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1.
Interv Neuroradiol ; : 1591019919896940, 2020 Jan 10.
Artigo em Inglês | MEDLINE | ID: mdl-31924102

RESUMO

PURPOSE: Diabetes mellitus indicated poor clinical prognosis for patients with acute ischemic stroke. Furthermore, diabetes mellitus could also impact the hemostatic system, while its influence on the histological composition of thrombus is unclear. METHODS: Consecutive patients with retrieved clots were included. Histologic staining for thrombus included hematoxylin and eosin, Martius Scarlet Blue, immunohistochemistry for von Willebrand factor. The differences in clot composition were compared according to diabetes mellitus history or hyperglycemia (≥7.8 mmol/L) on admission. RESULTS: A total of 52 patients were included; half of them were diagnosed as diabetes mellitus previously. Diabetic patients showed higher serum glucose on admission (8.90 vs. 7.40, p = 0.012). The baseline characteristics (expect smoking history and thrombus location), procedural, and clinical outcomes were similar between diabetic patients and nondiabetic patients. As for histologic composition, thrombus in patients with diagnosed diabetes mellitus had more fibrin (44.2% vs. 28.3%, p = 0.004) and fewer red blood cells (26.0% vs. 42.9%, p = 0.013) and equivalent content of platelets (24.0% vs. 21.5%, p = 0.694) and von Willebrand factor (0.041 vs. 0.031, p = 0.234) than patients without diabetes mellitus. However, there was no statistical difference in the content of red blood cells (41.6% vs. 27.3%, p = 0.105), fibrin (37.6% vs. 34.3%, p = 0.627), platelets (21.2% vs. 24.2%, p = 0.498), and von Willebrand factor (0.038 vs. 0.034, p = 0.284) between patients with or without hyperglycemia on admission. CONCLUSION: Clots in diabetic patients had more fibrin and fewer erythrocyte components compared with patients without diabetes mellitus, while hyperglycemia on admission did not show association with clot composition. Further studies are needed to confirm these results.

2.
Angew Chem Int Ed Engl ; 59(4): 1548-1551, 2020 Jan 20.
Artigo em Inglês | MEDLINE | ID: mdl-31750968

RESUMO

Applications of zeolites in catalysis are plagued by strong diffusion resistance, which results from limitations to molecular transport in micropores, across external crystal surfaces, but also across internal interfaces. The first type of diffusion resistance is well understood, the second is receiving increasing attention, while the diffusion barriers at internal interfaces remain largely unclear. We take Pt/Beta catalyzed isomerization of n-heptane as the model system to explore the role of internal diffusion barriers in zeolite catalysis. The two as-synthesized Pt/Beta catalysts have an identical Pt loading, similar Beta particle size and acidity, but different internal structures. A Pt/Beta crystal with no observable internal interfaces can be 180 % higher in activity and 22 % higher in selectivity than its counterpart with numerous internal interfaces. This can only be attributed to the strong transport barriers across internal interfaces, as supported by directly comparing the apparent diffusivities of the two Beta samples.

3.
Biochem Biophys Res Commun ; 523(2): 389-397, 2020 Mar 05.
Artigo em Inglês | MEDLINE | ID: mdl-31870550

RESUMO

The development of head and neck squamous cell carcinoma (HNSCC) is a complex pathological process and many cellular and molecular events may occur. The ubiquitin conjugating enzyme E2 (UBE2C) was found to play an oncogenic role in several human cancers. However, its functional role in HNSCC tumorigenesis remains unknown. In this study, UBE2C gene expression in HNSCC was first evaluated using the data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. The connection between UBE2C gene expression and patients' survival rates of HNSCC and other human cancers was also investigated. Liquid chromatography with tandem mass spectrometry was used to identify differentially expressed proteins, including UBE2C, between UMSCC1 oral cancer cells and normal human oral keratinocytes (NHOKs). Immunohistochemistry (IHC) was used to verify the differential expression of UBE2C protein between HNSCC and adjacent control tissues. Cell cycle analysis, MTT, colony formation, Transwell migration, and Matrigel invasion assays were used to study the effect of UBE2C downregulation on the malignant phenotypes of HNSCC cells. The bioinformatic analysis of the proteins interacting with UBE2C in HNSCC cells was also performed. Based on the data obtained from the cancer databases and our in vitro studies, we found that UBE2C was overexpressed in HNSCC and patients with high UBE2C expression suffered a remarkably worse overall survival rate than those with low UBE2C expression, and a similar observation was found in a number of other human cancers. UBE2C was also found to be overexpressed in HNSCC cells versus normal human oral keratinocytes and inhibition of UBE2C expression significantly suppressed the malignant phenotypes of HNSCC cells in vitro. The bioinformatic analysis indicated that UBE2C may be involved in head and neck tumorigenesis through the mediation of important pathways such as ubiquitin mediated proteolysis, proteasome, and cell cycle. In conclusion, our results suggest that UBE2C is consistently upregulated in many human solid tumors. It promotes HNSCC progression and may serve as a potential prognostic biomarker in HNSCC. Future studies are warranted to unveil the underlying molecular pathways of UBE2C in HNSCC.

