417 research outputs found

    急性曼陀罗中毒患者临床护理观察

    Get PDF
    Mandala is used medicinally to treat cough and asthma, conscious sedation. Entire individual plant is poisonous, and the toxic substances are hyoscyamine and scopolamine and atropine, etc. It is a rare case that patients were poisoned by Mandala in clinical practice. More reports were about the cases that patients were poisoned by seeds, fruit, leaf and flower. The toxicity would stimulate and restrain the central nervous system successively, block the reactions of acetylcholine, resist and paralyze the parasympathetic nerve. The paper discusses continuous blood purification treatment and clinical nursing of mandala poisoning patients by case analysis.曼陀罗内服可用来平喘止咳,镇静麻醉。曼陀罗全株有毒,毒性物质为莨菪碱、东莨菪碱和阿托品等。在临床中遇到的曼陀罗中毒罕见。有病例报道多为误食曼陀罗种子、果实、叶、花所致,其毒性作用是对中枢神经先兴奋后抑制,阻断乙酰胆碱反应,对抗和麻痹副交感神经。本文通过病例分析,探讨如何对曼陀罗中毒患者行连续性血液净化治疗、临床护理

    Adenovirus 11p downregulates CD46 early in infection

    Get PDF
    AbstractAdenovirus 11 prototype (Ad11p), belonging to species B, uses CD46 as an attachment receptor. CD46, a complement regulatory molecule, is expressed on all human nucleated cells. We show here that Ad11p virions downregulate CD46 on the surface of K562 cells as early as 5min p.i. Specific binding to CD46 by the Ad11p fiber knob was required to mediate downregulation. The complement regulatory factors CD55 and CD59 were also reduced to a significant extent as a consequence of Ad11p binding to K562 cells. In contrast, binding of Ad7p did not result in downregulation of CD46 early in infection. Thus, the presumed interaction between Ad7p and CD46 did not have the same consequences as the Ad11p–CD46 interaction, the latter virus (Ad11p) being a promising gene therapy vector candidate. These findings may lead to a better understanding of the pathogenesis of species B adenovirus infections

    Multiscale Combined Model Based on Run-Length-Judgment Method and Its Application in Oil Price Forecasting

    Get PDF
    Forecasting of oil price is an important area of energy market research. Based on the idea of decomposition-reconstruction-integration, this paper built a new multiscale combined forecasting model with the methods of empirical mode decomposition (EMD), artificial neural network (ANN), support vector machine (SVM), and time series methods. While building the model, we proposed a new idea to use run length judgment method to reconstruct the component sequences. Then this model was applied to analyze the fluctuation and trend of international oil price. Oil price series was decomposed and reconstructed into high frequency, medium frequency, low frequency, and trend sequences. Different features of fluctuation can be explained by irregular factors, season factors, major events, and long-term trend. Empirical analysis showed that the multiscale combined model obtained the best forecasting result compared with single models including ARIMA, Elman, SVM, and GARCH and combined models including ARIMA-SVM model and EMD-SVM-SVM method

    Changes in Volatile Profiles and Activity of Hydroperoxide Lyase and Alcohol Dehydrogenase During the Development of Cabernet Sauvignon Grapes (Vitis vinifera L.)

    Get PDF
    In this study we focused on the development of Cabernet Sauvignon grapes and investigated changes in theactivity of alcohol dehydrogenase (ADH) and hydroperoxide lyase (HPL) in different tissues. We sampledgrape skin at four, six, seven, eight, nine, 10, 12, 14 and 16 weeks after anthesis; developing flowers whenblooming at 0%, 5%, 50%, and 90%; and leaves at two and four weeks before anthesis and at two, four,six, eight, nine, and 10 weeks after anthesis. We also examined the type and fluctuation of volatile contents.ADH activity increased with the development of flowers and grape skins, which led to the increasing oftypes and concentration of alcohols. Low levels of 9-HPL led to low concentrations of C9 compounds.According to this paper, C6 compounds became abundant with the development of grape berries, while theactivity of 13-HPL kept at a low level in the flowers and grape skins. There might have been a high level of13-HPL activity from the end of flowering until fruit setting that we did not detect. Furthermore, similarC6 and C5 compounds were detected across all tissues, including hexanal, (E)-2-hexenal, (Z)-3-hexenal,(Z)-2-penten-1-ol, (Z)-3-hexen-1-ol, 1-hexanol and 3-hexen-1-ol. Generally speaking, the concentrations ofC6 and C5 compounds could be used as the criterion of maturation of the three grape tissues

    Antiaging Effect of Pine Pollen in Human Diploid Fibroblasts and in a Mouse Model Induced by D-Galactose

    Get PDF
    The present paper was designed to investigate the effect of pine pollen against aging in human diploid fibroblast 2BS cells and in an accelerated aging model, which was established by subcutaneous injections with D-galactose daily for 8 weeks in C57BL/6J mice. Pine pollen (1 mg/mL and 2 mg/mL) is proved to delay the replicative senescence of 2BS cells as evidenced by enhanced cell proliferation, decreased SA-β-Gal activity, and reversed expression of senescence-associated molecular markers, such as p53, p21Waf1, p16INK4a, PTEN, and p27Kip1 in late PD cells. Besides, pine pollen reversed D-galactose-induced aging effects in neural activity and inflammatory cytokine levels, as indicated by improved memory latency time and reduced error rate in step-down test and decreased concentrations of IL-6 and TNF-α in model mice. Similar to the role of AGEs (advanced glycation endproducts) formation inhibitor aminoguanidine (AG), pine pollen inhibited D-galactose-induced increment of AGEs levels thus reversed the aging phenotypes in model mice. Furthermore, the declined antioxidant activity was obviously reversed upon pine pollen treatment, which may account for its inhibitory effect on nonenzymatic glycation (NEG) in vivo. Our finding presents pine pollen as an attractive agent with potential to retard aging and attenuate age-related diseases in humans

    Immune Cells in the BBB Disruption After Acute Ischemic Stroke: Targets for Immune Therapy?

