Showing papers by "Giorgio Battaglia published in 2014"

Progressive brain damage, synaptic reorganization and NMDA activation in a model of epileptogenic cortical dysplasia.

Abstract: Whether severe epilepsy could be a progressive disorder remains as yet unresolved. We previously demonstrated in a rat model of acquired focal cortical dysplasia, the methylazoxymethanol/pilocarpine - MAM/pilocarpine - rats, that the occurrence of status epilepticus (SE) and subsequent seizures fostered a pathologic process capable of modifying the morphology of cortical pyramidal neurons and NMDA receptor expression/localization. We have here extended our analysis by evaluating neocortical and hippocampal changes in MAM/pilocarpine rats at different epilepsy stages, from few days after onset up to six months of chronic epilepsy. Our findings indicate that the process triggered by SE and subsequent seizures in the malformed brain i) is steadily progressive, deeply altering neocortical and hippocampal morphology, with atrophy of neocortex and CA regions and progressive increase of granule cell layer dispersion; ii) changes dramatically the fine morphology of neurons in neocortex and hippocampus, by increasing cell size and decreasing both dendrite arborization and spine density; iii) induces reorganization of glutamatergic and GABAergic networks in both neocortex and hippocampus, favoring excitatory vs inhibitory input; iv) activates NMDA regulatory subunits. Taken together, our data indicate that, at least in experimental models of brain malformations, severe seizure activity, i.e., SE plus recurrent seizures, may lead to a widespread, steadily progressive architectural, neuronal and synaptic reorganization in the brain. They also suggest the mechanistic relevance of glutamate/NMDA hyper-activation in the seizure-related brain pathologic plasticity.

Role of Proton Pump Inhibitor on Esophageal Carcinogenesis and Pancreatic Acinar Cell Metaplasia Development: An Experimental In Vivo Study

Abstract: Chronic gastro-duodenal reflux in the esophagus is a major risk for intestinal metaplasia and Barrett's adenocarcinoma. A role for chronic use of proton pump inhibitor (PPI) in the increased incidence of esophageal adenocarcinoma in Western countries has been previously suggested. The aim of this work was to study the effect of chronic administration of omeprazole (a proton pump inhibitor) per os in a model of reflux induced esophageal carcinogenesis. One week after esophago-gastro-jejunostomy, 115 Sprague-Dawley rats were randomized to receive 10 mg/Kg per day of omeprazole or placebo, 5 days per week. The esophago-gastric specimens were collected 28 ± 2 weeks after randomization and analyzed in a blinded fashion. Mortality and esophageal metaplasia rates did not differ between the two groups (p = 0.99 for mortality, p = 0.36 for intestinal metaplasia and p = 0.66 for multi-layered epithelium). Gastric pancreatic acinar cell metaplasia (PACM) was more frequently observed in PPI-treated rats (p = 0.003). Severe ulcer lesions significantly prevailed in the placebo group (p = 0.03). Locally invasive esophageal epithelial neoplasia were observed in 23/39 PPI-treated versus 14/42 placebo-animals (p = 0.03). In conclusion, chronic omeprazole treatment improved the healing of esophageal ulcerative lesions. Locally invasive neoplastic lesions and PACM prevailed among PPI-treated animals. However, neither an effect on the overall mortality nor on the incidence of pre-neoplastic lesions was observed in this work.

An unusual behavioural and motor paroxysmal disorder caused by insulinoma-related hypoglycemia: A possible cause of epilepsy misdiagnosis

Abstract: 1. IntroductionInsulinoma is a common cause of hypoglycemia in patientswithout systemic illness. The clinical diagnosis of hypoglycemia isgenerally based on Whipple’s triad: i.e. neuroglycopenic andautonomic symptoms, a low plasma glucose concentration at thetime of symptoms, and symptom relief when the hypoglycemia iscorrected. Neurological disorders are frequently misdiagnosed,

Timing and protocols of endoscopic follow-up in operated patients after esophageal surgery

Abstract: After esophagectomy, the surgical defect is reconstructed to form an esophageal conduit to maintain the continuity of digestive tract. The reconstruction requires the transposition of stomach (gastric pull-up), intestinal graft, or musculocutaneous graft to replace the esophagus. Despite continuous refinements over decades, this technique is still associated with high risk of graft-related complications such as necrosis, leakage, fistula, strictures, or impaction. Local recurrence of primary esophageal cancer and development of metachronous cancers in the remnant esophagus are constant risks for neoplastic patients undergoing esophagectomy. Failure to detect these complications during follow-up may lead to severe or even fatal outcomes. Therefore, a rigorous postoperative surveillance is always justified. Being a safe tool with versatile diagnostic and therapeutic utilities, endoscopy deserves a central role in the physician’s armamentarium in the postoperative management of esophageal reconstruction.