Clin Cosmet Investig Dermatol
January 2025
Purpose: To investigate the correlation between the presence of the Koebner phenomenon (KP) and clinical features of patients with vitiligo.
Patients And Methods: The clinical characteristic data, including age, age of onset, disease duration, gender, clinical stage, clinical type, family history, and comorbid immune-related diseases, of 1472 patients with/without KP were analyzed with SPSS 17.0 software.
Transition metal sulfides, despite their abundance of electrochemically active sites, often demonstrate inadequate rate performance and mechanical stability. The development of a multi-dimensional hierarchical architecture has proven to be an effective approach to address the limitations associated with sulfides. In the present study, MoNiCo-S nanorods featuring hierarchical micro-/nano-structures were successfully synthesized through a straightforward methodology that involved "in situ growth-etching-vulcanization".
View Article and Find Full Text PDFThe role of heparin in sepsis therapy has been widely debated. The controversy surrounding heparin's use as an anticoagulant in sepsis may stem from differences in sepsis definitions, study designs, timing and dosage of drug administration, treatment duration, complications, and patient severity. In this study, we aimed to determine the optimal timing and dosage of heparin in patients with sepsis, identify specific subgroups that could benefit from heparin therapy, and explore laboratory markers to assess its efficacy.
View Article and Find Full Text PDFBackground: The aim of this study was to investigate the clinical characteristics of severe pneumonia caused by human bocavirus (HBoV) infection to explore the associated risk factors.
Methods: We conducted a retrospective review of data from children hospitalized with HBoV pneumonia. Based on the severity of pneumonia, patients were categorized into severe pneumonia and non-severe pneumonia groups.
The carboxyl terminus of Hsc70-interacting protein (CHIP) is pivotal for managing misfolded and aggregated proteins via chaperone networks and degradation pathways. In a preclinical rodent model of CHIP-related ataxia, we observed that CHIP mutations lead to increased levels of phosphodiesterase 9A (PDE9A), whose role in this context remains poorly understood. Here, we investigated the molecular mechanisms underlying the role of PDE9A in CHIP-related ataxia and demonstrated that CHIP binds to PDE9A, facilitating its polyubiquitination and autophagic degradation.
View Article and Find Full Text PDF