31 research outputs found

    Depressive Syndromes in Autoimmune Disorders of the Nervous System: Prevalence, Etiology, and Influence

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    Autoimmune diseases of the nervous system (ADNS) consist of a group of severely disabling disorders characterized by abnormal immune attack against protein components of the nervous system. This type of attack behavior may occur in the central or peripheral nervous system, and in the neuromuscular junction, resulting in neuronal damage, axonal injury, demyelination or destruction of the neuromuscular junction. While the neurological deficits of patients with ADNS have received significant research attention, the manifestation of depression tends to be ignored. In fact, depressive manifestation is common in ADNS and adds significant burden upon patients suffering from this disease. Here, we systematically reviewed the current literature to highlight the prevalence, etiology and influence of depressive manifestation in ADNS. Most autoimmune diseases of the nervous system are discussed in this paper, from multiple sclerosis, acute disseminated encephalomyelitis and autoimmune encephalitis to acute myelitis, neuromyelitis optica, Guillain-Barré syndrome and myasthenia gravis. Depressive symptoms usually develop as a comorbidity during the course of disease, but sometimes exist as a primary presentation of the disease. Psychosocial factors, long periods of disablement and chronic pain are the three most common causes of depressive symptoms in many chronic conditions, particularly in peripheral neuropathy. Furthermore, the higher prevalence of depressive symptoms in ADNS suggests that immunological dysregulation may contribute to the elevated morbidity of depression. Finally, structural lesions of the brain, and some medications for ADNS, are also thought to precipitate depressive states in ADNS

    Concept for a Future Super Proton-Proton Collider

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    Following the discovery of the Higgs boson at LHC, new large colliders are being studied by the international high-energy community to explore Higgs physics in detail and new physics beyond the Standard Model. In China, a two-stage circular collider project CEPC-SPPC is proposed, with the first stage CEPC (Circular Electron Positron Collier, a so-called Higgs factory) focused on Higgs physics, and the second stage SPPC (Super Proton-Proton Collider) focused on new physics beyond the Standard Model. This paper discusses this second stage.Comment: 34 pages, 8 figures, 5 table

    Predictive value of the resistance of the probe to pass through the lesion in the diagnosis of peripheral pulmonary lesions using radial probe endobronchial ultrasound with a guide sheath

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    BackgroundTransbronchial lung biopsy guided by radial probe endobronchial ultrasonography with a guide sheath (EBUS-GS-TBLB) is becoming a significant approach for diagnosing peripheral pulmonary lesions (PPLs). We aimed to explore the clinical value of the resistance of the probe to pass through the lesion in the diagnosis of PPLs when performing EBUS-GS-TBLB, and to determine the optimum number of EBUS-GS-TBLB.MethodsWe performed a prospective, single-center study of 126 consecutive patients who underwent EBUS-GS-TBLB for solid and positive-bronchus-sign PPLs where the probe was located within the lesion from September 2019 to May 2022. The classification of probe resistance for each lesion was carried out by two bronchoscopists independently, and the final result depended on the bronchoscopist responsible for the procedures. The primary endpoint was the diagnostic yield according with the resistance pattern. The secondary endpoints were the optimum number of EBUS-GS-TBLB and factors affecting diagnostic yield. Procedural complications were also recorded.ResultsThe total diagnostic yield of EBUS-GS-TBLB was 77.8%, including 83.8% malignant and 67.4% benign diseases (P=0.033). Probe resistance type II displayed the highest diagnostic yield (87.5%), followed by type III (81.0%) and type I (61.1%). A significant difference between the diagnostic yield of malignant and benign diseases was detected in type II (P = 0.008), whereas others did not. Although most of the malignant PPLs with a definitive diagnosis using EBUS-GS-TBLB in type II or type III could be diagnosed in the first biopsy, the fourth biopsy contributed the most sufficient biopsy samples. In contrast, considerably limited tissue specimens could be obtained for each biopsy in type I. The inter-observer agreement of the two blinded bronchoscopists for the classification of probe resistance was excellent (κ = 0.84).ConclusionThe probe resistance is a useful predictive factor for successful EBUS-GS-TBLB diagnosis of solid and positive-bronchus-sign PPLs where the probe was located within the lesion. Four serial biopsies are appropriate for both probe resistance type II and type III, and additional diagnostic procedures are needed for type I

    Transcriptome Analysis of H2O2-Treated Wheat Seedlings Reveals a H2O2-Responsive Fatty Acid Desaturase Gene Participating in Powdery Mildew Resistance

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    Hydrogen peroxide (H2O2) plays important roles in plant biotic and abiotic stress responses. However, the effect of H2O2 stress on the bread wheat transcriptome is still lacking. To investigate the cellular and metabolic responses triggered by H2O2, we performed an mRNA tag analysis of wheat seedlings under 10 mM H2O2 treatment for 6 hour in one powdery mildew (PM) resistant (PmA) and two susceptible (Cha and Han) lines. In total, 6,156, 6,875 and 3,276 transcripts were found to be differentially expressed in PmA, Han and Cha respectively. Among them, 260 genes exhibited consistent expression patterns in all three wheat lines and may represent a subset of basal H2O2 responsive genes that were associated with cell defense, signal transduction, photosynthesis, carbohydrate metabolism, lipid metabolism, redox homeostasis, and transport. Among genes specific to PmA, ‘transport’ activity was significantly enriched in Gene Ontology analysis. MapMan classification showed that, while both up- and down- regulations were observed for auxin, abscisic acid, and brassinolides signaling genes, the jasmonic acid and ethylene signaling pathway genes were all up-regulated, suggesting H2O2-enhanced JA/Et functions in PmA. To further study whether any of these genes were involved in wheat PM response, 19 H2O2-responsive putative defense related genes were assayed in wheat seedlings infected with Blumeria graminis f. sp. tritici (Bgt). Eight of these genes were found to be co-regulated by H2O2 and Bgt, among which a fatty acid desaturase gene TaFAD was then confirmed by virus induced gene silencing (VIGS) to be required for the PM resistance. Together, our data presents the first global picture of the wheat transcriptome under H2O2 stress and uncovers potential links between H2O2 and Bgt responses, hence providing important candidate genes for the PM resistance in wheat

