Ionizing irradiation is a widely applied therapeutic method for the majority of solid malignant neoplasms, including brain tumors where, depending on localization, this might often be the only feasible primary intervention.Without doubt, it has been proved to be a fundamental tool available in the battlefield against cancer, offering a clear survival benefit in most cases. However, numerous studies have associated tumor irradiation with enhanced aggressive phenotype of the remaining cancer cells. A cell population manages to survive after the exposure, either because it receives sublethal doses and/or because it successfully utilizes the repair mechanisms. The biology of irradiated cells is altered leading to up-regulation of genes that favor cell survival, invasion and angiogenesis. In addition, hypoxia within the tumor mass limits the cytotoxicity of irradiation, whereas irradiation itself may worsen hypoxic conditions, which also contribute to the generation of resistant cells. Activation of cell surface receptors, such as the epidermal growth factor receptor, utilization of signaling pathways, and over-expression of cytokines, proteases and growth factors, for example the matrix metalloproteinases and vascular endothelial growth factor, protect tumor and non-tumor cells from apoptosis, increase their ability to invade to adjacent or distant areas, and trigger angiogenesis. This review will try to unfold the various molecular events and interactions that control tumor cell survival, invasion and angiogenesis and which are elicited or influenced by irradiation of the tumor mass, and to emphasize the importance of combining irradiation therapy with molecular targeting.
Patient: Male, 80Final Diagnosis: Unilateral complicated Herpetic Simplex Virus 1 KeratitisSymptoms: Visual impairmentMedication: Anti-herpetic treatment • Anti-VEGF • Cyclosporine A • Matrix regeneration therapyClinical Procedure: Amniotic membrane and limbal stem cell transplantationSpecialty: OphthalmologyObjective:Management of emergency careBackground:Keratitis caused by herpes simplex virus (HSV) can have detrimental effects on the cornea leading to loss of vision. Modern therapies can contribute to the prevention of anatomical and functional damage.Case Report:An 80-year-old male with complicated HSV-1 keratitis of the left eye (confirmed diagnosis after microbiological investigation) presented three months after antiviral treatment with corneal blurring, severe epitheliopathy, thinning of the stroma, and neovascularization. At the time he was referred, the visual acuity of his left eye was very low, as he could only count fingers at a one-foot distance. He was initially started on oral acyclovir (800 mg once daily) and topical poly-carboxymethyl glucose sulfate; afterwards he underwent amniotic membrane (AM) transplantation and localized treatment with anti-VEGF factors. One month after the AM transplantation there was an obvious improvement of the corneal surface. Ophthalmic suspension of cyclosporine-A 1% was also added to his treatment. After three months, a transplantation of stem cells (deriving from the sclerocorneal junction of his right eye) was carried out at the sclerocorneal junction, as the corneal damage and neovascularization was more severe at this anatomical area. Four months after the last surgery, his visual acuity was 1/10 (note, he had a history of an old vascular episode) and the cornea was sufficiently clear with no signs of epitheliopathy and almost complete subsidence of the neovascularization.Conclusions:Transplantation of AM and stem cells in combination with anti-VEGF factors and topical administration of cyclosporine-A 1% and poly-carboxymethyl glucose sulfate (a regenerative factor of corneal matrix) contributed substantially in the management of herpetic keratitis complications.
These findings demonstrate a significant arteriolar vasodilation after intravitreal juxta-arteriolar L-lactate microinjection in eyes with experimental BRVO in the affected areas. L-lactate microinjection can reverse the arteriolar vasoconstriction that occurs in acute experimental BRVO.
Purpose After branch retinal vein occlusion (BRVO), the retinal territory affected by the occlusion becomes hypoxic and the arterioles crossing this territory are often constricted. The purpose of the current experimental animal study is to investigate the effect of intravitreal juxta‐arteriolar microinjection of L‐lactate on the retinal arteriolar diameter following acute BRVO in minipigs. Methods Under general anesthesia, 9 eyes of 9 minipigs were evaluated. Argon laser endo‐photocoagulation was used to create BRVO. Two hours after BRVO, an intravitreal juxta‐arteriolar microinjection of 50 µl L‐lacate 1 mM (pH=7.4) was performed. The procedure was recorded in real time and retinal arteriolar diameter changes were measured in vivo using a Retinal Vessel Analyzer. Results Two hours after BRVO, the retinal arteriolar diameter decreased from 210 ± 16 AU to 183 ± 14 AU in the affected territories (p=0.04). Five minutes following L‐lactate juxta‐arteriolar microinjection, the retinal arteriolar diameter increased to 241 ± 16 AU (p< 0.01). The vasodilatory effect of L‐lactate persisted and remained significant till the end of the study period (243 ± 15 AU at 30 min, p<0.01). Conclusion We measured a significant vasodilation after intravitreal juxta‐arteriolar L‐lactate microinjection in eyes with experimental BRVO. L‐lactate microinjection can be of potential interest in acute BRVO, reversing the arteriolar vasoconstriction, thus leading to increase of the retinal arteriolar blood flow and possibly to improvement of the retinal cellular function in the occluded territory.
Introduction: Herpes simplex virus-1 (HSV-1) encephalitis, the most common and potentially life-threatening type of encephalitis, may rarely present as a stroke mimic. Prompt diagnosis is of paramount importance for the timely initiation of antiviral treatment and to avert intravenous thrombolysis.Case Report: A 60-year-old man with a history of lone paroxysmal atrial fibrillation without prior antithrombotic treatment was admitted due to mild gait unsteadiness and intermittent dysarthria of acute onset. On admission, the patient was afebrile, whereas neurological examination revealed only a mild pronator drift on the left. Brain magnetic resonance imaging (MRI) showed an extensive right temporo-occipital and thalamic lesion with restricted diffusion and 3 small-sized hemorrhagic foci. Brain MRangiography did not show large vessel stenosis or occlusion. On the basis of careful observation and the depiction of several imaging discrepancies, such as early vasogenic edema and hemorrhagic transformation, as well as uncus involvement, but also the lack of significant neurological deficits despite the size of the brain lesion we suspected viral encephalitis which was confirmed by the detection of HSV-1 DNA in the cerebrospinal fluid. Conclusion:HSV-encephalitis might occasionally result in the development of unilateral brain MRI lesions with extensive cytotoxic edema, resembling an acute ischemic stroke. Therefore, HSV-encephalitis must be considered in the differential diagnosis of acute ischemic stroke with atypical presentation. The presence of a significant dissociation between the brain MRI lesion volume and the neurological deficits, as well as certain brain MRI imaging discrepancies might serve as "red flags" to extend the diagnostic workup.
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