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Identification of antigenic sites on proteins is of vital importance for developing synthetic peptide vaccines, immunodiagnostic tests and antibody production. Currently, most of the prediction algorithms rely on amino acid propensity scales using a sliding window approach. These methods are oversimplified and yield poor predicted results in practice. In this paper, a novel scale, called the amino acid pair (AAP) antigenicity scale, is proposed that is based on the finding that B-cell epitopes favor particular AAPs. It is demonstrated that, using SVM (support vector machine) classifier, the AAP antigenicity scale approach has much better performance than the existing scales based on the single amino acid propensity. The AAP antigenicity scale can reflect some special sequence-coupled feature in the B-cell epitopes, which is the essence why the new approach is superior to the existing ones. It is anticipated that with the continuous increase of the known epitope data, the power of the AAP antigenicity scale approach will be further enhanced.

Particulate matter (PM) has been associated with increased pulmonary and cardiovascular mortality and morbidity. Additionally, PM is known to exacerbate asthma. However, whether ambient PM exposure contributes to the onset of asthma, especially in non-atopic children and adults, is less conclusive. The current study aimed to evaluate the effects of size-fractioned PM on lung immune responses in healthy BALB/c mice. We collected PM10, PM2.5, PM1 and PM0.1 samples from October 2012 to August 2013 in the Taipei Basin. These PM samples were representative of urban traffic pollution. The samples were extracted and sonicated in phosphate-buffered saline (PBS). Female BALB/c mice were exposed to the samples via intratracheal instillation at three different doses: 1.75 mg/kg (35 μg/per mouse), 5 mg/kg (100 μg/per mouse), and 12.5 mg/kg (250 μg/per mouse). The mice were exposed on days 0 and 7, and PBS alone was used as a control. Following the exposures, the expression profiles of inflammatory cells and cytokines in bronchoalveolar lavage fluid (BALF) were assessed. Exposure to PM10 resulted in inflammatory responses, including the recruitment of neutrophils and the induction of T helper 1 (Th1) cell-related cytokine release, such as TNF-α and IFN-γ. Furthermore, an allergic immune response, including the recruitment of eosinophils and the up-regulation of T helper 2 (Th2) cell-related cytokine release, such as IL-5 and IL-13, was also observed in the BALF of mice exposed to PM10. Our study showed that exposure to PM alone caused mixed Th1/Th2 inflammatory responses in healthy mice. These findings support the hypothesis that PM may contribute to the onset of asthma.

Manipulating the state of a logical quantum bit (qubit) usually comes at the expense of exposing it to decoherence. Fault-tolerant quantum computing tackles this problem by manipulating quantum information within a stable manifold of a larger Hilbert space, whose symmetries restrict the number of independent errors. The remaining errors do not affect the quantum computation and are correctable after the fact. Here we implement the autonomous stabilization of an encoding manifold spanned by Schrödinger cat states in a superconducting cavity. We show Zeno-driven coherent oscillations between these states analogous to the Rabi rotation of a qubit protected against phase flips. Such gates are compatible with quantum error correction and hence are crucial for fault-tolerant logical qubits.

The chemical compound 1,2-dichloroethane (DCE), or ethylene dichloride, is an industrial very short-lived substance (VSLS) whose major use is as a feedstock in the production chain of polyvinyl chloride (PVC). Like other chlorinated VSLSs, transport of DCE (and/or its atmospheric oxidation products) to the stratosphere could contribute to ozone depletion there. However, despite annual production volumes greatly exceeding those of more prominent VSLSs (e.g. dichloromethane), global DCE observations are sparse; thus, the magnitude and distribution of DCE emissions and trends in its atmospheric abundance are poorly known. In this study, we performed an exploratory analysis of the global DCE budget between 2002 and 2020. Combining bottom-up data on annual production and assumptions around fugitive losses during production and feedstock use, we assessed the DCE source strength required to reproduce atmospheric DCE observations. We show that the TOMCAT/SLIMCAT 3-D chemical transport model (CTM) reproduces DCE measurements from various aircraft missions well, including HIPPO (2009–2011), ATom (2016–2018), and KORUS-AQ (2016), along with surface measurements from Southeast Asia, when assuming a regionally varying production emission factor in the range of 0.5 %–1.5 %. Our findings imply substantial fugitive losses of DCE and/or substantial emissive applications (e.g. solvent use) that are poorly reported. We estimate that DCE's global source increased by ∼ 45 % between 2002 (349 ± 61 Gg yr−1) and 2020 (505 ± 90 Gg yr−1), with its contribution to stratospheric chlorine increasing from 8.2 (± 1.5) to ∼ 12.9 (± 2.4) ppt Cl (where ppt denotes parts per trillion) over this period. DCE's relatively short overall tropospheric lifetime (∼ 83 d) limits, although does not preclude, its transport to the stratosphere, and we show that its impact on ozone is small at present. Annually averaged, DCE is estimated to have decreased ozone in the lower stratosphere by up to several parts per billion (< 1 %) in 2020, although a larger effect in the springtime Southern Hemisphere polar lower stratosphere is apparent (decreases of up to ∼ 1.3 %). Given strong potential for growth in DCE production tied to demand for PVC, ongoing measurements would be of benefit to monitor potential future increases in its atmospheric abundance and its contribution to ozone depletion.