4.
J Cancer ; 10(27): 6915-6924, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31839827

RESUMO

Objective: Since the introduction in 2004, global usage of e-cigarettes (ECs) has risen exponentially. However, the risks of ECs on oral health are uncertain. The purpose of this study is to understand if EC aerosol exposure impacts the gene pathways of normal human oral keratinocytes (NHOKs), particularly the unfolded protein response (UPR) pathway. Materials and methods: EC aerosols were generated reproducibly with a home-made puffing device and impinged into the culture medium for NHOKs. DNA microarrays were used to profile the gene expression changes in NHOKs treated with EC aerosols, and the Ingenuity Pathway Analysis (IPA) was used to reveal signaling pathways altered by the EC aerosols. Quantitative PCR was used to validate the expression changes of significantly altered genes. Results: DNA microarray profiling followed by IPA revealed a number of signaling pathways, such as UPR, cell cycle regulation, TGF-ß signaling, NRF2-mediated oxidative stress response, PI3K/AKT signaling, NF-κB signaling, and HGF signaling, activated by EC aerosols in NHOKs. The UPR pathway genes, C/EBP homologous protein (CHOP), activating transcription factor 4 (ATF4), X box binding protein 1 (XBP1), and inositol-requiring enzyme 1 alpha (IRE1α) were all significantly up-regulated in EC aerosol-treated NHOKs whereas immunoglobulin heavy-chain binding protein (BIP) and PRKR-like ER kinase (PERK) were slightly up-regulated. qPCR analysis results were found to be well correlated with those from the DNA microarray analysis. The most significantly changed genes in EC aerosol-treated NHOKs versus untreated NHOKs were CHOP, ATF4, XBP1, IRE1α and BIP. Meanwhile, Western blot analysis confirmed that CHOP, GRP78 (BIP), ATF4, IRE1α and XBP1s (spliced XBP1) were significantly up-regulated in NHOKs treated with EC aerosols. Conclusion: Our results indicate that EC aerosols up-regulate the UPR pathway genes in NHOKs, and the induction of UPR response is mediated by the PERK - EIF2α - ATF4 and IRE1α - XBP1 pathways.

5.
BMC Cardiovasc Disord ; 19(1): 261, 2019 Nov 26.
Artigo em Inglês | MEDLINE | ID: mdl-31771529

RESUMO

BACKGROUND: High risk of embolic events exists in both patients with chronic atrial fibrillation (AF) and patients in the perioperative period of ablation (effective treatment for AF). Therefore, anticoagulant therapy is important. Oral anticoagulants can be divided into two major categories: vitamin K antagonists (VKAs) and non-vitamin K antagonist oral anticoagulants (NOACs). VKAs, represented by warfarin, have been widely used as traditional anticoagulants, whereas NOACs have been used in clinical practice, but their anticoagulant effects and side effects are still the focus of research. We used a meta-analysis to compare the incidence of left atrial thrombi (LAT) between different anticoagulants. METHODS: We searched PubMed, EMBASE, Web of Science, and the Cochrane Library databases for observational studies that compared the transesophageal echocardiography (TEE) findings for patients treated with NOACs and VKAs. The incidence of LAT and dense spontaneous echocardiographic contrast (dense SEC) were extracted as the basis of the meta-analysis. RESULTS: Fifteen studies were included in the meta-analysis. We found that patients anticoagulated with NOACs and VKAs had similar incidence of LAT (OR = 0.74, 95%CI: 0.55-1.00). After excluding the heterogeneous article by sensitivity analysis, we found the incidence of LAT in patients anticoagulated with NOACs is lower than VKAs (OR = 0.59, 95%CI: 0.42-0.84). The results of subgroup analysis showed that the incidence of LAT among three types of NOACs have no significant difference (dabigatran vs. rivaroxaban, OR = 1.16 [0.75, 1.81]; rivaroxaban vs. apixaban, OR = 0.97 [0.54, 1.74]; dabigatran vs. apixaban, OR = 1.09 [0.55, 2.16]). CONCLUSION: Patients anticoagulated with NOACs may have lower incidence of LAT than VKAs. The incidence of LAT among different type of NOACs are similar.

