Case report on tuberous sclerosis: a rare cause of seizure

We report a case of tuberous sclerosis in a 19 years old teenage patient with generalized tonic-clonic seizure. MRI brain showed linear CSF filled structure with surrounding gliosis extending from the frontal horn of right lateral ventricle to the pial surface of right frontal lobe-postoperative change. Multiple small T2/ FLAIR hyper-intensities without diffusion restriction in bilateral frontal temporal parietal and left occipital lobes, predominantly involving the cortex and sub-cortical white matter and small focus of calcification in left parietal peri-ventricular white matter. He was treated with valproic acid, sodium valproate and levetiracetam and showed prompt improvement. Epilepsy in tuberous sclerosis complex is a group of genetic disorders manifesting in childhood. Secondary causes of tuberous sclerosis should be suspected when there is abrupt onset in adulthood. The case highlights an uncommon case of epilepsy in tuberous sclerosis in young adult patient

Modulatory effect of Tinospora cordifolia extract on Cd-induced oxidative stress in Wistar rats

Background: Cadmium (Cd), a nonessential heavy metal, is a major environmental and public health concern. Oxidative stress plays an important role in Cd-induced kidney dysfunction. Tinospora cordifolia, a medicinal plant rich in phytochemicals, possesses antioxidant activity. The objective of the present study was to assess the protective effect of Tinospora cordifolia-stem methanolic extract (TCE) on Cd-induced nephrotoxicity in Wistar rats. Methods: Male Wistar rats were administered ∼5 mg/kg body weight Cd orally and 100 mg/kg body weight TCE for 28 days. At the end of Cd and TCE treatment, biochemical assays were performed in serum and tissue homogenate. Results: Cd-induced oxidative stress in the kidney resulted in increased levels of lipid peroxidation and protein carbonyl content with a significant decrease in cellular antioxidants, such as reduced GSH, SOD, CAT, GPX, and GST. Cd-induced nephrotoxicity was further confirmed by marked changes in the histology of the kidney and increased levels of kidney markers. Additionally, Cd-treated rats showed alterations in membrane-bound ATPase activity and decreased levels of tissue glycoproteins. Cotreatment with TCE considerably reduced the biochemical alterations in serum and renal tissue induced by Cd, and also restored ATPase activity and glycoproteins to near normal levels. Conclusion: Our results suggested that TCE with its antioxidant effect offered cytoprotection against Cd-induced toxicity in kidneys by restoring the altered cellular antioxidants and renal markers. TCE treatment for 28 days reversed ATPase activity and tissue glycoprotein levels. These results revealed the protective effect of TCE on Cd-induced toxicity in kidneys and oxidative stress