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Catalytic hydrogenation of CO2 has great potential to significantly reduce CO2 and contribute to green economy by converting CO2 into a variety of useful products. The goal of this study is to assess and compare the techno-economic and environmental measures of CO2 catalytic conversion to methanol and Fischer–Tropsch-based fuels. More specifically, two separate process models were developed using a process modeler: direct catalytic conversion of CO2 to Fischer–Tropsch-based liquid fuel/high-calorie SNG and direct catalytic conversion of CO2 to methanol. The unit production cost for each process was analyzed and compared to conventional liquid fuel and methanol production processes. CO2 emissions for each process were assessed in terms of global warming potential. The cost and environmental analyses results of each process were used to compare and contrast both routes in terms of economic feasibility and environmental friendliness. The results of both the processes indicated that the total CO2 emissions were significantly reduced compared with their respective conventional processes.

Background and Objectives: Postoperative delirium (POD) is a transient but significant complication in geriatric patients following hip or femur surgery. POD occurs in 19–65% of patients after hip surgeries, with notable risks associated with augmented morbidity, mortality, and prolonged hospitalization. The perioperative administration of benzodiazepines, particularly midazolam, is associated with an increased incidence of POD. Remimazolam, a novel ultra-short-acting benzodiazepine, has potential benefits, such as hemodynamic stability and ease of reversal, but its effect on POD occurrence remains unclear. Materials and Methods: This retrospective study investigated patients who were aged 65 years old and older who underwent hip or femur surgery. Following the application of exclusion criteria, 502 patients were grouped according to whether anesthesia was maintained with remimazolam (R group) or sevoflurane (S group). Data regarding patients’ baseline characteristics, anesthetic details, and postoperative outcomes, including the incidence of POD, were gathered and analyzed. Propensity score matching and logistic regression were conducted to identify factors associated with POD and compare outcomes between the two groups. Results: Among the 502 patients, POD was observed in 161 (32%). The POD incidence was not statistically significantly different between the groups (p = 1.000). A multivariable logistic regression analysis indicated that remimazolam was not a determinant of POD (p = 0.860), whereas being male and polypharmacy were (p = 0.022; p = 0.047). Initial disparities in age and comorbid conditions between the groups were rectified through matching, demonstrating that remimazolam had a similar POD risk to sevoflurane. Conclusions: This study showed that remimazolam did not exacerbate the risk of POD in elderly patients undergoing hip or femur surgery. Remimazolam is a reliable anesthetic option for this vulnerable demographic. Also, this study’s results indicated that polypharmacy and being male are POD risk factors, suggesting that meticulous perioperative medication management may help alleviate the risk of POD.

In the adult brain, neurogenesis occurs in the subgranular zone of the dentate gyrus (DG), where high levels of vesicular zinc are localized in the presynaptic terminals. To determine whether zinc has a role in modulating hippocampal neurogenesis under normal or pathologic conditions, we manipulated the level of vesicular zinc experimentally. To reduce hippocampal vesicular zinc, rats were either fed a zinc-deficient diet or treated with a zinc chelator, clioquinol (CQ). The number of progenitor cells and immature neurons was decreased significantly in the DG after 6 weeks of dietary zinc deprivation. Conversely, the number of progenitor cells and immature neurons was restored after a 2-week reversal to a normal zinc-containing diet. Similarly, a 1-week treatment with the zinc chelator, CQ, reduced the number of progenitor cells. The results of our previous study showed that hypoglycemia increased hippocampal neurogenesis. This study shows that zinc chelation reduced hypoglycemia-induced progenitor cell proliferation and neurogenesis. Finally, the role of vesicular zinc on neurogenesis was further assessed in zinc transporter 3 (ZnT3) gene deleted mice. Zinc transporter 3 knockout (KO) mice had significantly fewer proliferating progenitor cells and immature neurons after hypoglycemia. Our data provide converging evidence in support of the essential role zinc has in modulating hippocampal neurogenesis.

