Arteriovenous fistulae of the superficial temporal artery are rare, and their principal cause is traumas. Complications include pulsatile mass, headache, hemorrhage and deformities that compromise esthetics. Treatment can be performed using conventional surgery or endovascular methods. The authors describe a case of a 44-year-old male patient who developed a large pulsating mass, extending from the preauricular region to the right parietotemporal and frontal regions after a motorcycle accident. The treatment chosen was complete surgical removal of the pulsatile mass and ligature of the vessels feeding the fistula.Keywords: arteriovenous fistulae; superficial temporal artery; trauma. ResumoAs fístulas arteriovenosas de artéria temporal superficial são raras, sendo o trauma sua etiologia principal. Suas complicações incluem massa pulsátil, cefaleia, hemorragia e deformidade estética. O tratamento pode ser realizado por cirurgia convencional ou endovascular. Os autores relatam o caso de um paciente de 44 anos que evoluiu com massa pulsátil extensa desde região pré-auricular até região parietotemporal e frontal direita após acidente motociclístico. Optou-se por remoção cirúrgica completa da massa pulsátil e ligadura dos vasos nutridores da fístula.Palavras-chave: fístula arteriovenosa; artéria temporal superficial; trauma.

Cancer stem cells (CSCs) are responsible for tumor initiation and progression. Toll-like receptors (TLRs) are highly expressed in cancer cells and associated with poor prognosis. However, a linkage between CSCs and TLRs is unclear, and potential intervention strategies to prevent TLR stimulation-induced CSC formation and underlying mechanisms are lacking. Here, we demonstrate that stimulation of toll-like receptor 3 (TLR3) promotes breast cancer cells toward a CSC phenotype in vitro and in vivo. Importantly, conventional NF-κB signaling pathway is not exclusively responsible for TLR3 activation-enriched CSCs. Intriguingly, simultaneous activation of both β-catenin and NF-κB signaling pathways, but neither alone, is required for the enhanced CSC phenotypes. We have further identified a small molecule cardamonin that can concurrently inhibit β-catenin and NF-κB signals. Cardamonin is capable of effectively abolishing TLR3 activation-enhanced CSC phenotypes in vitro and successfully controlling TLR3 stimulation-induced tumor growth in human breast cancer xenografts. These findings may provide a foundation for developing new strategies to prevent the induction of CSCs during cancer therapies.

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Opioids have been widely applied in clinics as one of the most potent pain relievers for centuries, but their abuse has deleterious physiological effects beyond addiction. We previously reported that opioids inhibit cell growth and trigger apoptosis in lymphocytes. However, the underlying mechanism by which microglia apoptosis in response to opioids is not yet known. In this study, we show that morphine induces microglia apoptosis and caspase-3 activation in an opioid-receptor dependent manner. Morphine decreased the levels of microglia phosphorylated Akt (p-Akt) and p-GSK-3β (glycogen synthase kinase 3 beta) in an opioid receptor dependent manner. More interestingly, GSK-3β inhibitor SB216763 significantly increases morphine-induced apoptosis in both BV-2 microglia and mouse primary microglial cells. Moreover, co-treatment of microglia with SB216763 and morphine led to a significant synergistic effect on the level of phospho-p38 mitogen-activated protein kinase (MAPK). In addition, inhibition of p38 MAPK by its specific inhibitor SB203580 significantly inhibited morphine-induced apoptosis and caspase-3 activation. Taken together, our data clearly demonstrates that morphine induced apoptosis in microglial cells, which is mediated via GSK-3β and p38 MAPK pathways.

Recurrent leakage of the irritating cyst contents and subsequent chemical inflammatory response may be responsible for the high-density on CT scans and the cystic nature. A correct histological diagnosis is important because, in contrast to typical ECs and other lesions, HIECs are more prone to spread intra-operatively and result in severe aseptic meningitis.