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  • 机译 多发性骨髓瘤合并继发性骨髓增生异常综合征患者由根瘤菌引起的小脑累及的传播性毛霉菌病:1例报告
    摘要:Mucormycosis is an angioinvasive fungal infection with a high mortality rate. Patients with hematological malignancies following voriconazole therapy are at high risk from mucormycosis. Here, the present study reports on a 68-year-old man diagnosed with multiple myeloma and secondary myelodysplastic syndrome, who was infected with disseminated mucormycosis with cerebellum involvement confirmed by mycological culture and histopathological examination. For patients with hematological malignancies who are receiving antifungal therapy, an opportunistic infection of mucormycosis should be considered if a ‘breakthrough’ infection occurs in the predilection sites (such as the sinuses, lungs, skin, brain and gastrointestinal tract). It is difficult to diagnose mucormycosis because of the limited reliable detection methods, and because mucormycosis often presents with an acute onset and progresses rapidly, particularly in immunocompromised patients. Antifungal therapy with amphotericin B or posaconazole should be started as soon as possible considering the empirical diagnosis.
  • 机译 miR-552在肝细胞癌中的下调抑制细胞迁移和侵袭,并通过RUNX3促进细胞凋亡
    摘要:Research conducted previously has indicated that microRNAs (miRs) have potential effects on the pathogenesis of hepatocellular carcinoma (HCC). The biological functions of miR-552 have been well documented in colon cancer; however, the role of miR-552 in HCC remains unclear. The present study evaluated the effects of miR-552 in HCC physiology, using HCC cell lines as model. An miR-552 inhibitor was transfected into HCC cell lines to knock down the expression of miR-552. Reverse transcription-quantitative PCR and western blot analysis were used to detect the expression of miR-552 and Runt-related transcription factor 3 (RUNX3), respectively. MTT assay was used to analyze cell viability, whilst Transwell and wound-healing assay were used to investigate cell migration. Flow cytometry was performed to measure cell apoptosis. The direct association between RUNX3 and miR-552 was evaluated using dual luciferase reporter assay. The expression of miR-552 was significantly elevated in HCC tumor tissues compared with the adjacent healthy samples. Additionally, transfection with the miR-552 inhibitor decreased cell viability and migration. miR-552 knockdown also increased HCC cell apoptosis in vitro. In conclusion, these results suggest that miR-552 has an oncogenic function in HCC and is a potential biomarker for detecting HCC.
  • 机译 MicroRNA-146a通过抑制炎症和氧化应激来预防脑出血
    摘要:The present study aimed to investigate the role of microRNA-146a (miR-146a) in intracerebral hemorrhage (ICH), and to further assess its underlying mechanism. An ICH rat model was established in the current study and 1 h following ICH induction, rats were treated with or without an miR-146a mimic. A total of 3 days following ICH induction, rat neurological score, brain water content and neuronal apoptosis were measured via flow cytometry. Levels of pro-inflammatory cytokines tumor necrosis factor-α and interleukin-1β were detected via ELISA and certain biomarkers of oxidative stress, including malondialdehyde, superoxide dismutase and glutathione peroxidase, were also determined in current study. The expression of genes and proteins were detected in current study via reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. software and a dual luciferase reporter assay were used to confirm the association between miR-146a and TRAF6. The results of the current study revealed that miR-146a was significantly downregulated in ICH rats, and its overexpression reduced neurological damage and brain edema, as evidenced by decreased neurological scores and brain water content. Results from further analyses demonstrated that the overexpression of miR-146a inhibited neuronal apoptosis, reduced pro-inflammatory cytokine production and prevented oxidative stress in ICH rats. In addition, it was revealed that the upregulation of miR-146a repressed the TRAF6/NF-κB pathway in the brain tissue of ICH rats. TRAF6 was also determined to be a target of miR-146a. In conclusion, these data indicated that miR-146a protects against ICH by inhibiting inflammation and oxidative stress.
