Interstitial ectopic pregnancy is a rare type of tubal pregnancy that poses diagnostic challenge. It is associated with the highest risk of massive, uncontrollable bleeding and can result in uterine rupture in the second trimester. This is a rare case of unruptured interstitial ectopic diagnosed in the first trimester by ultrasonography and managed medically with systemic methrotrexate and serial ultrasound monitoring.`

No abstract

No abstract

Background: Although ethanol exerts its neurotoxic effect on the brain through inflammatory and oxidative processes, the effect of Riboceine on the brain following ethanol neurotoxicity is yet to be elucidated. Therefore, this study was designed to evaluate the effects of riboceine on the cellular, behavioral, and molecular impairments induced by ethanol toxicity in rats. Methods: A total of 24 male Wistar rats weighing between 160-170 grams were used for the study, and were divided into four groups of six rats each. After completion of the administration of ethanol and riboceine, and testing for motor impairment, the rats were sacrificed. The cerebellum was excised and processed for oxidative stress analyses, based on oxidative stress markers and histological examinations. The immunohistochemical expression of astrocytes in the cerebellum was examined, using Glial Fibrillary Acidic Protein (GFAP) stain. Results: This study demonstrated that ethanol-induced neurotoxicity in the cerebellum, characterized by increased oxidative stress profile, astrocyte activation, and neuronal death in the cerebellum, especially the Purkinje layer. Necrosis, significant decrease in Superoxide Dismutase (SOD), Catalase (CAT) and Gluathione (GSH) activities (P<0.05) as well as astrogliosis was associated with ethanol treatment. However, riboceine was observed to significantly increase the cerebellar SOD, CAT and GSH activities with significantly reduced Malondialdehyde (MDA) levels (P<0.05). It also attenuated the histomorphological alteration of the cerebellum and reduced the cerebellar astrocytes activation following ethanol-induced neurotoxicity, thus leading to the attenuation of motor impairment. Conclusion: Riboceine attenuated motor impairment caused by chronic ethanol-induced neurotoxicity, suggestive of its anti-oxidative and anti-inflammatory properties.

Understanding the bidirectional relationship in the cellular and molecular mechanisms associated with testosterone deprivation and cognitive activities has become a high-priority goal. Testosterone has been shown to have effects in the nervous system, ranging from targeting gene expression to modulating neurotransmission. This study therefore evaluated the modulatory role of ascorbic acid in the hippocampus of orchiectomized rats. Twenty-one adult male Wistar rats with an average weight of 170g±10g were randomly assigned into three groups of seven rats each; the control, orchiectomized (orchiectomy+flutamide, 11 mg/kg body weight, bw), and ascorbic acid (orchiectomy+flutamide, 11 mg/kg bw + ascorbic acid, 100 mg/kg bw). Treatment was by oral gavage and lasted for 30 days. Nitrosative stress and neuroinflammatory analysis, hormonal, histological and immunohistochemical expression of astrocytes in the hippocampus were examined. Results showed significantly increased expression of acetylcholinesterase, inducible nitric oxide synthase, and tumour necrotic factor-alpha in the hippocampus of orchiectomized animals. There was altered cytoarchitectural morphology evidenced by reduced Nissl profiles in neuronal axons and dendrites, which corresponded to apoptotic changes, and increased expression of reactive astrocytes suggesting neuronal damage. Nitrosative stress and inflammatory perturbations were well modulated in animals treated with ascorbic acid with unaltered hippocampal morphology. The results indicated that decline in brain androgen activities caused inflammatory and oxidative stress-driven alterations in the hippocampus, while ascorbic acid supplementation offered therapeutic value by modulating neurochemicals and scavenging free radicals in the hippocampus.