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Abstract Background Quelling microglial-induced excessive neuroinflammation is a potential treatment strategy across neurological disorders, including traumatic brain injury (TBI), and can be achieved by thalidomide-like drugs albeit this approved drug class is compromised by potential teratogenicity. Tetrafluorobornylphthalimide (TFBP) and tetrafluoronorbornylphthalimide (TFNBP) were generated to retain the core phthalimide structure of thalidomide immunomodulatory imide drug (IMiD) class. However, the classical glutarimide ring was replaced by a bridged ring structure. TFBP/TFNBP were hence designed to retain beneficial anti-inflammatory properties of IMiDs but, importantly, hinder cereblon binding that underlies the adverse action of thalidomide-like drugs. Methods TFBP/TFNBP were synthesized and evaluated for cereblon binding and anti-inflammatory actions in human and rodent cell cultures. Teratogenic potential was assessed in chicken embryos, and in vivo anti-inflammatory actions in rodents challenged with either lipopolysaccharide (LPS) or controlled cortical impact (CCI) moderate traumatic brain injury (TBI). Molecular modeling was performed to provide insight into drug/cereblon binding interactions. Results TFBP/TFNBP reduced markers of inflammation in mouse macrophage-like RAW264.7 cell cultures and in rodents challenged with LPS, lowering proinflammatory cytokines. Binding studies demonstrated minimal interaction with cereblon, with no resulting degradation of teratogenicity-associated transcription factor SALL4 or of teratogenicity in chicken embryo assays. To evaluate the biological relevance of its anti-inflammatory actions, two doses of TFBP were administered to mice at 1 and 24 h post-injury following CCI TBI. Compared to vehicle treatment, TFBP reduced TBI lesion size together with TBI-induction of an activated microglial phenotype, as evaluated by immunohistochemistry 2-weeks post-injury. Behavioral evaluations at 1- and 2-weeks post-injury demonstrated TFBP provided more rapid recovery of TBI-induced motor coordination and balance impairments, versus vehicle treated mice. Conclusion TFBP and TFNBP represent a new class of thalidomide-like IMiDs that lower proinflammatory cytokine generation but lack binding to cereblon, the main teratogenicity-associated mechanism. This aspect makes TFBP and TFNBP potentially safer than classic IMiDs for clinical use. TFBP provides a strategy to mitigate excessive neuroinflammation associated with moderate severity TBI to, thereby, improve behavioral outcome measures and warrants further investigation in neurological disorders involving a neuroinflammatory component. Graphical Abstract

Abstract In this study, the electrochemical characteristics of an anode fabricated using exfoliated graphite (EG), which is mass‐produced using an electrochemical method, are evaluated to verify the potential of EG as a conductive additive. EG exhibits high electrical conductivity because of the sp2 bonding on the two‐dimensional plane; this conductivity provides a stable electrical pathway and promotes electron transfer in the anode. Furthermore, the small number of graphene layers in EG provide excellent mechanical properties (elastic modulus, tensile strength), which suppresses the volume expansion of the anode during lithiation; therefore, EG‐based anode exhibits high capacity retention and charge/discharge cycle stability. The EG with a large specific surface area improves energy density by decreasing the amount of the additive by more than 70% compared to conventional conductive additives and by simultaneously increasing the amount of the active material. The capacity of the electrode with 3.0 wt% EG reaches 376 mAh/g even after 200 cycles at 0.2 C and 99% of its initial reversible capacity. The rate performance of the electrode with 3.0 wt% EG was about 370 mAh/g at 5.0 C. These results confirm that EG can be used as a conductive additive to overcome the limitations of existing commercial conductive agents.

A new type of silicon oxide-based carbon composite (SiOx@C) was developed to solve the prevalent challenges associated with conventional anode materials, such as pronounced volume fluctuations and inadequate electrical conductivity. The control of oxidation of SiOx was optimized to suppress the excessive formation of the solid electrolyte interphase (SEI) layer and eliminate the short circuits caused by volume variation. In addition, a uniform carbon layer could be formed on the surface of silicon oxide via the rotational chemical vapor deposition (r-CVD) method to improve electrical conductivity. The SiOx@C composites prevented the structural collapse caused by the volume variation of silicon with the buffering effect of the SEI layer produced by repeated charging and discharging. The discharge capacity was found to increase as the oxidation decreased. Particularly, the sample subjected to a reduction process at 700 °C for the SiOx-5h@C exhibited capacities ≥870 mAh g − 1 and excellent stability after 100 cycles at the current speed of 0.2 C.