  • 机译 妊娠糖尿病中lncRNA MEG3表达异常的机制
    • 作者:Hailing Zhang
    • 刊名:Experimental and Therapeutic Medicine
    • 2019年第5期
    摘要:Gestational diabetes mellitus (GDM) is a common metabolic condition during pregnancy. Long non-coding RNAs (lncRNAs) have been found to seve critical roles in GDM development; however, the role of lncRNA maternally expressed gene 3 (MEG3) in GDM remains unclear. Therefore, the aim of the present study was to investigate the expression and role of MEG3 in GDM, and to further explore the underlying mechanism. The levels of lncRNA MEG3 in the blood and placental villous tissues of pregnant women with GDM was measured using reverse transcription-quantitative PCR. Bioinformatics analysis and dual luciferase reporter assays were performed to investigate the association between lncRNA MEG3 and microRNA (miR)-345-3p. Transfection was subsequently performed on HTR-8/SVneo cells, a human chorionic trophoblast cell line, to assess the role of lncRNA MEG3 in GDM. In particular, cell viability, cellular migratory/invasive ability and cell apoptosis were analyzed using MTT assay, Transwell assay and flow cytometry, respectively. Compared with pregnant women without GDM, lncRNA MEG3 levels were significantly elevated in the blood and placental villous tissues of GDM pregnant women. miR-345-3p was identified to be a direct target of lncRNA MEG3 using dual luciferase reporter assay, which was found to be reduced in pregnant women with GDM. Further analysis demonstrated that lncRNA MEG3 overexpression significantly inhibited HTR-8/SVneo cell viability, and prevented cell migration and invasion in addition to inducing cell apoptosis. In contrast, lncRNA MEG3 knockdown significantly enhanced HTR-8/SVneo cell viability, promoted cell migration/invasion and reduced cell apoptosis. Inhibiting miR-345-3p expression negated all the observed physiological effects of lncRNA MEG3 knockdown on HTR-8/SVneo cells. In conclusion, lncRNA MEG3 levels were abnormally upregulated in GDM, which participated in the development and progression of GDM by regulating human chorionic trophoblast cell physiology. Therefore, lncRNA MEG3 may be a potential diagnostic and therapeutic target for GDM.
  • 机译 利多卡因通过调节MAPK / ERK /NF-κB信号通路保护H9c2细胞免受缺氧诱导的损伤
    • 作者:Haibin JinJin Yu
    • 刊名:Experimental and Therapeutic Medicine
    • 2019年第5期
    摘要:The aim of the present study was to investigate the effect of Lidocaine on hypoxia-induced injury in cardiomyoblasts whilst exploring the associated molecular mechanism. In the present study, hypoxia was induced in H9c2 cells to establish an in vitro model of myocardial infarction. The cells were treated with lidocaine (0.5, 1, 5, 10 mM) for 48 h under hypoxic conditions. Cell viability and apoptosis levels were determined by MTT assay and flow cytometry, and ELISA was used to measure the levels of inflammatory cytokines released. A creatine kinase isoenzyme/cardiac troponin I detection kit was used to show that lidocaine significantly reduced hypoxia-induced cardiac troponin 1 and creatine kinase-muscle/brain release in a dose-dependent manner. Mitochondrial viability staining suggested that lidocaine significantly enhanced mitochondrial viability under hypoxic conditions. Lidocaine also significantly reduced hypoxia-induced apoptosis and increased H9c2 viability in a dose-dependent manner. Additionally, under hypoxic conditions, lidocaine dose-dependently promoted Bcl-2 expression, while decreasing Bax and caspase-3 expression in H9c2 cells. ELISA and reverse transcription quantitative PCR were used to detect the levels of tumor necrosis factor (TNF-α), interleukin (IL)-1β and IL-6 released by H9c2 cells. Results showed that lidocaine markedly reduced the hypoxia-induced expression levels of IL-1β, TNF-α and IL-6 in a dose-dependent manner. In addition, protein levels of phosphorylated (p)-ERK1/2 and NF-κB p-p65 were analyzed by western blotting, and results indicated that lidocaine significantly increased the protein levels of p-ERK1/2 and decreased the protein level of NF-κB p-p65 in a dose-dependent manner under hypoxic conditions. These data suggested that lidocaine might protect cardiomyoblasts from hypoxia-induced injury via activation of the mitogen activated protein kinase/ERK/NF-κB signaling pathway.
