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1.
Front Microbiol ; 12: 719599, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34803940

RESUMO

Increasing evidences suggest that the gut microbiota have their contributions to the hypertension, but the metagenomic characteristics and potential regulating mechanisms in primary hypertension patients taking antihypertension drugs are not clear yet. We carried out a metagenomic analysis in 30 primary hypertension patients taking antihypertension medications and eight healthy adults without any medication. We found that bacterial strains from species, such as Bacteroides fragilis, Bacteroides vulgatus, Escherichia coli, Klebsiella pneumoniae, and Streptococcus vestibularis, were highly increased in patients; and these strains were reported to generate glycan, short-chain fatty acid (SCFA) and trimethylamine (TMA) or be opportunistic pathogens. Meanwhile, Dorea longicatena, Eubacterium hallii, Clostridium leptum, Faecalibacterium prausnitzii, and some other strains were greatly decreased in the patient group. The Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis found that ortholog groups and pathways related to glycan biosynthesis and multidrug resistance were significantly increased in the patient group, and some of the hub genes related to N-glycan biosynthesis were increased in the patient group, while those related to TMA precursor metabolism and amino acid metabolism both increased and decreased in the patient group. Metabolites tested by untargeted liquid chromatography-mass spectrometry (LC-MS) proved the decrease of acetic acid, choline, betaine, and several amino acids in patients' fecal samples. Moreover, meta-analysis of recent studies found that almost all patients were taking at least one kind of drugs that were reported to regulate adenosine monophosphate-activated protein kinase (AMPK) pathway, so we further investigated if AMPK regulated the metagenomic changes by using angiotensin II-induced mouse hypertensive model on wild-type and macrophage-specific AMPK-knockout mice. We found that the changes in E. coli and Dorea and glycan biosynthesis-related orthologs and pathways were similar in our cohort and hypertensive wild-type mice but reversed after AMPK knockout. These results suggest that the gut microbiota-derived glycan, SCFA, TMA, and some other metabolites change in medication-taking primary hypertension patients and that medications might promote gut microbiota glycan biosynthesis through activating macrophage-AMPK.

2.
Int J Psychophysiol ; 170: 112-120, 2021 12.
Artigo em Inglês | MEDLINE | ID: mdl-34699862

RESUMO

Although both originality and value are considered necessary criteria to identify creative ideas, little is known about how original and valuable ideas are generated in the human brain. To reveal how people monitor and control ongoing processing in the pursuit of original and valuable ideas, high-density electroencephalography (EEG) was used to record electrophysiological signals when participants were performing chunk decomposition tasks via novel-appropriate, novel-inappropriate, ordinary-appropriate and ordinary-inappropriate pathways. The results showed that approximately 100 ms after the problem was presented, novel pathways showed increased theta synchronization in the frontal sites compared to ordinary pathways. Novel pathways were associated with increased alpha desynchronization over the entire brain scale. These theta and alpha oscillations likely indicated rapid monitoring and effective control of novel processing in thinking. In the latter stages of problem solving, particularly during the 2000-2600-ms intervals, increased theta synchronization with decreased alpha desynchronization was found between novel-inappropriate and novel-appropriate pathways, which likely indicated slow monitoring and less control of inappropriate processing in novel thinking. The findings demonstrated the dynamic monitoring and control mechanism in the pursuit of original and valuable ideas.