    Get PDF
    Blood-Brain Barrier (BBB) disruption is an important pathophysiological process of acute ischemic stroke (AIS), resulting in devastating malignant brain edema and hemorrhagic transformation. The rapid activation of immune cells plays a critical role in BBB disruption after ischemic stroke. Infiltrating blood-borne immune cells (neutrophils, monocytes, and T lymphocytes) increase BBB permeability, as they cause microvascular disorder and secrete inflammation-associated molecules. In contrast, they promote BBB repair and angiogenesis in the latter phase of ischemic stroke. The profound immunological effects of cerebral immune cells (microglia, astrocytes, and pericytes) on BBB disruption have been underestimated in ischemic stroke. Post-stroke microglia and astrocytes can adopt both an M1/A1 or M2/A2 phenotype, which influence BBB integrity differently. However, whether pericytes acquire microglia phenotype and exert immunological effects on the BBB remains controversial. Thus, better understanding the inflammatory mechanism underlying BBB disruption can lead to the identification of more promising biological targets to develop treatments that minimize the onset of life-threatening complications and to improve existing treatments in patients. However, early attempts to inhibit the infiltration of circulating immune cells into the brain by blocking adhesion molecules, that were successful in experimental stroke failed in clinical trials. Therefore, new immunoregulatory therapeutic strategies for acute ischemic stroke are desperately warranted. Herein, we highlight the role of circulating and cerebral immune cells in BBB disruption and the crosstalk between them following acute ischemic stroke. Using a robust theoretical background, we discuss potential and effective immunotherapeutic targets to regulate BBB permeability after acute ischemic stroke

    The gastrointestinal-brain-microbiota axis: a promising therapeutic target for ischemic stroke

    Get PDF
    Ischemic stroke is a highly complex systemic disease characterized by intricate interactions between the brain and gastrointestinal tract. While our current understanding of these interactions primarily stems from experimental models, their relevance to human stroke outcomes is of considerable interest. After stroke, bidirectional communication between the brain and gastrointestinal tract initiates changes in the gastrointestinal microenvironment. These changes involve the activation of gastrointestinal immunity, disruption of the gastrointestinal barrier, and alterations in gastrointestinal microbiota. Importantly, experimental evidence suggests that these alterations facilitate the migration of gastrointestinal immune cells and cytokines across the damaged blood-brain barrier, ultimately infiltrating the ischemic brain. Although the characterization of these phenomena in humans is still limited, recognizing the significance of the brain-gastrointestinal crosstalk after stroke offers potential avenues for therapeutic intervention. By targeting the mutually reinforcing processes between the brain and gastrointestinal tract, it may be possible to improve the prognosis of ischemic stroke. Further investigation is warranted to elucidate the clinical relevance and translational potential of these findings

    Green Tea Polyphenol Epigallocatechin-3-Gallate Promotes Reendothelialization in Carotid Artery of Diabetic Rabbits by Reactivating Akt/eNOS Pathway

    Get PDF
    Background: Epigallocatechin gallate (EGCG) is the most abundant catechin in green tea and has proven benefits on endothelial cells in diabetes. However, it remains unclear whether EGCG could improve function of late endothelial progenitor cells (L-EPCs) in diabetes.Methods: Thirty-six rabbits were randomized into six groups. Thirty diabetic rabbits were induced by a single dose of alloxan (100 mg/kg injection intraperitoneally). All of them were given intragastrically EGCG (50 mg/kg/day) or saline for 7 days after carotid injury. In autotransfusion experiment, L-EPCs were cultured with pre-treated EGCG (40 μM for 72 h) and then were injected into the site of injured vascular. Proliferation and migration of EGCG pre-treated L-EPCs in high glucose condition were assessed by EDU incorporation assay and modified Boyden chamber assay, respectively. The mRNA and protein expression of Akt-eNOS pathway were detected by real-time PCR and western blot.Results: Reendothelialization rate in injured carotid artery of diabetic rabbits was augmented in the EGCG group (50 mg/kg/d for 7 days) compared with the non-EGCG group (74.2 ± 4.6% vs. 25.6 ± 5.9%, P < 0.001). EGCG pre-treated L-EPCs autologous transfusion also accelerated the diabetic rabbits’ carotid reendothelialization compared with the diabetic sham-operated group (65.6 ± 8.5% vs. 32.9 ± 5.0%, P = 0.011). In vitro studies showed, 40 μM EGCG treatment for 72 h recovered L-EPCs’ proliferation and migration, as well as restored the phosphorylation level of Akt and eNOS blocked by high glucose condition.Conclusion: EGCG accelerated reendothelialization in diabetic rabbits after carotid injury in part by reactivating the Akt/eNOS pathway, which might contribute to recovering proliferation and migration of L-EPCs impaired by high glucose
    corecore