  • 机译 老年认知功能障碍小鼠下丘脑DNA羟甲基化的表征
    • 作者:Jiang ZhongWei Xu
    • 刊名:Experimental and Therapeutic Medicine
    • 2019年第5期
    摘要:Post-operative cognitive dysfunction (POCD) is a common syndrome characterized by perioperative cerebral damage in elderly patients, including cognitive impairment and memory loss. Recent studies have revealed that anesthesia is one of the key causes of POCD. Ubiquitin-like with PHD and ring finger domains 2 (Uhrf2) has been reported to play a crucial role in regulating DNA methylation and hydroxymethylation, which are closely connected with memory building and erasure. However, whether narcotic drugs can affect Uhrf2 to impact on DNA methylation and hydroxymethylation in POCD is poorly understood. In this study, a POCD model was established in elderly mice through sevoflurane treatment, and these mice were found to have compromised levels of global DNA 5′-hydroxymethylcytosine (5hmC) and Uhrf2 in the hippocampus and the amygdaloid nucleus, when compared with non-POCD and control mice. The results of immunoprecipitation and quantitative PCR revealed that 5hmC modification of the promoters of genes associated with neural protection and development, such as glial cell-derived neurotrophic factor, brain derived neurotrophic factor, glucocorticoid receptor and acyl-CoA sythetase short chain family member 2, was reduced in the hippocampus of POCD mice when compared with non-POCD and control mice. Taken together, the findings of the present study suggest that loss of 5hmC, in the hippocampus and the amygdaloid nucleus modulated by Uhrf2 suppression, may result in the learning and memory ability impairment seen in mice with POCD.
  • 机译 胆管癌相关竞争性内源RNA网络的综合分析
    摘要:Cholangiocarcinoma (CCA) is the second most common type of primary malignancy of the liver. Certain long non-coding RNAs (lncRNAs) have been demonstrated to have key roles in tumor pathogenesis by binding to microRNAs (miRNAs). However, the competing endogenous RNA (ceRNA) network of CCA remains to be fully determined. In the present study, the RNA expression profiles for CCA were downloaded from The Cancer Genome Atlas and further analyzed. A total of 318 differentially expressed (DE) lncRNAs, 87 DE miRNAs and 3,851 DE mRNAs were identified from 36 CCA samples and 9 adjacent non-tumor samples (for lncRNAs and miRNAs, fold change ≥2.5 and P<0.01; for mRNAs, fold change ≥2 and P<0.01). Further bioinformatics analyses were performed and the ceRNA network for CCA was constructed, which included 16 lncRNAs, 55 miRNAs and 373 mRNAs. Survival analysis of all genes in the network revealed that high expression of the mRNAs fucosyltransferase 4 (P<0.005) and huntingtin-interacting protein 1 related (P<0.001) has a positive impact on the overall survival of patients with CAA. Furthermore, the lncRNAs H19 and PVT1, and the miRNAs Homo sapiens (hsa)-miR-16-5p and hsa-miR-424-5p, together with peroxisome proliferator-activated receptors, may also have important roles in the pathogenesis of CCA. The present study provided data to further the understanding of and research into the molecular mechanisms implicated in CCA.