6.
Artigo em Inglês | MEDLINE | ID: mdl-31745672

RESUMO

Emerging evidence suggests that long non-coding RNAs (lncRNAs) are critical regulators of diverse biological processes, including adipogenesis. Despite being considered an ideal animal model for studying adipogenesis, little is known about the roles of lncRNAs in the regulation of rabbit preadipocyte differentiation. In the present study, visceral preadipocytes isolated from newborn rabbits were cultured in vitro and induced for differentiation, and global lncRNA expression profiles of adipocytes collected at days 0, 3, and 9 of differentiation were analyzed by RNA-seq. A total of 2066 lncRNAs were identified from nine RNA-seq libraries. Compared to protein-coding transcripts, lncRNA transcripts exhibited characteristics of a longer length and lower expression level. Furthermore, 486 and 357 differentially expressed (DE) lncRNAs were identified when comparing day 3 vs. day 0 and day 9 vs. day 3, respectively. Target genes of DE lncRNAs were predicted by the cis-regulating approach. Prediction of functions revealed that DE lncRNAs when comparing day 3 vs. day 0 were involved in gene ontology (GO) terms of developmental growth, growth, developmental cell growth, and stem cell proliferation, and involved in Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of PI3K-Akt signaling pathway, fatty acid biosynthesis, and the insulin signaling pathway. The DE lncRNAs when comparing day 9 vs. day 3 were involved in GO terms that associated with epigenetic modification and were involved in the KEGG pathway of cAMP signaling pathway. This study provides further insight into the regulatory function of lncRNAs in rabbit visceral adipose and facilitates a better understanding of different stages of preadipocyte differentiation.

7.
ACS Nano ; 13(11): 13065-13082, 2019 Nov 26.
Artigo em Inglês | MEDLINE | ID: mdl-31682760

RESUMO

The widespread use of metal oxide nanoparticles (MOx NPs) poses a risk of exposure that may lead to adverse health effects on humans. Even though a number of toxicological methodologies are available for assessing nanotoxicity, the effect of MOx NPs on cell metabolism in vitro and in vivo remains largely unknown, especially under the exposure to low-dose or supposedly low-toxicity MOx NPs. In this study, liquid chromatography-mass spectrometry (LC-MS) based metabolomics was used to reveal significantly altered metabolites and metabolic pathways in human bronchial epithelial cells exposed to four different types of MOx NPs (ZnO, SiO2, TiO2, and CeO2) at both high (25 µg/mL) and low (12.5 µg/mL) doses. We demonstrated that high-dose ZnO NPs caused severe cytotoxicity with altered metabolism of amino acids, nucleotides, nucleosides, tricarboxylic acid cycle, lipids, inflammation/redox, and fatty acid oxidation, as well as the elevation of toxic and DNA damage related metabolites. Fewer metabolomic alterations were induced by low-dose ZnO NPs. However, most metabolites significantly altered by high-dose ZnO NPs were also slightly changed by low-dose ZnO NPs. On the other hand, the cells exposed to SiO2, TiO2, and CeO2 NPs at either high or low dose displayed low cytotoxicity with similar metabolomic alterations, although each type of NPs induced distinct changes of certain metabolites. These three NPs significantly affected the metabolic pathways of sphingosine-1-phosphate, fatty acid oxidation, folate cycle, inflammation/redox, and lipid metabolism. In addition, dose-dependent effects were observed for a number of metabolites significantly altered by respective MOx NPs. Representative metabolites of the significantly altered metabolic pathways were successfully validated in vitro using enzymatic assays. More importantly, these representative metabolites were further validated in a mouse model after lung exposure to respective NPs, indicating that in vitro metabolomic findings may be used to effectively predict the toxicological effects in vivo. Despite functional assay results demonstrating that the changes in cellular functions were largely reflected by the metabolomic alterations, LC-MS-based metabolomics was sensitive enough to detect the subtle metabolomic changes when functional cellular assays showed no significant difference. Collectively, our studies have unveiled potential metabolic mechanisms of MOx NP-induced nanotoxicity in lung epithelial cells and demonstrated the sensitivity and feasibility of using metabolomic signatures to understand and predict nanotoxicity in vivo.

8.
Clin Neurol Neurosurg ; 186: 105543, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31627063

RESUMO

OBJECTIVES: Cerebrovascular atherosclerotic stenosis (CAS) and intracranial aneurysm (IA) have a common underlying arterial pathology and common risk factors, but the clinical significance of CAS in IA rupture (IAR) is unclear. This study aimed to investigate the effect of CAS on the risk of IAR. PATIENTS AND METHODS: A total of 336 patients with 507 sacular IAs admitted at our center were included. Univariable and multivariable logistic regression analyses were performed to determine the association between IAR and the angiographic variables for CAS. We also explored the differences in CAS in patients aged <65 and ≥65 years. RESULTS: In all the patient groups, moderate (50%-70%) cerebrovascular stenosis was significantly associated with IAR (odds ratio [OR], 3.4; 95% confidence interval [CI], 1.8-6.5). Single cerebral artery stenosis was also significantly associated with IAR (OR, 2.3; 95% CI, 1.3-3.9), and intracranial stenosis may be a risk factor for IAR (OR, 1.8; 95% CI, 1.0-3.2). In addition, IAs with lobulation may be at a higher risk for rupture than IAs with regular shape (OR, 2.6; 95% CI, 1.1-5.8; P = 0.026), although the same was not true of aneurysms with a daughter sac (OR, 1.8; 95% CI, 0.9-3.7; P = 0.098). Bifurcation location (OR, 2.4; 95% CI, 1.5-3.8; P < 0.001) was significantly associated with aneurysmal rupture. For the patient subgroup aged <65 years, rupture risk was higher for aneurysms with moderate stenosis (OR, 3.4; 95% CI, 1.8-6.5). For patients aged ≥65 years, single-artery stenosis (OR, 1.9; 95% CI, 1.2-3.0) was statistically associated with IAR. CONCLUSIONS: We observed substantial differences in the severity of atherosclerotic stenosis, parent-artery stenosis, number of stenotic arteries, and intracranial/extracranial stenosis as indicators between ruptured and unruptured aneurysms. CAS is significantly associated with the risk of intracranial aneurysm rupture, whether in patients aged ≥65 years or <65 years. These findings indicate the clinical significance of CAS in IAR.

