A Study on the Impact of Financial Literacy and Digital Capabilities on Entrepreneurial Intention: Mediating Effect of Entrepreneurship.

In the post-COVID-19 era, the content of work and the necessary skills are rapidly changing due to the digital transformation of the way people work. Entrepreneurial adaptability and digital capability are the most necessary competencies for exploring opportunities and quickly turning them into a professional career amid a crisis. Financial literacy is also essential for expanding skills in economic and social life. The purpose of this study is to verify the influence of university students' financial literacy and digital capability on entrepreneurial intention and the mediating effect of entrepreneurship. To this end, a survey was conducted on university students in Busan and Gyeongnam, and a sample of 162 respondents was verified using SPSS 28.0. As a result of the study, it was found that financial literacy had a partially positive effect on entrepreneurship and entrepreneurial intention. Digital capability was found to have a positive effect on entrepreneurship and entrepreneurial intention. It was found that entrepreneurship had a partially positive effect on entrepreneurial intention. It was found that entrepreneurship had a partially positive mediating effect between financial literacy and entrepreneurial intention. It was found that entrepreneurship had a positive mediating effect between digital capability and entrepreneurial intention. As a result of this study, it was confirmed that financial literacy, digital capability, and entrepreneurship are very important competencies for university students to adapt to new trends and promote start-ups in a rapidly changing job environment after COVID-19, suggesting the need for further education.

Hemodynamic performance evaluation of neonatal ECMO double lumen cannula using fluid-structure interaction.

Extra corporeal membrane oxygenation (ECMO) is an artificial oxygenation facility, employed in situations of cardio-pulmonary failure. Some diseases i.e., acute respiratory distress syndrome, pulmonary hypertension, corona virus disease (COVID-19) etc. affect oxygenation performance of the lungs thus requiring the need of artificial oxygenation. Critical care teams used ECMO technique during the COVID-19 pandemic to support the heart and lungs of COVID-19 patients who had an acute respiratory or cardiac failure. Double Lumen Cannula (DLC) is one of the most critical components of ECMO as it resides inside the patient and, connects patient with external oxygenation circuit. DLC facilitates delivery and drainage of blood from the patient's body. DLC is characterized by delicate balance of internal and external flows inside a limited space of the right atrium (RA). An optimal performance of the DLC necessitates structural stability under biological and hemodynamic loads, a fact that has been overlooked by previously published studies. In the past, many researchers experimentally and computationally investigated the hemodynamic performance of DLC by employing Eulerian approach, which evaluate instantaneous blood damage without considering blood shear exposure history (qualitative assessment only). The present study is an attempt to address the aforementioned limitations of the previous studies by employing Lagrangian (quantitative assessment) and incorporating the effect of fluid-structure interaction (FSI) to study the hemodynamic performance of neonatal DLC. The study was performed by solving three-dimensional continuity, momentum, and structural mechanics equation(s) by numerical methods for the blood flow through neonatal DLC. A two-way coupled FSI analysis was performed to analyze the effect of DLC structural deformation on its hemodynamic performance. Results show that the return lumen was the most critical section with maximum pressure drop, velocity, shear stresses, and blood damage. Recirculation and residence time of blood in the right atrium (RA) increases with increasing blood flow rates. Considering the structural deformation has led to higher blood damage inside the DLC-atrium system. Maximum Von-Mises stress was present on the side edges of the return lumen that showed direct proportionality with the blood flow rate.

Deep learning-based optimization of a microfluidic membraneless fuel cell for maximum power density via data-driven three-dimensional multiphysics simulation.