  • 机译 黄芪甲苷IV调节NF-κB介导的肝星状细胞的衰老和凋亡,从而抑制PDGF-BB诱导的活化
    摘要:Activated hepatic stellate cells (HSCs) are the principal effectors during hepatic fibrosis, which is characterized by the accumulation of extracellular matrix. Therefore, present therapies and investigations into hepatic fibrosis mainly focus on the suppression of activated HSCs. Astragaloside IV (ASIV) is an effective constituent extracted from the plant Astragalus membranaceus and has exhibited anti-fibrotic properties in hepatic fibrosis. However, its protective mechanism against hepatic fibrosis is not fully understood. The present study aimed to investigate the mechanistic role of ASIV on rat HSC-T6 cells activated with platelet-derived growth factor (PDGF)-BB. HSC-T6 cells were activated using PDGF-BB and subsequently treated with ASIV (final concentrations of 20 and 40 µg/ml) for 48 h. ASIV treatment decreased the expression of α1 type I collagen, α-smooth muscle actin and fibronectin on mRNA and protein levels, suggesting that ASIV suppresses PDGF-BB-induced HSC-T6 activation. Senescence-associated β-galactosidase activity, p21, high-mobility group AT-hook 1 and p53, common biomarkers of senescence, were upregulated by ASIV treatment. In addition, the expression of telomerase reverse transcriptase was reduced. ASIV promoted apoptosis of PDGF-BB-activated HSC-T6 cells. The NF-κB signaling pathway, which controls cellular senescence and apoptosis, was demonstrated to be stimulated by ASIV by increasing p65, p52, p50 and inhibitor of NF-κB kinase α expression levels, and by suppressing the expression of NF-κB inhibitor α. Taken together, these results demonstrated that ASIV promoted cellular senescence and apoptosis by activating the NF-κB pathway to suppress PDGF-BB-induced HSC-T6 activation; with potential implications for the treatment of hepatic fibrosis.
  • 机译 通过血管成形术,支架和支架移植物治疗失败的动静脉透析移植物:两年通畅率和成本效益分析
    摘要:The objective of this prospective randomized single-center study was to compare primary and secondary patency rates, number of percutaneous transluminal angioplasty (PTA) interventions and cost-effectiveness among PTA, deployment of a stent, or a stent graft in the treatment of failing arteriovenous dialysis grafts (AVG) due to restenosis in the venous anastomosis or the outflow vein. Altogether 60 patients with failing AVG and restenosis in the venous anastomosis or the outflow vein were randomly assigned to either PTA, placement of a stent (E-Luminexx®) or stent graft (Fluency Plus®). After the procedure, patients with stent or stent graft received dual antiplatelet therapy for the next three months. Follow-up angiography was scheduled at 3, 6, and 12 months unless requested earlier due to suspected stenosis or malfunction of the access. Subsequently, angiography was performed only if requested by the clinician. During a median follow-up of 22.4 (IQR=5.7) months patients with PTA, stent, or stent graft required 3.1±1.7, 2.5±1.7, or 1.7±2.1 (P=0.031) secondary PTA interventions. The primary patency rates were 0, 18 and 65% at 12 months and 0, 18 and 37% at 24 months in the PTA, stent, and stent graft group respectively (P<0.0001). The cost of the procedures in the first two years was €7,900±€3,300 in the PTA group, €8,500±€4,500 in the stent group, and €7,500±€6,200 in the stent graft group (P=0.45). We conclude that the treatment of failing dialysis vascular access by the deployment of a stent graft significantly improves its primary patency rates and decreases the number of secondary PTA interventions; however, the reduction in costs for maintaining AVG patency is not significant.
