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1.
J Nanosci Nanotechnol ; 20(5): 3105-3116, 2020 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-31635654

RESUMO

The Z-scheme Bi2WO6/NaBiO3 nanocomposites were first fabricated by a facile hydrothermal method, and were then characterized by X-ray diffraction, transmission electron microscopy, scanning electron microscopy, energy dispersive spectrometer, Fourier-transform-infrared spectroscopy, X-ray photoelectron spectroscopy and N2 adsorption-desorption. The as-prepared Bi2WO6/NaBiO3 nanocomposites exhibit outstanding photocatalytic activity and recyclability. A 98.4% photodegradation of 2,3-dichlorophenol (50 mg·L-1) was attained in the presence of Bi2WO6/NaBiO3 (1:10) under the visible-light irradiation in 30 min. In particular, the photocatalytic mechanism has been discussed in detail, based on four aspects: (1) oxidative species, (2) photoelectrochemical performance, (3) conduction band and valence band energy levels and (4) possible transition states and reactions. In conclusion, O-2 is the main active oxidative species in the Bi2WO6/NaBiO3 nanocomposite. The material has higher photocurrent and visible light adsorption but lower electron-hole pairs recombination, which contributes to distinguished photocatalytic efficiency. The Z-scheme photocatalytic path was proposed and the possible degradation process and routes have been summarized.

2.
Appl Opt ; 58(27): 7375-7378, 2019 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-31674386

RESUMO

In this paper, an integrated processing method was demonstrated to fabricate the polymer-based thermo-optic (TO) switch with low power consumption. The characteristic parameters of the switch were carefully designed and simulated. The air trench structure was exploited to reduce the power consumption, which can be formed with the waveguide simultaneously by the integrated processing method. Moreover, the introduced polymer/silica hybrid waveguide structure can also improve the response time of the device. A typical fabricated switch presented a low switching power of 5.2 mW. The measured switching rise time and fall time are 192.2 and 201.1 µs, respectively.

3.
Appl Opt ; 58(27): 7609-7614, 2019 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-31674416

RESUMO

This paper proposes an accommodative intraocular lens (IOL), which consists of a two-element Alvarez lens and an aspheric lens for changing focal power and refractive power, respectively. The four-freeform-surface Alvarez lens is optimized for a multiple field of view; further, the aspheric lens also corrects the aberrations induced by the corneal asphericity of the human eye over the whole range of accommodation. A simulation using optical design software demonstrates its excellent performance in that the values of the modulation transfer function at 100 cycles/mm all reach ∼0.4 with a ±5° field of view for 3 and 5 mm pupils.

4.
Artigo em Inglês | MEDLINE | ID: mdl-31677784

RESUMO

Oxidative stress and cardiomyocyte apoptosis contributed to the progression of doxorubicin (Dox)-induced cardiotoxicity. Recent studies identified microRNA-22 (miR-22) as a cardiac- and skeletal muscle-enriched microRNA that functioned as a key regulator in stress-induced cardiac injury. The present study aimed to investigate the role and possible mechanism of miR-22 on Dox-induced oxidative stress and cardiomyocyte apoptosis. Mice were exposed to reduplicative injections of Dox (i.p., 4 mg/kg) weekly for consecutive 4 weeks to generate Dox-induced cardiotoxicity. Herein, we found that miR-22 level was significantly increased in murine hearts subjected to chronic Dox treatment. MiR-22 inhibition attenuated oxidative stress and cardiomyocyte apoptosis in vivo and in vitro, thereby preventing Dox-induced cardiac dysfunction. Mechanistically, we observed that miR-22 directly bound to the 3'-UTR of Sirt1 and caused SIRT1 downregulation. Conversely, miR-22 antagomir upregulated SIRT1 expression and SIRT1 inhibitor abolished the beneficial effects of miR-22 antagomir. In conclusion, miR-22 inhibition prevented oxidative stress and cardiomyocyte apoptosis via upregulating SIRT1 and miR-22 might be a new target for treating Dox-induced cardiotoxicity.