3.
Psych J ; 10(1): 96-111, 2021 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-32985116

RESUMO

Although the innovative designs deliver, superior customer value has long been noted. However, the emotional experience of innovative products brings remains mostly unknown. This work focuses on two kinds of innovative products: function innovation (FI) and design innovation (DI), to uncover the mystery of the emotional experience, these two types of innovative designs bring. Participants in Study 1 were required to subjectively report their practical, emotional experience of the two kinds of innovative designs. The result showed that the emotional experience of innovation products might be a mixture of emotionality. Also, FI and DI products may cause different emotional experiences performance. Multidimensional scaling was employed in Study 2 to simplify the dimensions of these reported emotions to investigate the difference of emotion dimensions distribution that FI and DI brings. The results showed that DI products mainly reflected strong arouse than FI in positive emotions. However, DI product brings more negative emotions than positive emotions. Whereas, FI product did not show the quantitative differences between positive and negative emotions. In Study 3, the difference between FI and DI in emotion intensity was investigated, and the result indicates that both FI and DI products can bring high-intensity positive emotion. However, the DI brings higher intensity negative emotion and lower intensity positive emotion than FI. These studies demonstrate the first direct evidence of the essence of the difference between FI and DI emotion experience and suggest possible guidance for consumers to avoid the effect of the emotions when choosing innovative products.


Assuntos
Criatividade , Emoções , Humanos
4.
Data Brief ; 30: 105538, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32346572

RESUMO

Creativity is critical for human development and social progress. There is a growing interest in studies on the neural mechanism of creativity with functional magnetic resonance imaging (fMRI). However, it is hard to investigate the neural basis of creativity as high-level cognitive processing in the human brain. Based on the two-fundamental feature of novelty and usefulness in creativity [1], [2], [3], [4], [5]. We could reveal the neural mechanism of creativity to investigate how the novelty and usefulness processing during creativity activity. The dataset contains two-part of data. First, online scanning data includes the fMRI scans and T1-weighted anatomical scans acquired under participants comprehend the three type of creative designs. The creative design includes familiar and useful design (FU), novel and useless design (NS), novel and useful design (NU). Participants were asked to comprehend each design throughout the entire 6 s and respond to a usefulness evaluation for every design via pressing the yes or no button. The three types of designs were pseudo-random presented during scanning. Second, post-test data includes the behavioral data of novelty and usefulness evaluation in a 5-scaled test using the same creative design pictures in fMRI scanning by the same group of participants. The dataset is meant to be used to assess the neural basis of novelty and usefulness features processing in creativity; it also allows for empirical investigation of how the neural bases responses to the different novel signal (e.g., usefulness signal and useless signal), the human brain distinguishes the familiar or novel signal. The dataset is a supplement to the research findings in the "The function of the hippocampus and middle temporal gyrus in forming new associations and concepts during the processing of novelty and usefulness features in creative designs" published in NeuroImage [6].

5.
Neuroimage ; 214: 116751, 2020 07 01.
Artigo em Inglês | MEDLINE | ID: mdl-32194284

RESUMO

Creative thought relies on the reorganization of existing knowledge to generate novel and useful concepts. However, how these new concepts are formed, especially through the processing of novelty and usefulness (which are usually regarded as the key properties of creativity), is not clear. Taking familiar and useful (FU) objects/designs as the starting point or fundamental baseline, we modified them into novel and useless (NS) objects/designs or novel and useful (NU) ones (i.e., truly creative ones) to investigate how the features of novelty and usefulness are processed (processing of novelty: NU minus FU; processing of usefulness: NU minus NS). Specifically, we predicted that the creative integration of novelty and usefulness entails not only the formation of new associations, which could be critically mediated by the hippocampus and adjacent medial temporal lobe (MTL) areas, but also the formation of new concepts or categories, which is supported by the middle temporal gyrus (MTG). We found that both the MTL and the MTG were involved in the processing of novelty and usefulness. The MTG showed distinctive patterns of information processing, reflected by strengthened functional connectivity with the hippocampus to construct new concepts and strengthened functional connectivity with the executive control system to break the boundaries of old concepts. Additionally, participants' subjective evaluations of concept distance showed that the distance between the familiar concept (FU) and the successfully constructed concept (NU) was larger than that between the FU and the unsuccessfully constructed concept (NS), and this pattern was found to correspond to the patterns of their neural representations in the MTG. These findings demonstrate the critical mechanism by which new associations and concepts are formed during novelty and usefulness processing in creative design; this mechanism may be critically mediated by the hippocampus-MTG connection.