  • 机译 同型半胱氨酸通过下调血管内皮生长因子的表达来抑制人脐静脉内皮细胞的活力和迁移能力
    摘要:The current study aimed to explore the effect of homocysteine (Hcy) on the viability and migration ability of human umbilical vein endothelial cells (HUVECs), as well as to examine the underlying mechanism. The association between the expression level of Hcy and lower extremity deep vein thrombosis (DVT) was detected in clinical samples collected from patients. In addition, the effect of Hcy on the viability and migration ability of HUVECs was detected by cell counting kit-8 and Transwell assays, respectively, while vascular endothelial growth factor (VEGF) expression was measured in order to verify the effect of Hcy on VEGF. The results indicated that the serum Hcy levels in DVT patients were significantly increased. In vitro experiments also confirmed that Hcy was able to significantly inhibit the viability and migration ability of HUVECs, and downregulate the expression of VEGF in these cells. Furthermore, the inhibitory effect of Hcy on HUVEC viability and migration ability was achieved by downregulating the expression of VEGF using small interfering RNA transfection. In conclusion, Hcy inhibited the viability and migration ability of HUVECs by downregulating the expression of VEGF. This may underlie the high incidence of DVT in patients with hyperhomocysteinemia.
  • 机译 综合生物信息学分析揭示LINC01093 / miR-96-5p / ZFAND5 /NF-κB信号轴在肝细胞癌中的作用
    摘要:Hepatocellular carcinoma (HCC) is a significant health burden worldwide and its pathogenesis remains to be fully elucidated. One of the means by which long non-coding (lnc)RNAs regulate gene expression is by interacting with micro (mi)RNAs and acting as competing endogenous (ce)RNAs. lncRNAs have important roles in various diseases. The aim of the present study was to examine the potential roles of lncRNAs in HCC. The RNA expression profiles of 21 paired tissues of HCC and adjacent non-tumor tissues were obtained from the Gene Expression Omnibus database. The differentially expressed RNAs were analyzed using the DESeq package in R. Expression validation and survival analysis of selected RNAs were performed using Gene Expression Profile Interactive Analysis and/or Kaplan-Meier Plotter. The target genes of the miRNAs were predicted using lncBase or TargetScan. Functional analyses were performed using the Database for Annotation, Visualization and Integrated Discovery, and regulatory networks were determined using Cytoscape. Long intergenic non-protein coding RNA 1093 (LINC01093) was identified as one of the most significantly downregulated lncRNAs in HCC tissues. Downregulated expression of LINC01093 was associated with poor prognosis. A ceRNA network involving LINC01093, miR-96-5p and zinc finger AN1-type containing 5 (ZFAND5) was established. According to functional analyses, NF-κB signaling was implicated in the regulatory network for HCC. The present study revealed that a LINC01093/miR-96-5p/ZFAND5/NF-κB signaling axis may have an important role in the pathogenesis of HCC, and further investigation of this axis may provide novel insight into the development and progression of HCC.
  • 机译 乌司他丁联合轻度低温治疗对大鼠心肺复苏后肠屏障功能障碍的影响
    摘要:The aim of the present study was to investigate the effect of ulinastatin (UTI) alone or combined with mild therapeutic hypothermia (MTH) on intestinal barrier dysfunction following cardiopulmonary resuscitation (CPR) in rats. A total of 25 adult male Sprague-Dawley rats were randomly organized into five groups: Sham; control; UTI; MTH; and the combined group. The latter four groups were induced with the asphyxiated cardiac arrest rat model and treated with different interventions. After 6 h of treatment, the intestinal tissues of the rats were examined by electron microscopy, and the levels of intestinal malondialdehyde (MDA) and superoxide dismutase (SOD) were determined. The results of the present study indicated that the target temperature had successfully been attained in MTH and the combined group, and the other three groups of rats all survived at a normal temperature. In the rats treated with UTI or MTH, the epithelial cells exhibited pathological changes in their tight junctions and epithelial cell surface microvilli compared with the sham group. In the rats treated with a combination of UTI and MTH, whilst the epithelial cells exhibited a few slight changes, including mitochondrial edema, they were largely similar to the normal epithelial cells. However, there were significant differences in the levels of MDA and SOD between the different treatment groups. UTI combined with MTH may serve a protective role by suppressing oxidative stress in the small intestinal mucosa following CPR in rats compared with either UTI or MTH treatment alone.
