Environmental pollution with vanadium may pose neurotoxicity threats to known unique neural attributes (cognition and olfaction) of the African giant rat (AGR). This rodent lives within the same ecological zones with the human populace thus, experimental investigations on the effect of vanadium on this rodent may mirror latent epidemiological scenario on the human populace. This work was designed to evaluate the neurotoxic effect of vanadium on the hippocampal neuronal infrastructure and circuitry, and provide cellular correlates to its notable pathologies in the AGR. Adult male AGRs were dosed daily with 3mg/kg body sodium metavanadate for 14days and harvested brains were processed for histology Using Nissl and Golgi staining techniques with stereological analysis. we demonstrated the effect of vanadium on AGR neuronal architecture of the hippocampal trisynaptic loop as a probable cellular mechanism of vanadium-induced memory deficits. Specifically, the most notable pathologies were seen in the dentate gyrus and CA3 with significant decrease in neuronal density, disruption of the cytoarchitecture, and loss of dendritic arborizations and axonal extensions. while hippocampal subfields CA2 and CA4 show region-specific resistance to the vanadium-induced neurotoxicity. The selective vulnerability to the vanadium-induced neurotoxicity is adduced. Given the unique neural attributes of the AGR and their translational benefits, as sniff rats it then becomes expedient to note the impact of environmental pollution (in this case vanadium) on their performance index. It is also proposed that this indigenous rodent may be a suitable model for evaluating memory pathologies in ecological studies of neurotoxicities.

Environmental pollution with vanadium may pose neurotoxicity threats to known unique neural attributes (cognition and olfaction) of the African giant rat (AGR). This rodent lives within the same ecological zones as the human populace. Thus, experimental investigations on the effect of vanadium on this rodent may mirror latent epidemiological scenarios in the human populace. This work was designed to evaluate the neurotoxic effect of vanadium on the hippocampal neuronal infrastructure and circuitry and provide cellular correlates to its significant pathologies in the AGR. Twelve adult male AGRs were assigned into two groups (n = 6/group; vanadium and control). They were dosed daily with 3 mg/kg body sodium metavanadate and sterile water for 14 days, respectively, and harvested brains were processed for histology. Using Nissl and Golgi staining techniques with stereological analysis, we demonstrated the effect of vanadium on AGR neuronal architecture of the hippocampal trisynaptic loop as a probable cellular mechanism of vanadium-induced memory deficits. Specifically, the most significant pathologies were seen in the dentate gyrus and CA3, with significantly decreased neuronal density disrupted cytoarchitecture and loss of dendritic arborisations and axonal extensions. At the same time, hippocampal subfields CA2 and CA4 showed region-specific resistance to vanadium-induced neurotoxicity. Furthermore, the selective vulnerability to vanadium-induced neurotoxicity is adduced. This work has demonstrated the neurotoxic effect of vanadium on the hippocampal subfields and circuitry in the AGR and highlighted its probable impact on their translational purposes. This rodent may be a suitable model for evaluating memory pathologies in neurotoxicological studies

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Understanding neuronal firing patterns and long-term potentiation (LTP) induction in studying learning, memory, and neurological diseases is critical. However, recently, despite the rapid advancement in neuroscience, we are still constrained by the experimental design, detection tools for exploring the mechanisms and pathways involved in LTP induction, and detection ability of neuronal action potentiation signals. This review will reiterate LTP-related electrophysiological recordings in the mammalian brain for nearly 50 years and explain how excitatory and inhibitory neural LTP results have been detected and described by field- and single-cell potentials, respectively. Furthermore, we focus on describing the classic model of LTP of inhibition and discuss the inhibitory neuron activity when excitatory neurons are activated to induce LTP. Finally, we propose recording excitatory and inhibitory neurons under the same experimental conditions by combining various electrophysiological technologies and novel design suggestions for future research. We discussed different types of synaptic plasticity, and the potential of astrocytes to induce LTP also deserves to be explored in the future.

Every year, the United States spends close to 18% of its gross domestic product on health care-a value that far surpasses that of any other developed nation. 1 Surgical expenditure accounts for nearly one-third of this national spending. 1 This cost has been projected to increase in coming years, as demand for additional operating rooms and procedural facilities continues to grow.Improving perioperative productivity and efficiency in the operating room is one approach that may help to reduce unnecessary costs for the hospital and the patient. 1,2 Furthermore, beyond the concrete financial savings, improving operating room efficiency can also increase operating room throughput, improve patient safety, and lead to greater staff and patient satisfaction (Fig. 1).Historically, quality improvement (QI) or process improvement models such as the Plan-Do-Study-Act model, the Focus-Analyze-Develop-Execute (FADE) model, and the Team Strategies and Tools to Enhance Performance and Patient Safety model have been used to increase productivity and eliminate inefficiencies within health care. 3,4 Alternative QI methodologies that are Background: Improving perioperative efficiency helps reduce unnecessary surgical expenditure, increase operating room throughput, improve patient safety, and enhance staff and patient satisfaction. Lean Six Sigma (LSS) is a quality improvement model that has been successfully applied to eliminate inefficiencies in the business sector but has not yet been widely adopted in medicine. This study investigates the adaptation of LSS to improve operative efficiency for plastic surgery procedures. Methods: The authors followed the define, measure, analyze, improve, and control phases to implement LSS. The key outcome measures gathered were operative times, including the cut-to-close time, and the total time the patient spent in the operating room. Results:The study included a total of 181 patients who underwent immediate bilateral deep inferior epigastric perforator flap breast reconstruction between January of 2016 and December of 2019. The LSS interventions were associated with a decrease in total operative time from 636.36 minutes to 530.35 minutes, and a decrease in the time between incision to closure from 555.16 minutes to 458.85 minutes for a bilateral mastectomy with immediate deep inferior epigastric artery flap breast reconstruction. Conclusions: This study demonstrates that LSS is useful to improve perioperative efficiency during complex plastic surgery procedures. The workflow of the procedure was improved by determining the optimal spatial positioning and distinct roles for each surgeon and preparing surgeon-specific surgical trays. Two process maps were developed to visualize the positioning of the surgeons during each stage of the procedure and depict the parallel workflow that helped improve intraoperative efficiency.