The Egyptian Cardiothoracic Surgeon (ECTS - E-Journal)
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Vasculogenic Mimicry in Small Cell Lung Cancer
No full textBackgroundSmall cell lung cancer (SCLC) accounts for ~15% of lung cancer cases worldwide and despite initial responses to chemotherapy, most patients relapse with drug resistant disease. Targeting tumour vasculature in SCLC produced disappointing results and angiogenesis-independent tumour vascularisation pathways, including vasculogenic mimicry (VM), warrant further investigation. VM is the ability of aggressive tumour cells to form fluid conducting vascular channel-like structures. We sought to determine the role of VM in SCLC and explore the function of VE-Cadherin, a VM-associated protein in vitro and in SCLC Circulating Tumour Cells (CTCs).MethodVM was evaluated using CD31/periodic acid-Schiff (PAS) staining in a tissue micro-array (TMA) from 41 limited stage SCLC chemo-naive patients and in tumours from 11 Circulating Tumour Cell (CTC) Derived Explant (CDX) models1. Laser Capture Microdissection (LCM) and Copy Number Analysis (CNA) were performed on CDX samples which were enriched for VM. The role of VE-Cadherin in VM was evaluated in vitro and in ISET filtered CTCs stained by IF for DAPI, CD45, cytokeratin and VE-Cadherin. ResultsIn the TMA, VM score >10% correlated with poor OS (13.0 v 23.8 months, log rank p=0.025). VM was present in CDX models and CNA confirmed its SCLC origin. VM cells exhibited a distinct molecular signature. In vitro VE-Cadherin was essential for network formation in Matrigel and 37/38 SCLC patients contained a sub-population of VE-Cadherin expressing CTCs where the VM score ranged from 0 - 100% (median 11%, mean 21%).ConclusionWe present the first evidence of VM in SCLC which correlates with poor OS and with findings in other cancers. VM is present in CDX models and CNA confirms that VM vessels originate from tumour, and bear a unique molecular signature. VE-Cadherin is required in SCLC for VM in vitro and VE-Cadherin co-expression was found in CTC sub-populations in SCLC
Heckscher Reloaded? Mercantilism, the State and Europe’s Transition to Industrialization (1600–1900)
No full textSeeking teachers’ views regarding literacy resources in Gaelic medium education. Final Report. Soillse research network.
No full textIs distal fibular fracture an absolute contraindication to free fibular flap harvesting? A review of evidence in the literature and illustration by a successful case.
No full textDespite the advantages of a fibula flap, many surgeons would often be hesitant in its use in patients with a history of distal fibular fracture. The chief concern is the potential vascular damage sustained during the injury. From our experience, however, we noticed that the blood supply of various components of a fibula flap rarely relies on its distal part alone. Avoiding the use of this flap may unnecessarily forgo the optimal reconstructive option in many patients. Free fibula flap was harvested from a 41-year-old man who had a history of left fibula fracture 10 years before surgery. The fracture was treated with open reduction with internal fixation. The plate was removed 1 year after the trauma surgery. We used this fractured and healed fibula to reconstruct the intraoral and mandibular defect after tumor extirpation. The harvesting process was straight-forward and the flap survived uneventfully. On the basis of our experience and current evidence in the literature, we believe that a history of previous fibular fracture should not be considered as an absolute contraindication for free fibular flap harvesting. With a good knowledge of the lower limb anatomy and appropriate patient selection, the fibular flap can still be a safe option that incurs no additional risk. © 2014 Wiley Periodicals, Inc
Enhancing electron affinity and tuning band gap in donor-acceptor organic semiconductors by benzothiadiazole directed C-H borylation
No full textTRPV1 expression and function in splenic dendritic cells: a potential role in immune homeostasis
No full textNeuro-immune interactions, particularly those driven by neuropeptides, are increasingly implicated in immune responses. For instance triggering calcium channel Transient Receptor Potential Vanilloid 1 (TRPV1) on sensory nerves induces the release of CGRP (calcitonin gene related peptide), a neuropeptide known to moderate dendritic cell activation and TH1 polarisation. Despite observations that CGRP is not confined to the nervous system, few studies have addressed the possibility that immune cells can respond to well documented ‘neural’ ligands independently of peripheral nerves. Here we have identified functionally relevant TRPV1 on primary antigen presenting cells of the spleen and have demonstrated both calcium influx and CGRP release in three separate strains of mice using natural agonists. Furthermore, we have shown downregulation of activation markers CD80/86 on dendritic cells, and upregulation of IL6 and IL10 in response to CGRP treatment. We suggest that dendritic cell responses to neural ligands can amplify neuropeptide release, but more importantly that variability in CGRP release across individuals may have important implications for immune cell homeostasis
