187 research outputs found

    Two cases of pyogenic liver abscess due to Klebsiella pneumoniae in immunocompetent children

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    Pyogenic liver abscess (PLA) can be caused by bacteria entering the liver via the portal vein or primary bacteremia, or it can be cryptogenic. Recently, Klebsiella pneumoniae has been increasingly found as a PLA pathogen. PLA due to this bacterium often leads to formation of extrahepatic abscesses. The treatment of choice is dual therapy with insertion of percutaneous catheter drainage and antibiotic therapy. We report 2 cases of PLA due to K. pneumoniae in immunocompetent children. We successfully treated patient 1 with percutaneous catheter drainage for 18 days and 6-week course of antibiotic therapy. Patient 2 was treated with percutaneous needle aspiration and antibiotic therapy for the same period. In both patients, the PLAs showed the ultrasound-confirmed resolutions after the dual therapy

    Comparative study of the treatment outcomes of osteoporotic compression fractures without neurologic injury using a rigid brace, a soft brace, and no brace : a prospective randomized controlled non-inferiority trial

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    BACKGROUND:The efficacy of brace application for the treatment of osteoporotic compression fractures remains unclear. The purpose of this study was to compare the treatment outcomes in patients with osteoporotic compression fractures with regard to whether the patients had no braces, rigid braces, or soft braces.METHODS:We randomly assigned sixty patients with acute one-level osteoporotic compression fractures within three days of injury to the no-brace, soft-brace, and rigid-brace groups through 1:1:1 allocation. The primary outcome was the baseline adjusted Oswestry Disability Index score at twelve weeks after compression fracture. The non-inferior margin of the Oswestry Disability Index was set at an average of 10 points.RESULTS:The baseline adjusted Oswestry Disability Index score at twelve weeks after compression fracture in the no-brace group was not inferior to that in the soft-brace or rigid-brace groups. The mean adjusted Oswestry Disability Index score was 35.95 points (95% confidence interval, 25.42 to 46.47 points) in the no-brace group and 37.83 points (95% confidence interval, 26.77 to 48.90 points) in the soft-brace group, with a difference of -1.88 points (95% confidence interval, -7.02 to 9.38 points) between the groups. Similarly, the mean adjusted Oswestry Disability Index score was 35.95 points (95% confidence interval, 25.42 to 46.47 points) in the no-brace group and 33.54 points (95% confidence interval, 23.79 to 43.29 points) in the rigid-brace group, with a difference of 2.41 points (95% confidence interval, -7.86 to 9.27 points) between the groups. During the follow-up assessment period, there was no significant difference among the groups for the overall Oswestry Disability Index scores (p = 0.260), visual analog scale for pain scores for back pain (p = 0.292), and anterior body compression ratios (p = 0.237). However, the Oswestry Disability Index scores and the visual analog scale scores for back pain significantly improved with time after the fractures (p < 0.001), and the body compression ratios significantly decreased with time in all three groups (p < 0.001).CONCLUSIONS:The Oswestry Disability Index scores for the treatment of compression fractures without a brace were not inferior to those with soft or rigid braces. Moreover, the improvement in back pain and progression of anterior body compression were similar among the three groups.OAIID:oai:osos.snu.ac.kr:snu2014-01/102/0000004226/15SEQ:15PERF_CD:SNU2014-01EVAL_ITEM_CD:102USER_ID:0000004226ADJUST_YN:NEMP_ID:A079510DEPT_CD:801CITE_RATE:4.309DEPT_NM:의학과SCOPUS_YN:NCONFIRM:

    House of Commons Library: Briefing paper: Number 07147, 13 April 2018: School places in England: applications, allocations and appeals

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    Background: We previously reported that ginsenoside Re (GRe) attenuated against methamphetamine (MA)-induced neurotoxicity via anti-inflammatory and antioxidant potentials. We also demonstrated that dynorphin possesses anti-inflammatory and antioxidant potentials against dopaminergic loss, and that balance between dynorphin and substance P is important for dopaminergic neuroprotection. Thus, we examined whether GRe positively affects interactive modulation between dynorphin and substance P against MA neurotoxicity in mice. Methods: We examined changes in dynorphin peptide level, prodynorphin mRNA, and substance P mRNA, substance P-immunoreactivity, homeostasis in enzymatic antioxidant system, oxidative parameter, microglial activation, and pro-apoptotic parameter after a neurotoxic dose of MA to clarify the effects of GRe, prodynorphin knockout, pharmacological inhibition of κ-opioid receptor (i.e., nor-binaltorphimine), or neurokinin 1 (NK1) receptor (i.e., L-733,060) against MA insult in mice. Results: GRe attenuated MA-induced decreases in dynorphin level, prodynorphin mRNA expression in the striatum of wild-type (WT) mice. Prodynorphin knockout potentiated MA-induced dopaminergic toxicity in mice. The imbalance of enzymatic antioxidant system, oxidative burdens, microgliosis, and pro-apoptotic changes led to the dopaminergic neurotoxicity. Neuroprotective effects of GRe were more pronounced in prodynorphin knockout than in WT mice. Nor-binaltorphimine, a κ-opioid receptor antagonist, counteracted against protective effects of GRe. In addition, we found that GRe significantly attenuated MA-induced increases in substance P-immunoreactivity and substance P mRNA expression in the substantia nigra. These increases were more evident in prodynorphin knockout than in WT mice. Although, we observed that substance P-immunoreactivity was co-localized in NeuN-immunreactive neurons, GFAP-immunoreactive astrocytes, and Iba-1-immunoreactive microglia. NK1 receptor antagonist L-733,060 or GRe selectively inhibited microgliosis induced by MA. Furthermore, L-733,060 did not show any additive effects against GRe-mediated protective activity (i.e., antioxidant, antimicroglial, and antiapoptotic effects), indicating that NK1 receptor is one of the molecular targets of GRe. Conclusions: Our results suggest that GRe protects MA-induced dopaminergic neurotoxicity via upregulatgion of dynorphin-mediated κ-opioid receptor and downregulation of substance P-mediated NK1 R

    Application of self-assembly peptides targeting the mitochondria as a novel treatment for sorafenib-resistant hepatocellular carcinoma cells

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    Currently, there is no appropriate treatment option for patients with sorafenib-resistant hepatocellular carcinoma (HCC). Meanwhile, pronounced anticancer activities of newly-developed mitochondria-accumulating self-assembly peptides (Mito-FF) have been demonstrated. This study intended to determine the anticancer effects of Mito-FF against sorafenib-resistant Huh7 (Huh7-R) cells. Compared to sorafenib, Mito-FF led to the generation of relatively higher amounts of mitochondrial reactive oxygen species (ROS) as well as the greater reduction in the expression of antioxidant enzymes (P &lt; 0.05). Mito-FF was found to significantly promote cell apoptosis while inhibiting cell proliferation of Huh7-R cells. Mito-FF also reduces the expression of antioxidant enzymes while significantly increasing mitochondrial ROS in Huh7-R cells. The pro-apoptotic effect of Mito-FFs for Huh7-R cells is possibly caused by their up-regulation of mitochondrial ROS, which is caused by the destruction of the mitochondria of HCC cells
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