Single-Trial EEG-fMRI Reveals the Generation Process of the Mismatch Negativity

Although research on the mismatch negativity (MMN) has been ongoing for 40 years, the generation process of the MMN remains largely unknown. In this study, we used a single-trial electro-encephalography (EEG)-functional magnetic resonance imaging (fMRI) coupling method which can analyze neural activity with both high temporal and high spatial resolution and thus assess the generation process of the MMN. We elicited the MMN with an auditory oddball paradigm while recording simultaneous EEG and fMRI. We divided the MMN into five equal-durational phases. Utilizing the single-trial variability of the MMN, we analyzed the neural generators of the five phases, thereby determining the spatiotemporal generation process of the MMN. We found two distinct bottom-up prediction error propagations: first from the auditory cortex to the motor areas and then from the auditory cortex to the inferior frontal gyrus (IFG). Our results support the regularity-violation hypothesis of MMN generation

Clinical spectrum and gene mutations in a Chinese cohort with anoctaminopathy

Recessive mutations in anoctamin-5 (ANO5) are causative for limb-girdle muscular dystrophy (LGMD) 2L and non-dysferlin Miyoshi-like distal myopathy (MMD3). ANDS mutations are highly prevalent in European countries; however it is not common in patients of Asian origin, and there is no data regarding the Chinese population. We retrospectively reviewed the clinical manifestations and gene mutations of Chinese patients with anoctaminopathy. A total of five ANDS mutations including four novel mutations and one reported mutation were found in four patients from three families. No hotspot mutation was found. Three patients presented with presymptomatic hyperCKemia and one patient had limb muscle weakness. Muscle imaging of lower limbs showed preferential adductor magnus and medial gastrocnemius involvement. No hotspot mutation has been identified in Chinese patients to date. (C) 2019 Elsevier B.V. All rights reserved.Peer reviewe

CRISPR-cas system:biological function in microbes and its use to treat antimicrobial resistant pathogens

The development of antibiotic resistance in bacteria is a major public health threat. Infection rates of resistant pathogens continue to rise against nearly all antimicrobials, which has led to development of different strategies to combat the antimicrobial resistance. In this review, we discuss how the newly popular CRISPR-cas system has been applied to combat antibiotic resistance in both extracellular and intracellular pathogens. We also review a recently developed method in which nano-size CRISPR complex was used without any phage to target themecAgene. However, there is still challenge to practice these methods in field against emerging antimicrobial resistant pathogens

Trust, individual income and nation’s wealth

本文將信任作為新的變數,加入到消費者最優問題當中;分別基於RBC模型和AK模型的框架,推导了信任對於個人以及社會經濟表現的影響.兩個模型的數學解都預測信任會正向影響社會的產出水平,但在信任是否影響經濟的成長速度這一命題上得出了不同的結論.利用跨國數據和中國省級數據進行實證研究,我們發現信任應當有收入效果,但沒有成長效果;特別的,我們還發現信任和人力資本之間具有相互促進的內在關係.在個人收入層面, 我們利用中國的調查資料, 也同時驗證了信任對於個人所得的正向效果.This paper presents two modified models in which social trust is constructed in the representative household’s budget constraint. The solutions of both models predict that trust is positively related with the overall output, while the predictions for the growth effect of trust are ambiguous. Using the cross-country data and Chinese province data, we find our result of empirical analysis suggests that trust should only has income effect but no growth effect. Furthermore, we find there’s an important mutually enhancing relationship between human capital and trust. On individual level, the positive income-trust relationship is further verified using the Chinese survey data

Effect of the environment in Antarctica on immune function and electroencephalogram

An observation on the changes of immune function (serum immunoglobulin, lymphocyte transformation) and electroencephalogram were carried out when the explorers were residing in Antarctica for a long time. Serum IgM, IgG decreased by the end of twelve months residing in Antarctica. It were only 40%; 38% (P < 0.1) of the previous value before leaving for Antarctica. Serum IgA increased first and then return to its previous value before leaving for Antarctica. When they returned back to Beijing for 2 months serum IgA was lower than that before leaving (P < 0.05). Lymphocyte transformation rate decreased to 45% (P < 0.05) of its previous level before leaving for Antarctica. The low lymphocyte transformation rate lasted for 2 months after return. But the variation of Ig level and lymphocyte transformation rate were small in the control group at different seasons. It is obviously that the significant change of Lg level and lymphocyte transformation rate of explorers residing in Antarctica is the result of special environment. The desynchronization process on electroencephalogram (EEG) increased. The frequency and index of beta-wave band increased during their stay in Antarctica. There is a close relationship between the decrease of lymphocyte transformation rate and the increase of the index and amplitude of beta-band on EEG. It indicated that the decrease of immunity (especially cell mediated immunity) resulted from living under stress for a long time