Most somatic mutations that arise during normal development are present at low levels in single or multiple tissues depending on the developmental stage and affected organs. However, the effect of human developmental stages or mutations of different organs on the features of somatic mutations is still unclear. Here, we performed a systemic and comprehensive analysis of low-level somatic mutations using deep whole-exome sequencing (average read depth ~500×) of 498 multiple organ tissues with matched controls from 190 individuals. Our results showed that early clone-forming mutations shared between multiple organs were lower in number but showed higher allele frequencies than late clone-forming mutations [0.54 vs. 5.83 variants per individual; 6.17% vs. 1.5% variant allele frequency (VAF)] along with less nonsynonymous mutations and lower functional impacts. Additionally, early and late clone-forming mutations had unique mutational signatures that were distinct from mutations that originated from tumors. Compared with early clone-forming mutations that showed a clock-like signature across all organs or tissues studied, late clone-forming mutations showed organ, tissue, and cell-type specificity in the mutation counts, VAFs, and mutational signatures. In particular, analysis of brain somatic mutations showed a bimodal occurrence and temporal-lobe-specific signature. These findings provide new insights into the features of somatic mosaicism that are dependent on developmental stage and brain regions.

Highlights Ultrathin and defect-free graphene ink is prepared through a high-throughput fluid dynamics process, resulting in a high exfoliation yield (53.5%) and a high concentration (47.5 mg mL−1). A screen-printed graphene conductor exhibits a high electrical conductivity of 1.49 × 104 S m−1 and good mechanical flexibility. An electrochemical sodium ion sensor based on graphene ink exhibits an excellent potentiometric sensing performance in a mechanically bent state. Real-time monitoring of sodium ion concentration in sweat is demonstrated. Abstract Conductive inks based on graphene materials have received significant attention for the fabrication of a wide range of printed and flexible devices. However, the application of graphene fillers is limited by their restricted mass production and the low concentration of their suspensions. In this study, a highly concentrated and conductive ink based on defect-free graphene was developed by a scalable fluid dynamics process. A high shear exfoliation and mixing process enabled the production of graphene at a high concentration of 47.5 mg mL−1 for graphene ink. The screen-printed graphene conductor exhibits a high electrical conductivity of 1.49 × 104 S m−1 and maintains high conductivity under mechanical bending, compressing, and fatigue tests. Based on the as-prepared graphene ink, a printed electrochemical sodium ion (Na+) sensor that shows high potentiometric sensing performance was fabricated. Further, by integrating a wireless electronic module, a prototype Na+-sensing watch is demonstrated for the real-time monitoring of the sodium ion concentration in human sweat during the indoor exercise of a volunteer. The scalable and efficient procedure for the preparation of graphene ink presented in this work is very promising for the low-cost, reproducible, and large-scale printing of flexible and wearable electronic devices.

The immunomodulatory imide drug (IMiD) class, which includes the founding drug member thalidomide and later generation drugs, lenalidomide and pomalidomide, has dramatically improved the clinical treatment of specific cancers, such as multiple myeloma, and it combines potent anticancer and anti-inflammatory actions. These actions, in large part, are mediated by IMiD binding to the human protein cereblon that forms a critical component of the E3 ubiquitin ligase complex. This complex ubiquitinates and thereby regulates the levels of multiple endogenous proteins. However, IMiD-cereblon binding modifies cereblon’s normal targeted protein degradation towards a new set of neosubstrates that underlies the favorable pharmacological action of classical IMiDs, but also their adverse actions—in particular, their teratogenicity. The ability of classical IMiDs to reduce the synthesis of key proinflammatory cytokines, especially TNF-α levels, makes them potentially valuable to reposition as drugs to mitigate inflammatory-associated conditions and, particularly, neurological disorders driven by an excessive neuroinflammatory element, as occurs in traumatic brain injury, Alzheimer’s and Parkinson’s diseases, and ischemic stroke. The teratogenic and anticancer actions of classical IMiDs are substantial liabilities for effective drugs in these disorders and can theoretically be dialed out of the drug class. We review a select series of novel IMiDs designed to avoid binding with human cereblon and/or evade degradation of downstream neosubstrates considered to underpin the adverse actions of thalidomide-like drugs. These novel non-classical IMiDs hold potential as new medications for erythema nodosum leprosum (ENL), a painful inflammatory skin condition associated with Hansen’s disease for which thalidomide remains widely used, and, in particular, as a new treatment strategy for neurodegenerative disorders in which neuroinflammation is a key component.

