ABSTRACT
Diabetes mellitus (DM), a prevalent metabolic disorder, is associated with widespread damage to bodily systems, notably causing significant dysfunction within the peripheral and central nervous systems (CNS). The primary objective of this study is to explore the extent of DM's impact on cognitive and behavioral functions and to evaluate the therapeutic potential of ethanol leaf extracts from Ziziphus jujuba (ZJ) and Eclipta alba (EA) in mitigating these adverse effects. Utilizing an established animal model, we aimed to determine the effectiveness of these plant extracts in ameliorating the cognitive impairments commonly seen in diabetic states. In our experimental framework, we allocated Wistar rats (n=6 per group) into eight different groups, inducing DM through alloxan administration. The intervention groups were treated orally with either the standard antidiabetic drug glibenclamide or varying doses of ZJ and EA extracts over periods of seven and 21 days. Throughout the study, we carefully tracked fluctuations in blood glucose levels, noting considerable decreases, particularly following the 21-day treatment interval. Post-treatment, the rats' cognitive functions were assessed using the Morris water maze (MWM) test. This evaluation revealed significant cognitive enhancement in the diabetic rats administered with ZJ and EA extracts, with these groups displaying reduced latency in finding the submerged platform, indicative of improved learning and memory. These observations were statistically significant (p<0.01). The findings underscore the hypoglycemic effects of ZJ and EA extracts and suggest their viability as cognitive enhancers in the context of DM. The protective effects of these extracts against cognitive decline caused by DM are clear. They add important new information to the research on natural phytochemicals for managing chronic diseases. This study opens new avenues for the application of these substances in treating neurocognitive disorders associated with DM.
ABSTRACT
Introduction Cell phone usage has tremendously increased, and to make usage comfortable, accessories such as Bluetooth earphones are available. But still, most people use cell phones for a long period of time by flexing their elbows near their ears. When the users flex the elbow to hold the phone near the ear, this results in increased pressure over the ulnar nerve since the ulnar nerve runs superficially at the level of the elbow. The extensive pressure over the ulnar nerve may result in nerve compression, which results in cubital tunnel syndrome, recently called the cell phone elbow. Hence, this study was undertaken to assess the ulnar nerve function among cell phone users in relation to the duration of usage. Materials and methods Young healthy volunteers (n = 30) aged between 20 and 25 years were selected for the study in order to prevent age-related neuropathic changes. After getting a history of mobile phone usage, the subjects were asked about neural symptoms such as tingling, numbness, and pain while using cell phones. Ulnar nerve function was assessed by Froment's sign and Wartenberg's sign. An ulnar nerve conduction study was done. Results Seventy percent of the subjects (n = 21) out of the 30 subjects participating in the study reported tingling and numbness during mobile phone usage. But Froment's sign and Wartenberg's sign were negative for all the subjects. There was a significant positive correlation (r = 0.913 and r = 0.8253) between the duration of mobile phone use and latency and a negative correlation (r = -0.8439) with conduction velocity. Conclusion The malposition of the elbow during prolonged cell phone use results in ulnar nerve entrapment. The continuous usage of cell phones without rest by flexing the elbow causes nerve compression. This can be taken as a warning sign to prevent further damage.
ABSTRACT
Being a "behavioral disorder," autism spectrum disorder (ASD) is difficult to manage because its precise etiology is uncertain. In order to better understand the pathophysiology of autism and explore various therapeutic approaches, animal models are developed. Animal models of autism caused by valproate during pregnancy exhibit strong construct validity and reliability. Hence, this study was done among autism-induced rats with the aim of identifying the behavioral and biochemical assays. Pregnant rats were administered sodium valproate on the 12th day of gestation, while control pregnant rats received normal saline. The rats' offspring that received normal saline during intrauterine life were grouped as control, and the rats' offspring that received valproate were grouped as autism-induced. From postnatal day (PND) 21, behavioral assessments were done by using the Y maze (repetitive behavior) and the T maze (social behavior). The estimation of antioxidant profile (malondialdehyde {MDA}, glutathione {GSH}, catalase (CAT), and superoxide dismutase {SOD}), proinflammatory markers (tumor necrosis factor {TNF} alpha, transforming growth factor {TGF} beta, interleukin {IL} 6, and IL-1 beta), neurotransmitters (gamma-aminobutyric acid {GABA} and serotonin), and brain-derived neurotrophic factor (BDNF) in the hippocampal region was done. Oxidative stress, increased proinflammatory markers, and increased serotonin were recorded in the autism group. Rats with autism had a significant decrease in GABA and BDNF levels. These biochemical alterations can be correlated with clinical features of autism to diagnose and manage the disorder at the earliest.