  • 机译 麻风树碱抑制耐甲氧西林的金黄色葡萄球菌的抗药性
    摘要:Bacterial resistance to antimicrobial agents, including multidrug resistance, is an increasing problem in the treatment of infectious diseases. The development of resistance-modifying agents represents a potential strategy to alleviate the spread of bacterial resistance to antibiotics. A checkerboard microdilution assay was used to determine the synergy of jatrorrhizine and the antibiotic, norfloxacin (NFX). A bacterial ethidium bromide efflux assay, reverse transcription semi-quantitative polymerase chain reaction analysis and molecular docking study were performed. The three-dimensional structure of NorA multidrug efflux pump (NorA) was generated using a multiple threading approach. A murine thigh infection model was used to evaluate the in vivo synergistic effect. As a natural product, jatrorrhizine exhibited little antibacterial activity against methicillin-resistant Staphylococcus aureus (MRSA) SA1199B with a minimum inhibitory concentration (MIC) of 64 mg/l. According to the investigations of the mechanism, jatrorrhizine significantly inhibited bacterial drug efflux and the expression of NorA in the mRNA level as it can bind to NorA by hydrogen-bonds, hydrophobic and electrostatic interactions. The in vivo synergistical bactericidal activity of jatrorrhizine and NFX against MRSA was confirmed in a murine thigh infection model. As a novel resistance-modifying agent, jatrorrhizine exhibited in vitro and in vivo synergistic activities against MRSA, and inhibited bacterial drug efflux. The effects were mediated by the suppression of NorA mRNA expression and/or interactions with NorA efflux pump. These data support the hypothesis that jatrorrhizine is a potential agent for therapeutic use in infections caused by MRSA.
  • 机译 肌酸可以预防脂多糖诱导的小鼠急性肺损伤
    摘要:Acute respiratory distress syndrome is a well-known inflammatory disease associated with high rates of morbidity and mortality due to a lack of effective treatment methods. Carnosic acid (CA) is a phenolic diterpene compound that serves a central role in cytoprotective responses to inflammation. In the present study, the protective mechanism of CA on acute lung injury (ALI) induced by lipopolysaccharide (LPS) was investigated. Mice were randomly assigned to the following five groups: Control group, LPS group, and LPS plus CA groups (at 10, 20 and 40 mg/kg doses). Following pre-treatment with vehicle or CA, ALI was induced by the administration of LPS. At 6 h after LPS treatment, mice were sacrificed and lung tissues were harvested for histologic analysis and the determination of wet-to-dry ratio, myeloperoxidase activity and toll-like receptor 4 (TLR4) and NF-κB expression. Additionally, the levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) were determined in bronchoalveolar lavage fluid (BALF) and lung tissues, as well as the rate of apoptosis of the isolated neutrophils from BALF. The alleviation of LPS-induced ALI by CA was confirmed by histologic results and a reduction in the wet-to-dry ratio of lung tissues. Additionally, CA was revealed to significantly suppress the inhibitory effect of LPS on neutrophil apoptosis and the promoting effects of LPS on IL-1β, IL-6, TNF-α, TLR4 and NF-κB expression, and NF-κB phosphorylation. The current results indicated that CA protects against LPS-induced ALI via a mechanism that inhibits inflammation.
  • 机译 lncRNA-miRNA-mRNA网络的构建,以确定lncRNA在牛皮癣中的调节作用
    摘要:Psoriasis is a chronic inflammatory skin disorder that impairs the quality of life of affected patients. Emerging studies indicate that certain long non-coding RNAs (lncRNAs) have important roles in psoriasis. However, the exact functions of lncRNAs and their regulatory mechanisms as competitive endogenous RNAs (ceRNAs) in psoriasis have remained to be fully elucidated. In the present study, differentially expressed lncRNAs, microRNAs (miRNAs) and mRNAs were identified by analyzing public datasets, and a psoriasis-associated lncRNA-miRNA-mRNA network was constructed based on the ceRNA theory. Furthermore, previously validated abnormally expressed miRNAs in psoriasis were identified by a systematic literature search in the PubMed and Web of Science databases, and a specific miRNA-associated lncRNA-miRNA-mRNA sub-network was extracted. Furthermore, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed using DAVID 6.8. A total of 253 lncRNAs, 106 miRNAs and 1,156 mRNAs were identified as being differentially expressed between psoriasis skin and healthy control skin. The present study identified two key lncRNAs that may potentially have a role in the pathogenesis of psoriasis: and Prader Willi/Angelman region RNA 6. This integrative analysis enhances the understanding of the molecular mechanism of psoriasis and may provide novel therapeutic targets for the treatment of psoriasis.