5.
Artigo em Inglês | MEDLINE | ID: mdl-31677795

RESUMO

Adipose tissue hypoxia occurs early in obesity and is associated with increased tissue macrophages and systemic inflammation that impacts muscle insulin responsiveness. We investigated how hypoxia interacted with adipocyte-macrophage crosstalk and inflammatory cytokine release, using co-culture and conditioned media (CM). Murine primary adipocytes from lean or obese mice were cultured under normoxic (21% O2) or hypoxic (1% O2) conditions. RAW264.7 macrophages were incubated under normoxic or hypoxic conditions with or without adipocyte conditioned media. Macrophage and adipocyte-macrophage co-culture CM were also collected. We found hypoxia did not elicit direct cytokine release from macrophages. However, adipocyte CM or adipocyte co-culture, synergistically stimulated TNFα and MCP-1 release from macrophages that was not further impacted by hypoxia. Exposure of muscle cells to elevated cytokines led to reduced insulin and muscle stress/inflammatory signaling. We conclude hypoxia or obesity induces release of inflammatory TNFα and MCP-1 from mice primary adipocytes but the two environmental conditions do not synergize to worsen macrophage signal transduction or insulin responsiveness.

6.
Artigo em Inglês | MEDLINE | ID: mdl-31678621

RESUMO

OBJECTIVE: Angiopoietin-1 (Ang-1), a secreted protein, mainly regulates angiogenesis. Ang-1 has been shown to promote the development of atherosclerosis, whereas little is known about its effects on lipid metabolism and inflammation in this process. METHOD: Ang-1 was transfected into ApoE-/- mice via lentiviral vector or incubated with THP-1 derived macrophages. Oil red O and HE staining were performed to measure the size of atherosclerotic plaques in ApoE-/- mice. Immunofluorescence was employed to show the expression of target proteins in aorta. [3H] labeled cholesterol was performed to examine the efficiency of cholesterol efflux and reverse cholesterol transport (RCT) both in vivo and vitro. Western blot and qPCR were used to quantify target proteins both in vivo and vitro. ELISA detected the levels of pro-inflammatory cytokines in mouse peritoneal macrophage. RESULTS: Our data showed that Ang-1 augmented atherosclerotic plaques formation and inhibited cholesterol efflux. The binding of Ang-1 to Tie2 resulted in downregulation of LXRα, ABCA1 and ABCG1 expression via inhibiting the translocation of TFE3 into nucleus. In addition, Ang-1 decreased serum HDL-C levels and reduced reverse cholesterol transport (RCT) in ApoE-/- mice. Furthermore, Ang-1 induced lipid accumulation followed by increasing TNF-α, IL-6, IL-1ß,and MCP-1 produced by MPMs, as well as inducing M1 phenotype macrophage marker iNOS and CD86 expression in aorta of ApoE-/- mice. CONCLUSION: Ang-1 has an adverse effect on cholesterol efflux by decreasing the expression of ABCA1 and ABCG1 via Tie2/TFE3/LXRα pathway, thereby promoting inflammation and accelerating atherosclerosis progression.