Assuntos
Criatividade , Hipocampo/fisiologia , Lobo Temporal/fisiologia , Mapeamento Encefálico/métodos , Feminino , Humanos , Masculino , Adulto Jovem
6.
Eur Heart J ; 41(26): 2456-2468, 2020 07 07.
Artigo em Inglês | MEDLINE | ID: mdl-31821481

RESUMO

AIMS: Obesity is a risk factor of abdominal aortic aneurysm (AAA). Inflammatory cytokine interleukin-18 (IL18) has two receptors: IL18 receptor (IL18r) and Na-Cl co-transporter (NCC). In human and mouse AAA lesions, IL18 colocalizes to its receptors at regions rich in adipocytes, suggesting a role of adipocytes in promoting IL18 actions in AAA development. METHODS AND RESULTS: We localized both IL18r and NCC in human and mouse AAA lesions. Murine AAA development required both receptors. In mouse AAA lesions, IL18 binding to these receptors increased at regions enriched in adipocytes or adjacent to perivascular adipose tissue. 3T3-L1 adipocytes enhanced IL18 binding to macrophages, aortic smooth muscle cells (SMCs), and endothelial cells by inducing the expression of both IL18 receptors on these cells. Adipocytes also enhanced IL18r and IL18 expression from T cells and macrophages, AAA-pertinent protease expression from macrophages, and SMC apoptosis. Perivascular implantation of adipose tissue from either diet-induced obese mice or lean mice but not that from leptin-deficient ob/ob mice exacerbated AAA development in recipient mice. Further experiments established an essential role of adipocyte leptin and fatty acid-binding protein 4 (FABP4) in promoting IL18 binding to macrophages and possibly other inflammatory and vascular cells by inducing their expression of IL18, IL18r, and NCC. CONCLUSION: Interleukin-18 uses both IL18r and NCC to promote AAA formation. Lesion adipocyte and perivascular adipose tissue contribute to AAA pathogenesis by releasing leptin and FABP4 that induce IL18, IL18r, and NCC expression and promote IL18 actions.


Assuntos
Adipócitos , Aneurisma da Aorta Abdominal , Interleucina-18 , Animais , Aneurisma da Aorta Abdominal/etiologia , Modelos Animais de Doenças , Células Endoteliais , Camundongos , Camundongos Endogâmicos C57BL , Receptores de Interleucina-18 , Transdução de Sinais
7.
Neural Plast ; 2018: 3479059, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30013595

RESUMO

In contrast to cognitive emotion regulation theories that emphasize top-down control of prefrontal-mediated regulation of emotion, in traditional Chinese philosophy and medicine, different emotions are considered to have mutual promotion and counteraction relationships. Our previous studies have provided behavioral evidence supporting the hypotheses that "fear promotes anger" and "sadness counteracts anger"; this study further investigated the corresponding neural correlates. A basic hypothesis we made is the "internal versus external orientation" assumption proposing that fear could promote anger as its external orientation associated with motivated action, whereas sadness could counteract anger as its internal or homeostatic orientation to somatic or visceral experience. A way to test this assumption is to examine the selective involvement of the posterior insula (PI) and the anterior insula (AI) in sadness and fear because the posterior-to-anterior progression theory of insular function suggests that the role of the PI is to encode primary body feeling and that of the AI is to represent the integrative feeling that incorporates the internal and external input together. The results showed increased activation in the AI, parahippocampal gyrus (PHG), posterior cingulate (PCC), and precuneus during the fear induction phase, and the activation level in these areas could positively predict subsequent aggressive behavior; meanwhile, the PI, superior temporal gyrus (STG), superior frontal gyrus (SFG), and medial prefrontal cortex (mPFC) were more significantly activated during the sadness induction phase, and the activation level in these areas could negatively predict subsequent feelings of subjective anger in a provocation situation. These results revealed a possible cognitive brain mechanism underlying "fear promotes anger" and "sadness counteracts anger." In particular, the finding that the AI and PI selectively participated in fear and sadness emotions was consistent with our "internal versus external orientation" assumption about the different regulatory effects of fear and sadness on anger and aggressive behavior.