A deep learning-based method for optimizing a membraneless microfluidic fuel cell (MMFC)performance by combining the artificial neural network (ANN) and genetic algorithm (GA) was for the first time introduced. A three-dimensional multiphysics model that had an accuracy equivalent to experimental results (R2 = 0.976) was employed to generate the ANN's training data. The constructed ANN is equivalent to the simulation (R2 = 0.999) but with far better computation resource efficiency as the ANN's execution time is only 0.041 s. The ANN model is then used by the GA to determine the inputs (microchannel length = 10.040 mm, width = 0.501 mm, height = 0.635 mm; temperature = 288.210 K, cell voltage = 0.309 V) that lead to the maximum power density of 0.263 mWcm-2 (current density of 0.852 mAcm-2) of the MMFC. The ANN-GA and numerically calculated maximum power densities differed only by 0.766%.

Changes in Cyclin D1, cdk4, and Their Associated Molecules in Ischemic Pyramidal Neurons in Gerbil Hippocampus after Transient Ischemia and Neuroprotective Effects of Ischemic Preconditioning by Keeping the Molecules in the Ischemic Neurons.

Inadequate activation of cell cycle proteins including cyclin D1 and cdk4 is involved in neuronal cell death induced by diverse pathological stresses, including transient global brain ischemia. The neuroprotective effect of ischemic preconditioning is well-established, but the underlying mechanism is still unknown. In this study, we examined changes in cyclin D1, cdk4, and related molecules in cells or neurons located in Cornu Ammonis 1 (CA1) of gerbil hippocampus after transient ischemia for 5 min (ischemia and reperfusion) and investigated the effects of IPC on these molecules after ischemia. Four groups were used in this study as follows: sham group, ischemia group, IPC plus (+) sham group, and IPC+ischemia group. IPC was developed by inducing 2-min ischemia at 24 h before 5-min ischemia (real ischemia). Most pyramidal cells located in CA1 of the ischemia group died five days after ischemia. CA1 pyramidal cells in the IPC+ischemia group were protected. In the ischemia group, the expressions of cyclin D1, cdk4, phosphorylated retinoblastoma (p-Rb), and E2F1 (a transcription factor regulated by p-Rb) were significantly altered in the pyramidal cells with time after ischemia; in the IPC+ischemia group, they were controlled at the level shown in the sham group. In particular, the expression of p16INK4a (an endogenous cdk inhibitor) in the ischemia group was reversely altered in the pyramidal cells; in the IPC+TI group, the expression of p16INK4a was not different from that shown in the sham group. Our current results indicate that cyclin D1/cdk4-related signals may have important roles in events in neurons related to damage/death following ischemia and reperfusion. In particular, the preservation of p16INK4a by IPC may be crucial in attenuating neuronal death/damage or protecting neurons after brain ischemic insults.

Development of Er3+, Yb3+ Co-Doped Y2O3 NPs According to Yb3+ Concentration by LP-PLA Method: Potential Further Biosensor.

As diagnostic biosensors for analyzing fluids from the human body, the development of inorganic NPs is of increasing concern. For one, nanoceramic phosphors have been studied to meet the increasing requirements for biological, imaging, and diagnostic applications. In this study, Y2O3 NPs co-doped with trivalent rare earths (erbium and ytterbium) were obtained using a liquid phase-pulsed laser ablation (LP-PLA) method after getting high density Er, Yb:Y2O3 ceramic targets by Spark plasma sintering (SPS). Most NPs are under 50 nm in diameter and show high crystallinity of cubic Y2O3 structure, containing (222), (440), and (332) planes via HR-TEM. Excitation under a 980 nm laser to a nanoparticle solution showed 525 and 565 nm green, and 660 nm red emissions. The green emission intensity increased and decreased with increasing Yb3+ additive concentration, when the red spectrum continuously strengthened. Utilizing this study's outcome, we suggest developing technology to mark invisible biomolecules dissolved in a solvent using UC luminescence of Er3+, Yb3+ co-doped Y2O3 NPs by LP-PLA. The LP-PLA method has a potential ability for the fabrication of UC NPs for biosensors with uniform size distribution by laser parameters.

Homogeneous and Multiphase Analysis of Nanofluids Containing Nonspherical MWCNT and GNP Nanoparticles Considering the Influence of Interfacial Layering.

