Scientific reports
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High density lipoprotein cholesterol (HDL-C) has been reported as a significant indicator of systemic inflammation. The association underlying HDL-C and persistent organ failure (POF), pancreatic necrosis (PNec) and mortality in acute pancreatitis (AP) has not been evaluated. From 2007 to 2016, consecutive AP patients with admission lipid profiles assessment were included in this study. ⋯ Moreover, there was a positive trend for the association across increasing HDL-C quartiles and POF, PNec and mortality after multivariable analysis (p values were <0.001, <0.001 and 0.043, respectively). The AUC of HDL-C for the outcomes were comparable to that of Ranson score for diagnosing POF (0.778 vs. 0.678; P < 0.001), PNec (0.734 vs. 0.701; P = 0.143) and mortality (0.768 vs. 0.745; P = 0.516). Decreased HDL-C value is an independent risk factor for the incidence of POF, PNec and in-hospital mortality in AP.
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Cervical radiculopathy has become an increasing problem worldwide. Conservative treatment options have been recommended in many reviews on cervical radiculopathy, ranging from different types of physiotherapy to waiting for remission by natural history. No multimodal pain management concept (MPM) on an inpatient basis has been evaluated. ⋯ MPM seems to be an efficient short-term approach to treating cervical radiculopathy. Cervical translaminar epidural steroid injection is an important part of this concept. In the absence of a clear indication for surgery, MPM represents a treatment option.
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Recent evidence indicates that motor cortex stimulation (MCS) is a potentially effective treatment for chronic neuropathic pain. However, the neural mechanisms underlying the attenuated hyperalgesia after MCS are not completely understood. In this study, we investigated the neural mechanism of the effects of MCS using an animal model of neuropathic pain. ⋯ Interestingly, inhibition of protein kinase M zeta (PKMζ), a regulator of synaptic plasticity, in the ACC blocked the effects of repetitive MCS. Histological and molecular studies showed a significantly increased level of glial fibrillary acidic protein (GFAP) expression in the ACC after peripheral neuropathy, and neither MCS treatment nor ZIP administration affected this increase. These results suggest that repetitive MCS can attenuate the mechanical allodynia in neuropathic pain, and that the activation of PKMζ in the ACC may play a role in the modulation of neuropathic pain via MCS.
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Verteporfin (VP), a light-activated drug used in photodynamic therapy for the treatment of choroidal neovascular membranes, has also been shown to be an effective inhibitor of malignant cells. Recently, studies have demonstrated that, even without photo-activation, VP may still inhibit certain tumor cell lines, including ovarian cancer, hepatocarcinoma and retinoblastoma, through the inhibition of the YAP-TEAD complex. In this study, we examined the effects of VP without light activation on human glioma cell lines (LN229 and SNB19). ⋯ In addition, we observed that expression of VEGFA and the pluripotent marker Oct-4 were also decreased. Verteporfin did not alter the Akt survival pathway or the mTor pathway but there was a modest increase in LC3-IIB, a marker of autophagosome biogenesis. This study suggests that verteporfin should be further explored as an adjuvant therapy for the treatment of glioblastoma.
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Succinyl Coenzyme A synthetase (SCS) is a key mitochondrial enzyme. Defected SCS ADP-forming β subunit (SCS A-β) is linked to lethal infantile Leigh or leigh-like syndrome. However, the impacts of SCS A-β deficiency on mitochondria specifically in neurons have not yet been comprehensively investigated. ⋯ Our data also suggest that the deregulation of mitochondrial nucleoside diphosphate kinase (NDPK) together with defects in mitochondrial transcription factors including mitochondrial DNA pol γ and Twinkle contribute to SCS A-β deficiency-mediated mtDNA instability. Furthermore, we have found that SCS A-β deficiency has detrimental influence on neuronal mitochondrial dynamics. Put together, the results have furnished our knowledge on the pathogenesis of SCS A-β deficiency-related mitochondrial diseases and revealed the vital role of SCS A-β in maintaining neuronal mitochondrial quality control and neuronal physiology.