Although numerous epidemiological studies revealed an association between ambient fine particulate matter (PM 2.5 ) exposure and Alzheimer’s disease (AD), the PM 2.5 -induced neuron toxicity and associated mechanisms were not fully elucidated. The present study assessed brain toxicity in 6-month-old female triple-transgenic AD (3xTg-AD) mice following subchronic exposure to PM 2.5 via an inhalation system. The treated mice were whole-bodily and continuously exposed to real-world PM 2.5 for 3 months, while the control mice inhaled filtered air. Changes in cognitive and motor functions were evaluated using the Morris Water Maze and rotarod tests. Magnetic resonance imaging analysis was used to record gross brain volume alterations, and tissue staining with hematoxylin and eosin, Nissl, and immunohistochemistry methods were used to monitor pathological changes in microstructures after PM 2.5 exposure. The levels of AD-related hallmarks and the oxidative stress biomarker malondialdehyde (MDA) were assessed using Western blot analysis and liquid chromatography-mass spectrometry, respectively. Our results showed that subchronic exposure to environmental levels of PM 2.5 induced obvious neuronal loss in the cortex of exposed mice, but without significant impairment of cognitive and motor function. Increased levels of phosphorylated-tau and MDA were also observed in olfactory bulb or hippocampus after PM 2.5 exposure, but no amyloid pathology was detected, as reported in previous studies. These results revealed that a relatively lower level of PM 2.5 subchronic exposure from the environmental atmosphere still induced certain neurodegenerative changes in the brains of AD mice, especially in the olfactory bulb, entorhinal cortex and hippocampus, which is consistent with the nasal entry and spreading route for PM exposure. Systemic factors may also contribute to the neuronal toxicity. The effects of PM 2.5 after a more prolonged exposure period are needed to establish a more comprehensive picture of the PM 2.5 -mediated development of AD.

The powder of the hematite sample was isothermally reduced with a hydrogen-water vapor gas mixture at 1023K-1273K. The results indicate that the overall reduction process of hematite can be divided into three stages (Fe2O3-Fe3O4-FeO-Fe) each of which should be investigated. At 1023K, the average reaction rate decreased by 53.6% in stage 1 when the water vapor content of the reaction gas increased from 0% to 50%, and it decreased by about 77.2% in stage 2. However, in stage 3, when the water vapor content increased only from 0% to 20%, it decreased by about 78.1%. The results also show that the influence of water vapor on the reduction reaction increases with increasing reaction temperature in all stages of the reduction reaction. The microstructure of the reduction products showed that they still had some holes; that did not seriously block the channel for hydrogen diffusion. Various models were considered to further clarify the influence of water vapor in the reduction stage The range of apparent activation energy of the different stages obtained by the model fitting was about 20-70 kJ/mol, which also confirmed the absence of the solid-state diffusion phenomenon.

