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1.
Cancer Lett ; 469: 498-509, 2020 Jan 28.
Artigo em Inglês | MEDLINE | ID: mdl-31765736

RESUMO

Emerging evidences show that dysregulation of circadian genes is closely associated with tumorigenesis. However, whether circadian genes regulate the reprogramming of metabolism in tumor cells is largely unknown. Here, we showed that NPAS2, one of the core circadian molecules, significantly contributed to the reprogramming of glucose metabolism mainly through two mechanisms. On the one hand, NPAS2 upregulated the expression of glycolytic genes GLUT1, HK2, GPI, ALDOA, ENO2, PKM2 and MCT4. On the other hand, NPAS2 downregulated the expression of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α). Mechanistically, HIF-1α was found to be a direct transcriptional target of NPAS2, which mediated both the upregulation of glycolytic genes and downregulation of mitochondrial biogenesis in HCC cells. In addition, we found that upregulation of NPAS2 expression was mainly due to the downregulation of miR-199b-5p. In vitro and in vivo assays further indicated that HIF-1α-mediated reprogramming of glucose metabolism played a critical role in NPAS2-regulated growth and metastasis of HCC cells. Our findings demonstrate that NPAS2 plays a critical role in glucose metabolism reprogramming, suggesting that NPAS2 may serve as a potential therapeutic target in HCC.

2.
J Cell Biochem ; 121(1): 443-457, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31231887

RESUMO

Accumulating findings reveal that long noncoding RNAs (lncRNAs) as crucial regulatory molecules serve vital functions in the progression of hepatocellular carcinoma (HCC). This study aims to investigate the biological roles and mechanisms of lncRNA HOXD cluster antisense RNA 1 (HOXD-AS1) in HCC cells based on transcriptome analysis. The Cancer Genome Atlas data analysis and experimental validation showed that HOXD-AS1 was increased in HCC tissues/cell lines and positively relevant to histologic grade. The subcellular localization results indicated HOXD-AS1 was dispersed both in the nucleus as well as the cytoplasm of HCC cells. In vitro loss-of-function experiments revealed that silencing of HOXD-AS1 could dramatically suppress the proliferation, migration, and invasion, and induce S or/and G2/M phase cell cycle arrest as well as apoptosis of Bel-7402 and MHCC97H cells accompanying the changes in expression levels of cyclin B1, cyclin D1, BCL-2, BAX, and MMP2. In vivo assay also showed that HOXD-AS1 silencing could markedly reduce xenograft tumor volume and weight of HCC cells. Transcriptome and bioinformatic analysis indicated that a total of 1103 genes were significantly altered by HOXD-AS1 silencing, of which 132 genes exhibited a significant correlation with HOXD-AS1 expression in HCC tissues. Gene Ontology (GO) enrichment analysis revealed differentially expressed genes were remarkably enriched in several cancer-related biological processes (cell proliferation, cell cycle, apoptosis, migration, angiogenesis, and hypoxic response). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis indicated that HOXD-AS1 has the potential to affect p53, tumor necrosis factor (TNF), mitogen-activated protein kinase (MAPK) pathway, and Western blot results further validated that HOXD-AS1 silencing could inhibit the MEK/ERK pathway in Bel-7402 cells. Collectively, HOXD-AS1, as an oncogenic lncRNA, might exert crucial functions in HCC progression and serve as a potential diagnostic biomarker and therapeutic target for HCC.

3.
J Cell Physiol ; 235(3): 1948-1961, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31552677

RESUMO

Acute pancreatitis (AP) is an inflammatory disorder initiated by activation of pancreatic zymogens, leading to pancreatic injury and systemic inflammatory response. MicroRNAs (miRNAs) have emerged as important regulators of gene expression and key players in human physiological and pathological processes. Discoveries over the past decade have confirmed that altered expression of miRNAs is implicated in the pathogenesis of AP. Indeed, a number of miRNAs have been found to be dysregulated in various cell types involved in AP such as acinar cells, macrophages, and lymphocytes. These aberrant miRNAs can regulate acinar cell necrosis and apoptosis, local and systemic inflammatory response, thereby contributing to the initiation and progression of AP. Moreover, patients with AP possess unique miRNA signatures when compared with healthy individuals or those with other diseases. In view of their stability and easy detection, therefore, miRNAs have the potential to act as biomarkers for the diagnosis and assessment of patients with AP. In this review, we provide an overview of the novel cellular and molecular mechanisms underlying the roles of miRNAs during the disease processes of AP, as well as the potential diagnosis and therapeutic biomarkers of miRNAs in patients with AP.