  • 机译 根据小关节关节炎的严重程度,关节内腰椎小关节皮质激素注射的结果
    摘要:Lumbar facet joint osteoarthritis (FJOA) caused by degenerative change(s) is considered to be the main cause of facet joint-origin low back pain (LBP). Intra-articular lumbar facet joint (IA LFJ) corticosteroid injection is widely used for controlling pain induced by FJOA. In the current study, the outcomes of IA LFJ corticosteroid injection were evaluated according to the severity of FJOA. A total of 50 patients who received IA LFJ corticosteroid injections for the treatment of LFJ pain were recruited. Patients were classified into three groups according to the severity of FJOA, which was indicated during a lumbar axial MRI. A total of 10 patients were assigned to group A (patients with mild FJOA), 27 to group B (patients with moderate FJOA) and 13 to group C (patients with severe FJOA). Pain intensity was evaluated using a numerical rating scale (NRS) prior to treatment and at 1, 2 and 3 months after treatment. A total of 26 (52%) patients experienced successful treatment outcomes (defined as >50% reduction in NRS score at 3 months). Patients in all groups demonstrated a significant decrease in NRS scores at 1, 2 and 3 months after IA LFJ corticosteroid injection compared with the pre-treatment score (P<0.001). However, the effect of IA LFJ corticosteroid injection was not significantly different among the three groups (P=0.889). The results demonstrated that facet joint-origin LBP was significantly reduced after IA LFJ corticosteroid injection, regardless of the severity of FJOA. The results of the current study indicated that IA LFJ corticosteroid injection is a beneficial clinical option for managing LBP caused by FJOA.
  • 机译 经皮肾镜取石术治疗肾出血时,最初的超选择性肾动脉栓塞治疗失败:危险因素分析
    摘要:Superselective renal arterial embolization (SRAE) is a well-established method for the treatment of severe hemorrhage following percutaneous nephrolithotomy (PCNL). However, there remains a significant rate of failures requiring repeat SRAE or nephrectomy. To identify risk factors for initial treatment failure of SRAE, the data of patients who had undergone SRAE for severe bleeding due to PCNL between August 2005 and June 2016 were retrospectively analyzed. A total of 98 patients required SRAE for bleeding control following PCNL. Renal arteriography revealed pseudoaneurysm in 65 patients, arteriovenous fistula in 6 patients, and a combination of both in 11 patients. Free extravasation was observed in 11 patients; 8 of these patients exhibited coexisting pseudoaneurysm. Vascular aberration/tortuosity was identified in 10 patients. A total of 17 patients (17.3%) experienced initial treatment failure and underwent repeat SRAE. Multivariate analysis identified percutaneous tract size, number of bleeding sites and vascular aberration/tortuosity as significant predictors of initial treatment failure. The results from the present study suggested that repeated SRAE is preferred for patients who have experienced initial treatment failure with recurrent hemorrhage following PCNL. Large tract size, multiple bleeding sites and renal vascular aberration/tortuosity were significantly associated with increased risk of initial treatment failure of SRAE. These data may assist interventional radiologists in the planning and execution of SRAE in the treatment of PCNL.