Background Recurrent/moderate (R/M) hypoglycemia is common in type 1 diabetes. Although mild or moderate hypoglycemia is not life-threatening, if recurrent, it may cause cognitive impairment. In the present study, we sought to determine whether R/M hypoglycemia leads to neuronal death, dendritic injury, or cognitive impairment. Methods The experiments were conducted in normal and in diabetic rats. Rats were subjected to moderate hypoglycemia by insulin without anesthesia. Oxidative stress was evaluated by 4-Hydroxy-2-nonenal immunostaining and neuronal death was determined by Fluoro-Jade B staining 7 days after R/M hypoglycemia. To test whether oxidative injury caused by NADPH oxidase activation, an NADPH oxidase inhibitor, apocynin, was used. Cognitive function was assessed by Barnes maze and open field tests at 6 weeks after R/M hypoglycemia. Results The present study found that oxidative injury was detected in the dendritic area of the hippocampus after R/M hypoglycemia. Sparse neuronal death was found in the cortex, but no neuronal death was detected in the hippocampus. Significant cognitive impairment and thinning of the CA1 dendritic region was detected 6 weeks after hypoglycemia. Oxidative injury, cognitive impairment, and hippocampal thinning after R/M hypoglycemia were more severe in diabetic rats than in non-diabetic rats. Oxidative damage in the hippocampal CA1 dendritic area and microglial activation were reduced by the NADPH oxidase inhibitor, apocynin. Conclusion The present study suggests that oxidative injury of the hippocampal CA1 dendritic region by R/M hypoglycemia is associated with chronic cognitive impairment in diabetic patients. The present study further suggests that NADPH oxidase inhibition may prevent R/M hypoglycemia-induced hippocampal dendritic injury.

Traumatic brain injury (TBI) is one of the most devastating injuries experienced by military personnel, as well as the general population, and can result in acute and chronic complications such as cognitive impairments. Since there are currently no effective tools for the treatment of TBI, it is of great importance to determine the mechanisms of neuronal death that characterize this insult. Several studies have indicated that TBI-induced neuronal death arises in part due to excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), which results in nicotinamide adenine dinucleotide (NAD+) depletion and subsequent energy failure. In this study, we investigated whether intranasal administration of NAD+ could reduce neuronal death after TBI. Rats were subjected to a weight-drop TBI model that induces cortical and hippocampal neuronal death. The intranasal administration of NAD+ (20 mg/kg) immediately after TBI protected neurons in CA1, CA3, and dentate gyrus of the hippocampus, but not in the cortex. In addition, delayed microglial activation normally seen after TBI was reduced by NAD+ treatment at 7 days after insult. Neuronal superoxide production and PARP-1 accumulation after TBI were not inhibited by NAD+ treatment, indicating that reactive oxygen species (ROS) production and PARP-1 activation are events that occur upstream of NAD+ depletion. This study suggests that intranasal delivery of NAD+ represents a novel, inexpensive, and non-toxic intervention for preventing TBI-induced neuronal death.

Hypoglycemia-induced cerebral neuropathy can occur in patients with diabetes who attempt tight control of blood glucose and may lead to cognitive dysfunction. Accumulating evidence from animal models suggests that hypoglycemia-induced neuronal death is not a simple result of glucose deprivation, but is instead the end result of a multifactorial process. In particular, the excessive activation of poly (ADP-ribose) polymerase-1 (PARP-1) consumes cytosolic nicotinamide adenine dinucleotide (NAD+), resulting in energy failure. In this study, we investigate whether lactate administration in the absence of cytosolic NAD+ affords neuroprotection against hypoglycemia-induced neuronal death. Intraperitoneal injection of sodium L-lactate corrected arterial blood pH and blood lactate concentration after hypoglycemia. Lactate administered without glucose was not sufficient to promote electroencephalogram recovery from an isoelectric state during hypoglycemia. However, supplementation of glucose with lactate reduced neuronal death by ∼80% in the hippocampus. Hypoglycemia-induced superoxide production and microglia activation was also substantially reduced by administration of lactate. Taken together, these results suggest an intriguing possibility: that increasing brain lactate following hypoglycemia offsets the decrease in NAD+ due to overactivation of PARP-1 by acting as an alternative energy substrate that can effectively bypass glycolysis and be fed directly to the citric acid cycle to maintain cellular ATP levels.

Hypothermia reduces neuronal damage after cerebral ischemia and traumatic brain injury, while hyperthermia exacerbates damage from these insults. Previously we have shown that temperature-dependent modulation of excitotoxic neuronal death is mediated in part by temperature-dependent changes in the synaptic release/translocation of Zn2+. In this study, we hypothesize that brain temperature also affects hypoglycemia-induced neuronal death by modulation of vesicular Zn2+ release from presynaptic terminals. To test our hypothesis, we used a rat model of insulin-induced hypoglycemia. Here we found that hypoglycemia-induced neuronal injury was significantly affected by brain temperature, that is, hypothermia inhibited while hyperthermia aggravated neuronal death. To investigate the mechanism of temperature-dependent neuronal death after hypoglycemia, we measured zinc release/translocation, reactive oxygen species (ROS) production, and microglia activation. Here we found that hypoglycemia-induced Zn2+ release/translocation, ROS production, and microglia activation were inhibited by hypothermia but aggravated by hyperthermia. Even when the insult was accompanied by hyperthermic conditions, zinc chelation inhibited ROS production and microglia activation. Zinc chelation during hyperthermia reduced neuronal death, superoxide production, and microglia activation, which was comparable to the protective effects of hypothermia. We conclude that neuronal death after hypoglycemia is temperature-dependent and is mediated by increased Zn2+ release, superoxide production, and microglia activation.