The practical implication of nanofluids is essentially dependent on their accurate modelling, particularly in comparison with the high cost of experimental investigations, yet the accuracy of different computational approaches to simulate nanofluids remains controversial to this day. Therefore, the present study is aimed at analysing the homogenous, multiphase Eulerian-Eulerian (volume of fluid, mixture, Eulerian) and Lagrangian-Eulerian approximation of nanofluids containing nonspherical nanoparticles. The heat transfer and pressure drop characteristics of the multiwalled carbon nanotubes (MWCNT)-based and multiwalled carbon nanotubes/graphene nanoplatelets (MWCNT/GNP)-based nanofluids are computed by incorporating the influence of several physical mechanisms, including interfacial nanolayering. The accuracy of tested computational approaches is evaluated by considering particle concentration and Reynolds number ranges of 0.075-0.25 wt% and 200-470, respectively. The results demonstrate that for all nanofluid combinations and operational conditions, the Lagrangian-Eulerian approximation provides the most accurate convective heat transfer coefficient values with a maximum deviation of 5.34% for 0.25 wt% of MWCNT-water nanofluid at the largest Reynolds number, while single-phase and Eulerian-Eulerian multiphase models accurately estimate the thermal fields of the diluted nanofluids at low Reynolds numbers, but overestimate the results for denser nanofluids at high Reynolds numbers.

Comparative evaluation of ballet-type and conventional stent graft configurations for endovascular aneurysm repair: A CFD analysis.

PURPOSE: Cross limb stent graft (SG) configuration technique for endovascular aneurysm repair (EVAR) is employed for splayed aortic bifurcations to avoid device kinking and smoothen cannulation. The present study investigates three types of stent graft (SG) configurations for endovascular aneurysm repair (EVAR) in abdominal aortic aneurysm. A computational fluid dynamic analysis was performed on the pulsatile non-Newtonian flow characteristics in three ideally modeled geometries of abdominal aortic (AA) SG configurations. METHODS: The three planar and crosslimb SG configurations were ideally modeled, namely, top-down nonballet-type, top-down ballet-type, and bottom-up nonballet-type configurations. In top-down SG configuration, most of the device is deployed in the main body in the vicinity of renal artery and the limbs are extended to the iliac artery. While in the bottom-up configuration, some of the SG device is deployed in the main body, the limbs are deployed in aortic bifurcation, and the extra stent graft of the main body is extended to the proximal aorta until the below of the renal artery. The effects of non-Newtonian pulsatile flow on the wall stresses and flow patterns of the three models were investigated and compared. Moreover, the average wall shear stress (AWSS), oscillatory shear stress index (OSI), absolute helicity, pressure distribution, graft displacement and flow visualization plots were analyzed. RESULTS: The top-down ballet-type showed less branch blockage effect than the top-down nonballet-type models. Furthermore, the top-down ballet-type configuration showed an increased tendency to sustain high WSS and higher helicity characteristics than that of the bottom-up and top-down non-ballet type configurations. However, displacement forces of the top-down ballet-type configuration were 40% and 9.6% higher than those of the bottom-up and top-down nonballet-type configurations, respectively. CONCLUSIONS: Some complications such as graft tearing, thrombus formation, limb disconnection during long term follow up periods might be relevant to hemodynamic characteristics according to the configurations of EVAR. Hence, the reported data required to be validated with the clinical results.

Experimental pretreatment with YES-10®, a plant extract rich in scutellarin and chlorogenic acid, protects hippocampal neurons from ischemia/reperfusion injury via antioxidant role.