4.
Neural Netw ; 121: 161-168, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31563699

RESUMO

User response prediction makes a crucial contribution to the rapid development of online advertising system and recommendation system. The importance of learning feature interactions has been emphasized by many works. Many deep models are proposed to automatically learn high-order feature interactions. Since most features in advertising systems and recommendation systems are high-dimensional sparse features, deep models usually learn a low-dimensional distributed representation for each feature in the bottom layer. Besides traditional fully-connected architectures, some new operations, such as convolutional operations and product operations, are proposed to learn feature interactions better. In these models, the representation is shared among different operations. However, the best representation for each operation may be different. In this paper, we propose a new neural model named Operation-aware Neural Networks (ONN) which learns different representations for different operations. Our experimental results on two large-scale real-world ad click/conversion datasets demonstrate that ONN consistently outperforms the state-of-the-art models in both offline-training environment and online-training environment.

5.
Int J Cancer ; 146(1): 169-180, 2020 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-31090062

RESUMO

Our previous study demonstrated that heterogeneous nuclear ribonucleoprotein AB (HNRNPAB) is a key gene that facilitates metastasis of hepatocellular carcinoma (HCC). However, the molecular mechanisms behind this relationship are not fully understood. In our study, we utilized long-noncoding RNA (lncRNA) microarrays to identify a HNRNPAB-regulated lncRNA named lnc-ELF209. Our findings from chromatin immunoprecipitation assays indicate that HNRNPAB represses lnc-ELF209 transcription by directly binding to its promoter region. We also analyzed clinical samples from HCC patients and cell lines with quantitative real-time polymerase chain reactions, RNA in situ hybridization and immunohistochemistry, and found that there is a negative relationship between HNRNPAB and lnc-ELF209 expression. Up/downregulation assays and rescue assays indicate that lnc-ELF209 inhibits cell migration, invasion and epithelial-mesenchymal transition regulated by HNRNPAB. This suggests a new regulatory mechanism for HNRNPAB-promoted HCC progression. RNA pull-down and LC-MS/MS were used to determine triosephosphate isomerase, heat shock protein 90-beta and vimentin may be involved in the tumor-suppressed function of lnc-ELF209. Furthermore, we found lnc-ELF209 could stabilize TPI protein expression. We also found that lnc-ELF209 overexpression in HCCLM3 cell resulted in a lower rate of lung metastatic, which suggested a less aggressive HCC phenotype. Collectively, these findings offer new insights into the regulatory mechanisms that underlie HNRNPAB cancer-promoting activities and demonstrate that lnc-ELF209 is a HNRNPAB-regulated lncRNA that may play an important role in the inhibition of HCC progression.

6.
Sci Total Environ ; 698: 134298, 2020 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-31505343

RESUMO

Many studies have examined the acute toxicity of nanoparticles (NPs) towards model bacteria. In this study, we report the time-dependent effects of ZnO NPs on native, selected Zn-resistant and dominant bacteria in estuarine waters. An initial inhibition of bacterial growth followed by a recovery at 24 h was observed, and this rebound phenomenon was particularly notable when the raw water samples were treated with relatively high ZnO NP concentrations (1 and 10 mg/L).By comparing the groups treated with Zn2+, Zn2+ was shown to largely explain the acute cytotoxic effect of ZnO NPs on bacteria in raw waters. Furthermore, similar to the native bacteria, especially the dominant bacteria, the viability of Escherichia coli (E. coli) decreased with the increasing treatments time and the concentrations of ZnO NPs in water with different salinities. Moreover, the expression of Zn-resistance genes including zntA and zntR in E. coli suggested that the Zn-resistance system in E. coli can be activated to defend against the stress of Zn2+ released from ZnO NPs, and salinity may promote this process in estuarine aquatic systems. Thus, the effect of ZnO NPs on bacteria in estuarine water bodies is likely determined by the synergistic effect of environmental salinity and dissolved Zn ions. As such, our findings are of high relevance and importance for understanding the ecological disturbances caused by anthropogenic NPs in estuarine environments.

