Unusual presentation of a multiple sclerosis case involving central retinal artery occlusion

The term intermediate uveitis (IU) refers to a subgroup of uveitis in which the vitreous is the site of greatest inflammation. Patients with multiple sclerosis (MS) have a greater frequency of IU compared with the general population.The IU associated with MS is characterized by the presence of pars planitis (occasionally accompanied by anterior uveitis) and the presence of peripheral retinal vasculitis in the form of periphlebitis (venous sheathing) in 6–26% of patients.We present a patient with an unusual initial presentation of MS involving central retinal artery occlusion (CRAO) in the right eye (RE).Although retinal vascular changes are asymptomatic in the majority of MS patients, the spectrum of impairment ranges from simple peripheral retina periphlebitis to the presence of peripheral occlusive retinal vasculitis in 6.5% of patients.This atypical case may represent an extreme of the spectrum of retinal vasculitis associated with demyelinating disease.     

Inhibition of HMGcoA reductase by atorvastatin prevents and reverses MYC-induced lymphomagenesis

Statins are a class of drugs that inhibit 3-hydroxy-3-methylglutaryl-coenzyme A (HMGcoA) reductase, a critical enzyme in the mevalonate pathway. Several reports document that statins may prevent different human cancers. However, whether or not statins can prevent cancer is controversial due to discordant results. One possible explanation for these conflicting conclusions is that only some tumors or specific statins may be effective. Here, we demonstrate in an in vivo transgenic model in which atorvastatin reverses and prevents the onset of MYC-induced lymphomagenesis, but fails to reverse or prevent tumorigenesis in the presence of constitutively activated K-Ras (G12D). Using phosphoprotein fluorescence-activated cell sorter (FACS) analysis, atorvastatin treatment was found to result in the inactivation of the Ras and ERK1/2 signaling pathways associated with the dephosphorylation and inactivation of MYC. Correspondingly, tumors with a constitutively activated K-Ras (G12D) did not exhibit dephosphorylation of ERK1/2 and MYC. Atorvastatin's effects on MYC were specific to the inhibition of HMGcoA reductase, as treatment with mevalonate, the product of HMG-CoA reductase activity, abrogated these effects and inhibited the ability of atorvastatin to reverse or suppress tumorigenesis. Also, RNAi directed at HMGcoA reductase was sufficient to abrogate the neoplastic properties of MYC-induced tumors. Thus, atorvastatin, by inhibiting HMGcoA reductase, induces changes in phosphoprotein signaling that in turn prevent MYC-induced lymphomagenesis.