A porous carbon foam (P-CF) with high porosity and large pore volume is developed to offer an efficient scaffold for radionuclides adsorption/decontamination. The three-dimensional (3D) porous structure can be easily formed by carbonization of petroleum pitch. During the heat treatment process, the volatile components from the petroleum pitch create highly interconnected pores without any templates, blowing and foaming agents. In addition, Prussian Blue (PB) nanoparticles are introduced onto the surface of the P-CF by a simple hydrothermal method. By combining the enhanced binding affinity to radionuclides with the increased porosity, the synthesized PB@P-CF exhibits the enhanced adsorption capacity for the Cesium ion (133Cs). This study provides a feasible way to utilize residual oil for preparing functionalized porous carbon-based adsorbents for the removal of radionuclides from aqueous solutions. The superior adsorption behaviors of the PB@P-CF make them promising candidates for radioactive materials adsorption/decontamination.

Traumatic brain injury (TBI) is a major risk factor for several neurodegenerative disorders, including Parkinson’s disease (PD) and Alzheimer’s disease (AD). Neuroinflammation is a cause of later secondary cell death following TBI, has the potential to aggravate the initial impact, and provides a therapeutic target, albeit that has failed to translate into clinical trial success. Thalidomide-like compounds have neuroinflammation reduction properties across cellular and animal models of TBI and neurodegenerative disorders. They lower the generation of proinflammatory cytokines, particularly TNF-α which is pivotal in microglial cell activation. Unfortunately, thalidomide-like drugs possess adverse effects in humans before achieving anti-inflammatory drug levels. We developed F-3,6′-dithiopomalidomide (F-3,6′-DP) as a novel thalidomide-like compound to ameliorate inflammation. F-3,6′-DP binds to cereblon but does not efficiently trigger the degradation of the transcription factors (SALL4, Ikaros, and Aiolos) associated with the teratogenic and anti-proliferative responses of thalidomide-like drugs. We utilized a phenotypic drug discovery approach that employed cellular and animal models in the selection and development of F-3,6’-DP. F-3,6′-DP significantly mitigated LPS-induced inflammatory markers in RAW 264.7 cells, and lowered proinflammatory cytokine/chemokine levels in the plasma and brain of rats challenged with systemic LPS. We subsequently examined immunohistochemical, biochemical, and behavioral measures following controlled cortical impact (CCI) in mice, a model of moderate TBI known to induce inflammation. F-3,6′-DP decreased CCI-induced neuroinflammation, neuronal loss, and behavioral deficits when administered after TBI. F-3,6′-DP represents a novel class of thalidomide-like drugs that do not lower classical cereblon-associated transcription factors but retain anti-inflammatory actions and possess efficacy in the treatment of TBI and potentially longer-term neurodegenerative disorders.

Micro-plate or microcell UO2–Mo is considered a promising accident tolerant fuel candidate for water-cooled power reactors. In this work, we evaluated the anticipated oxidation behavior of a UO2–Mo system under high-temperature steam to understand the impact of Mo oxidation on the fuel degradation mechanism in the event of steam ingress through cracks in the cladding. The equilibrium oxygen compositions of UO2 and Mo in various steam atmospheres relevant to reactor operating conditions were predicted using thermodynamic calculations and then compared with previous results. The oxidation behavior of UO2–Mo pellets was discussed through thermodynamic calculations and in terms of kinetic parameters such as oxygen diffusion, fuel temperature profile, and pellet microstructure. Mo oxidation was found to have an insignificant effect on pellet integrity in a cladding leakage scenario under normal reactor operating conditions.

