Cerebral vasculitis is characterized by inflammation of the walls of blood vessels and may affect vessels of any size. The pathogenesis of vasculitis remains poorly understood. Vasculitis may affect large vessels (Takayasu arteritis, giant cell arteritis), medium-sized vessels (Kawasaki disease, polyarteritis nodosa), small vessels (immunoglobulin A vasculitis, microscopic polyangiitis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis), or variable-sized vessels (Behçet disease, Cogan syndrome). Primary angiitis of the central nervous system (CNS) is an idiopathic disorder with no evidence of generalized inflammation that may simulate reversible cerebral vasoconstriction syndromes. Vasculitis may be secondary to systemic disease, infection, malignancy, drug use, or radiation therapy. Imaging findings vary from small ischemic changes to frank infarction, hemorrhage, and white matter edema and may show contrast material enhancement. The cerebral arteries may demonstrate a beaded appearance with variable degrees of stenosis, occlusion, and contrast enhancement of the vessel wall. Correlation of imaging findings with clinical presentation and laboratory test results helps establish the diagnosis of CNS vasculitis.

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Background: Testicular cancer is a public health problem. The goal of this study was to demonstrate the efficacy of quercetin treatment on N-nitroso-N-methyl-urea (MNU)-induced testicular carcinogenesis alone or in combination with cisplatin-treatment. Methods: In total 70 adult male albino rats were categorized into six groups, control, quercetin-treatment (10 mg/kg body weight), cisplatin-treatment (2 mg/kg. body weight), cisplatin and quercetin-treatment, MNU-treatment, MNU plus quercetin-treatment and MNU plus quercetin and cisplatin-treatment. Treatment with quercetin and/or cisplatin was performed after 2 months of MNU induced testicular carcinogenesis. The studied groups were euthanized and sacrificed and their testes were examined for gene expression, biochemical, histological and immunohistochemically analysis, inflammation and apoptosis of germ cells. Results: The fertility of the rats subjected to MNU carcinogenesis was impaired following cisplatin and/or quercetin-treatment. Cisplatin-treatment reduced the fertility rate and improved after quercetin-treatment. Quercetin-treatment decreased the sharp increase in RNA expression of BAX and MPO in both cisplatin-toxicated testes and after MNU carcinogenesis induction. In addition, the testicular levels of testosterone and SOD increased in parallel with depletion of MDA, IL-6, AFP and caspase-3 levels in MNU and/or cisplatin-treatment after -quercetin-treatment. The testicular structure of the cisplatin-treated group recovered their dividing germ and sperm differentiation after-quercetin-treatment. While, there was a great appearance of flourishing germ cell of MNU carcinogenesis post quercetin therapy, there was still a lack of sperm differentiation. Conclusion: Quercetin-treatment showed increased cisplatin activity and decreased testicular carcinogenesis due to anti-neoplastic and antioxidant activities.

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