Erigeron annuus (L.) PERS. (EALP) and Clematis mandshurica RUPR. (CMR) have been used in traditional remedies due to their medicinal effects. Recently, we reported that pretreatment with 200 mg/kg of YES-10® (a combination of extracts from leaves of EALP and CMR) displayed neuroprotective effects against brain ischemia and reperfusion injury. The present study analyzed the major ingredients of YES-10® and investigated whether neuroprotection from YES-10® was dependent upon antioxidant effects in the cornu ammonis 1 (CA1) field in the gerbil hippocampus, after transient forebrain ischemia for 5 min. YES-10® was demonstrated to predominantly contain scutellarin and chlorogenic acid. Pretreatment with YES-10® significantly increased protein levels and the immunoreactivity of copper/zinc-superoxide dismutase (SOD1) and manganese-superoxide dismutase (SOD2) was in the pyramidal neurons of the hippocampal CA1 field when these were examined prior to transient ischemia induction. The increased SODs in CA1 pyramidal neurons following YES-10® treatment were maintained after ischemic injury. In this case, the CA1 pyramidal neurons were protected from ischemia-reperfusion injury. Oxidative stress was significantly attenuated in the CA1 pyramidal neurons, and this was determined by 4-hydroxy-2-nonenal immunohistochemistry and dihydroethidium histofluorescence staining. Taken together, the results indicated that YES-10® significantly attenuated transient ischemia-induced oxidative stress and may be utilized for developing a protective agent against ischemic insults.

Pycnogenol® Supplementation Attenuates Memory Deficits and Protects Hippocampal CA1 Pyramidal Neurons via Antioxidative Role in a Gerbil Model of Transient Forebrain Ischemia.

Pycnogenol® (an extract of the bark of French maritime pine tree) is used for dietary supplement and known to have excellent antioxidative efficacy. However, there are few reports on neuroprotective effect of Pycnogenol® supplementation and its mechanisms against ischemic injury following transient forebrain ischemia (TFI) in gerbils. Now, we examined neuroprotective effect and its mechanisms of Pycnogenol® in the gerbils with 5-min TFI, which evokes a significant death (loss) of pyramidal cells located in the cornu ammonis (CA1) region of gerbil hippocampus from 4-5 days post-TFI. Gerbils were pretreated with 30, 40, and 50 mg/kg of Pycnogenol® once a day for 7 days before TFI surgery. Treatment with 50 mg/kg, not 30 or 40 mg/kg, of Pycnogenol® potently protected learning and memory, as well as CA1 pyramidal cells, from ischemic injury. Treatment with 50 mg/kg Pycnogenol® significantly enhanced immunoreactivity of antioxidant enzymes (superoxide dismutases and catalase) in the pyramidal cells before and after TFI induction. Furthermore, the treatment significantly reduced the generation of superoxide anion, ribonucleic acid oxidation and lipid peroxidation in the pyramidal cells. Moreover, interestingly, its neuroprotective effect was abolished by administration of sodium azide (a potent inhibitor of SODs and catalase activities). Taken together, current results clearly indicate that Pycnogenol® supplementation can prevent neurons from ischemic stroke through its potent antioxidative role.

Laminarin Attenuates Ultraviolet-Induced Skin Damage by Reducing Superoxide Anion Levels and Increasing Endogenous Antioxidants in the Dorsal Skin of Mice.

A number of studies have demonstrated that marine carbohydrates display anti-oxidant, anti-melanogenic, and anti-aging activities in the skin. Laminarin (LA), a low-molecular-weight polysaccharide, is found in brown algae. The benefits of LA in ultraviolet B (UVB) induced photodamage of the skin have not been reported. The aim of this study was to investigate the effects of pre-treated LA on histopathological changes and oxidative damage in mouse dorsal skin on day 5, following repeated UVB exposure. Histopathology, Western blot analysis and immunohistochemical studies showed that epidermal thickness in the UVB group was significantly increased; however, the thickness in the UVB group treated with LA (LA/UVB group) was less compared with that of the UVB group. Collagen fibers in the dermis of the UVB group were significantly decreased and destroyed, whereas, in the LA/UVB group, the density of collagen fibers was significantly increased compared with that of the UVB group. Oxidative stress due to superoxide anion production measured via dihydroethidium fluorescence staining was dramatically increased in the UVB group, whereas in the LA/UVB group, the oxidative stress was significantly decreased. Expressions of SOD1, glutathione peroxidase and catalase were markedly reduced in the UVB group, whereas in the LA/UVB group, they were significantly higher along with SOD2 than in the control group. Taken together, our results indicate that LA pretreatment prevents or attenuates skin damage, by decreasing oxidative stress and increasing antioxidant enzymes in mouse dorsal skin.