7.
Phys Rev Lett ; 123(21): 217002, 2019 Nov 22.
Artigo em Inglês | MEDLINE | ID: mdl-31809164

RESUMO

We report first-principles and strongly correlated calculations of the newly discovered heavy fermion superconductor UTe_{2}. Our analyses reveal three key aspects of its magnetic, electronic, and superconducting properties that include (i) a two-leg ladder-type structure with strong magnetic frustrations, which might explain the absence of long-range orders and the observed magnetic and transport anisotropy, (ii) quasi-two-dimensional Fermi surfaces composed of two separate electron and hole cylinders with similar nesting properties as in UGe_{2}, which may potentially promote magnetic fluctuations and help to enhance the spin-triplet pairing, and (iii) a unitary spin-triplet pairing state of strong spin-orbit coupling at zero field, with point nodes presumably on the heavier hole Fermi surface along the k_{x} direction, in contrast to the previous belief of nonunitary pairing. Our proposed scenario is in excellent agreement with latest thermal conductivity measurement and provides a basis for understanding the peculiar magnetic and superconducting properties of UTe_{2}.

8.
Hum Mol Genet ; 2019 Dec 09.
Artigo em Inglês | MEDLINE | ID: mdl-31813995

RESUMO

Huntington's disease (HD) is a neurodegenerative disorder caused by an expanded polyglutamine (polyQ) tract in the huntingtin (HTT) protein. Mutant HTT (mHTT) toxicity is caused by its aggregation/oligomerisation. The striatum is the most vulnerable region, although all brain regions undergo neuronal degeneration in the disease. Here we show that the levels of Bim, a BH3-only protein, are significantly increased in HD human post-mortem and HD mouse striata, correlating with neuronal death. Bim reduction ameliorates mHTT neurotoxicity in HD cells. In the HD mouse model, heterozygous Bim knockout significantly mitigates mHTT accumulation and neuronal death, ameliorating disease-associated phenotypes and lifespan. Therefore, Bim could contribute to the progression of HD.

9.
Breast Cancer Res ; 21(1): 131, 2019 Nov 29.
Artigo em Inglês | MEDLINE | ID: mdl-31783895

RESUMO

BACKGROUND: Breast cancer is a leading cause of cancer-related death for women in the USA. Thus, there is an increasing need to investigate novel prognostic markers and therapeutic methods. Inflammation raises challenges in treating and preventing the spread of breast cancer. Specifically, the nuclear factor kappa b (NFκB) pathway contributes to cancer progression by stimulating proliferation and preventing apoptosis. One target gene of this pathway is PTGS2, which encodes for cyclooxygenase 2 (COX-2) and is upregulated in 40% of human breast carcinomas. COX-2 is an enzyme involved in the production of prostaglandins, which mediate inflammation. Here, we investigate the effect of Singleminded-2s (SIM2s), a transcriptional tumor suppressor that is implicated in inhibition of tumor growth and metastasis, in regulating NFκB signaling and COX-2. METHODS: For in vitro experiments, reporter luciferase assays were utilized in MCF7 cells to investigate promoter activity of NFκB and SIM2. Real-time PCR, immunoblotting, immunohistochemistry, and chromatin immunoprecipitation assays were performed in SUM159 and MCF7 cells. For in vivo experiments, MCF10DCIS.COM cells stably expressing SIM2s-FLAG or shPTGS2 were injected into SCID mice and subsequent tumors harvested for immunostaining and analysis. RESULTS: Our results reveal that SIM2 attenuates the activation of NFκB as measured using NFκB-luciferase reporter assay. Furthermore, immunostaining of lysates from breast cancer cells overexpressing SIM2s showed reduction in various NFκB signaling proteins, as well as pAkt, whereas knockdown of SIM2 revealed increases in NFκB signaling proteins and pAkt. Additionally, we show that NFκB signaling can act in a reciprocal manner to decrease expression of SIM2s. Likewise, suppressing NFκB translocation in DCIS.COM cells increased SIM2s expression. We also found that NFκB/p65 represses SIM2 in a dose-dependent manner, and when NFκB is suppressed, the effect on the SIM2 is negated. Additionally, our ChIP analysis confirms that NFκB/p65 binds directly to SIM2 promoter site and that the NFκB sites in the SIM2 promoter are required for NFκB-mediated suppression of SIM2s. Finally, overexpression of SIM2s decreases PTGS2 in vitro, and COX-2 staining in vivo while decreasing PTGS2 and/or COX-2 activity results in re-expression of SIM2. CONCLUSION: Our findings identify a novel role for SIM2s in NFκB signaling and COX-2 expression.