Traumatic brain injury (TBI) is a neurodegenerative disorder for which no effective pharmacological treatment is available. Glucagon-like peptide 1 (GLP-1) analogues such as Exenatide have previously demonstrated neurotrophic and neuroprotective effects in cellular and animal models of TBI. However, chronic or repeated administration was needed for efficacy. In this study, the pharmacokinetics and efficacy of PT302, a clinically available sustained-release Exenatide formulation (SR-Exenatide) were evaluated in a concussive mild (m)TBI mouse model. A single subcutaneous (s.c.) injection of PT302 (0.6, 0.12, and 0.024 mg/kg) was administered and plasma Exenatide concentrations were time-dependently measured over 3 weeks. An initial rapid regulated release of Exenatide in plasma was followed by a secondary phase of sustained-release in a dose-dependent manner. Short- and longer-term (7 and 30 day) cognitive impairments (visual and spatial deficits) induced by weight drop mTBI were mitigated by a single post-injury treatment with Exenatide delivered by s.c. injection of PT302 in clinically translatable doses. Immunohistochemical evaluation of neuronal cell death and inflammatory markers, likewise, cross-validated the neurotrophic and neuroprotective effects of SR-Exenatide in this mouse mTBI model. Exenatide central nervous system concentrations were 1.5% to 2.0% of concomitant plasma levels under steady-state conditions. These data demonstrate a positive beneficial action of PT302 in mTBI. This convenient single, sustained-release dosing regimen also has application for other neurological disorders, such as Alzheimer's disease, Parkinson's disease, multiple system atrophy and multiple sclerosis where prior preclinical studies, likewise, have demonstrated positive Exenatide actions.

Neuroinflammation represents a common trait in the pathology and progression of the major psychiatric and neurodegenerative disorders. Neuropsychiatric disorders have emerged as a global crisis, affecting 1 in 4 people, while neurological disorders are the second leading cause of death in the elderly population worldwide (WHO, 2001; GBD 2016 Neurology Collaborators, 2019). However, there remains an immense deficit in availability of effective drug treatments for most neurological disorders. In fact, for disorders such as depression, placebos and behavioral therapies have equal effectiveness as antidepressants. For neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease, drugs that can prevent, slow, or cure the disease have yet to be found. Several non-traditional avenues of drug target identification have emerged with ongoing neurological disease research to meet the need for novel and efficacious treatments. Of these novel avenues is that of neuroinflammation, which has been found to be involved in the progression and pathology of many of the leading neurological disorders. Neuroinflammation is characterized by glial inflammatory factors in certain stages of neurological disorders. Although the meta-analyses have provided evidence of genetic/proteomic upregulation of inflammatory factors in certain stages of neurological disorders. Although the mechanisms underpinning the connections between neuroinflammation and neurological disorders are unclear, and meta-analysis results have shown high sensitivity to factors such as disorder severity and sample type, there is significant evidence of neuroinflammation associations across neurological disorders. In this review, we summarize the role of neuroinflammation in psychiatric disorders such as major depressive disorder, generalized anxiety disorder, post-traumatic stress disorder, and bipolar disorder, as well as in neurodegenerative disorders, such as Parkinson’s disease and Alzheimer’s disease, and introduce current research on the potential of immunomodulatory imide drugs (IMiDs) as a new treatment strategy for these disorders.

(1) Background: An important concomitant of stroke is neuroinflammation. Pomalidomide, a clinically available immunomodulatory imide drug (IMiD) used in cancer therapy, lowers TNF-α generation and thus has potent anti-inflammatory actions. Well-tolerated analogs may provide a stroke treatment and allow evaluation of the role of neuroinflammation in the ischemic brain. (2) Methods: Two novel pomalidomide derivatives, 3,6′-dithiopomalidomide (3,6′-DP) and 1,6′-dithiopomalidomide (1,6′-DP), were evaluated alongside pomalidomide in a rat middle cerebral artery occlusion (MCAo) stroke model, and their anti-inflammatory actions were characterized. (3) Results: Post-MCAo administration of all drugs lowered pro-inflammatory TNF-α and IL1-β levels, and reduced stroke-induced postural asymmetry and infarct size. Whereas 3,6′- and 1,6′-DP, like pomalidomide, potently bound to cereblon in cellular studies, 3,6′-DP did not lower Ikaros, Aiolos or SALL4 levels—critical intermediates mediating the anticancer/teratogenic actions of pomalidomide and IMiDs. 3,6′-DP and 1,6′-DP lacked activity in mammalian chromosome aberration, AMES and hERG channel assays –critical FDA regulatory tests. Finally, 3,6′- and 1,6′-DP mitigated inflammation across rat primary dopaminergic neuron and microglia mixed cultures challenged with α-synuclein and mouse LPS-challenged RAW 264.7 cells. (4) Conclusion: Neuroinflammation mediated via TNF-α plays a key role in stroke outcome, and 3,6′-DP and 1,6′-DP may prove valuable as stroke therapies and thus warrant further preclinical development.