Melatonin, N-aceyl-5-methoxytryptamine, is the main secretory product of the pineal gland and has neuroprotective effects on several brain injuries, including ischemic stroke. In the present study, we hypothesized that exogenous melatonin may decrease hypoglycemia-induced neuronal death through the prevention of superoxide generation. To test our hypothesis, hypoglycemia was induced by injecting human insulin (10 U/kg, i.p.) in rats. Melatonin injection was started immediately after hypoglycemia (10 mg/kg, i.p.). The first melatonin injection was performed at the end of a 30-min isoelectric EEG period. The second and third injections were administered at 1 and 3 h after the first injection. Reactive oxygen species generation, as detected by dihydroethidium staining, was significantly reduced by melatonin treatment. Neuronal injury was reduced by the treatment of melatonin in the hippocampal CA1 and dentate granule cells. Microglia activation was robust in the hippocampus after hypoglycemia, which was almost completely prevented by melatonin treatment. Hypoglycemia-induced cognitive impairment was also significantly prevented by melatonin treatment. The present study suggests that melatonin has therapeutic potential to prevent hypoglycemia-induced brain injury.

Diabetic patients who attempt strict management of blood glucose levels frequently experience hypoglycemia. Severe and prolonged hypoglycemia causes neuronal death and cognitive impairment. There is no effective tool for prevention of these unwanted clinical sequelae. Minocycline, a second-generation tetracycline derivative, has been recognized as an anti-inflammatory and neuroprotective agent in several animal models such as stroke and traumatic brain injury. In the present study, we tested whether minocycline also has protective effects on hypoglycemia-induced neuronal death and cognitive impairment. To test our hypothesis we used an animal model of insulin-induced acute hypoglycemia. Minocycline was injected intraperitoneally at 6 hours after hypoglycemia/glucose reperfusion and injected once per day for the following 1 week. Histological evaluation for neuronal death and microglial activation was performed from 1 day to 1 week after hypoglycemia. Cognitive evaluation was conducted 6 weeks after hypoglycemia. Microglial activation began to be evident in the hippocampal area at 1 day after hypoglycemia and persisted for 1 week. Minocycline injection significantly reduced hypoglycemia-induced microglial activation and myeloperoxidase (MPO) immunoreactivity. Neuronal death was significantly reduced by minocycline treatment when evaluated at 1 week after hypoglycemia. Hypoglycemia-induced cognitive impairment is also significantly prevented by the same minocycline regimen when subjects were evaluated at 6 weeks after hypoglycemia. Therefore, these results suggest that delayed treatment (6 hours post-insult) with minocycline protects against microglial activation, neuronal death and cognitive impairment caused by severe hypoglycemia. The present study suggests that minocycline has therapeutic potential to prevent hypoglycemia-induced brain injury in diabetic patients.

The mechanism of hypoglycemia-induced neuronal death has been extensively studied since a Swedish scientist, Roland Auer, developed a rat model of insulin-induced hypoglycemia one quarter of a century ago. Currently, mounting data derived from these studies are making it possible to propose an ever more complete mechanism of hypoglycemia-induced neuron death. Although salient differences between the two insults do exist, the pattern and progression of neuron death after acute/severe hypoglycemia have been observed to share many similarities with ischemia-induced neuron death. One important consideration is that the divalent cation zinc is a common neurotoxic factor in both conditions. For the last decade, our laboratory has offered evidence for the hypothesis that synaptic vesicular zinc release and subsequent translocation into the postsynaptic neuron are key upstream events in both neurological injuries of ischemia and hypoglycemia. The release of vesicular zinc from presynaptic terminals depends on nitric oxide production, which is initiated by glucose reperfusion after hypoglycemia. Postsynaptic intracellular influx of zinc after hypoglycemia increases reactive oxygen species production and PARP-1 activation, which eventually leads to neuronal death. Thus, hypoglycemia-induced neuronal death is not simply caused by a lack of neuronal glucose availability but rather by sequential zinc-mediated events that impinge upon the process of neuronal death. This paper focuses on the role of zinc in hypoglycemia-induced neuron death; first, the temporal events of zinc release and translocation after severe hypoglycemia; second, the role of zinc on reactive oxygen species production; and third, the role of zinc on poly(ADP-ribose) polymerase 1 activation. Here, we also speculate on possible intervention strategies to prevent hypoglycemia-induced neuronal death.