Laminarin Pretreatment Provides Neuroprotection against Forebrain Ischemia/Reperfusion Injury by Reducing Oxidative Stress and Neuroinflammation in Aged Gerbils.

Laminarin is a polysaccharide isolated from brown algae that has various biological and pharmacological activities, such as antioxidant and anti-inflammatory properties. We recently reported that pretreated laminarin exerted neuroprotection against transient forebrain ischemia/reperfusion (IR) injury when we pretreated with 50 mg/kg of laminarin once a day for seven days in adult gerbils. However, there have been no studies regarding a neuroprotective effect of pretreated laminarin against IR injury in aged animals and its related mechanisms. Therefore, in this study, we intraperitoneally inject laminarin (50 mg/kg) once a day to aged gerbils for seven days before IR (5-min transient ischemia) surgery and examine the neuroprotective effect of laminarin treatment and the mechanisms in the gerbil hippocampus. IR injury in vehicle-treated gerbils causes loss (death) of pyramidal neurons in the hippocampal CA1 field at five days post-IR. Pretreatment with laminarin effectively protects the CA1 pyramidal neurons from IR injury. Regarding the laminarin-treated gerbils, production of superoxide anions, 4-hydroxy-2-nonenal expression and pro-inflammatory cytokines [interleukin(IL)-1ß and tumor necrosis factor-α] expressions are significantly decreased in the CA1 pyramidal neurons after IR. Additionally, laminarin treatment significantly increases expressions of superoxide dismutase and anti-inflammatory cytokines (IL-4 and IL-13) in the CA1 pyramidal neurons before and after IR. Taken together, these findings indicate that laminarin can protect neurons from ischemic brain injury in an aged population by attenuating IR-induced oxidative stress and neuroinflammation.

YES-10, A Combination of Extracts from Clematis mandshurica RUPR. and Erigeron annuus (L.) PERS., Prevents Ischemic Brain Injury in A Gerbil Model of Transient Forebrain Ischemia.

: Clematis mandshurica RUPR. (CMR) and Erigeron annuus (L.) PERS. (EALP) have pharmacological effects including anti-inflammatory activity and been used in traditional medicines in Asia. However, neuroprotective effects of CMR and/or EALP extracts against brain ischemic insults have never been addressed. Thus, the aim of this study was to examine neuroprotective effects of YES-10, a combination of extracts from CMR and EALP (combination ratio, 1:1), in the hippocampus following ischemia/reperfusion in gerbils. Protection of neurons was investigated by cresyl violet staining, fluoro-jade B histofluorescence staining and immunohistochemistry for neuronal nuclei. In addition, attenuation of gliosis was studied by immunohistochemistry for astrocytic and microglial markers. Treatments with 50 or 100 mg/kg YES-10 failed to protect neurons in the hippocampus after ischemia/reperfusion injury. However, administration of 200 mg/kg YES-10 protected neurons from ischemia/reperfusion injury and attenuated reactive gliosis. These findings strongly suggest that a combination of extracts from CMR and EALP can be used as a prevention approach/drug against brain ischemic damage.

Post-treatment with oxcarbazepine confers potent neuroprotection against transient global cerebral ischemic injury by activating Nrf2 defense pathway.