Traumatic brain injury (TBI) causes mortality and disability worldwide. It can initiate acute cell death followed by secondary injury induced by microglial activation, oxidative stress, inflammation and autophagy in brain tissue, resulting in cognitive and behavioral deficits. We evaluated a new pomalidomide (Pom) analog, 3,6’-dithioPom (DP), and Pom as immunomodulatory agents to mitigate TBI-induced cell death, neuroinflammation, astrogliosis and behavioral impairments in rats challenged with controlled cortical impact TBI. Both agents significantly reduced the injury contusion volume and degenerating neuron number evaluated histochemically and by MRI at 24 hr and 7 days, with a therapeutic window of 5 hr post-injury. TBI-induced upregulated markers of microglial activation, astrogliosis and the expression of pro-inflammatory cytokines, iNOS, COX-2, and autophagy-associated proteins were suppressed, leading to an amelioration of behavioral deficits with DP providing greater efficacy. Complementary animal and cellular studies demonstrated DP and Pom mediated reductions in markers of neuroinflammation and α-synuclein-induced toxicity.

A microcell UO2 pellet, as an accident-tolerant fuel pellet, is being developed to enhance the accident tolerance of nuclear fuels under accident conditions as well as the fuel performance under normal operation conditions.Improved capture-ability for highly radioactive and corrosive fission product (Cs and I) is the distinct feature of a ceramic microcell UO2 pellet, and the enhanced pellet thermal conductivity is that of a metallic microcell UO2 pellet. The fuel temperature can be effectively decreased by enhanced thermal conductivity.In this study, the material concepts of metallic and ceramic microcell UO2 pellets were designed, and the fabrication process of microcell UO2 pellets embodying the designed concept was developed. We successfully implemented the microcell UO2 pellets and produced microcell UO2 pellets.In addition, an assessment of the out-of-pile properties of a microcell UO2 pellet was performed, and the in-reactor performance and behavior of the developed microcell pellets were evaluated through a Halden irradiation test. According to the expectations, the excellent performance of the microcell UO2 pellets was confirmed by the online measurement data of the Halden irradiation test. Keywords: Accident-Tolerant Fuel, Fission Product Retention, Halden Irradiation Test, Microcell UO2 Pellet, Thermal Conductivity

PURPOSE The purpose of this study was verifying effects of 8 weeks of inspiratory muscle training on pulmonary function and maximum inspiratory pressure and skill-related physical fitness in women. METHODS Participants were divided into two group; an inspiratory muscle training group (IMT, n = 8 ) and a placebo control group (CON, n = 8 ). The IMT group carried out inspiratory muscle training six days per week, 30 times a day. ‘Paired t-test’ for comparison between before and after result in each group. And ‘independent sample t-test’ for comparison value of before and after result in each groups (SPSS 23.0 Ver.). RESULTS As a results regarding maximum inspiratory pressure, IMT was shown to have a significant effect on peak S-index and peak inspiratory flow(PIF)(p< .001). IMT induced a significant improvement in Sit-up and Shuttle run(p< .01). CONCLUSIONS The results of the present study indicate that IMT is able to improve maximum inspiratory pressure and skill-related physical fitness in women. future studies should attempt to implement variations in methodology including, using male subjects, exercising for a different period of time and evaluating other fitness outcomes.