9.
Anal Cell Pathol (Amst) ; 2019: 3815786, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31534898

RESUMO

Aim: Microvessel density is a marker of tumor angiogenesis activity for development and metastasis. Our preliminary study showed that ginsenoside Rg3 (Rg3) induces apoptosis in hepatocellular carcinoma (HCC) in vitro. The aim of this study was to investigate the cross-link for apoptosis induction and antiangiogenesis effect of Rg3 on orthotopic HCC in vivo. Methods: The murine HCC cells Hep1-6 were implanted in the liver of mouse. With oral feeding of Rg3 (10 mg/kg once a day for 30 days), the quantitative analysis of apoptosis was performed by using pathology and a transmission electron microscope and microvessel density was quantitatively measured by immunohistochemical staining of the CD105 antibody. The mice treated with Rg3 (n = 10) were compared with the control (n = 10) using Kaplan-Meier analysis. Animal weight and tumor weight were measured to determine the toxicity of Rg3 and antitumor effect on an orthotopic HCC tumor model. Results: With oral feeding of Rg3 daily in the first 30 days on tumor implantation, Rg3 significantly decreased the orthotopic tumor growth and increased the survival of animals (P < 0.05). Rg3-treated mice showed a longer survival than the control (P < 0.05). Rg3 treatment induced apoptosis and inhibited angiogenesis. They contributed to the tumor shrinkage. Rg3 initialized the tumor apoptotic progress, which then weakened the tumor volume and its capability to produce the vascularized network for further growth of the tumor and remote metastasis. Conclusion: Rg3 inhibited the activation of microtumor vessel formation in vivo besides its apoptosis induction. Rg3 may be used as an adjuvant agent in the clinical HCC treatment regimen.

10.
Stem Cells Int ; 2019: 1705629, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31467558

RESUMO

Adipose stem cells (ASCs) are an attractive cell source for treating many human diseases including osteoporosis. However, the molecular mechanisms accounting for ASC osteogenesis are poorly known. In this study, ASCs were first isolated from the fat tissues from the patients with osteoporosis. The global transcriptome profile between osteogenic differentiated ASCs and undifferentiated ASCs was compared using RNA sequencing (RNA-seq). Then, bioinformatic analysis was performed to reveal the central genes and pathways that regulated the osteogenic differentiation of ASCs. One of the interested genes C5AR1 was chosen for further investigation. A total of 1521 upregulated and 3020 downregulated genes were identified between the ASCs with osteogenic induction and controls. Functional gene ontology analysis revealed that these significantly differentially expressed genes (DEGs) were associated with cell cycle, protein binding, and nucleotide binding. Pathway analysis showed that many canonical pathways, such as the MAPK signaling pathway and the PI3K-AKT pathway, might actively be involved in regulating osteogenic differentiation of ASCs. A total of three subnetworks and 20 central nodes were identified by the protein-protein interaction analysis. In addition, the expression level of C5AR1 was significantly increased during osteogenic differentiation of ASCs. The downregulation of C5AR1 dramatically reduced the expression levels of osteogenic differentiation biomarkers and calcium nodule formation capacity. Collectively, we have provided a number of novel genes and pathways that might be indispensable for ASC osteogenic differentiation. Manipulating the levels of this candidate gene might contribute to the osteoporosis therapy.

11.
ACS Appl Mater Interfaces ; 11(33): 29569-29578, 2019 Aug 21.
Artigo em Inglês | MEDLINE | ID: mdl-31361117

RESUMO

Circulating tumor cells (CTCs) in blood is the direct cause of tumor metastasis. The isolation and detection of CTCs in the whole blood is very important and of clinical value in early diagnosis, postoperative review, and personalized treatment. It is difficult to separate all types of CTCs that efficiently rely on a single path due to cancer cell heterogenicity. Here, we designed a new kind of "filter chip" for the retention of CTCs with very high efficiency by integrating the effects of cell size and specific antigens on the surface of tumor cells. The filter chip consists of a semicircle arc and arrays and can separate large-scale CTC microspheres, which combined with CTCs automatically. We synthesized interfacial zinc oxide coating with nanostructure on the surface of the microsphere to increase the specific surface area to enhance the capturing efficiency of CTCs. Microspheres, trapped in the arrays, would entrap CTCs, too. The combination of the three kinds of strategies resulted in more than 90% capture efficiency of different tumor cell lines. Furthermore, it is easy to find and isolate the circulating tumor cells from the chip as tumor cells would be fixed inside the structure of a filter chip. To avoid the high background contamination when a few CTCs are surrounded by millions of nontarget cells, a digital detection method was applied to improve the detection sensitivity. The CTCs in the whole blood were specifically labeled by the antibody-DNA conjugates and detected via the DNA of the conjugates with a signal amplification. The strategy of the antibody-functional microsphere-integrated microchip for cell sorting and detection of CTCs may find broad implications that favor the fundamental cancer biology research, the precise diagnosis, and monitoring of cancer in the clinics.