Assuntos
Afeto/fisiologia , Ira/fisiologia , Encéfalo/fisiologia , Medo/fisiologia , Medo/psicologia , Pesar , Adulto , Encéfalo/diagnóstico por imagem , China , Emoções/fisiologia , Feminino , Humanos , Imageamento por Ressonância Magnética/métodos , Masculino , Autorrelato , Adulto Jovem
9.
Mol Cell Biochem ; 445(1-2): 67-78, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29243066

RESUMO

Excessive mechanical stretch induces production of proinflammatory mediators in cardiac fibroblasts, which could act as inflammatory supporter cells in heart failure. Accumulation evidence and our previous studies suggest that serum-glucocorticoid-regulated kinase 1 (SGK1) contributes to cardiac remodeling and fibrosis, development of heart failure. However, the role and mechanism of SGK1 in mechanical stretch-induced inflammation of cardiac fibroblasts remain unclear. Here, cardiac fibroblasts isolated from wild-type (WT) and SGK1 knockout (SGK1-/-) mice were stimulated by 18% cyclic stretch, under static condition as the control. The results showed that mechanical stretch increased SGK1 expression and activation in WT cardiac fibroblasts but not its isoform, SGK2 or SGK3 expression. Bio-Plex array revealed hyperstretch could enhance chemokines release in WT cardiac fibroblasts, but SGK1 knockout significantly attenuated chemokines production through blocking activation of nuclear factor-kappa B (NF-κB). Moreover, supernatants from WT cardiac fibroblasts subjected to hyperstretch promoted macrophage migration, enhanced expression of macrophage-derived profibrotic mediators, whereas supernatants from SGK1 deficiency suppressed these effects. Although SGK1 did not directly affect mechanical stretch-induced myofibroblast differentiation, SGK1 activation of cardiac fibroblasts facilitated myofibroblast differentiation through the upregulation of the profibrotic mediators secreted by macrophages. These results suggest that SGK1 may play a critical role in the inflammatory cascade of cardiac fibroblasts triggered by mechanical stretch; SGK1 could be used as a potential target for treatment of cardiac fibrosis and heart failure.


Assuntos
Fibroblastos/citologia , Proteínas Imediatamente Precoces/fisiologia , Inflamação/fisiopatologia , Miocárdio/enzimologia , Estresse Mecânico , Animais , Células Cultivadas , Quimiocinas/biossíntese , Meios de Cultura , Ativação Enzimática , Fibroblastos/enzimologia , Fibrose/patologia , Insuficiência Cardíaca/patologia , Proteínas Imediatamente Precoces/genética , Proteínas Imediatamente Precoces/metabolismo , Mediadores da Inflamação/metabolismo , Macrófagos/citologia , Macrófagos/metabolismo , Masculino , Camundongos , Camundongos Knockout , Miocárdio/citologia , /metabolismo
10.
Biochim Biophys Acta Mol Basis Dis ; 1864(1): 1-10, 2018 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-28986310

