04, P=3.04×10−5, PFDR=0.015), CD8br NKT %T cell (OR=1.08, 95%CI: 1.04~1.12, P=9.33×10−5, PFDR=0.023), and CD8br NKT %lymphocyte (OR=1.08, 95%CI: 1.03~1.12, P=3.59×10−4, PFDR=0.066). Furthermore, ADHD showed no statistical effects on immunophenotypes. It’s worth noting that 20 phenotypes exist where ADHD’s appearance could diminish 85% of immune cells, including FSC-A in myeloid DC (β= -0.278, 95% CI: 0.616~0.931, P=0.008), CD3 in CD45RA- CD4+ (β= -0.233, 95% CI: 0.654~0.960, P=0.017), CD62L- monocyte AC (β=0.227, 95% CI: 0.038~1.518, P=0.019), CD33 in CD33br HLA DR+ CD14dim (β= -0.331, 95% CI: 0.543~0.950, P=0.020), and CD25 in CD39+ resting Treg (β=0.226, 95% CI: 1.522, P=0.022), and FSC-A in monocytes (β= -0.255, 95% CI: 0.621~0.967, P=0.234), among others.ConclusionStudies indicate that the immune system’s response influences the emergence of ADHD. The findings greatly improve our understanding of the interplay between immune responses and ADHD risk, aiding in the development of treatment strategies from an immunological perspective.

To prove that calcium alginate beads can be used as scaffolds during in vitro culture.

ContextCortisol, a hormone regulated by the hypothalamic-pituitary-adrenal (HPA) axis, has been linked to attention deficit hyperactivity disorder (ADHD). The nature of the relationship between cortisol and ADHD, and whether it is causal or explained by reverse causality, remains a matter of debate.ObjectiveThis study aims to evaluate the bidirectional causal relationship between morning plasma cortisol levels and ADHD.MethodsThis study used a bidirectional 2-sample Mendelian randomization (MR) design to analyze the association between morning plasma cortisol levels and ADHD using genetic information from the authoritative Psychiatric Genomics Collaboration (PGC) database (n = 55,347) and the ADHD Working Group of the CORtisol NETwork (CORNET) Consortium (n = 12,597). MR analyses were employed: inverse variance weighting (IVW), MR-Egger regression, and weighted medians. OR values and 95% CI were used to evaluate whether there was a causal association between morning plasma cortisol levels on ADHD and ADHD on morning plasma cortisol levels. The Egger-intercept method was employed to test for level pleiotropy. Sensitivity analysis was performed using the “leave-one-out” method, MR pleiotropy residual sum, and MR pleiotropy residual sum and outlier (MR-PRESSO).ResultsFindings from bidirectional MR demonstrated that lower morning plasma cortisol levels were associated with ADHD (ADHD-cortisol OR = 0.857; 95% CI, 0.755–0.974; P = 0.018), suggesting there is a reverse causal relationship between cortisol and ADHD. However, morning plasma cortisol levels were not found to have a causal effect on the risk of ADHD (OR = 1.006; 95% CI, 0.909–1.113; P = 0.907), despite the lack of genetic evidence. The MR-Egger method revealed intercepts close to zero, indicating that the selected instrumental variables had no horizontal multiplicity. The “leave-one-out” sensitivity analysis revealed stable results, with no instrumental variables significantly affecting the results. Heterogeneity tests were insignificant, and MR-PRESSO did not detect any significant outliers. The selected single-nucleotide polymorphisms (SNPs) F were all >10, indicating no weak instrumental variables. Thus, the overall MR analysis results were reliable.ConclusionThe study findings suggest a reverse causal relationship between morning plasma cortisol levels and ADHD, with low cortisol levels associated with ADHD. No genetic evidence was found to support a causal relationship between morning plasma cortisol levels and the risk of ADHD. These results suggest that ADHD may lead to a significant reduction in morning plasma cortisol secretion.

Key Clinical Message: This case illustrates that under comprehensive management of individual and clinical needs, urgent‐start peritoneal dialysis can be performed safely without bleeding complications in patients with hemophilia A who developed end‐stage renal disease. Patients in these cases can benefit from synthetic strategy. Hemophilia A is a serious inherited bleeding disorder resulting from a deficiency of coagulation factor VIII (FVIII). Chronic kidney disease (CKD) involvement in hemophilia is relatively rare, but there has been an upward trend in the survival time of patients with prolonged hemophilia. Although peritoneal dialysis (PD) is often used as the first treatment modality for renal replacement treatment, limited data are available on comprehensive management in the hemophilia A population, especially for urgent‐start PD. A 56‐year‐old man who had hemophilia A, was diagnosed with CKD 3 years ago and developed end‐stage renal disease was admitted to our hospital after contracting pneumonia and undergoing subsequent Type I respiratory failure. Urgent‐start PD improved his condition and health outcomes, and protected his residual renal function. This case is the first study of a Chinese male patient with hemophilia A who developed end‐stage renal disease. We summarize the clinical treatment and nursing care strategies of urgent‐start PD in a hemophilia A patient with end‐stage renal disease. This case illustrates that under comprehensive management of individual and clinical needs, urgent‐start PD can be performed safely without bleeding complications in patients with hemophilia A. [ABSTRACT FROM AUTHOR]

The reactivity of the open-shell Gd@C2v-C82 with different charge states towards benzyl bromide was investigated. [Gd@C2v-C82]3− exhibited enhanced activity relative to Gd@C2v-C82 and [Gd@C2v-C82]−. The structural characterizations, including MALDI-TOF MS, UV-vis-NIR, and single crystal X-ray diffraction, indicate the formation of isomeric benzyl monoadducts of Gd@C2v-C82. All three monoadducts contain 1:1 mirror-symmetric enantiomers. Additionally, the addition of the benzyl group and its specific position result in distinct electrochemical behavior of the products compared to the parent Gd@C2v-C82. Theoretical studies demonstrate that only [Gd@C2v-C82]3− has a HOMO energy level that matches well with the LUMO energy level of the PhCH2 radical, providing a rationalization for the observed significantly different reactivity. [ABSTRACT FROM AUTHOR]