Assuntos
Anticorpos/química , Microfluídica/métodos , Microesferas , Células Neoplásicas Circulantes , Óxido de Zinco/química , Células HeLa , Humanos , Células MCF-7 , Nanofios/química
12.
J Exp Clin Cancer Res ; 38(1): 138, 2019 Mar 29.
Artigo em Inglês | MEDLINE | ID: mdl-30922366

RESUMO

BACKGROUND: SOX11 is a transcription factor that plays an important role in mantle cell lymphoma development. However, its functional role in head and neck squamous cell carcinoma (HNSCC) remains unknown. METHODS: Protein expression was measured with Western blotting, immunohistochemistry or quantitative proteomics, and gene expression was measured with quantitative RT-PCR. Functional role of SOX11 in HNSCC was evaluated with MTS/apoptosis, migration, invasion assays and a xenograft model. A SOX11-targeting gene, SDCCAG8, was confirmed with chromatin immunoprecipitation (ChIP), luciferase reporter and rescue assays. RESULTS: SOX11 was up-regulated in recurrent versus primary HNSCC and in highly invasive versus low invasive HNSCC cell lines. Silencing SOX11 in HNSCC cell lines significantly inhibited the cell proliferation, migration, invasion and resistance to Cisplatin, and vice versa. Quantitative proteomic analysis of SOX11-silencing HNSCC cells revealed a number of differentially expressed proteins, including a down-regulated tumor antigen SDCCAG8. Silencing of SDCCAG8 in HNSCC cells also significantly inhibited the cell proliferation, migration and invasion, and vice versa. ChIP assays demonstrated that endogenous SOX11 strongly bound to Sdccag8 gene promoter in highly invasive HNSCC cells. When over-expressed in low invasive HNSCC cells, wild type SOX11 but not mutant SOX11 induced the promoter activity of Sdccag8 and significantly induced the expression of SDCCAG8. However, exogenous mutant SOX11 abolished the expression of SDCCAG8 in highly invasive HNSCC cells. In addition, the inhibitory effects of SOX11 knockdown were partially rescued by over-expression of SDCCAG8 in HNSCC cells. CONCLUSION: Collectively, our findings indicate SOX11 promotes HNSCC progression via the regulation of SDCCAG8.


Assuntos
Autoantígenos/metabolismo , Carcinoma de Células Escamosas/patologia , Neoplasias de Cabeça e Pescoço/patologia , Proteínas de Neoplasias/metabolismo , Fatores de Transcrição SOXC/metabolismo , Regulação para Cima , Animais , Autoantígenos/genética , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/metabolismo , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Progressão da Doença , Regulação Neoplásica da Expressão Gênica , Neoplasias de Cabeça e Pescoço/genética , Neoplasias de Cabeça e Pescoço/metabolismo , Humanos , Camundongos , Proteínas de Neoplasias/genética , Transplante de Neoplasias , Fatores de Transcrição SOXC/genética
13.
J Reconstr Microsurg ; 35(7): 499-504, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30836413

RESUMO

BACKGROUND: End-to-end, end-to-side, and side-to-side microvascular anastomoses are the main types of vascular bypass grafting used in microsurgery and neurosurgery. Currently, there has been no animal model available for practicing all three anastomoses in one operation. The aim of this study was to develop a novel animal model that utilizes the rat abdominal aorta (AA), common iliac arteries (CIAs), and the median sacral artery (MSA) for practicing these three types of anastomosis. METHODS: Eight adult Sprague-Dawley rats were anesthetized and then laparotomized. The AA, MSA, and bilateral CIAs were exposed and separated from the surrounding tissues. The length and diameter of each artery were measured. The relatively long segment of the AA without major branches was selected to perform end-to-end anastomosis. One side of the CIAs (or AA) and MSA were used for end-to-side anastomosis. The bilateral CIAs were applied to a side-to-side and another end-to-side anastomosis. RESULTS: Anatomical dissection of the AA, CIAs, and MSA was successfully performed on eight Sprague-Dawley rats; four arterial-to-arterial anastomoses were possible for each animal. The AA trunk between the left renal artery and right iliolumbar arteries was 15.60 ± 0.76 mm in length, 1.59 ± 0.15 mm in diameter, for an end-to-end anastomosis. The left CIA was 1.06 ± 0.08 mm in diameter, for an end-to-side anastomosis with the right CIA. The MSA was 0.78 ± 0.07 mm in diameter, for another end-to-side anastomosis with the right CIA or AA. After finishing end-to-side anastomosis in the proximal part of bilateral CIAs, the distal portion was juxtaposed for an average length of 5.6 ± 0.25 mm, for a side-to-side anastomosis. CONCLUSION: This model can comprehensively and effectively simulate anastomosis used in revascularization procedures and can provide more opportunities for surgical education, which may lead to more routine use in microvascular anastomosis training.