  • 机译 外源性脑源性神经营养因子减轻大鼠蛛网膜下腔出血后神经元凋亡和神经功能缺损
    摘要:Brain-derived neurotrophic factor (BDNF) is a growth factor crucial for neuronal survival, while its role in subarachnoid hemorrhage (SAH)-induced neuronal apoptosis remains unclear. The aim of the present study was to investigate whether administering exogenous BDNF can protect against neuronal apoptosis and neurological deficits following SAH in a rat model. The BDNF level was found to be significantly decreased in the basal cortex at 6, 12, 24, 48 and 72 h following SAH. Exogenous BDNF significantly decreased the expression of Bax and reduced activation of caspase-3 and caspase-9 and the number of apoptotic neurons. Moreover, exogenous BDNF treatment significantly improved the neurological deficits at 72 h and long-term behavioral deficits (day 14) following SAH in a rat model. These findings indicate that exogenous BDNF attenuated SAH-induced neuronal injury in rats.
  • 机译 金雀异黄素联合吉非替尼对肝细胞癌Hep3B细胞的抑制作用
    摘要:Combination therapy is an important method for treating advanced hepatocellular carcinoma (HCC). Gefitinib is an epidermal growth factor receptor (EGFR) inhibitor, which has profound effects on HCC. The purpose of the present study was to investigate the effects of genistein in combination with gefitinib on the proliferation and apoptosis of HCC cells and the associated mechanism. Cell counting kit-8 assay was performed to calculate the IC50 values and cytotoxicity, whilst flow cytometry was used to assess cell apoptosis. Protein expression was detected using western blot analysis. The IC50 of genistein and gefitinib on Hep3B cells were calculated to be 128.078 and 13.657 µM, respectively. Genistein in combination with gefitinib significantly inhibited cell viability, promoted apoptosis and reduced EGFR, vascular endothelial growth factor receptor and platelet-derived growth factor receptor phosphorylation. Genistein in combination with gefitinib promoted the expression of cleaved caspase-3 and cleaved poly ADP-ribose polymerase. In addition, combined treatment of genistein and gefitinib strongly inhibited the activation of the Akt/Erk/mTOR signaling pathway. In conclusion, findings from the present study suggest that genistein in combination with gefitinib inhibit HCC cell proliferation and promote apoptosis by inhibiting the Akt/Erk/mTOR pathway.
  • 机译 在COPD患者的运动训练中确定补充氧疗是否有益:系统评价和荟萃分析
    摘要:Exercise training is an integral component of the pulmonary rehabilitation program for patients with chronic obstructive pulmonary disease (COPD). The aim of this study was to systematically search the published literature and analyze the evidence on the efficacy of supplemental oxygen in improving outcomes during exercise training in patients with COPD. The PubMed, Scopus, Cochrane Central Register of Controlled Trials (CENTRAL) and Google scholar databases were searched electronically for articles in the English language published up to May, 2019. In total, 7 trials were included in this systematic review and meta-analysis. There was considerable heterogeneity amongst the included studies. Meta-analysis indicated no significant difference in power (random: MD = −2.38; 95% CI, −5.79 to 1.03; P=0.86) and maximum energy expenditure (VO2 max) (random: MD = −0.01; 95% CI, −0.06 to 0.07; P=0.45) between the oxygen and control groups on maximal exercise testing. Qualitative analysis of the included studies revealed no benefits of supplemental oxygen in improving exercise capacity and dyspnea scores. Data on the quality of life assessed by the Chronic Respiratory Disease Questionnaire was pooled for 95 participants in the study group and 91 participants in the control group. The results indicated no beneficial effects of supplemental oxygen in improving quality of life outcomes (random: MD = −0.09; 95% CI, −0.16 to −0.01; P=0.59). On the whole, the findings of this study indicate that supplemental oxygen during the exercise training of patients with COPD does not improve exercise capacity, dyspnea scores and quality of life. However, the quality of the evidence is weak. Multi-center randomized controlled trials with homogenous methodology and intervention are required to provide stronger evidence on this subject.

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