In patients with Takayasu arteritis, carotid artery recanalization via endovascular surgery combined with immunosuppressive therapy is effective and can be performed safely and repeatedly. The improvement in carotid artery blood flow supplying the central nervous system relieves symptoms of cerebral ischemia and is associated with an improved quality of life.
Eosinophilic esophagitis is characterized by eosinophil predominant inflammation in the esophagus. How eosinophils migrate and infiltrate into the esophagus, however, is less clear. Our previous study demonstrated mast cell activation led to eosinophil infiltration in the esophagus. Prostaglandin D2 (PGD2) is an important mediator released from activated mast cells. The present study aims to determine whether PGD2 induces eosinophil infiltration into the esophagus via a DP2 receptor-dependent mechanism. Using an in vivo guinea pig model, PGD2, DP1 agonist, or DP2 agonist were injected into the esophagus. Esophageal tissues were removed 2-hour after injections and proceeded to either H-E staining or immunofluorescent-staining of eosinophil major basic protein (MBP) to compare each treatment-induced eosinophil infiltration in the esophagus. In a separate study, ovalbumin-sensitized guinea pigs were pretreated with either DP2 or DP1 antagonists, followed by inhalation of ovalbumin to induce mast cell activation. Esophageal tissues were then processed for immunofluorescent-staining of MBP. PGD2 injection in the esophagus led to an increase of eosinophil infiltration in esophageal epithelium at the injection site as revealed by H-E staining. Increased infiltration of eosinophils was further confirmed by the increased presence of MBP-labeled immuno-positive (MBP-LI) cells in esophageal epithelium. Injection with DP2 agonist 15(R)-PGD2, but not DP1 agonist BW 245C, mimicked the PGD2-induced response. In ovalbumin-sensitized animals, antigen inhalation increased MBP-LI cells in esophageal epithelium. Pretreatment with DP2 antagonist BAY-u3405, but not DP1 antagonist BW 868C, inhibited the antigen inhalation-induced increase of MBP-LI cells in esophageal epithelium. These data support the hypothesis that PGD2 induces eosinophil trafficking into the esophageal epithelium via a DP2-mediated pathway, suggesting a role of DP2 antagonist in the prevention of eosinophilic esophagitis.
Takayasu's arteritis (TA) is a chronic, idiopathic, inflammatory disease affecting the aorta and its branches. To date, only one case involving abdominal aortic thrombosis due to TA has been reported. After bilateral artificial subclavian-iliac bypass, a case of abdominal aortic thrombosis due to TA received a delayed diagnosis in a 44-year-old Chinese male who experienced recurrent episodes of heart failure and uncontrolled hypertension with claudication of two extremities. Abdominal color Doppler sonography and computed tomography aortography (CTA) showed occlusion of the abdominal aorta and bilateral renal artery stenosis. After vascular bypass and during 1 year follow-up, his cardiac function improved and blood pressure was well controlled, with reduced serum creatinine. Postoperative CTA still showed abdominal aortic thrombosis resulting in arterial occlusion extending from the left renal artery initial segment level to the bilateral common iliac artery and the bifurcation of the renal artery, except for the vascular bypass. Abdominal aortic thrombosis due to TA is very rare and potentially life threatening, probably becoming an atherosclerosis risk factor. Doppler sonography and CTA results are important for diagnosis. Artificial vascular bypass can be used for TA in debilitated patients with diffuse aortic disease.
Aim: The differentiation of hair follicle stem cells (HFSCs) into hair follicle cells has potential clinical applications for cutaneous burns. However, the mechanisms regulating the differentiation of HFSCs into hair follicular papilla or epidermal cells are currently not clear. This study investigated the role of the Wnt/β-catenin pathway and its crosstalk with other signaling components during this differentiation process. Methods: Lithium chloride (LiCl, 10 mmol/L) and keratinocyte growth factor (KGF, 10 µg/L) were used to induce HFSC differentiation, validated by immunofluorescence analysis. The mRNA expression of β-catenin, adenomatous polyposis coli, glycogen synthase kinase-3β (GSK-3β), axin, and lymphoid enhancer factor-1 after 3, 5, 7, and 9 days were measured to evaluate the role of the Wnt/βcatenin pathway. Results: During LiCl-induced HFSC differentiation into hair follicle cells, the Wnt/ β-catenin signaling pathway was activated and the expression of GSK-3β, a vital component of the degradation compound, was inhibited. This led to increased cytoplasmic β-catenin expression, nuclear translocation, and subsequent target gene transcription. By contrast, KGF induced the differentiation of HFSCs into epidermal cells and did not affect the expression of β-catenin. This data indicates that LiCl and KGF distinctly regulate the differentiation of HFSCs into hair follicle and epidermal cells, respectively. Furthermore, the Wnt/β-catenin signaling pathway is predominantly involved in hair follicle differentiation. Conclusion: these results demonstrate that LiCl can be used to differentiate HFSCs into hair follicle cells in vitro, which has important therapeutic applications for treating patients with cutaneous damage.
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