Assuntos
Anastomose Cirúrgica/educação , Microcirurgia/educação , Procedimentos Cirúrgicos Vasculares/educação , Animais , Masculino , Modelos Animais , Ratos , Ratos Sprague-Dawley
14.
World J Surg Oncol ; 17(1): 3, 2019 Jan 03.
Artigo em Inglês | MEDLINE | ID: mdl-30606195

RESUMO

BACKGROUND: Although pathological evaluation has been considered an effective evaluation method, some problems still exist in practice. Therefore, we explored whether there are more reasonable and practical pathological evaluation criteria for neoadjuvant chemotherapy in patients with advanced gastric cancer. Here, we aim to determine pathological judgment criteria for neoadjuvant chemotherapy in patients with advanced gastric cancer. METHODS: Eighty-seven patients with cT2-4 or cN+ were enrolled in this study. Pathological factors for overall survival (OS) were investigated using univariate and multivariate analyses, and the pathological criteria for neoadjuvant chemotherapy were then determined. RESULTS: A total of 87 patients underwent 3-4 cycles of neoadjuvant chemotherapy, with 67 (77.0%), 15 (17.2%), and 5 (5.8%) receiving Folfox6, Xelox, and SOX regimens, respectively. All patients showed different levels of graded histological regression (GHR) of the primary tumor, with a ≥ 50% regression rate of 50.6%. The univariate analysis showed that GHR ≥ 50% (p = 0.022), 66.7% (p = 0.013), and 90% (p = 0.028) were significantly correlated with OS. The multivariate analysis demonstrated that ypTNM (II/III) stage was significantly associated with OS compared with ypTNM (0+I) stage [HR = 3.553, 95% CI 1.886-6.617; HR = 3.576, 95% CI 1.908-6.703, respectively] and that the Lauren classification of diffuse type was also an independent risk factor for OS compared with the intestinal type (HR = 3.843, 95% CI 1.443-10.237). CONCLUSIONS: The Lauren classification and ypTNM stage after neoadjuvant chemotherapy are independent prognostic factors in advanced gastric cancer. A GHR ≥ 50%/< 50% can be used as the primary criterion for advanced gastric cancer after neoadjuvant chemotherapy to determine postoperative adjuvant chemotherapy regimens.


Assuntos
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Terapia Neoadjuvante/métodos , Seleção de Pacientes , Neoplasias Gástricas/terapia , Estômago/patologia , Feminino , Seguimentos , Gastrectomia , Humanos , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Prognóstico , Estudos Retrospectivos , Estômago/cirurgia , Neoplasias Gástricas/mortalidade , Neoplasias Gástricas/patologia , Análise de Sobrevida , Resultado do Tratamento
15.
Methods Mol Biol ; 1901: 103-112, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30539572

RESUMO

Primary Sjögren's syndrome (pSS) is a systemic autoimmune disease marked by dry mouth/dry eye symptoms as a result of the destruction of the salivary and lacrimal glands. Patients with pSS may be at risk for the development of mucosa-associated lymphoid tissue (MALT) lymphoma. Testing of autoantibodies in the oral fluid of patients with pSS or MALT lymphoma using immunoassays may lead to a simple and noninvasive clinical tool for diagnostic or prognostic applications. In this chapter, we describe the procedures and protocols for determining autoantibodies to salivary gland antigens with proteomics-related methods, including 2D gel electrophoresis, liquid chromatography-tandem mass spectrometry (LC-MS/MS), Western blotting, protein microarray, and enzyme-linked immunosorbent assay (ELISA).


Assuntos
Antígenos/imunologia , Autoanticorpos/análise , Glândulas Salivares/imunologia , Eletroforese em Gel Bidimensional , Ensaio de Imunoadsorção Enzimática , Humanos , Análise Serial de Proteínas , Saliva/metabolismo , Proteínas e Peptídeos Salivares/metabolismo
16.
Lipids Health Dis ; 17(1): 271, 2018 Nov 28.
Artigo em Inglês | MEDLINE | ID: mdl-30486837