Background Air pollution, especially fine particulate matter (PM), can cause brain damage, cognitive decline, and an increased risk of neurodegenerative disease, especially alzheimer’s disease (AD). Typical pathological findings of amyloid and tau protein accumulation have been detected in the brain after exposure in animal studies. However, these observations were based on high levels of PM exposure, which were far from the WHO guidelines and those present in our environment. In addition, white matter involvement by air pollution has been less reported. Thus, this experiment was designed to simulate the true human world and to discuss the possible white matter pathology caused by air pollution. Results 6 month-old female 3xTg-AD mice were divided into exposure and control groups and housed in the Taipei Air Pollutant Exposure System (TAPES) for 5 months. The mice were subjected to the Morris water maze test after exposure and were then sacrificed with brain dissection for further analyses. The mean mass concentration of PM 2.5 during the exposure period was 13.85 μg/m 3 . After exposure, there was no difference in spatial learning function between the two groups, but there was significant decay of memory in the exposure group. Significantly decreased total brain volume and more neuronal death in the cerebral and entorhinal cortex and demyelination of the corpus callosum were noted by histopathological staining after exposure. However, there was no difference in the accumulation of amyloid or tau on immunohistochemistry staining. For the protein analysis, amyloid was detected at significantly higher levels in the cerebral cortex, with lower expression of myelin basic protein in the white matter. A diffuse tensor image study also revealed insults in multiple white matter tracts, including the optic tract. Conclusions In conclusion, this pilot study showed that even chronic exposure to low PM 2.5 concentrations still caused brain damage, such as gross brain atrophy, cortical neuron damage, and multiple white matter tract damage. Typical amyloid cascade pathology did not appear prominently in the vulnerable brain region after exposure. These findings imply that multiple pathogenic pathways induce brain injury by air pollution, and the optic nerve may be another direct invasion route in addition to olfactory nerve.

In 1989, Manning, Patel, and Borchardt wrote a review of protein stability (Manning et al., Pharm. Res. 6:903-918, 1989), which has been widely referenced ever since. At the time, recombinant protein therapy was still in its infancy. This review summarizes the advances that have been made since then regarding protein stabilization and formulation. In addition to a discussion of the current understanding of chemical and physical instability, sections are included on stabilization in aqueous solution and the dried state, the use of chemical modification and mutagenesis to improve stability, and the interrelationship between chemical and physical instability.

Air pollution is typically at its lowest in Taiwan during summer. The mean concentrations of PM10, PM2.5, and daytime ozone (08:00–17:00 LST) during summer (June–August) over central Taiwan were 35–40 µg m−3, 18–22 µg m−3, and 30–42 ppb, respectively, between 2004 and 2019. Sampling analysis revealed that the contribution of organic carbon (OC) to PM2.5 could have exceeded 30 % in urban and inland mountain sites during July in 2017 and 2018. Frequent episodes of air quality deterioration occur over the western plains of Taiwan when an easterly typhoon circulation interacts with the complex topographic structure of the island. We explored an episode of air quality deterioration that was associated with a typhoon between 15 and 17 July 2018 using the Weather Research Forecasting with Chemistry (WRF-Chem) model. The results indicated that the continual formation of low-pressure systems or typhoons in the area between Taiwan and Luzon island in the Philippines provided a strong easterly ambient flow, which lasted for an extended period between 15 and 17 July. The interaction between the easterly flow and Taiwan's Central Mountain Range (CMR) resulted in stable weather conditions and weak wind speed in western Taiwan during the study period. Numerical modeling also indicated that a lee side vortex easily formed, and the wind direction could have changed from southwesterly to northwesterly over central Taiwan because of the interaction between the typhoon circulation and the CMR. The northwesterly wind coupled with a sea breeze was conducive to the transport of air pollutants from the coastal upstream industrial and urban areas to the inland area. The dynamic process for the wind direction changed given a reasonable explanation for why the observed SO42- became the major contributor to PM2.5 during the episode. SO42- contribution proportions (%) to PM2.5 at the coastal, urban, and mountain sites were 9.4 µg m−3 (30.5 %), 12.1 µg m−3 (29.9 %), and 11.6 µg m−3 (29.7 %), respectively. Moreover, the variation of the boundary layer height had a strong effect on the concentration level of both PM2.5 and ozone. The lee vortex and land–sea breeze, as well as the boundary layer development, were the key mechanisms in air pollutant accumulation and transport. As typhoons frequently occur around Taiwan during summer and fall, their effect on the island's air quality merits further research attention.

Accurate automatic spike detection is highly beneficial to clinical assessment of epileptic electroencephalogram (EEG) data. In this paper, a new two-stage approach is proposed for epileptic spike detection. First, the k-point nonlinear energy operator (k-NEO) is adopted to detect all possible spike candidates, then a newly proposed spike model with slow wave features is applied to these candidates for spike classification. Experimental results show that the proposed system, using the AdaBoost classifier, outperforms the conventional method in both two- and three-class EEG pattern classification problems. The proposed system not only achieves better accuracy for spike detection, but also provides new ability to differentiate between spikes and spikes with slow waves. Though spikes with slow waves occur frequently in epileptic EEGs, they are not used in conventional spike detection. Identifying spikes with slow waves allows the proposed system to have better capability for assisting clinical neurologists in routine EEG examinations and epileptic diagnosis.