7.
J Ethnopharmacol ; : 112354, 2019 Nov 02.
Artigo em Inglês | MEDLINE | ID: mdl-31689480

RESUMO

ETHNOPHARMACOLOGICAL RELEVANCE: Fufang Chuanxiong capsule consists of Angelica sinensis radix and Chuanxiong rhizome, which are used in the traditional Chinese medicine for the treatment of coronary artery disease, and Xinyue capsule is composed of panax quinquefolius saponin extracted from leaves and stems of Panax quinquefolium L, which has the functions of anti-myocardial ischemia, improving myocardial energy metabolism and inhibiting apoptosis of cardiomyocytes. OBJECTIVE: To observe the role of Chinese herbal medicines in the cardiovascular outcome among patients with acute coronary syndrome (ACS) and renal insufficiency after percutaneous coronary intervention (PCI). METHODS: The subjects came from the 5C trial (chictr.org number: chictr-trc-07000021), post-PCI patients suffered from ACS with mild-to-moderate renal insufficiency (30 mL•min-1•1.73 m-2 < estimated glomerular filtration rate≤89 mL•min-1•1.73 m-2) included. The study population consisted of 215 subjects in the control group who were treated with western medicine standard therapy, and 211 subjects in the treatment group who were treated with Chinese herbal medicines (Fufang Chuanxiong Capsule and Xinyue Capsule) for 6 months on the basis of western medicine standard therapy. All were followed for 1 year. The primary endpoint included the composite of cardiac death, nonfatal recurrent myocardial infarction, and ischemia-driven revascularization. Secondary endpoint included the composite of stroke, congestive heart failure, and readmission for ACS. The serum creatinine and estimated glomerular filtration rate (eGFR) were evaluated. RESULTS: After 1 year follow-up of two groups, there were 16 cases of primary endpoint in the control group and 6 cases of primary endpoint in the treatment group [absolute risk reduction (ARR): 0.046, 95%CI: 0.004-0.088; relative risk (RR): 0.38, 95%CI: 0.15-0.96, P = 0.040]. There were 15 cases of secondary endpoint in the control group and 5 cases of secondary endpoint in the treatment (ARR: 0.041, 95%CI: 0.006-0.086; RR: 0.34, 95%CI: 0.13-0.92, P = 0.033). The eGFR in the treatment group was significantly higher than that in the control group (75.19 ±â€¯16.74 mL min-1·1.73 m-2 VS 72.03 ±â€¯14.96 mL min-1·1.73 m-2, P < 0.05). The eGFR in the treatment group was significantly higher after the intervention with Chinese herbal medicines than that before intervention (72.27 ±â€¯11.83 mL min-1·1.73 m-2 VS 75.19 ±â€¯16.74 mL min-1·1.73 m-2, P < 0.05). CONCLUSION: Chinese herbal medicines plus western medicine standard therapy improved clinical outcomes in patients with ACS and mild-to-moderate renal insufficiency. Additionally, this study also demonstrated Chinese herbal medicines were useful in deferring decline of renal function.

8.
Artigo em Inglês | MEDLINE | ID: mdl-31675454

RESUMO

Autophagy and cellular senescence are two critical responses of mammalian cells to stress and may have a direct relationship given that they respond to the same set of stimuli, including oxidative stress, DNA damage, and telomere shortening. Mesenchymal stem cells (MSCs) have emerged as reliable cell sources for stem cell transplantation and are currently being tested in numerous clinical trials. However, the effects of autophagy on MSC senescence and corresponding mechanisms have not been fully evaluated. Several studies demonstrated that autophagy level increases in aging MSCs and the downregulation of autophagy can delay MSC senescence. which is inconsistent with most studies that showed autophagy could play a protective role in stem cell senescence. To further study the relationship between autophagy and MSC senescence and explore the effects and mechanisms of premodulated autophagy on MSC senescence, we induced the up- or downregulation of autophagy by using rapamycin (Rapa) or 3-methyladenine, respectively, before MSC senescence induced by D-galactose (D-gal). Results showed that pretreatment with Rapa for 24 hours remarkably alleviated MSC aging induced by D-gal and inhibited ROS generation. p-JNK and p-38 expression were also clearly decreased in the Rapa group. Moreover, the protective effect of Rapa on MSC senescence can be abolished by enhancing the level of ROS, and p38 inhibitor can reverse the promoting effect of H2 O2 on MSC senescence. In summary, the present study indicates that autophagy plays a protective role in MSC senescence induced by D-gal, and ROS/JNK/p38 signaling plays an important mediating role in autophagy-delaying MSC senescence.

10.
Aging (Albany NY) ; 112019 Nov 07.
Artigo em Inglês | MEDLINE | ID: mdl-31699956

RESUMO

Exosomes secreted by bone marrow mesenchymal stem cells (BMSCs) promote osteosarcoma cell proliferation and migration, while the underlying mechanism remains unknown. Since the long non-coding RNA PVT1 has been reported to be upregulated in osteosarcoma cells and contributes to its growth and metastasis, we aim to investigate whether BMSC-derived exosomes promote osteosarcoma growth and metastasis via transporting PVT1 into osteosarcoma cells. The PVT1 expression in BMSC-derived exosomes was markedly higher than that in osteosarcoma cell-derived exosomes. The co-culturing of BMSC-derived exosomes and osteosarcoma cells (Saos-2, MG-63, and MNNG/HOS cell lines) significantly raised PVT1 expression of osteosarcoma cells. The direct binding between PVT1 and the oncogenic protein ERG was confirmed using RNA immunoprecipitation and RNA pull-down assays, and the transported PVT1 promotes osteosarcoma cell proliferation and migration via inhibiting degradation and ubiquitination of ERG. PVT1 also increased ERG expression through sponging miR-183-5p. In summary, our findings indicated that BMSC-derived exosomes encapsulate PVTl and transport it into osteosarcoma cells, and the transported PVT1 promotes tumor growth and metastasis by inhibiting ubiquitination and promoting expression of ERG in osteosarcoma cells. These data provide a novel insight into the mechanism of BMSC-derived exosomes in affecting osteosarcoma progression.

