(J Am Acad Dermatol 2009;61:294-302 )”
“Tuberous sclerosis c

(J Am Acad Dermatol 2009;61:294-302.)”
“Tuberous sclerosis complex (TSC) is a genetic disorder caused by inactivating mutations in the TSC1 or TSC2 genes and characterized by slow-growing tumors in multiple organs. Of the affected individuals, 10% display subependymal giant cell astrocytomas (SEGAs), which can lead to Selleckchem STI571 substantial neurological morbidity. The TSC1/TSC2 protein complex is a negative regulator of the mTOR pathway. Hence, mutations in these genes in preclinical models are associated

with increased mTOR pathway activation and heightened sensitivity to mTOR inhibitors. We hereby report our experience with RAD001 (Everolimus) therapy, a novel mTOR inhibitor, in inducing a dramatic regression of SEGAs.\n\nA patient with TSC and SEGAs was treated with 10 mg/day oral RAD001. MRIs and neuro-ophtalmological exams were performed

before and at regular intervals following the initiation of therapy.\n\nThe lesions exhibited significant regression in several tumor locations and stabilization in others, accompanied with an improvement of his visual status. Treatment was well tolerated for 11 months but was than discontinued due to hypertension and elevated CPK, without evidence for rhabdomyolysis. Yet, during 9 months following the AG-014699 supplier interruption of therapy, SEGAs remained unchanged.\n\nOral RAD001 demonstrated preliminary encouraging results as treatment of astrocytomas associated with TSC. These preliminary results were recently supported by the Novartis announcement of the phase II study of RAD001 for SEGAs, which was not published yet. According to their statement, 75% of the patients showed reduction of SEGAs’ volume following treatment with RAD001. Based on these results, RAD001 may be an alternative to surgery in selected patients with TSC and SEGAs.”
“It is well known that fish caudal fins can be completely regenerated after fin amputation. Although much research on fin regeneration has been

carried out, there have been very few reports regarding fin Epigenetics inhibitor regeneration after tail amputation. In this study, we used grass carp, common carp, koi carp, and zebrafish as experimental organisms. Some caudal fins could be distinctly regenerated in 2 weeks after tail amputation. After all-trans-retinoic acid treatment and tail amputation, zebrafish were unable to regenerate caudal fins that could be seen with the naked eye. However, after tail amputation, more than half of the zebrafish tested were able to regenerate caudal fins. Caudal fin regeneration depended on the presence of musculature and endoskeleton at the site of amputation. These caudal fins arose from segments of the endoskeleton, which contrast with currently accepted knowledge. J. Exp. Zool. (Mol. Dev. Evol.) 312B:762-769, 2009. (C) 2009 Wiley-Liss, Inc.”
“Resistance is increasing to several critical antimicrobials used to treat Salmonella typhimurium infection, urging people to search for new antimicrobial agents.

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