RESUMO

BACKGROUND: The rabbit is widely used as an important experimental model for biomedical research, and shows low adipose tissue deposition during growth. Long non-coding RNAs (lncRNAs) are associated with adipose growth, but little is known about the function of lncRNAs in the rabbit adipose tissue. METHODS: Deep RNA-sequencing and comprehensive bioinformatics analyses were used to characterize the lncRNAs of rabbit visceral adipose tissue (VAT) at 35, 85 and 120 days after birth. Differentially expressed (DE) lncRNAs were identified at the three growth stages by DESeq. The cis and trans prediction ways predicted the target genes of the DE lncRNAs. To explore the function of lncRNAs, Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed on the candidate genes. RESULTS: A total of 991,157,544 clean reads were generated after RNA-Seq of the three growth stages, of which, 30,353 and 107 differentially expressed (DE) lncRNAs were identified. Compared to the protein-coding transcripts, the rabbit lncRNAs shared some characteristics such as shorter length and fewer exons. Cis and trans target gene prediction revealed, 43 and 64 DE lncRNAs respectively, corresponding to 72 and 20 protein-coding genes. GO enrichment and KEGG pathway analyses revealed that the candidate DE lncRNA target genes were involved in oxidative phosphorylation, glyoxylate and dicarboxylate metabolism, and other adipose growth-related pathways. Six DE lncRNAs were randomly selected and validated by q-PCR. CONCLUSIONS: This study is the first to profile the potentially functional lncRNAs in the adipose tissue growth in rabbits, and contributes to our understanding of mammalian adipogenesis.


Assuntos
Tecido Adiposo/crescimento & desenvolvimento , Desenvolvimento Embrionário/genética , Genoma/genética , RNA Longo não Codificante/genética , Adipogenia/genética , Tecido Adiposo/metabolismo , Animais , Perfilação da Expressão Gênica , Regulação da Expressão Gênica no Desenvolvimento/genética , Sequenciamento de Nucleotídeos em Larga Escala , RNA Mensageiro/genética , Coelhos , Análise de Sequência de RNA
17.
Sci Rep ; 8(1): 14497, 2018 09 27.
Artigo em Inglês | MEDLINE | ID: mdl-30262919

RESUMO

Several members of the EPH kinase family and their ligands are involved in blood pressure regulation, and such regulation is often sex- or sex hormone-dependent, based on animal and human genetic studies. EPHB6 gene knockout (KO) in mice leads to hypertension in castrated males but not in un-manipulated KO males or females. To assess whether this finding in mice is relevant to human hypertension, we conducted a human genetic study for the association of EPHB6 and its two ligands, EFNB1 and EFNB3, with hypertension in hypogonadic patients. Seven hundred and fifty hypertensive and 750 normotensive Han Chinese patients, all of whom were hypogonadic, were genotyped for single nucleotide polymorphisms (SNPs) within the regions of the genes, plus an additional 50 kb 5' of the genes for EPHB6, EFNB1 and EFNB3. An imputed insertion/deletion polymorphism, rs35530071, was found to be associated with hypertension at p-values below the Bonferroni-corrected significance level of 0.0024. This marker is located 5' upstream of the EFNB3 gene start site. Previous animal studies showed that while male EFNB3 gene knockout mice were normotensive, castration of these mice resulted in hypertension, corroborating the results of the human genetic study. Considering the significant associations of EFNB3 SNPs with hypertension in hypogonadic males and supporting evidence from castrated EFNB3 KO mice, we conclude that loss-of-function variants of molecules in the EPHB6 signaling pathway in the presence of testosterone are protective against hypertension in humans.


Assuntos
Efrina-B1/genética , Efrina-B3/genética , Hipertensão/genética , Hipogonadismo/genética , Polimorfismo de Nucleotídeo Único , Receptores da Família Eph/genética , Adulto , Animais , Grupo com Ancestrais do Continente Asiático , China , Humanos , Hipertensão/patologia , Hipertensão/fisiopatologia , Hipogonadismo/patologia , Hipogonadismo/fisiopatologia , Masculino , Camundongos , Camundongos Knockout , Pessoa de Meia-Idade
18.
Cell Physiol Biochem ; 49(5): 1804-1812, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30231244

RESUMO

BACKGROUND/AIMS: Microbes reside in a number of body sites, including the oral cavity, and are associated with the progression of many systemic diseases. In this study, we aimed to investigate the effects of gout and hyperuricemia (HUA) on the composition of oral microbiomes. METHODS: Analysis of the oral microbiota from 12 gout patients, 11 HUA patients, and 19 healthy control subjects was performed using a deep sequencing approach, and validation of significant changes in Prevotella intermedia and Serratia marcescens in new patient cohorts was performed using quantitative PCR (qPCR). RESULTS: Our analysis indicated that both gout and HUA significantly altered the composition of the oral microbiome in patients. Patients with gout or HUA had significantly greater levels of salivary Prevotella intermedia but significantly lower levels of Serratia marcescens than healthy control subjects. CONCLUSION: We demonstrated the association between the oral microbiome and gout and HUA for the first time. In particular, 16S sequencing and qPCR analysis revealed significantly higher levels of oral Prevotella intermedia in gout/HUA patients, which suggests that these patients might be at risk for the development of periodontitis.