11.
Clin Sci (Lond) ; 133(20): 2045-2059, 2019 Oct 30.
Artigo em Inglês | MEDLINE | ID: mdl-31654061

RESUMO

BACKGROUND: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. METHODS: Purified recombinant human inhibitor of κB kinase subunit ß (IKKß) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. RESULTS: We showed that hydrogen sulfide (H2S) inhibited IKKß activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKß activity directly via sulfhydrating IKKß at cysteinyl residue 179 (C179) in purified recombinant IKKß protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKß inactivation. Furthermore, to demonstrate the significance of IKKß sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKß. In purified IKKß protein, C179S mutation of IKKß abolished H2S-induced IKKß sulfhydration and the subsequent IKKß inactivation. In human PAECs, C179S mutation of IKKß blocked H2S-inhibited IKKß activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKß abolished the inhibitory effect of H2S on IKKß activation and pulmonary vascular inflammation and remodeling. CONCLUSION: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKß via sulfhydrating IKKß at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

12.
Mol Cancer ; 18(1): 148, 2019 Oct 27.
Artigo em Inglês | MEDLINE | ID: mdl-31656200

RESUMO

BACKGROUND: As an important means of communication, exosomes play an important role in the development of hepatocellular carcinoma (HCC). METHODS: Bioinformatics analysis, dual-luciferase reporter assays, methylation-specific quantitative PCR, and ChIP-PCR analysis were used to gain insight into the underlying mechanism of miR-21 in HCC. RESULTS: The detection of miRNAs in exosomes of HCC showed that miR-21 expression in exosomes was positively correlated with the expression level of miR-21 in cells and negatively correlated with the expression of its target genes PTEN, PTENp1 and TETs. HCC cell-derived exosomes could increase miR-21 and p-Akt expression in HCC cells and downregulate the expression of PTEN, PTENp1 and TETs. MiR-21 inhibitors or PTENp1 overexpression vectors could weaken the effect of the abovementioned exosomes and simultaneously weaken their role in promoting cell proliferation and migration and inhibiting apoptosis. Further studies showed that miR-21 not only directly regulated the expression of PTEN, PTENp1 and TETs but also increased the methylation level of the PTENp1 promoter by regulating the expression of TETs, thereby inhibiting the expression of PTENp1 and further downregulating the expression of PTEN. CONCLUSIONS: Exosomal miR-21 can regulate the expression of the tumor suppressor genes PTEN and PTENp1 in various ways and affect the growth of HCC cells.

13.
J Lipid Res ; 2019 Oct 29.
Artigo em Inglês | MEDLINE | ID: mdl-31662443

RESUMO

CXC chemokine ligand 12 (CXCL12) is a member of CXC chemokine family and mainly acts on cell chemotaxis. CXCL12 also elicits a pro-atherogenic role, but the molecular mechanisms have not been fully defined yet. We aimed to reveal if and how CXCL12 promoted atherosclerosis via regulating lipid metabolism. In vitro, our data showed that CXCL12 reduced ABCA1 expression and it-mediated cholesterol efflux from THP-1-derived macrophages to apoA-I. Data from the Luciferase reporter gene and Chromatin immunoprecipitation assays revealed that TCF21 stimulated transcription of ABCA1 via binding to its promoter region, which was repressed by CXCL12. We found that CXCL12 increased the levels of phosphorylated GSK3ß and phosphorylation of ß-catenin at the position Thr120. Inactivation of GSK3ß or ß-catenin increased expression of TCF21 and ABCA1. Further, knockdown or inhibition of CXCR4 (CXC chemokine receptor 4) blocked the effects of CXCL12 on TCF21 and ABCA1 expression and phosphorylation of GSK3ß and ß-catenin. In vivo, overexpression of CXCL12 in Apoe-/- mice via lentivirus enlarged atherosclerotic lesion area and increased macrophage infiltration in atherosclerotic plaques. We further found that overexpression of CXCL12 reduced the efficiency of reverse cholesterol transport and plasma HDL-C levels, decreased ABCA1 expression in aorta and mouse peritoneal macrophages (MPMs), and suppressed cholesterol efflux from MPMs to apoA-I in Apoe-/- mice. Collectively, these findings suggest that CXCL12 interacts with CXCR4 and then activates the GSK-3ß/ß-cateninT120/TCF21 signaling pathway to inhibit ABCA1-dependent cholesterol efflux from macrophages and aggravate atherosclerosis. Targeting CXCL12 may be a novel and promising strategy for the prevention  of atherosclerosis.