    A review of the role of cav-1 in neuropathology and neural recovery after ischemic stroke

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    Abstract Ischemic stroke starts a series of pathophysiological processes that cause brain injury. Caveolin-1 (cav-1) is an integrated protein and locates at the caveolar membrane. It has been demonstrated that cav-1 can protect blood–brain barrier (BBB) integrity by inhibiting matrix metalloproteases (MMPs) which degrade tight junction proteins. This article reviews recent developments in understanding the mechanisms underlying BBB dysfunction, neuroinflammation, and oxidative stress after ischemic stroke, and focuses on how cav-1 modulates a series of activities after ischemic stroke. In general, cav-1 reduces BBB permeability mainly by downregulating MMP9, reduces neuroinflammation through influencing cytokines and inflammatory cells, promotes nerve regeneration and angiogenesis via cav-1/VEGF pathway, reduces apoptosis, and reduces the damage mediated by oxidative stress. In addition, we also summarize some experimental results that are contrary to the above and explore possible reasons for these differences

    Neutron beam line design of a white neutron source at CSNS

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    China Spallation Neutron Source (CSNS), which is under construction, is a large scientific facility dedicated mainly for multi-disciplinary research on material characterization using neutron scattering techniques. The CSNS Phase-I accelerator will deliver a proton beam with an energy of 1.6 GeV and a pulse repetition rate of 25 Hz to a tungsten target, and the beam power is 100 kW. A white neutron source using the back-streaming neutrons through the incoming proton beam channel was proposed and is under construction. The back-streaming neutrons which are very intense and have good time structure are very suitable for nuclear data measurements. The white neutron source includes an 80-m neutron beam line, two experimental halls, and also six different types of spectrometers. The physics design of the beam line is presented in this paper, which includes beam optics and beam characterization simulations, with the emphasis on obtaining extremely low background. The first-batch experiments on nuclear data measurements are expected to be conducted in late 2017

    Neutron beam line design of a white neutron source at CSNS

    No full text
    China Spallation Neutron Source (CSNS), which is under construction, is a large scientific facility dedicated mainly for multi-disciplinary research on material characterization using neutron scattering techniques. The CSNS Phase-I accelerator will deliver a proton beam with an energy of 1.6 GeV and a pulse repetition rate of 25 Hz to a tungsten target, and the beam power is 100 kW. A white neutron source using the back-streaming neutrons through the incoming proton beam channel was proposed and is under construction. The back-streaming neutrons which are very intense and have good time structure are very suitable for nuclear data measurements. The white neutron source includes an 80-m neutron beam line, two experimental halls, and also six different types of spectrometers. The physics design of the beam line is presented in this paper, which includes beam optics and beam characterization simulations, with the emphasis on obtaining extremely low background. The first-batch experiments on nuclear data measurements are expected to be conducted in late 2017

    Endothelial H2S-AMPK dysfunction upregulates the angiocrine factor PAI-1 and contributes to lung fibrosis

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    Dysfunction of the vascular angiocrine system is critically involved in regenerative defects and fibrosis of injured organs. Previous studies have identified various angiocrine factors and found that risk factors such as aging and metabolic disorders can disturb the vascular angiocrine system in fibrotic organs. One existing key gap is what sense the fibrotic risk to modulate the vascular angiocrine system in organ fibrosis. Here, using human and mouse data, we discovered that the metabolic pathway hydrogen sulfide (H2S)-AMP-activated protein kinase (AMPK) is a sensor of fibrotic stress and serves as a key mechanism upregulating the angiocrine factor plasminogen activator inhibitor-1 (PAI-1) in endothelial cells to participate in lung fibrosis. Activation of the metabolic sensor AMPK was inhibited in endothelial cells of fibrotic lungs, and AMPK inactivation was correlated with enriched fibrotic signature and reduced lung functions in humans. The inactivation of endothelial AMPK accelerated lung fibrosis in mice, while the activation of endothelial AMPK with metformin alleviated lung fibrosis. In fibrotic lungs, endothelial AMPK inactivation led to YAP activation and overexpression of the angiocrine factor PAI-1, which was positively correlated with the fibrotic signature in human fibrotic lungs and inhibition of PAI-1 with Tiplaxtinin mitigated lung fibrosis. Further study identified that the deficiency of the antioxidative gas metabolite H2S accounted for the inactivation of AMPK and activation of YAP-PAI-1 signaling in endothelial cells of fibrotic lungs. H2S deficiency was involved in human lung fibrosis and H2S supplement reversed mouse lung fibrosis in an endothelial AMPK-dependent manner. These findings provide new insight into the mechanism underlying the deregulation of the vascular angiocrine system in fibrotic organs
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