10.
Biomolecules ; 9(12)2019 Nov 28.
Artigo em Inglês | MEDLINE | ID: mdl-31795147

RESUMO

Secondary metabolites of lichens are promising bioresources for candidate anti-cancer drugs. Accordingly, several approaches have been proposed for screening these molecules for novel anti-cancer lead compounds. In this study, we found that a non-toxic concentration of physciosporin, a compound isolated from Pseudocyphellaria granulata, significantly decreased colony formation on soft agar and spheroid formation by CSC221 cancer stem-like cells. Physciosporin also decreased spheroid formation in other colorectal cancer cell lines, including DLD1, Caco2, and HT29. Aldehyde dehydrogenase-1 (ALDH1), the most important cancer stem marker, was sharply downregulated at both the protein and mRNA level following treatment with physciosporin. Physciosporin also decreased the transcriptional activity of the glioma-associated oncogene homolog zinc finger protein (Gli), as well as the Hes1 and CSL promoters, in reporter assays. Moreover, the drug significantly suppressed spheroid formation in CSC221 cells overexpressing Gli1/2 or EN1 (an S2-cleaved but membrane-tethered form of human Notch1) but did not suppress spheroid formation in cells overexpressing both Gli1/2 and ∆EN1, suggesting that physciosporin suppresses colon cancer cell stemness through the Sonic hedgehog and Notch signaling pathways. Together, these results demonstrate for the first time that physciosporin is a potent inhibitor of colorectal cancer cell stemness.

11.
Hum Genomics ; 13(1): 63, 2019 Dec 05.
Artigo em Inglês | MEDLINE | ID: mdl-31806011

RESUMO

BACKGROUND: Mandibulofacial dysostosis with microcephaly (MFDM) is characteristic of multiple skeletal anomalies comprising craniofacial anomalies/dysplasia, microcephaly, dysplastic ears, choanal atresia, and short stature. Heterozygous loss of function variants of EFTUD2 was previously reported in MFDM; however, the mechanism underlying EFTUD2-associated skeletal dysplasia remains unclear. RESULTS: We identified a novel frameshift variant of EFTUD2 (c.1030_1031delTG, p.Trp344fs*2) in an MFDM Chinese patient with craniofacial dysmorphism including ear canal structures and microcephaly, mild intellectual disability, and developmental delay. We generated a zebrafish model of eftud2 deficiency, and a consistent phenotype consisting of mandibular bone dysplasia and otolith loss was observed. We also showed that EFTUD2 deficiency significantly inhibited proliferation, differentiation, and maturation in human calvarial osteoblast (HCO) and human articular chondrocyte (HC-a) cells. RNA-Seq analysis uncovered activated TP53 signaling with increased phosphorylation of the TP53 protein and upregulation of five TP53 downstream target genes (FAS, STEAP3, CASP3, P21, and SESN1) both in HCO and in eftud2-/- zebrafish. Additionally, inhibition of p53 by morpholino significantly reduced the mortality of eftud2-/- larvae. CONCLUSIONS: Our results confirm a novel de novo variant of the EFTUD2 gene and suggest that EFTUD2 may participate in the maturation and differentiation of osteoblasts and chondrocytes, possibly via activation of the TP53 signaling pathway. Thus, mutations in this gene may lead to skeletal anomalies in vertebrates.