14.
Turk J Med Sci ; 49(5): 1590-1598, 2019 Oct 24.
Artigo em Inglês | MEDLINE | ID: mdl-31652042

RESUMO

Background/aim: Cyclosporine A (CsA), a traditional immunosuppressive compound, has been reported to specifically prevent isch-emia reperfusion tissue injury via apoptosis pathway. This study aimed to explore the renoprotective effects of CsA on the kidneys of rabbits undergoing renal pelvic perfusion. Materials and methods: A total of 30 rabbits were randomly assigned into a control group (n = 6) and an experimental group (n = 24). The experimental group underwent a surgical procedure that induced severe hydronephrosis and was then stochastically divided into 4 groups (S1, S1', S2, and S2'), consisting of 6 rabbits each. Groups S1 and S1' were perfused with 20 mmHg of fluid, while groups S2 and S2' were perfused with 60 mmHg of fluid. Administration to groups S1' and S2' was done intravenously, with CsA once a day for 1 week before perfusion. In the control group, after severe hydronephrosis was induced, a sham operation was performed in a second laparoto-my. Acute kidney damage was evaluated using hematoxylin and eosin staining, in addition to analyzing the mitochondrial ultrastructure and mitochondrial membrane potential (MMP). The cytochrome C (CytC) and neutrophil gelatinase-associated lipocalin (NGAL) expression were examined immunohistochemically using Western blotting and reverse transcription-polymerase chain reaction. Results: It was found that the renal histopathological damage was ameliorated, mitochondrial vacuolization was lower, MMP was high-er, and the CytC and NGAL contents were decreased after drug intervention (groups S1' and S2') when compared to the experimental groups (S1 and S2). Furthermore, there was no difference between drug intervention groups S1' and S2'. Conclusion: These results suggest that CsA can attenuate renal damage from severe hydronephrosis induced by renal pelvic perfusion in rabbits. It plays a protective role in the acute kidney injury process, possibly through increased MMP and mitochondrial changes.

15.
Zhongguo Zhen Jiu ; 39(10): 1103-8, 2019 Oct 12.
Artigo em Chinês | MEDLINE | ID: mdl-31621265

RESUMO

Acupuncture figure is the model of human body for the learners and practitioners of acupuncture to learn and memorize the meridians points on the body surface in ancient time. The earliest bronze acupuncture figure was made in the fifth year of the North Song Dynasty and it had been cast continuously or even spread to overseas in the later dynasties. Specially, the imitation and production of bronze acupuncture figure in Japan in Edo Period were the most prominent. At present, the bronze acupuncture figure of the Edo era, with the complete and detailed historical background records, is preserved in the Tokyo National Museum of Japan and exhibited as a metal reticulated bronze figure. Such figure was named as Kanbun bronze acupuncture figure because it was cast during the Kanbun period. In the paper, the study achievements were collected on the Kanbun bronze acupuncture figure at home and abroad and its history was reviewed in terms of time feature, production background and producer. Based on the traditional Chinese thought and theory of acupuncture and moxibustion embodied by Kanbun bronze acupuncture figure, the value of the Kanbun bronze acupuncture figure in acupuncture and moxibustion was explored. Additionally, align with the introduction of Western medicine in Edo era in Japan and in consideration with the specific understanding on anatomical knowledge in Western medicine reflected by the bronze acupuncture figure, the value of the Western medicine was discussed. Finally, in view of the reticule structure of bronze acupuncture figure, the orientation and selection were analyzed under the influence of the eastern and western medicine in the Edo era, based on which, the motivation of the acceptance and creation of this bronze acupuncture figure in Japan was explored in the culture dissemination of medicine.

