Background: Preoperative neck ultrasonography (US) may detect nodal metastases of papillary thyroid carcinoma (PTC) but its utility in detecting metastases at specific neck subsites and levels is not known. We therefore evaluated preoperative US in detecting cervical metastases of PTC according to neck subsites and levels. Methods: Preoperative US was performed in 133 new patients to detect metastases at three central cervical subsites and five lateral cervical levels. All patients underwent total thyroidectomy and bilateral central neck dissection. Thirty-four patients with lateral nodal metastases underwent modified radical neck dissection. Results: Lymph node metastases to the central and lateral cervical compartments were identified in 57.9% and 25.6%, respectively. The sensitivity and specificity of US for detecting central nodal metastasis were 61.0% and 92.8%, respectively. In the lateral neck, US detected nonpalpable lymph node metastases in 6 of 34 patients (17.6%). Overall, US was >85.0% specific at all cervical subsites and levels. Conclusion: Preoperative US may detect cervical metastases of PTC and may assist in determining the necessity and extent of neck dissection in PTC patients.
Gasdermin E (GSDME)-mediated pyroptosis is induced in keratinocytes of UVB-challenged skin. The role of GSDME in UVB-caused skin damage remains unknown. To explore the role of GSDME in UVB-induced skin inflammation. We compared differences in skin appearance, histological features, keratinocyte death modalities, infiltration of immune cells, and levels of some inflammatory cytokines between Gsdme−/− mice and wild type (WT) mice after UVB exposure. We explored whether keratinocytes contribute to GSDME deficiency-caused aggravation of UVB-induced skin inflammation in GSDME knockdown keratinocyte cultured in vitro and keratinocyte-specific Gsdme conditional knockout mice. We used anti-Ly6G antibody to deplete neutrophils and explore their role in UVB-caused skin damage. Skin damage and neutrophils infiltration were aggravated in UVB-challenged Gsdme−/− mice, compared with UVB-challenged WT mice. Apoptosis and necroptosis, which were initiated together with GSDME-mediated pyroptosis in UVB-challenged WT mice, were not enhanced in UVB-challenged Gsdme−/− mice. Neutrophils activation indicators and its recruiting cytokines were increased in skin tissue of UVB-challenged Gsdme−/− mice. However, GSDME knockdown did not lead to the further increase of mRNA and secretion of TNF-α and IL-6 in UVB-challenged keratinocytes. Skin damage was not aggravated in UVB-challenged Gsdme cKO mice. Neutrophils depletion alleviated UVB-caused skin damage in WT mice and Gsdme−/− mice, and eliminated its aggravation in Gsdme−/− mice. This study demonstrates that GSDME plays a restrictive role in UVB-induced skin damage through inhibiting excessive recruitment and activation of neutrophils in the immune microenvironment in UVB-caused skin inflammation. However, keratinocytes might not contribute to this restrictive function.
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