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This article discusses a case of Adie's tonic pupil in a 37-year-old Asian woman with primary Sjögren syndrome. The patient presented with symptoms of dry eyes, dry mouth, bilateral dilated pupils, and blurred vision. Further examination revealed irregular shaped pupils and a sluggish response to light. The presence of Adie's tonic pupil was confirmed through pharmacological testing. The article emphasizes the importance of recognizing this rare manifestation of Sjögren syndrome for early diagnosis and proper management. [Extracted from the article]

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Objective: The present study was to investigate whether dihydroartemisinin (DHA), which is a highly effective and safe drug in the treatment of malaria, could be repurposed for the treatment of skin fibrosis and vascular dysfunction in systemic sclerosis (SSc). Methods: The value of DHA was determined using a bleomycin-induced model of skin fibrosis. mRNA transcriptome analysis was performed, and the targets of DHA on fibroblasts were identified. Immunofluorescence staining was used to identify dermal vessels undergoing endothelial-to-mesenchymal transition (EndoMT). Autophagic flux was detected by western blot and mRFP-GFP-LC3 adenovirus vector transfection. Results: Both systemic and topical administration of DHA decreased dermal thickness and collagen deposition and alleviated EndoMT in bleomycin-induced skin fibrosis mice model. Treatment of human umbilical vein endothelial cells (HUVECs) with TGF-β1 resulted in the acquisition of the activation marker (α-SMA) and loss of endothelial markers (CD31 and VE-cadherin), a process that was restored by DHA. DHA significantly suppressed skin fibroblast activation and collagen-1 production mainly through regulating PI3K-Akt pathway. DHA also induced fibroblast autophagic flux and that autophagy dependently suppressed collagen-1 production. Conclusion: The results of the present study revealed that oral and topical DHA administration ameliorated tissue fibrosis and protected dermal blood vessels from bleomycin-induced EndoMT. Our study has elucidated the value of repurposing DHA for the treatment of SSc. Key Points • Oral or topical usage of DHA alleviated dermal fibrosis and EndoMT in bleomycin-induced skin fibrosis mice models. • DHA autophagy dependently inhibited fibroblast activation and collagen deposition via PI3K-ATK pathway. • DHA inhibited EndoMT of HUVECs induced by TGF-β1 by the downregulation of α-SMA and the upregulation of CD31 and VE-cadherin. [ABSTRACT FROM AUTHOR]

Introduction: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies. Larger tumor size is widely acknowledged to be associated with increased lymph node (LN) metastatic potential. However, the quantitative relationships between tumor size and LN metastasis or survival remain unclear. This study aims to quantify the objective relationship between tumor size and the prevalence of LN metastases across a spectrum primary tumor size.Methods: The Surveillance, Epidemiology, and End Results (SEER) database was used to identify 9958 patients with resected PDAC without distant metastasis. The prevalence of LN metastases, LN ratio (LNR), and N2/N1 ratio were assessed amongst different tumor sizes, and the relationships were displayed by matched curves.Results: In the enrolled cohort, age, tumor site, grade, American Joint Committee on Cancer (AJCC) 8th node staging, tumor size, chemotherapy, and radiotherapy were identified as significant independent predictors for overall survival (OS) and cancer-specific survival (CSS). For tumors within 1-40 mm in size, the prevalence of node-positive disease is closely modelled using a logarithmic formula [0.249 × ln (size) + 0.452] × 100%. The prevalence plateaued between 70% and 80% beyond 40 mm. The mean LNR increased in a stepwise manner as tumor size increased from 1-5 mm (LNR = 0.024) to 41-45 mm (LNR = 0.177); then, beyond 45 mm, it plateaued near 0.170. N2/N1 ratio gradually increased along with tumor size from 1-5 mm (N2/N1 = 0.286) to 41-45 mm (N2/N1 = 1.016), and when tumor size reached to 41-45 mm or more, the ratio stabilized around 1.000. In addition, significant survival prediction by AJCC N staging was observed when tumors ranging between 16 and 45 mm in size.Conclusion: Regional LN involvement demonstrated a logarithmic growth with increasing tumor sizes in patients with resected PDAC . The probability of metastasis in each regional LN for resected PDAC with tumors greater than 40 mm in size was near 17.0% and their overall prevalence of LN metastasis was 70-80%. Among which, 50% of patients had an N2 stage. Such prediction may be a potential and promising tool for guiding lymphadenectomy in PDAC surgery. [ABSTRACT FROM AUTHOR]

Purpose of the Review: Over the years, our perceptions of fibrogenesis in systemic sclerosis (SSc) have advanced a lot. Herein, we review potential targets for SSc discovered in the past 3 years. Recent Findings: In recent years, metabolites have come into the limelight of SSc research. Anti-oxidants, promotor of adipogenesis, modulator of fatty acid metabolism, regulator of glucose homeostasis, and adenosine deaminase open a new door for SSc treatment. A mosaic of biolipids, especially cannabinoid receptor 2 agonist, represents a rational therapeutic approach in fibrosis. In terms of immune aspects, targeting chemokines or integrins for cell adhesion may become new approach to inhibiting fibrotic pathways. Epigenetic modulation of immune pathways has been uncovered much recently. Targeting histone modifications and lncRNAs has demonstrated therapeutic potential in SSc animal models. The classical JAK-STAT and interferon pathway drive great attention these years because of the promising potential for the drug repurposing of targeted therapies from arthritis to SSc. In fibrosis-associated developmental pathways, BMP, Hedgehog, and PU.1 are expected to offer new targets to restrain fibrosis. Summary: New targets involved in metabolic reprogramming, immunity, epigenetics together with developmental and apoptotic pathways open new avenues for therapeutic modulation in SSc. [ABSTRACT FROM AUTHOR]