12.
J Org Chem ; 2019 Dec 06.
Artigo em Inglês | MEDLINE | ID: mdl-31808693

RESUMO

Direct conversion of the readily available alkyl bromides and alcohols to value-added epoxides using DMSO under mild reaction conditions has been developed. Benzyl and allyl bromides, activated and unactivated alcohols all proceeded smoothly to give epoxides in high to excellent yield. Dimethyl sulfide, generated by DMSO oxidations, was in situ elaborated to form the substituted dimethyl sulfonium ylide species that participates in Corey-Chaykovsky epoxidation in domino and one pot fashion, respectively.

13.
Stem Cell Res Ther ; 10(1): 372, 2019 Dec 04.
Artigo em Inglês | MEDLINE | ID: mdl-31801626

RESUMO

BACKGROUND: Mesenchymal stem cells (MSCs) have been shown to alleviate acute lung injury (ALI) via paracrine hepatocyte growth factor (HGF) and to induce the differentiation of dendritic cells (DCs) into tolerogenic dendritic cells (DCregs) and participate in the immune response. However, whether MSCs induce the production of DCregs by secreting HGF to alleviate early ALI remains unclear. We observed that the protective effect of mouse bone marrow-derived MSCs against lipopolysaccharide (LPS)-induced ALI was achieved by inducing mature DCs (mDCs) to differentiate into DCregs, and its mechanism is related to the activation of the HGF/Akt pathway. METHODS: MSCs or MSCs with overexpression or knockdown of HGF were cocultured with DCs derived from mouse bone marrow using a Transwell system for 3 days. Moreover, we used MSCs or MSCs with overexpression or knockdown of HGF to treat LPS-induced ALI mice for 24 h. Flow cytometry was performed to measure the phagocytosis, accumulation, and maturation of DCs, as well as proliferation of T cells. Lung injury was estimated by lung wet weight to body weight ratio (LWW/BW) and histopathological analysis. Furthermore, we used the Akt inhibitor MK-2206 in a coculture system to elucidate the role of the HGF/Akt pathway in regulating the differentiation of DCs into regulatory DCs and relieving lung injury in early ALI mice. RESULTS: Immature DCs (imDCs) were induced to mature after 24 h of LPS (50 ng/ml) stimulation. MSCs or HGF induced the differentiation of mDCs into regulatory DCs characterized by low expression of MHCII, CD86, and CD40 molecules, strong phagocytic function, and the ability to inhibit T cell proliferation. The effect of MSCs on DCregs was enhanced with the increase in HGF secretion and was weakened with the decrease in HGF secretion. DCregs induced by recombinant HGF were attenuated by the Akt inhibitor MK-2206. Lung DC aggregation and mDC ratio increased in LPS-induced ALI mice, while treatment with MSCs decreased lung DC aggregation and maturation and alleviated lung pathological injury. High expression of the HGF gene enhanced the above effect of MSCs, while decreased expression of HGF weakened the above effect of MSCs. CONCLUSIONS: MSCs alleviate early ALI via paracrine HGF by inducing mDCs to differentiate into regulatory DCs. Furthermore, the mechanism of HGF-induced differentiation of mDCs into DCregs is related to the activation of the Akt pathway.

