440 research outputs found
Inhibitors and Activators of SOD, GSH‐Px, and CAT
Reactive oxygen species (ROS) is harmful to our health, and SOD, CAT, and GPX are the major antioxidant enzymes that defend us from effects of ROS. In medicine, food, and dairy industries, antioxidant enzymes often surround complex environments. For better utilization of these enzymes, the inhibitors (including competitive inhibitors and noncompetitive inhibitors) and activators of SOD, CAT, and GPX are descripted in detail in this chapter. Also, the structure and catalytic mechanism of these antioxidants are summarized
Effects of extraosseous talotarsal stabilization on the biomechanics of flexible flatfoot subtalar joints in children: a finite element study
Background: Objective of the study was to generate an experimental foundation for the clinical application of extraosseous talotarsal stabilization (EOTTS) in treatment of flexible flatfeet in children by investigating the biomechanical characteristics of flexible flatfoot and the effects of EOTTS on hindfoot biomechanics.Methods: Three-dimensional finite element models of the foot and ankle complex were generated from computer tomography images of a volunteer’s left foot in three states: normal, flexible flatfoot, and post-EOTTS. After validation by X-ray, simulated loads were applied to the three models in a neutral position with both feet standing.Results: In the flexible flatfoot model, the contact stress on the subtalar joint increased and contact areas decreased, resulting in abnormal stress distribution compared to the normal model. However, following treatment of the foot with EOTTS, these parameters returned to close to normal. Subtalar joint instability leads to a flexible flat foot. Based on this study, it is proposed that EOTTS can restore the normal function of the subtalar joint in and is an effective treatment for flexible flatfoot in children. We and many clinical data studies provide evidence for sinus tarsi implants in pediatric patients. It is showed that the formation of flexible flatfoot is induced by subtalar joint instability.Conclusions: Because of the EOTTS provides the best biomechanical solution to subtalar joint instability, the EOTTS became an effective form for subtalar joint instability treatment
Loss of FKBP5 Affects Neuron Synaptic Plasticity: An Electrophysiology Insight
FKBP5 (FKBP51) is a glucocorticoid receptor (GR) binding protein, which acts as a co-chaperone of heat shock protein 90 (HSP90) and negatively regulates GR. Its association with mental disorders has been identified, but its function in disease development is largely unknown. Long-term potentiation (LTP) is a functional measurement of neuronal connection and communication, and is considered one of the major cellular mechanisms that underlies learning and memory, and is disrupted in many mental diseases. In this study, a reduction in LTP in Fkbp5 knockout (KO) mice was observed when compared to WT mice, which correlated with changes to the glutamatergic and GABAergic signaling pathways. The frequency of mEPSCs was decreased in KO hippocampus, indicating a decrease in excitatory synaptic activity. While no differences were found in levels of glutamate between KO and WT, a reduction was observed in the expression of excitatory glutamate receptors (NMDAR1, NMDAR2B and AMPAR), which initiate and maintain LTP. The expression of the inhibitory neurotransmitter GABA was found to be enhanced in Fkbp5 KO hippocampus. Further investigation suggested that increased expression of GAD65, but not GAD67, accounted for this increase. Additionally, a functional GABAergic alteration was observed in the form of increased mIPSC frequency in the KO hippocampus, indicating an increase in presynaptic GABA release. Our findings uncover a novel role for Fkbp5 in neuronal synaptic plasticity and highlight the value of Fkbp5 KO as a model for studying its role in neurological function and disease development
Efficient CCA-Secure PKE from Identity-Based Techniques
Office of Research, Singapore Management Universit
The mouse and ferret models for studying the novel avian-origin human influenza A (H7N9) virus.
BackgroundThe current study was conducted to establish animal models (including mouse and ferret) for the novel avian-origin H7N9 influenza virus.FindingsA/Anhui/1/2013 (H7N9) virus was administered by intranasal instillation to groups of mice and ferrets, and animals developed typical clinical signs including body weight loss (mice and ferrets), ruffled fur (mice), sneezing (ferrets), and death (mice). Peak virus shedding from respiratory tract was observed on 2 days post inoculation (d.p.i.) for mice and 3-5 d.p.i. for ferrets. Virus could also be detected in brain, liver, spleen, kidney, and intestine from inoculated mice, and in heart, liver, and olfactory bulb from inoculated ferrets. The inoculation of H7N9 could elicit seroconversion titers up to 1280 in ferrets and 160 in mice. Leukopenia, significantly reduced lymphocytes but increased neutrophils were also observed in mouse and ferret models.ConclusionsThe mouse and ferret model enables detailed studies of the pathogenesis of this illness and lay the foundation for drug or vaccine evaluation
The roles of inflammasomes in cancer
Inflammation is a key characteristic of all stages of tumor development, including tumor initiation, progression, malignant transformation, invasion, and metastasis. Inflammasomes are an important component of the inflammatory response and an indispensable part of the innate immune system. Inflammasomes regulate the nature of infiltrating immune cells by signaling the secretion of different cytokines and chemokines, thus regulating the anti-tumor immunity of the body. Inflammasome expression patterns vary across different tumor types and stages, playing different roles during tumor progression. The complex diversity of the inflammasomes is determined by both internal and external factors relating to tumor establishment and progression. Therefore, elucidating the specific effects of different inflammasomes in anti-tumor immunity is critical for promoting the discovery of inflammasome-targeting drugs. This review focuses on the structure, activation pathway, and identification methods of the NLRP3, NLRC4, NLRP1 and AIM2 inflammasomes. Herein, we also explore the role of inflammasomes in different cancers and their complex regulatory mechanisms, and discuss current and future directions for targeting inflammasomes in cancer therapy. A detailed knowledge of inflammasome function and regulation may lead to novel therapies that target the activation of inflammasomes as well as the discovery of new drug targets
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