Oxcarbazepine (OXC), a voltage-gated sodium channel blocker, is an antiepileptic medication and used for the bipolar disorders treatment. Some voltage-gated sodium channel blockers have been demonstrated to display strong neuroprotective properties in models of cerebral ischemia. However, neuroprotective effects and mechanisms of OXC have not yet been reported. Here, we investigated the protective effect of OXC and its mechanisms in the cornu ammonis 1 subfield (CA1) of gerbils subjected to 5 min of transient global cerebral ischemia (tGCI). tGCI led to death of most pyramidal neurons in CA1 at 5 days after ischemia. OXC (100 and 200 mg/kg) was intraperitoneally administered once at 30 min after tGCI. Treatment with 200 mg/kg, not 100 mg/kg OXC, significantly protected CA1 pyramidal neurons from tGCI-induced injury. OXC treatment significantly decreased superoxide anion production, 4-hydroxy-2-nonenal and 8-hydroxyguanine levels in ischemic CA1 pyramidal neurons. In addition, the treatment restored levels of superoxide dismutases, catalase, and glutathione peroxidase. Furthermore, the treatment distinctly inhibited tGCI-induced microglia activation and significantly reduced levels of pro-inflammatory cytokines (interleukin-1ß and tumor necrosis factor-α). In particular, OXC treatment significantly enhanced expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream protein heme oxygenase-1 in ischemic CA1. The neuroprotective effects of OXC were abolished by brusatol (an inhibitor of Nrf2). Taken together, these results indicate that post-treatment of OXC can display neuroprotection against brain injuries following ischemic insults. This neuroprotection may be displayed by attenuation of oxidative stress and neuroinflammation, which can be mediated by activation of Nrf2 pathway.

Pre-Treatment with Laminarin Protects Hippocampal CA1 Pyramidal Neurons and Attenuates Reactive Gliosis Following Transient Forebrain Ischemia in Gerbils.

Transient brain ischemia triggers selective neuronal death/loss, especially in vulnerable regions of the brain including the hippocampus. Laminarin, a polysaccharide originating from brown seaweed, has various pharmaceutical properties including an antioxidant function. To the best of our knowledge, few studies have been conducted on the protective effects of laminarin against ischemic injury induced by ischemic insults. In this study, we histopathologically investigated the neuroprotective effects of laminarin in the Cornu Ammonis 1 (CA1) field of the hippocampus, which is very vulnerable to ischemia-reperfusion injury, following transient forebrain ischemia (TFI) for five minutes in gerbils. The neuroprotective effect was examined by cresyl violet staining, Fluoro-Jade B histofluorescence staining and immunohistochemistry for neuronal-specific nuclear protein. Additionally, to study gliosis (glial changes), we performed immunohistochemistry for glial fibrillary acidic protein to examine astrocytes, and ionized calcium-binding adaptor molecule 1 to examine microglia. Furthermore, we examined alterations in pro-inflammatory M1 microglia by using double immunofluorescence. Pretreatment with 10 mg/kg laminarin failed to protect neurons in the hippocampal CA1 field and did not attenuate reactive gliosis in the field following TFI. In contrast, pretreatment with 50 or 100 mg/kg laminarin protected neurons, attenuated reactive gliosis and reduced pro-inflammatory M1 microglia in the CA1 field following TFI. Based on these results, we firmly propose that 50 mg/kg laminarin can be strategically applied to develop a preventative against injuries following cerebral ischemic insults.

Altered Nurr1 protein expression in the hippocampal CA1 region following transient global cerebral ischemia.

Nuclear receptor related 1 protein (Nurr1), a member of the nuclear receptor 4 family of orphan nuclear receptors, has been reported to display anti­inflammatory properties. The present study investigated the alteration of Nurr1 immunoreactivity in the gerbil hippocampus proper following 5 min of transient global cerebral ischemia. In sham operated gerbils, Nurr1 immunoreactivity was observed in pyramidal neurons in all cornu ammonis 1­3 (CA1­3) subfields of the hippocampus proper. In ischemia­operated gerbils, Nurr1 immunoreactivity was altered in the CA1 subfield. Nurr1 immunoreactivity in CA1 pyramidal neurons gradually decreased until 2 days post­ischemia, and, at 4 days post­ischemia, Nurr1 immunoreactivity was concentrated in CA1 pyramidal neurons. Additionally, Nurr1 immunoreactivity was newly expressed in microglia in the CA1 subfield at 4 days post­ischemia. Conversely, in the CA2/3 subfield, time­dependent alteration of Nurr1 immunoreactivity was not identified at any time following ischemia. These results indicated that the alteration of Nurr1 expression in the CA1 subfield in the hippocampus may be associated with the death of CA1 pyramidal neurons.