14.
Dysphagia ; 2019 Dec 04.
Artigo em Inglês | MEDLINE | ID: mdl-31802198

RESUMO

The objective of this study is to investigate the changes in swallowing function after using an absorbable collagen biomembrane during anterior cervical spine surgery (ACSS). A prospective controlled study of patients who underwent two-level anterior cervical decompression and fusion (ACDF) with a zero-profile implant or single-level anterior cervical corpectomy and fusion (ACCF) with cage and plate fixation was performed in our hospital from January 2016. An absorbable collagen biomembrane was used after suturing the prevertebral fascia in the experimental groups. The thickness of prevertebral soft tissue (PST) was measured on lateral X-rays to determine the extent of swelling. In addition, the Bazaz grading system and the Swallowing-Quality of Life (SWAL-QOL) survey were used to assess the swallowing function. A total of 100 patients were included with a follow-up of 12 months. Significant differences in PST swelling were found between the experimental groups and control groups at 3 months, 6 months, and 12 months postoperatively (P < 0.05). Patients in the experimental groups had significantly increased SWAL-QOL scores compared with patients in the control groups at 3 months and 6 months after surgery (P < 0.05). A significant difference in the total incidence of dysphagia was observed at 3 months postoperatively between the experimental groups and control groups (P < 0.05). The application of absorbable collagen biomembrane in ACSS can reduce the total incidence of dysphagia and improve swallowing function early after surgery.

15.
Crit Care Med ; 2019 Dec 05.
Artigo em Inglês | MEDLINE | ID: mdl-31804299

RESUMO

OBJECTIVES: We performed a national cross-sectional survey to determine the epidemiologic characteristics of patients with sepsis in ICU in China. DESIGN: A cross-section survey study. SETTING: Forty-four hospitals in mainland China from December 1, 2015, to January 31, 2016. PATIENTS: All septic patients diagnosed according sepsis-1 criteria admitted to participating ICU. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: We recorded demographic, physiologic, and microbiological data with follow-up for 90 days or death, if sooner. The frequency of sepsis and 90-day mortality rate were computed, and the relationship with gross domestic product determined. Multivariate logistic regression analysis was used to determine risk factors for 90-day mortality in patients with sepsis. Two-thousand three-hundred twenty-two patients with sepsis were included in the analysis, of whom 786 patients (33.9%) had hospital-acquired sepsis. The most common infection site was the lung (68.2%), followed by abdomen (26.6%) and bloodstream (7.8%). The frequency of sepsis in the ICU was 20.6 cases per 100 ICU admissions (95% CI, 15.8-25.4) with a 90-day mortality of 35.5%. The proportion of sepsis, severe sepsis, and septic shock were 3.10%, 43.6%, and 53.3% with a 90-day mortality of 2.78%, 17.69%, and 51.94%, respectively. Older age, low body weight, higher Sequential Organ Failure Assessment score, the number of systemic inflammatory response syndrome criteria, comorbid with heart failure, hematologic cancer, immunosuppression, higher level of lactate, infection site (pneumonia and bloodstream) were associated with 90-day mortality. CONCLUSIONS: Sepsis affects a fifth of patients admitted to ICUs in mainland China with a 90-day mortality rate of 35.5%. Our findings indicate that a large burden of sepsis, and we need to focus on sepsis as a quality improvement target in China given the high mortality. In addition, further studies are needed to delineate the epidemiology of sepsis outside the ICU.

