Electronic transitions of platinum monoboride

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On the design and implementation of a high definition multi-view intelligent video surveillance system

This paper proposes a distributed architecture for high definition (HD) multi-view video surveillance system. It adopts a modular design where multiple intelligent Internet Protocol (IP)-based video surveillance cameras are connected to a local video server. Each server is equipped with storage and optional graphics processing units (GPUs) for supporting high-level video analytics and processing algorithms such as real-time decoding and tracking for the video captured. The servers are connected to the IP network for supporting distributed processing and remote data access. The DSP-based surveillance camera is equipped with realtime algorithms for streaming compressed videos to the server and performing simple video analytics functions. We also developed video analytics algorithms for security monitoring. Both publicly available data set and real video data that are captured under indoor and outdoor scenarios are used to validate our algorithms. Experimental results show that our distributed system can support real-time video applications with high definition resolution.published_or_final_versio

Association of proinflammatory cytokines and chemotherapy-associated cognitive impairment in breast cancer patients: a multi-centered, prospective, cohort study.

BackgroundExisting evidence suggests that proinflammatory cytokines play an intermediary role in postchemotherapy cognitive impairment. This is one of the largest multicentered, cohort studies conducted in Singapore to evaluate the prevalence and proinflammatory biomarkers associated with cognitive impairment in breast cancer patients.Patients and methodsChemotherapy-receiving breast cancer patients (stages I-III) were recruited. Proinflammatory plasma cytokines concentrations [interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, granulocyte-macrophage colony-stimulating factor, interferon-γ and tumor necrosis factor-α] were evaluated at 3 time points (before chemotherapy, 6 and 12 weeks after chemotherapy initiation). The FACT-Cog (version 3) was utilized to evaluate patients' self-perceived cognitive disturbances and a computerized neuropsychological assessment (Headminder) was administered to evaluate patients' memory, attention, response speed and processing speed. Changes of cognition throughout chemotherapy treatment were compared against the baseline. Linear mixed-effects models were applied to test the relationships of clinical variables and cytokine concentrations on self-perceived cognitive disturbances and each objective cognitive domain.ResultsNinety-nine patients were included (age 50.5 ± 8.4 years; 81.8% Chinese; mean duration of education = 10.8 ± 3.3 years). Higher plasma IL-1β was associated with poorer response speed performance (estimate: -0.78; 95% confidence interval (CI) -1.34 to -0.03; P = 0.023), and a higher concentration of IL-4 was associated with better response speed performance (P = 0.022). Higher concentrations of IL-1β and IL-6 were associated with more severe self-perceived cognitive disturbances (P = 0.018 and 0.001, respectively). Patients with higher concentrations of IL-4 also reported less severe cognitive disturbances (P = 0.022).ConclusionsWhile elevated concentrations of IL-6 and IL-1β were observed in patients with poorer response speed performance and perceived cognitive disturbances, IL-4 may be protective against chemotherapy-associated cognitive impairment. This study is important because cytokines would potentially be mechanistic mediators of chemotherapy-associated cognitive changes

VEGF(164)-mediated inflammation is required for pathological, but not physiological, ischemia-induced retinal neovascularization

Hypoxia-induced VEGF governs both physiological retinal vascular development and pathological retinal neovascularization. In the current paper, the mechanisms of physiological and pathological neovascularization are compared and contrasted. During pathological neovascularization, both the absolute and relative expression levels for VEGF(164) increased to a greater degree than during physiological neovascularization. Furthermore, extensive leukocyte adhesion was observed at the leading edge of pathological, but not physiological, neovascularization. When a VEGF(164)-specific neutralizing aptamer was administered, it potently suppressed the leukocyte adhesion and pathological neovascularization, whereas it had little or no effect on physiological neovascularization. In parallel experiments, genetically altered VEGF(164)-deficient (VEGF(120/188)) mice exhibited no difference in physiological neovascularization when compared with wild-type (VEGF(+/+)) controls. In contrast, administration of a VEGFk-1/Fc fusion protein, which blocks all VEGF isoforms, led to significant suppression of both pathological and physiological neovascularization. In addition, the targeted inactivation of monocyte lineage cells with clodronate-liposomes led to the suppression of pathological neovascularization. Conversely, the blockade of T lymphocyte-mediated immune responses with an anti-CD2 antibody exacerbated pathological neovascularization. These data highlight important molecular and cellular differences between physiological and pathological retinal neovascularization. During pathological neovascularization, VEGF(164) selectively induces inflammation and cellular immunity. These processes provide positive and negative angiogenic regulation, respectively. Together, new therapeutic approaches for selectively targeting pathological, but not physiological, retinal neovascularization are outlined