Assuntos
Gota/patologia , Microbiota , Boca/microbiologia , Prevotella intermedia/isolamento & purificação , Adulto , Idoso , Estudos de Casos e Controles , Feminino , Gota/microbiologia , Humanos , Hiperuricemia/microbiologia , Hiperuricemia/patologia , Masculino , Pessoa de Meia-Idade , Prevotella intermedia/genética , RNA Ribossômico 16S/química , RNA Ribossômico 16S/genética , RNA Ribossômico 16S/metabolismo , Serratia marcescens/genética , Serratia marcescens/isolamento & purificação
19.
Cell Physiol Biochem ; 47(6): 2498-2510, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29991018

RESUMO

BACKGROUND/AIMS: Interference with endothelial progenitor cell (EPC) neovascularization is a novel therapeutic target for neovascular-related diseases. Angiotensin Ⅱ (Ang Ⅱ) was found to enhance new vessel formation and aggravated neovascular-related diseases. In this study, we investigated the effects of Ang Ⅱ on EPC neovascular-related functions and explored the underlying mechanisms. METHODS: EPCs were cultured from bone marrow derived mononuclear cells. The effects of Ang Ⅱ on EPC proliferation, adhesion, migration, and in vitro tube formation were investigated using the MTT assay, adhesion assay, transwell chamber assay, and in vitro tube formation assay respectively. The underlying mechanisms were explored using Western blotting assay. RESULTS: EPC adhesion, migration and in vitro tube formation were promoted by Ang Ⅱ, and the effects were reversed by RhoA/Rho-associated kinases (ROCK) signaling pathway inhibitors including C3 exoenzyme, GGTI-286 and Y-27632. The active form of RhoA was up-regulated by Ang Ⅱ and this effect was abolished by C3 exoenzyme. Moreover, RhoA silencing resulted in a notable inhibition of EPC adhesion, migration and in vitro tube formation, suggesting that RhoA activation played a pivotal role in Ang Ⅱ angiogenic effect. The results also demonstrated that phosphorylation of p38 mitogen-activated protein kinase (MAPK) and c-Jun-NH2 kinase was elevated by Ang Ⅱ and attenuated by C3 exoenzyme, GGTI-286 and Y-27632. The enhancing effects of Ang Ⅱ on EPC adhesion, migration and in vitro vasculogenesis were reversed by p38 inhibitor SB202190 and JNK inhibitor SP600125. CONCLUSION: Ang Ⅱ may enhance EPC neovascular-related functions through activating RhoA/ ROCK and MAPK signaling pathway.


Assuntos
Angiotensina II/metabolismo , Movimento Celular , Células Progenitoras Endoteliais/metabolismo , Sistema de Sinalização das MAP Quinases , Neovascularização Patológica/metabolismo , Proteínas rho de Ligação ao GTP/metabolismo , Animais , Adesão Celular , Células Progenitoras Endoteliais/patologia , Masculino , Neovascularização Patológica/genética , Neovascularização Patológica/patologia , Ratos , Ratos Sprague-Dawley , Proteínas rho de Ligação ao GTP/genética
20.
Sci Rep ; 8(1): 10726, 2018 Jul 16.
Artigo em Inglês | MEDLINE | ID: mdl-30013094

RESUMO

Androgen plays a pivotal role in the progression of renal fibrosis. However, whether exogenous androgen treatment to aged male rats can improve the age-related renal fibrosis was not explored. In our study, the changes of morphological structure, renal fibrosis, ultrastructure and renal function, the expressions of extracellular matrix (ECM), matrix metalloproteinases (MMPs) and its tissue inhibitors of metalloproteinases (TIMPs), the expressions of tumor growth factor ß1 (TGF-ß1)/Smad signaling and oxidative stress parameters as well as nuclear factor erythroid 2-related factor 2-antioxidant response element (Nrf2-ARE) signaling were tested in kidney of aged male Wistar rats after subcutaneous testosterone propionate (TP, 2 mg/kg/d, 84-day) injection. Aged rats showed significantly renal histopathological changes, increased renal fibrosis, increased thickening of the glomerular basement membrane and the Bowman's capsule basement membrane, declined renal functional, increased ECM, lower expressions of MMP-2 and MMP-9 and higher expressions of TIMP-1 and TIMP-2 in renal tissues and higher expressions of TGF-ß1/Smad signaling, as well as lower expressions of Nrf2-ARE signaling compared to young rats. TP treatment significantly improved age-related above indexes. These results suggested that TP supplement may alleviate age-related renal fibrosis via suppression of TGF-ß1/Smad signaling and activation of Nrf2-ARE signaling in aged rats.


Assuntos
Envelhecimento/fisiologia , Regulação da Expressão Gênica/efeitos dos fármacos , Rim/patologia , Transdução de Sinais/efeitos dos fármacos , Propionato de Testosterona/administração & dosagem , Animais , Elementos de Resposta Antioxidante/genética , Fibrose , Regulação da Expressão Gênica/fisiologia , Rim/efeitos dos fármacos , Rim/ultraestrutura , Masculino , Microscopia Eletrônica de Transmissão , Modelos Animais , Fator 2 Relacionado a NF-E2/metabolismo , Ratos , Ratos Wistar , Transdução de Sinais/fisiologia , Proteínas Smad/metabolismo , Fator de Crescimento Transformador beta1/metabolismo
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