16.
Medicine (Baltimore) ; 98(49): e18085, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31804318

RESUMO

This was a prospective cohort study with a short-term follow-up. To explore whether age is a factor in the prognosis following high ligation and stripping (HLS) performed in an ambulatory care center. This study included 170 patients who underwent their first HLS for varicose veins in an ambulatory center from November 2016 to October 2017 at West China Hospital. The patients were categorized as two groups: the ≤60 years old group and the >60 years old group. We collected the two age groups data included Clinical, Etiology, Anatomy, and Pathophysiology (CEAP) classification, Venous Clinical Severity Score (VCSS), Visual Analogue Score (VAS), Aberdeen Varicose Veins Questionnaire (AVVQ), Quality of Recovery (QoR-15), and postoperative complications at predetermined time points. The clinical correlation between age and prognosis following HLS in an ambulatory care center was prospectively studied after adjusting for potential confounders. The distribution of age and prognosis were also compared in the AVVQ improvement and VCSS improvement of patients at 6 weeks and 6 months after surgery. Our research comprised a total of 170 patients (236 limbs), of which 86 (50.6%) patients were female and 66 (38.8%) patients received bilateral procedures. After multivariable risk adjustment for potential confounding factors, we observed that age was not associated with the improvement of AVVQ (OR 0.3, 95%CI (1.3, 0.7), P = .54) and VCSS (OR 0.2, 95%CI (0.2, 0.6) P = .38) at 6 months after HLS, as well as AVVQ (OR 0.5,95%CI (1.2, 2.2), P = .57) at 6 weeks after HLS. However, at 6 weeks after HLS, age was related to the improvement of VCSS (OR -0.6, 95%CI (1.2, 0.1), P = .03), with the >60 years old group having a lower VCSS improvement compared to the 60 years old group. In postoperative complications, there were no significant differences in terms of complications between the two age groups (all P value >.05). Therefore, in our opinion, age is not a barrier for good outcomes following HLS in an ambulatory care center.

17.
Medicine (Baltimore) ; 98(49): e18163, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31804330

RESUMO

RATIONALE: Non-traumatic bowel perforation caused by cytomegalovirus (CMV) and Mycobacterium avium complex (MAC) infections has become rare among patients with acquired immunodeficiency syndrome (AIDS) in the era of combination antiretroviral therapy (cART); however, CMV-associated and MAC-related immune reconstitution inflammatory syndrome (IRIS) has subsequently emerged owing to the wide use of integrase inhibitor-based regimens. Here we report a case of spontaneous perforation of the jejunum in a patient with human immunodeficiency virus (HIV) infection with good compliance to cART. PATIENT CONCERNS: A 32-year-old HIV-infected man developed CMV disease and DMAC infection, as unmasking IRIS, 3 days after the initiation of cART. After appropriate treatment for opportunistic infections, intermittent fever with enlarged lymph nodes in the abdomen occurred as paradoxical IRIS. The patient was administered prednisolone with subsequent tapering according to his clinical condition. DIAGNOSES: Unexpected perforation of hollow organ during the titration of steroid dose with clinical presentations of severe abdominal pain was diagnosed by chest radiography. INTERVENTIONS: He underwent surgical repair with peritoneal toileting smoothly. OUTCOMES: He was discharged well with a clean surgical wound on post-operative day 10. LESSONS: Bowel perforation may be a life-threatening manifestation of IRIS in the era of cART. Steroids should be avoided, if possible, to decrease the risk of bowel perforation, especially in IRIS occurred after opportunistic diseases involving the gastrointestinal tract.

18.
Insect Sci ; 2019 Dec 03.
Artigo em Inglês | MEDLINE | ID: mdl-31793737

RESUMO

Apoptosis play critical roles in multiple biological processes in multicellular organisms. Caspases are known as important participator and regulator of apoptosis. Here, four novel caspase genes of Spodoptera exigua were cloned and characterized, which were designated as SeCasp-1, SeCasp-6, SeCasp-7 and SeCasp-8. Analysis of the putative encoded protein sequences of these SeCasps indicated that SeCasp-1 and SeCasp-7 were possible homologues of executor caspases; SeCasp-8 was a possible homologue of initiator caspases; and SeCasp-6 was a unique caspase of S. exigua that shares low similarity with all the identified insect caspases. Based on baculovirus expression system analyses, SeCasp-1 exhibited similar caspase activity to human caspase-1, -3, -4, -6, -8 and -9; SeCasp-6 presented similar caspase activity to human caspase-2, -3, -4, -6, -8 and -9; SeCasp-7 exhibited similar caspase activity to human caspase-2, -3 and -6; and SeCasp-8 presented similar caspase activity only to human caspase-8. Induction with different chemicals revealed that SeCasp-1 showed extreme upregulation after 24 h in the treated fat body cell line (IOZCAS-Spex-II) of S. exigua. Developmental expression analysis revealed that SeCasp-1 was highly transcribed in the larval stages, while SeCasp-6, SeCasp-7, SeCasp-8 were down-regulated. The in vivo detection of the relative expression levels of SeCasps in S. eixgua larvae inoculated with different pathogens suggested that SeCasp-1 was sensitive to Bacillus thuringiensis infection and that SeCasp-6 was sensitive to baculovirus infection. SeCasp-7 and SeCasp-8 showed slight changes under either in vitro chemical apoptosis induction or in vivo pathogen infection. This article is protected by copyright. All rights reserved.