Improved HCN channels in pyramidal neurons and their new expression levels in pericytes and astrocytes in the gerbil hippocampal CA1 subfield following transient ischemia.

Hyperpolarization­activated cyclic nucleotide­gated (HCN) channels have been known to participate in the regulation of neuronal excitability, synaptic transmission and long­term potentiation in the hippocampus. The present study investigated transient ischemia­induced changes of HCN1 and HCN2 expressions in the Cornu Ammonis 1 (CA1) subfield of the hippocampus in gerbils subjected to 5 min transient global cerebral ischemia (tgCI). Neuronal death was exhibited in pyramidal neurons of the striatum pyramidale in the CA1 subfield 4 days after tgCI. HCN1 and HCN2 immunoreactivities were demonstrated in intact CA1 pyramidal neurons, and were transiently and markedly increased in the CA pyramidal neurons at 6 h after ischemia. Thereafter, they gradually decreased in a time­dependent manner. A total of 4 days after ischemia, HCN1 and HCN2 immunoreactivities were barely detected in the CA1 pyramidal neurons; however, HCN1 and HCN2 were began to be expressed in pericytes and astrocytes at 4 days after ischemia. The results indicated that HCN1 and HCN2 expression levels were apparently changed in the gerbil hippocampal CA1 subfield following tgCI and suggested that ischemia­induced alterations in HCN1 and HCN2 expression levels may be closely associated with the death of CA1 pyramidal neurons following 5 min of tgCI.

A 2-Min Transient Ischemia Confers Cerebral Ischemic Tolerance in Non-Obese Gerbils, but Results in Neuronal Death in Obese Gerbils by Increasing Abnormal mTOR Activation-Mediated Oxidative Stress and Neuroinflammation.

A brief episode of transient ischemia (TI) can confer cerebral ischemic tolerance against a subsequent severer TI under standard condition. The brain under obesity's conditions is more sensitive to ischemic injury. However, the impact of a brief episode of TI under obesity's conditions has not been fully addressed yet. Thus, the objective of this study was to determine the effect of a brief TI in the hippocampus of high-fat diet (HFD)-induced obese gerbils and related mechanisms. Gerbils were maintained on HFD or normal diet (ND) for 12 weeks and subjected to 2 min TI. HFD gerbils were heavier, with higher blood glucose, serum total cholesterol, triglycerides, and leptin levels. Massive loss of pyramidal neurons occurred in the hippocampal cornu ammonis 1 (CA1) field of HFD animals at 5 days after 2 min of TI, but 2 min of TI did not elicit death of pyramidal neurons in ND gerbils. The HFD group showed significantly increased levels of oxidative stress indicators (dihydroethidium and 4-hydroxynonenal) and proinflammatory cytokines (tumor necrosis factor-α and interleukin-1ß) and microglial activation in pre- and/or post-ischemic phases compared to the ND group. Levels of mammalian target of rapamycin (mTOR) and phosphorylated-mTOR in the CA1 field of the HFD group were also significantly higher than the ND group. On the other hand, inhibition of mTOR activation by rapamycin (an allosteric mTOR inhibitor) significantly attenuated neuronal death induced by HFD, showing reduction of HFD-induced increases of oxidative stress indicators and proinflammatory cytokines, and microglia activation. Taken together, a brief episode of TI can evoke neuronal death under obesity's conditions. It might be closely associated with an abnormal increase of mTOR activation-mediated, severe oxidative stress and neuroinflammation in pre- and/or post-ischemic phases.