RESUMO

Inflammation has emerged as a critical biological process contributing to hypertensive cardiac remodeling. Effective pharmacological treatments targeting the cardiac inflammatory response, however, are still lacking. Prior studies suggested that the serum- and glucocorticoid-inducible kinase (SGK1) plays a key role in inflammation and cardiac remodeling. Recently, a highly selective SGK1 inhibitor, EMD638683, was developed, though whether EMD638683 can prevent hypertension-induced cardiac fibrosis and the mechanisms by which this inhibitor may alter the disease process remain unknown. Using a murine Angiotension II (Ang II) infusion-induced hypertension model we found that EMD638683 treatment inhibited cardiac fibrosis and remodeling, with significant abatement of cardiac inflammation. EMD638683 was shown to suppress Ang II infusion-induced interleukin (IL)-1ß release, and substantially reduce nucleotide-binding oligomerization domain-like receptor with pyrin domain 3 (NLRP3) expression and caspase-1 activation in cardiac tissues. In vitro experiments revealed that EMD638683 ameliorated Ang II-stimulated IL-1ß secretion in macrophages by blocking NLRP3 inflammasome activation. By reducing IL-1ß production in macrophages, the transformation of fibroblasts to myofibroblasts was inhibited. The effects of EMD638683 on cardiac fibrosis were abolished by supplementation with exogenous IL-1ß. Administration of the NLRP3 inflammasome inhibitor MCC950 indicated that EMD638683 attenuated Ang II-induced cardiac inflammation and fibrosis by inhibiting the NLRP3 inflammasome/IL-1ß secretion axis. These findings indicate that the SGK1 inhibitor EMD638683 can negatively regulate NLRP3 inflammasome activation, and may represent a promising approach to the treatment of hypertensive cardiac damage.


Assuntos
Angiotensina II/farmacologia , Benzamidas/farmacologia , Coração/efeitos dos fármacos , Hidrazinas/farmacologia , Inflamassomos/efeitos dos fármacos , Miocardite/prevenção & controle , Miocárdio/patologia , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Animais , Cardiotônicos/farmacologia , Células Cultivadas , Citoproteção/efeitos dos fármacos , Fibrose/prevenção & controle , Inflamassomos/metabolismo , Inflamação/prevenção & controle , Camundongos , Camundongos Endogâmicos C57BL , Miocardite/patologia
11.
Int J Clin Exp Pathol ; 10(9): 9621-9626, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-31966840

RESUMO

Cervical cancer is a kind of female malignant tumor with increasing incidence recently. Macrophage migration inhibitory factor (MIF) is a major tumor facilitating factor. The previous study suggests that there was a correlation between MIF and migration or invasion of tumors. Epithelial mesenchymal transition (EMT) is the basis for tumor invasion and migration. Therefore, this study utilized MFI to treat cervical carcinoma Hela cells, and the mechanism of EMT was also further analyzed. Cervical carcinoma Hela cells were transfected with pFenesil MIF siRNA plasmids, following by real-time fluorescent quantitative PCR to detect MIF levels. MTT assay was then utilized for evaluate the proliferative activity of Hela cells after transfection. The cell invasion and migration were examined. The expression of E-cadherin and Vimentin were also detected. The results indicated that the MIF was positively expressed in Hela cells, whose MIF mRNA level was increased after the transfection (P<0.05). Compared to the control or blank group, the transfected group had elevated proliferative activity with elongated incubation time (P<0.05). Both invasion and migration functions of transfected cells were significantly potentiated (P<0.05) compared to the control or blank group. E-cadherin expression level was also decreased in experimental group. MIF was also expressed in cervical carcinoma Hela cells. Elevated MIF level could facilitate the cell invasion and migration, and elevate the Vimentin and decrease E-cadherin expression, thus facilitating EMT.

12.
Mol Immunol ; 82: 66-74, 2017 02.
Artigo em Inglês | MEDLINE | ID: mdl-28033540

RESUMO

Regulatory T cells (Tregs) are immune suppressive cells, but their roles in tumor growth have been elusive, depending on tumor type or site. Our prior study demonstrated a role of cathepsin S (CatS) in reducing Treg immunosuppressive activity. Therefore, CatS inhibition in Tregs may exacerbate tumor growth. Using mouse bladder carcinoma MB49 cell subcutaneous implant tumor model, we detected no difference in tumor growth, whether mice were given saline- or CatS inhibitor-treated Tregs. However, mice that received inhibitor-treated Tregs had fewer splenic and tumor Tregs, and lower levels of tumor and splenic cell proliferation than mice that received saline-treated Tregs. In vitro, inhibitor-treated Tregs showed lower proliferation and higher apoptosis than saline-treated Tregs when cells were exposed to MB49. In contrast, both types of Tregs showed no difference in proliferation when they were co-cultured with normal splenocytes. Inhibitor-treated Tregs had less apoptosis in splenocytes, but more apoptosis in splenocytes with MB49 conditioned media than saline-treated Tregs. In turn, we detected less proliferation and more apoptosis of MB94 cells after co-culture with inhibitor-treated Tregs, compared with saline-treated Tregs. B220+ B-cell, CD4+ T-cell, and CD8+ T-cell proliferation and apoptosis were also lower in splenocytes co-cultured with inhibitor-treated Tregs than with saline-treated Tregs. Under the same conditions, the addition of cancer cell-conditioned media greatly increased CD8+ T-cell proliferation and reduced CD8+ T-cell apoptosis. These observations suggest that CatS inhibition of Tregs may reduce overall T-cell immunity under normal conditions, but enhance CD8+ T-cell immunity in the presence of cancer cells.