Alternative Splicing of P/Q-Type Ca2+ Channels Shapes Presynaptic Plasticity

Alternative splicing of pre-mRNAs is prominent in the mammalian brain, where it is thought to expand proteome diversity. For example, alternative splicing of voltage-gated Ca2+ channel (VGCC) α1 subunits can generate thousands of isoforms with differential properties and expression patterns. However, the impact of this molecular diversity on brain function, particularly on synaptic transmission, which crucially depends on VGCCs, is unclear. Here, we investigate how two major splice isoforms of P/Q-type VGCCs (Cav2.1[EFa/b]) regulate presynaptic plasticity in hippocampal neurons. We find that the efficacy of P/Q-type VGCC isoforms in supporting synaptic transmission is markedly different, with Cav2.1[EFa] promoting synaptic depression and Cav2.1[EFb] synaptic facilitation. Following a reduction in network activity, hippocampal neurons upregulate selectively Cav2.1[EFa], the isoform exhibiting the higher synaptic efficacy, thus effectively supporting presynaptic homeostatic plasticity. Therefore, the balance between VGCC splice variants at the synapse is a key factor in controlling neurotransmitter release and presynaptic plasticity

Review and comparison of shearography and active thermography for nondestructive evaluation

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Impact of potential engine malfunctions on fuel consumption and gaseous emissions of a Euro VI diesel truck

© 2019 Elsevier Ltd Although new vehicles are designed to comply with specific emission regulations, their in-service performance would not necessarily achieve them due to wear-and-tear and improper maintenance, as well as tampering or failure of engine control and exhaust after-treatment systems. In addition, there is a lack of knowledge on how significantly these potential malfunctions affect vehicle performance. This study was therefore conducted to simulate the effect of various engine malfunctions on the fuel consumption and gaseous emissions of a 16-tonne Euro VI diesel truck using transient chassis dynamometer testing. The simulated malfunctions included those that would commonly occur in the intake, fuel injection, exhaust after-treatment and other systems. The results showed that all malfunctions increased fuel consumption except for the malfunction of EGR fully closed which reduced fuel consumption by 31%. The biggest increases in fuel consumption were caused by malfunctions in the intake system (16%–43%), followed by the exhaust after-treatment (6%–30%), fuel injection (4%–24%) and other systems (6%–11%). Regarding pollutant emissions, the effect of engine malfunctions on HC and CO emissions was insignificant, which remained unchanged or even reduced for most cases. An exception was EGR fully open which increased HC and CO emissions by 343% and 1124%, respectively. Contrary to HC and CO emissions, NO emissions were significantly increased by malfunctions. The largest increases in NO emissions were caused by malfunctions in the after-treatment system, ranging from 38% (SCR) to 1606% (DPF pressure sensor). Malfunctions in the fuel injection system (24%–1259%) and intercooler (438%–604%) could also increase NO emissions markedly. This study demonstrated clearly the importance of having properly functioning engine control and exhaust after-treatment systems to achieve the required performance of fuel consumption and pollutant emissions

Adult presentation of a rare mitochondrial tRNA Val gene mutation—an expanding clinical phenotype

\ua9 2024 The Author(s). European Journal of Neurology published by John Wiley & Sons Ltd on behalf of European Academy of Neurology.Background and purpose: Late-onset mitochondrial disorders are diagnostically challenging with significant heterogeneity in disease presentation. A case is reported of a 67-year-old gentleman who presented with a 3-month history of seizures, recurrent encephalopathy, ataxia and weight loss, preceded by recent initiation of haemodialysis for end-stage chronic kidney disease. Methods: Extensive work-up including serological, cerebrospinal fluid, magnetic resonance imaging and electroencephalography was performed. Whole exome sequencing and muscle biopsy confirmed the diagnosis. Results: Magnetic resonance imaging brain demonstrated a single non-enhancing T2 fluid attenuated inversion recovery hyperintense cortical/subcortical signal change in the right temporal lobe and cerebellar atrophy. Given the subacute presentation of uncertain aetiology, he was empirically treated for autoimmune/paraneoplastic encephalitis. Despite radiological resolution of the cortical abnormality 2 weeks later, there was no clinical improvement. Further collateral history unveiled a mildly ataxic gait and longstanding hearing loss suggestive of a genetic cause. Whole exome sequencing revealed a likely pathogenic, heteroplasmic mitochondrial DNA variant in the MT-TV gene, m.1659T>C, present at higher levels of heteroplasmy in muscle (91%) compared to other mitotic tissues. A high fat/protein diet and multivitamins including co-enzyme Q10 were commenced. Treatment of the nutritional deficiency and avoidance of intermittent fasting due to unreliable oral intake secondary to encephalopathy probably contributed to the clinical improvement seen over the ensuing few months, with resolution of his encephalopathy and return to his baseline gait and weight. Conclusion: An adult case is reported with an acute neurological presentation mimicking encephalitis, caused by a heteroplasmic m.1659T>C MT-TV variant, previously reported once in a child who displayed a different clinical phenotype

The Nucleosome Assembly Protein TSPYL2 Regulates the Expression of NMDA Receptor Subunits GluN2A and GluN2B

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