Traumatic brain injury (TBI) is a leading cause of disability and mortality worldwide. It can instigate immediate cell death, followed by a time-dependent secondary injury that results from disproportionate microglial and astrocyte activation, excessive inflammation and oxidative stress in brain tissue, culminating in both short- and long-term cognitive dysfunction and behavioral deficits. Within the brain, the hippocampus is particularly vulnerable to a TBI. We studied a new pomalidomide (Pom) analog, namely, 3,6′-dithioPom (DP), and Pom as immunomodulatory imide drugs (IMiD) for mitigating TBI-induced hippocampal neurodegeneration, microgliosis, astrogliosis and behavioral impairments in a controlled cortical impact (CCI) model of TBI in rats. Both agents were administered as a single intravenous dose (0.5 mg/kg) at 5 h post injury so that the efficacies could be compared. Pom and DP significantly reduced the contusion volume evaluated at 24 h and 7 days post injury. Both agents ameliorated short-term memory deficits and anxiety behavior at 7 days after a TBI. The number of degenerating neurons in the CA1 and dentate gyrus (DG) regions of the hippocampus after a TBI was reduced by Pom and DP. DP, but not Pom, significantly attenuated the TBI-induced microgliosis and DP was more efficacious than Pom at attenuating the TBI-induced astrogliosis in CA1 and DG at 7D after a TBI. In summary, a single intravenous injection of Pom or DP, given 5 h post TBI, significantly reduced hippocampal neurodegeneration and prevented cognitive deficits with a concomitant attenuation of the neuroinflammation in the hippocampus.

This study investigated the combined effects of proton irradiation and surface pre-treatment on the current characteristics of Gallium Nitride (GaN)-based metal-insulator-semiconductor high-electron-mobility-transistors (MIS-HEMTs) to evaluate the radiation hardness involved with the Silicon Nitride (SiN) passivation/GaN cap interface. The impact of proton irradiation on the static and dynamic current characteristics of devices with and without pre-treatment were analyzed with 5 MeV proton irradiation. In terms of transfer characteristics before and after the proton irradiation, the drain current of the devices without and with pre-treatment were reduced by an increase in sheet and contact resistances after the proton irradiation. In contrast with the static current characteristics, the gate-lag characteristics of the device with pre-treatment were significantly degenerated. In the device with pre-treatment, the hydrogen passivation for surface states of the GaN cap was formed by the pre-treatment and SiN deposition processes. Since the hydrogen passivation was removed by the proton irradiation, the newly created vacancies resulted in the degeneration of gate-lag characteristics. After nine months in an ambient atmosphere, the gate-lag characteristics of the device with pre-treatment were recovered because of the hydrogen recombination. These results demonstrated that the radiation hardness of MIS-HEMTs was affected by the SiN/GaN interface quality.

Abstract Mild blast traumatic brain injury (B-TBI) induced lasting cognitive impairments in novel object recognition and less severe deficits in Y-maze behaviors. B-TBI significantly reduced the levels of synaptophysin (SYP) protein staining in cortical (CTX) and hippocampal (HIPP) tissues. Treatment with exendin-4 (Ex-4) delivered by subcutaneous micro-osmotic pumps 48 hours prior to or 2 hours immediately after B-TBI prevented the induction of both cognitive deficits and B-TBI induced changes in SYP staining. The effects of a series of biaxial stretch injuries (BSI) on a neuronal derived cell line, HT22 cells, were assessed in an in vitro model of TBI. Biaxial stretch damage induced shrunken neurites and cell death. Treatment of HT22 cultures with Ex-4 (25 to 100 nM), prior to injury, attenuated the cytotoxic effects of BSI and preserved neurite length similar to sham treated cells. These data imply that treatment with Ex-4 may represent a viable option for the management of secondary events triggered by blast-induced, mild traumatic brain injury that is commonly observed in militarized zones.

In this work, Gallium Nitride (GaN)-based p-i-n diodes were designed using a computer aided design (TCAD) simulator for realizing a betavoltaic (BV) cell with a high output power density (Pout). The short-circuit current density (JSC) and open-circuit voltage (VOC) of the 17 keV electron-beam (e-beam)-irradiated diode were evaluated with the variations of design parameters, such as the height and doping concentration of the intrinsic GaN region (Hi-GaN and Di-GaN), which influenced the depletion width in the i-GaN region. A high Hi-GaN and a low Di-GaN improved the Pout because of the enhancement of absorption and conversion efficiency. The device with the Hi-GaN of 700 nm and Di-GaN of 1 × 1016 cm−3 exhibited the highest Pout. In addition, the effects of native defects in the GaN material on the performances were investigated. While the reverse current characteristics were mainly unaffected by donor-like trap states like N vacancies, the Ga vacancies-induced acceptor-like traps significantly decreased the JSC and VOC due to an increase in recombination rate. As a result, the device with a high acceptor-like trap density dramatically degenerated the Pout. Therefore, growth of the high quality i-GaN with low acceptor-like traps is important for an enhanced Pout in BV cell.