Mequindox Induced Genotoxicity and Carcinogenicity in Mice

Mequindox (MEQ), acting as an inhibitor of deoxyribonucleic acid (DNA) synthesis, is a synthetic heterocyclic N-oxides. To investigate the potential carcinogenicity of MEQ, four groups of Kun-Ming (KM) mice (50 mice/sex/group) were fed with diets containing MEQ (0, 25, 55, and 110 mg/kg) for one and a half years. The result showed adverse effects on body weights, feed consumption, hematology, serum chemistry, organ weights, relative organ weights, and incidence of tumors during most of the study period. Treatment-related changes in hematology, serum chemistry, relative weights and histopathological examinations revealed that the hematological system, liver, kidneys, and adrenal glands, as well as the developmental and reproductive system, were the main targets after MEQ administration. Additionally, MEQ significantly increased the frequency of micronucleated normochromatic erythrocytes in bone marrow cells of mice. Furthermore, MEQ increased the incidence of tumors, including mammary fibroadenoma, breast cancer, corticosuprarenaloma, haemangiomas, hepatocarcinoma, and pulmonary adenoma. Interestingly, the higher incidence of tumors was noted in M25 mg/kg group, the lowest dietary concentration tested, which was equivalent to approximately 2.25 and 1.72 mg/kg b.w./day in females and males, respectively. It was assumed that the lower toxicity might be a reason for its higher tumor incidence in M25 mg/kg group. This finding suggests a potential relationships among the dose, general toxicity and carcinogenicity in vivo, and further study is required to reveal this relationship. In conclusion, the present study demonstrates that MEQ is a genotoxic carcinogen in KM mice

Smart Ring: A Model of Node Failure Detection in High Available Cloud Data Center

Part 8: Web, Communication, and Cloud ComputingInternational audienceNowadays most of cloud data centers deploy high available system in order to provide continuous services, so it’s very important for a high available cluster to detect the node failure (physical machine failure) accurately and timely in a low bandwidth occupation way. However, compared to the traditional cluster environment, the scale of cloud data center increases rapidly with the use of virtualization, so traditional node failure detection models have already faced several new problems. In this paper, we present a three roles and two layers node failure detection model, named as Smart Ring, which fits cloud data center well and strikes a balance between accuracy, instantaneity and bandwidth occupation. It can simultaneously detect the status of physical machines and virtual machines and deal well with multiple nodes failure and network partition. Our experiment results show that Smart Ring has a better performance than most existing models

Image_7_Mequindox-Induced Kidney Toxicity Is Associated With Oxidative Stress and Apoptosis in the Mouse.JPEG

<p>Mequindox (MEQ), belonging to quinoxaline-di-N-oxides (QdNOs), is a synthetic antimicrobial agent widely used in China. Previous studies found that the kidney was one of the main toxic target organs of the QdNOs. However, the mechanisms underlying the kidney toxicity caused by QdNOs in vivo still remains unclear. The present study aimed to explore the molecular mechanism of kidney toxicity in mice after chronic exposure to MEQ. MEQ led to the oxidative stress, apoptosis, and mitochondrial damage in the kidney of mice. Meanwhile, MEQ upregulated Bax/Bcl-2 ratio, disrupted mitochondrial permeability transition pores, caused cytochrome c release, and a cascade activation of caspase, eventually induced apoptosis. The oxidative stress mediated by MEQ might led to mitochondria damage and apoptosis in a mitochondrial-dependent apoptotic pathway. Furthermore, upregulation of the Nrf2-Keap1 signaling pathway was also observed. Our findings revealed that the oxidative stress, mitochondrial dysfunction, and the Nrf2-Keap1 signaling pathway were associated with the kidney apoptosis induced by MEQ in vivo.</p

Mequindox-Induced Kidney Toxicity Is Associated With Oxidative Stress and Apoptosis in the Mouse

Mequindox (MEQ), belonging to quinoxaline-di-N-oxides (QdNOs), is a synthetic antimicrobial agent widely used in China. Previous studies found that the kidney was one of the main toxic target organs of the QdNOs. However, the mechanisms underlying the kidney toxicity caused by QdNOs in vivo still remains unclear. The present study aimed to explore the molecular mechanism of kidney toxicity in mice after chronic exposure to MEQ. MEQ led to the oxidative stress, apoptosis, and mitochondrial damage in the kidney of mice. Meanwhile, MEQ upregulated Bax/Bcl-2 ratio, disrupted mitochondrial permeability transition pores, caused cytochrome c release, and a cascade activation of caspase, eventually induced apoptosis. The oxidative stress mediated by MEQ might led to mitochondria damage and apoptosis in a mitochondrial-dependent apoptotic pathway. Furthermore, upregulation of the Nrf2-Keap1 signaling pathway was also observed. Our findings revealed that the oxidative stress, mitochondrial dysfunction, and the Nrf2-Keap1 signaling pathway were associated with the kidney apoptosis induced by MEQ in vivo