16.
Ther Innov Regul Sci ; : 2168479019875338, 2019 Oct 03.
Artigo em Inglês | MEDLINE | ID: mdl-31581817

RESUMO

For topically applied over-the-counter (OTC) products, the association of unwanted systemic exposure and adverse events may be difficult to ascertain without a recognition or determination of in vivo absorption. Evaluation of skin permeability using a validated in vitro permeation methodology can provide important information for both initial formulation selection and reformulation during the product life cycle. Additionally, a comparison of permeation rates between formulations using a validated methodology could reduce the number of nonclinical studies needed as part of reformulation. However, many in vitro permeation tests (IVPTs) have produced results with high variability and low reproducibility between study sites. It is unclear if this is due to a lack of a standardized protocol, or lack of control of multiple key experimental factors including skin source, preparation, receptor fluid, and study design. This review presents the authors perspective on the potential regulatory utility of IVPT and proposes steps to improve the accuracy and reproducibility of IVPT. The focus of this review is on topical dermatologic drugs with an initial emphasis on the OTC marketplace where reformulations are more common.

17.
Atherosclerosis ; 289: 143-161, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31518965

RESUMO

BACKGROUND AND AIMS: Krüppel-like factor 14 (KLF14) is known to play a role in atherosclerosis, but the underlying mechanisms are still largely unknown. The aim of our study was to explore the effects of KLF14 on lipid metabolism and inflammatory response, providing a potential target for lowering the risk of atherosclerosis-causing disease. METHODS AND RESULTS: mRNA and protein levels of KLF14 were significantly decreased in oxidized low-density lipoprotein (oxLDL)-treated macrophages and in the atherosclerotic lesion area. Chromatin immunoprecipitation (ChIP) and luciferase reporter gene assays were used to confirm that KLF14 positively regulated miR-27a expression by binding to its promoter. We also found that KLF14 could restored appropriate cellular lipid homeostasis and inflammatory responses via negatively regulating lipoprotein lipase (LPL) expression in THP1-derived macrophages through miR-27a. In addition, gypenosides (GP), a KLF14 activator, delayed the development of atherosclerosis in apolipoprotein E deficient (apoE-/-) mice. CONCLUSIONS: KLF14 plays an antiatherogenic role via the miR-27a-dependent down-regulation of LPL and subsequent inhibition of proinflammatory cytokine secretion and lipid accumulation.

18.
New Phytol ; 224(3): 1304-1315, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31494940

RESUMO

Interactions between mutualists, competitors, and antagonists have contrasting ecological effects that, sustained over generations, can influence micro- and macroevolution. Dissimilar benefits and costs for these interactions should cause contrasting co-diversification patterns between interacting clades, with prevalent co-speciation by mutualists, association loss by competitors, and host switching by antagonists. We assessed these expectations for a local assemblage of 26 fig species (Moraceae: Ficus), 26 species of mutualistic (pollinating), and 33 species of parasitic (galling) wasps (Chalcidoidea). Using newly acquired gene sequences, we inferred the phylogenies for all three clades. We then compared the three possible pairs of phylogenies to assess phylogenetic congruence and the relative frequencies of co-speciation, association duplication, switching, and loss. The paired phylogenies of pollinators with their mutualists and competitors were significantly congruent, unlike that of figs and their parasites. The distributions of macroevolutionary events largely agreed with expectations for mutualists and antagonists. By contrast, that for competitors involved relatively frequent association switching, as expected, but also unexpectedly frequent co-speciation. The latter result likely reflects the heterogeneous nature of competition among fig wasps. These results illustrate the influence of different interspecific interactions on co-diversification, while also revealing its dependence on specific characteristics of those interactions.