19.
BMC Evol Biol ; 19(1): 219, 2019 12 02.
Artigo em Inglês | MEDLINE | ID: mdl-31791235

RESUMO

BACKGROUND: Phylogenetic species trees are widely used in inferring evolutionary relationships. Existing software and algorithms mainly focus on phylogenetic inference. However, less attention has been paid to intermediate steps, such as processing extremely large sequences and preparing configure files to connect multiple software. When the species number is large, the intermediate steps become a bottleneck that may seriously affect the efficiency of tree building. RESULTS: Here, we present an easy-to-use pipeline named PhySpeTree to facilitate the reconstruction of species trees across bacterial, archaeal, and eukaryotic organisms. Users need only to input the abbreviations of species names; PhySpeTree prepares complex configure files for different software, then automatically downloads genomic data, cleans sequences, and builds trees. PhySpeTree allows users to perform critical steps such as sequence alignment and tree construction by adjusting advanced options. PhySpeTree provides two parallel pipelines based on concatenated highly conserved proteins and small subunit ribosomal RNA sequences, respectively. Accessory modules, such as those for inserting new species, generating visualization configurations, and combining trees, are distributed along with PhySpeTree. CONCLUSIONS: Together with accessory modules, PhySpeTree significantly simplifies tree reconstruction. PhySpeTree is implemented in Python running on modern operating systems (Linux, macOS, and Windows). The source code is freely available with detailed documentation (https://github.com/yangfangs/physpetools).

20.
Artigo em Inglês | MEDLINE | ID: mdl-31822385

RESUMO

OBJECTIVE: To present the pooled quantitative evidence of basic profiles, initial treatment strategies, and clinical outcomes in patients with isolated abdominal aortic dissection (IAAD). METHODS: A comprehensive systematic review and meta-analysis was performed of all available studies reporting IAAD, retrieved from the MEDLINE, Embase, and Cochrane Databases. The logistic normal random effect model was fitted using the generalised linear mixed model with random intercepts to calculate the pooled proportion estimates. RESULTS: Seventeen studies with 482 patients were included in this meta-analysis. Male smokers with hyperlipidaemia and hypertension were the most prominent basic profile. IAADs were predominantly spontaneous and infrarenal, and roughly half were acute and symptomatic. Approximately 67% [95% confidence interval (CI) 42-86%] of patients were managed initially conservatively. In the overall population, the 30 day all cause mortality was 3% (95% CI 1-5%) and the long term mortality during follow up was 8% (95% CI 5-14%). Re-intervention during follow up occurred in 8% (95% CI 5-15%) of patients. In the subgroup analysis, patients with conservative treatment had a 30 day mortality of 1% (95% CI 0-8%), a long term mortality of 5% (95% CI 1-29%), and a re-intervention rate of 18% (95% CI 10-29%). Patients with open surgery had a 30 day mortality of 9% (95% CI 0-82%), a long term mortality of 12% (95% CI 4-31%), and a re-intervention rate of 9% (95% CI 1-44%). Patients with endovascular repair had a 30 day mortality of 2% (95% CI 0-10%), a long term mortality of 5% (95% CI 2-13%), a re-intervention rate of 6% (95% CI 3-13%), and a persistent endoleak rate of 4% (95% CI 2-10%). CONCLUSION: Appropriate initial treatment strategies can be used to obtain acceptable clinical outcomes in patients with IAAD. Invasive intervention is necessary if patients match certain indications for intervention. Regular imaging surveillance should be provided for all patients, especially those treated conservatively.

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