Therapeutic hypothermia attenuates paraplegia and neuronal damage in the lumbar spinal cord in a rat model of asphyxial cardiac arrest.

Spinal cord ischemia can result from cardiac arrest. It is an important cause of severe spinal cord injury that can lead to serious spinal cord disorders such as paraplegia. Hypothermia is widely acknowledged as an effective neuroprotective intervention following cardiac arrest injury. However, studies on effects of hypothermia on spinal cord injury following asphyxial cardiac arrest and cardiopulmonary resuscitation (CA/CPR) are insufficient. The objective of this study was to examine effects of hypothermia on motor deficit of hind limbs of rats and vulnerability of their spinal cords following asphyxial CA/CPR. Experimental groups included a sham group, a group subjected to CA/CPR, and a therapeutic hypothermia group. Severe motor deficit of hind limbs was observed in the control group at 1 day after asphyxial CA/CPR. In the hypothermia group, motor deficit of hind limbs was significantly attenuated compared to that in the control group. Damage/death of motor neurons in the lumbar spinal cord was detected in the ventral horn at 1 day after asphyxial CA/CPR. Neuronal damage was significantly attenuated in the hypothermia group compared to that in the control group. These results indicated that therapeutic hypothermia after asphyxial CA/CPR significantly reduced hind limb motor dysfunction and motoneuronal damage/death in the ventral horn of the lumbar spinal cord following asphyxial CA/CPR. Thus, hypothermia might be a therapeutic strategy to decrease motor dysfunction by attenuating damage/death of spinal motor neurons following asphyxial CA/CPR.

CFD and kinetic-based modeling to optimize the sparger design of a large-scale photobioreactor for scaling up of biofuel production.

Microalgal biofuels have not yet achieved wide-spread commercialization, partially as a result of the complexities involved with designing and scaling up of their biosystems. The sparger design of a pilot-scale photobioreactor (120 L) was optimized to enable the scale-up of biofuel production. An integrated model coupling computational fluid dynamics and microalgal biofuel synthesis kinetics was used to simulate the biomass growth and novel biofuel production (i.e., bisabolene) in the photobioreactor. Bisabolene production from Chlamydomonas reinhardtii mutant was used as an example to test the proposed model. To select the optimal sparger configuration, a rigorous procedure was followed by examining the effects of sparger design parameters (number and diameter of sparger holes and gas flow rates) on spatially averaged bubble volume fraction, light intensity, friction velocity, power input, biomass concentration, and bisabolene production. The optimized sparger design increases the final biomass concentration by 18%, thereby facilitating the scaling up of biofuel production.

Parvalbumin-immunoreactive cells in the olfactory bulb of the pigeon: Comparison with the rat.

The olfactory bulb (OB) shows special characteristics in its phylogenetic cortical structure and synaptic pattern. In the OB, gamma-aminobutyric acid (GABA), as an inhibitory neurotransmitter, is secreted from GABAergic neurons which contain parvalbumin (a calcium-binding protein). Many studies on the distribution of parvalbumin-immunoreactive neurons in the rodent OB have been published but poorly reported in the avian OB. Therefore, in this study, we compared the structure of the OB and distribution of parvalbumin-immunoreactive neurons in the OB between the rat and pigeon using cresyl violet staining and immunohistochemistry for parvalbumin, respectively. Fundamentally, the pigeon OB showed layers like those of the rat OB; however, some layers were not clear like in the rat OB. Parvalbumin-immunoreactive neurons in the pigeon OB were predominantly distributed in the external plexiform layer like that in the rat OB; however, the neurons did not have long processes like those in the rat. Furthermore, parvalbumin-immunoreactive fibres were abundant in some layers; this finding was not shown in the rat OB. In brief, parvalbumin-immunoreactive neurons were found like those in the rat OB; however, parvalbumin-immunoreactive fibres were significantly abundant in the pigeon OB compared to those in the rat OB.