19.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue ; 31(8): 938-941, 2019 Aug.
Artigo em Chinês | MEDLINE | ID: mdl-31537215

RESUMO

OBJECTIVE: To investigate the assessment values of procalcitonin (PCT), lactic acid (LAC), sequential organ failure assessment (SOFA) score and acute physiology and chronic health evaluation II (APACHE II) score in patients with sepsis. METHODS: 140 patients with suspicious bacterial infection admitted to emergency department of Beijing Chaoyang Hospital of the Capital Medical University from August 2017 to June 2018 were enrolled. They were divided into three groups according to diagnostic criteria of Sepsis-3: non-sepsis group (n = 58), sepsis group (n = 66) and septic shock group (n = 16). The PCT, LAC, SOFA score, APACHE II score, 28-day prognosis, and positive detection rate of PCT and LAC were compared among three groups. Independent predictors of 28-day mortality were analyzed by Logistic regression; predictive values of PCT, LAC, SOFA score and APACHE II score for 28-day mortality in sepsis patients were analyzed by receiver operating characteristic (ROC) curve. RESULTS: PCT, LAC, SOFA score, APACHE II score at admission, and 28-day mortality in sepsis group and septic shock group were significantly higher than those in non-sepsis group, and PCT, LAC, APACHE II score, and 28-day mortality in sepsis shock group were further higher than those in sepsis group [PCT (µg/L): 38.1±12.6 vs. 4.6±2.3, LAC (mmol/L): 3.3±2.1 vs. 2.4±2.1, APACHE II score: 14.9±2.4 vs. 9.5±4.3, 28-day mortality: 75.0% vs. 24.2%, all P < 0.05]. The positive detection rate of PCT and LAC in sepsis group and septic shock group were higher than those in non-sepsis group (positive detection rate of PCT: 56.1%, 81.3% vs. 32.8%; positive detection rate of LAC: 42.4%, 62.5% vs. 13.7%; all P < 0.01). Logistic regression analysis showed that PCT, LAC, SOFA score and APACHE II score were independent predictors of 28-day mortality [PCT: odds ratio (OR) = 0.933, 95% confidence interval (95%CI) = 0.878-0.991; LAC: OR = 0.539, 95%CI = 0.347-0.838; SOFA score: OR = 0.291, 95%CI = 0.514-0.741; APACHE II score: OR = 0.808, 95%CI = 0.669-0.976; all P < 0.05]. ROC curve analysis showed that the area under ROC curve (AUC) of PCT, LAC, SOFA score and APACHE II score predicting 28-day mortality was 0.76, 0.86, 0.81 and 0.87, respectively. The assessment values of APACHE II score and LAC were higher than PCT in predicting 28-day mortality (Z1 = 2.56, Z2 = 2.45, both P < 0.01), and the performance of SOFA score was similar to PCT. CONCLUSIONS: PCT, LAC, SOFA score and APACHE II score were reliable indexes to evaluate disease severity for patients diagnosed with infection. The assessment values of APACHE II score and LAC in 28-day mortality were superior to SOFA score and PCT.


Assuntos
Ácido Láctico/metabolismo , Pró-Calcitonina/metabolismo , Sepse/metabolismo , APACHE , Humanos , Escores de Disfunção Orgânica , Prognóstico , Curva ROC
20.
Cell Death Dis ; 10(10): 701, 2019 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-31541079

RESUMO

Hepatoblastoma (HB) is the most common hepatic neoplasm in childhood and the therapeutic outcomes remain undesirable due to its recurrence and metastasis. Increasing evidence shows that dipeptidase 1 (DPEP1) has pivotal function in tumorigenesis in multiple tumors. However, the expression pattern, biological function, and underlying mechanism of DPEP1 in HB have not been reported. Here we showed that DPEP1 was significantly upregulated and was associated with poor prognosis in HB patients. In vitro and in vivo assays indicated that silencing DPEP1 significantly suppressed HB cell proliferation, migration, and invasion, while DPEP1 overexpression exhibited the opposite effect. In addition, we identified that DPEP1 was a direct target of microRNA-193a-5p (miR-193a-5p). Functional experiments demonstrated that overexpression of miR-193a-5p significantly inhibited cell proliferation and invasion of HB cells, while the inhibitory effect could be reversed by DPEP1 overexpression. Moreover, miR-193a-5p was decreased in HB tumor tissues and associated with a poor clinical prognosis. Mechanistically, our results indicated that the miR-193a-5p/DPEP1 axis participated to the progression of HB via regulating the PI3K/Akt/mTOR (phosphatidylinositol-3-kinase/Akt/mammalian target of rapamycin) signaling. In conclusion, our findings suggest that the miR-193a-5p /DPEP1 axis might be a good prognostic predictor and therapeutic target in HB.

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