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Subconjunctival administration of bevacizumab induced involution of new vessels, abolished inflammatory response, and resulted in return of corneal function. Furthermore, bevacizumab is a novel approach for the treatment of herpetic stromal keratitis.

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Objectives: The complexity of endovascular revascularization treatment (ERT) in acute ischemic stroke (IS) and the small number of patients eligible for that treatment justifies the development of Stroke Center networks with interhospital transfer of eligible patients. But it is possible that this approach generate “futile“ transfers (i.e. shift of patients who finally do not receive ET) generating unnecessary costs. Our aim is to analyze the frequency of “futile” transfers, the reasons for rejection for ERT and to identify the possible associated factors. Methods: We analyzed a prospective registry of ERT from a Stroke Network integrated by three hospitals with facilities for ERT for acute stroke patients. These hospitals share a common stroke protocol and have established a weekly rotatory shift with inter-hospital transference to the on-call center for ERT in those patients in whom this therapy is indicated, both primarily, after completing IV thrombolysis or in patients attended in outside hospitals (drip and shift). We analyzed: demographic data, vascular risk factors, stroke severity, frequency of prior intravenous thrombolysis, time from stroke onset and reasons for rejection. Study period: 1/02/2012 to 07/05/2013. Results: ERT protocol was activated in 199 patients, receiving ERT 129 (64.8%). 120 (60.3%) patients required inter-hospital transfer, among them 50 (41%) were not finally treated (futile transfer). These were more often male (74.1% vs. 25.9%, P = 0.04), with no differences in age, vascular risk factors, time-lapse from stroke onset or delay of inter-hospital transfer, baseline NIHSS, baseline ASPECTS or rate of prior intravenous thrombolysis between transferred patients treated with ERT and those non-treated. Reasons for rejection were: clinical improvement (16%), arterial recanalization (24%), clinical deterioration (8%); ASPECTS <7 in the 2nd TC (20%), absence of mismatch (20%); delay in shipment (2%), revocation of consent (1%). Conclusions: 40% of shipments for ERT are “futile”. None of the baseline patient characteristics predict this fact, being arterial recanalization and findings in a second imaging test done in the receiving hospital the main reasons for ERT rejection.

Air pollution is a serious environmental issue worldwide in developing countries’ megacities, affecting the population’s health, including the ocular surface, by predisposing or exacerbating other ocular diseases. Herpes simplex keratitis (HSK) is caused by the herpes simplex virus type 1 (HSV-1). The primary or recurring infection in the ocular site causes progressive corneal scarring that may result in visual impairment. The present study was designed to study the immunopathological changes of acute HSK under urban polluted air, using the acute HSK model combined with an experimental urban polluted air exposure from Buenos Aires City. We evaluated the corneal clinical outcomes, viral DNA and pro-inflammatory cytokines by RT-PCR and ELISA assays, respectively. Then, we determined the innate and adaptive immune responses in both cornea and local lymph nodes after HSV-1 corneal by immunofluorescence staining and flow cytometry. Our results showed that mice exposed to polluted air develop a severe form of HSK with increased corneal opacity, neovascularization, HSV-1 DNA and production of TNF-α, IL-1β, IFN-γ, and CCL2. A high number of corneal resident immune cells, including activated dendritic cells, was observed in mice exposed to polluted air; with a further significant influx of bone marrow-derived cells including GR1+ cells (neutrophils and inflammatory monocytes), CD11c+ cells (dendritic cells), and CD3+ (T cells) during acute corneal HSK. Moreover, mice exposed to polluted air showed a predominant Th1 type T cell response over Tregs in local lymph nodes during acute HSK with decreased corneal Tregs. These findings provide strong evidence that urban polluted air might trigger a local imbalance of innate and adaptive immune responses that exacerbate HSK severity. Taking this study into account, urban air pollution should be considered a key factor in developing ocular inflammatory diseases.