Molecular communications in the gut–brain axis, between the central nervous system and the gastrointestinal tract, are critical for maintaining healthy brain function, particularly in aging. Epidemiological analyses indicate type 2 diabetes mellitus (T2DM) is a risk factor for neurodegenerative disorders including Alzheimer's disease (AD) and Parkinson's diseases (PD) for which aging shows a major correlative association. Common pathophysiological features exist between T2DM, AD, and PD, including oxidative stress, inflammation, insulin resistance, abnormal protein processing, and cognitive decline, and suggest that effective drugs for T2DM that positively impact the gut–brain axis could provide an effective treatment option for neurodegenerative diseases. Glucagon-like peptide-1 (GLP-1)-based antidiabetic drugs have drawn particular attention as an effectual new strategy to not only regulate blood glucose but also decrease body weight by reducing appetite, which implies that GLP-1 could affect the gut–brain axis in normal and pathological conditions. The neurotrophic and neuroprotective effects of GLP-1 receptor (R) stimulation have been characterized in numerous in vitro and in vivo preclinical studies using GLP-1R agonists and dipeptidyl peptidase-4 inhibitors. Recently, the first open label clinical study of exenatide, a long-acting GLP-1 agonist, in the treatment of PD showed long-lasting improvements in motor and cognitive function. Several double-blind clinical trials of GLP-1R agonists including exenatide in PD and other neurodegenerative diseases are already underway or are about to be initiated. Herein, we review the physiological role of the GLP-1R pathway in the gut–brain axis and the therapeutic strategy of GLP-1R stimulation for the treatment of neurodegenerative diseases focused on PD, for which age is the major risk factor.

Hippocampal sclerosis (HS) is one of the most common features of intractable temporal lobe epilepsy. Generally it can be identified through brain magnetic resonance imaging (MRI) with high degree of sensitivity and specificity. Typical brain MRI findings of HS are hippocampal atrophy with hyperintense signal confined to the lesion. On the other hand cortical dysplasia exhibits blurring of the gray-white matter junction and abnormal white matter signal intensity. We present a case where preoperative brain MRI strongly suggested the presence of diffuse cortical dysplasia in the left temporal lobe but postoperative pathology revealed the temporal lesion to be unremarkable except for hippocampal sclerosis.

In this study, we developed lateral flow assay (LFA) biosensors for the detection of hepatitis B surface antigens using well-controlled gold nanoparticles (AuNPs). To enhance colorimetric signals, a seeded growth method was used for the preparation of size-controlled AuNPs with a narrow size distribution. Different sizes of AuNPs in the range of 342–137.8 nm were conjugated with antibodies and then optimized for the efficient detection of LFA biosensors. The conjugation stability was investigated by UV-vis spectroscopy of AuNP dispersion at various pH values and concentrations of antibody. Based on optimized conjugation conditions, the use of 42.7 ± 0.8 nm AuNPs exhibited superior performance for the detection of LFAs relative to other sizes of AuNPs.

Post-hemorrhagic hydrocephalus (PHH) in preterm infant is common, life-threatening and the main cause of bad developmental outcomes. Ventriculoperitoneal (VP) shunt is used as the ultimate treatment for PHH. Low birth weight and low gestational age are the combination of worse prognostic factors while the single most important prognostic factor of VP shunting is age. Aggressive and early intervention have better effect in intraventricular hemorrhage and intracranial pressures control. It reduces infection rate and brain damage resulted in delayed shunt insertion. It is extremely important to let PHH infants get older and gain weight to have internal organs to be matured before undergoing VP shunt. As premature infants undergo shunt after further growth, shunt-related complications would be reduced. So temporary surgical intervention is critical for PHH infants to have them enough time until permanently shunted. [ABSTRACT FROM AUTHOR]