ABSTRACT
BACKGROUND: Abdominal wall reconstruction (AWR) is a treatment option for structural defects of the abdominal wall. The most frequently cited publications related to AWR have not been quantitatively or qualitatively assessed. This bibliometric analysis characterizes and assesses the most frequently cited AWR publications, to identify trends, gaps, and guide future efforts for the international research community. METHODS: The 100 most cited publications in AWR were identified on Web of Science, across all available journal years (from May 1964 to December 2023). Study details, including the citation count, main content focus, and outcome measures, were extracted and tabulated from each publication. Oxford Centre for Evidence-Based Medicine levels of evidence (LOE) of each study were also assessed. RESULTS: The 100 most cited publications in AWR were cited by a total of 9674 publications. Citations per publication ranged from 43 to 414 (mean 96.7 ± 52.48). Most publications were LOE 3 (n = 60), representative of the large number of retrospective cohort studies. The number of publications for LOE 5, 4, 3, 2, and 1 was 21, 2, 60, 2, and 12, respectively. The main content focus was surgical technique in 44 publications followed by outcomes in 38 publications. Patient-reported outcome measures were used in 3 publications, and no publications reported validated esthetic outcome measures. CONCLUSIONS: Overall, 3 was the LOE for most frequently cited AWR publications, with more publications below LOE 3 than above LOE 3. Validated outcome measures and patient-reported outcome measures were infrequently incorporated in the studies evaluated.
ABSTRACT
BACKGROUND: Increasing evidence supports a key role for peripheral immune processes in the pathophysiology of Alzheimer's disease (AD), highlighting an intricate interplay between brain resident glial cells and both innate and adaptive peripheral immune effectors. We previously showed that regulatory T cells (Tregs) have a beneficial impact on disease progression in AD-like pathology, notably by modulating the microglial response associated with Aß deposits in a mouse model of amyloid pathology. Besides microglia, reactive astrocytes also play a critical role in neuroinflammatory processes associated with AD. Different phenotypes of reactive astrocytes have previously been characterized, including A1-like neurotoxic and A2-like neuroprotective subtypes. However, the precise impact of Tregs on astrocyte reactivity and phenotypes in AD still remains poorly defined. METHODS: We assessed the impact of Treg immunomodulation on astrocyte reactivity in a mouse model of AD-like amyloid pathology. Using 3D imaging, we carried out extensive morphological analyses of astrocytes following either depletion or amplification of Tregs. We further assessed the expression of several A1- and A2-like markers by immunofluorescence and RT-qPCR. RESULTS: Modulation of Tregs did not significantly impact the magnitude of global astrocyte reactivity in the brain nor in the close vicinity of cortical amyloid deposits. We did not observe changes in the number, morphology, or branching complexity of astrocytes according to immunomodulation of Tregs. However, early transient depletion of Tregs modulated the balance of reactive astrocyte subtypes, resulting in increased C3-positive A1-like phenotypes associated with amyloid deposits. Conversely, early depletion of Tregs decreased markers of A2-like phenotypes of reactive astrocytes associated with larger amyloid deposits. Intriguingly, modulation of Tregs also impacted the cerebral expression of several markers of A1-like subsets in healthy mice. CONCLUSIONS: Our study suggests that Tregs contribute to modulate and fine-tune the balance of reactive astrocyte subtypes in AD-like amyloid pathology, by dampening C3-positive astrocytes in favor of A2-like phenotypes. This effect of Tregs may partly relate to their capacity at modulating steady state astrocyte reactivity and homeostasis. Our data further highlight the need for refined markers of astrocytes subsets and strategy of analysis for better deciphering the complexity of astrocyte reactivity in neurodegeneration.