Assuntos
Carcinoma de Células de Transição/imunologia , Catepsinas/antagonistas & inibidores , Linfócitos T Reguladores/imunologia , Neoplasias da Bexiga Urinária/imunologia , Transferência Adotiva , Animais , Apoptose/imunologia , Carcinoma de Células de Transição/patologia , Proliferação de Células/efeitos dos fármacos , Técnicas de Cocultura , Cisteína Proteases/farmacologia , Modelos Animais de Doenças , Citometria de Fluxo , Tolerância Imunológica/imunologia , Imuno-Histoquímica , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Linfócitos T Reguladores/transplante , Neoplasias da Bexiga Urinária/patologia
13.
Oncotarget ; 7(10): 11553-66, 2016 Mar 08.
Artigo em Inglês | MEDLINE | ID: mdl-26872375

RESUMO

Laryngeal squamous cell carcinoma (LSCC) is a highly aggressive malignant cancer. The regulation of LSCC progression by long non-coding RNA (lncRNA) was not well understood. In this study, we reported that the lncRNA H19 was upregulated in LSCC. The expression levels of H19 were inversely correlated with the survival rate of LSCC patients. Knockdown of H19 expression inhibited LSCC cell migration, invasion and proliferation. We identified microRNA miR-148a-3p as an inhibitory target for H19. Overexpression of miR-148a-3p reduced LSCC migration, invasion and proliferation cell, while inhibition of miR-148a-3p did the opposite. The inhibition of LSCC progression induced by H19 knockdown required the activity of miR-148a-3p. We also identified DNA methyltransferase enzyme DNMT1 as a target of miR-148a-3p. Cellular DNA methylation levels were inhibited by both miR-148a-3p overexpression and H19 knockdown. In summary, our study demonstrated that the lncRNA H19 promoted LSCC progression via miR-148a-3p and DNMT1.


Assuntos
Carcinoma de Células Escamosas/metabolismo , DNA (Citosina-5-)-Metiltransferase 1/metabolismo , Neoplasias de Cabeça e Pescoço/metabolismo , Neoplasias Laríngeas/metabolismo , MicroRNAs/metabolismo , RNA Longo não Codificante/metabolismo , Animais , Sequência de Bases , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/patologia , Linhagem Celular Tumoral , Movimento Celular/fisiologia , Proliferação de Células/fisiologia , DNA (Citosina-5-)-Metiltransferase 1/genética , Metilação de DNA , Progressão da Doença , Feminino , Células HEK293 , Neoplasias de Cabeça e Pescoço/genética , Neoplasias de Cabeça e Pescoço/patologia , Humanos , Neoplasias Laríngeas/genética , Neoplasias Laríngeas/patologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , MicroRNAs/genética , Pessoa de Meia-Idade , RNA Longo não Codificante/genética , Carcinoma de Células Escamosas de Cabeça e Pescoço , Análise de Sobrevida , Transfecção , Regulação para Cima
14.
Arterioscler Thromb Vasc Biol ; 36(1): 69-77, 2016 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-26543094

RESUMO

OBJECTIVE: Asthma and abdominal aortic aneurysms (AAA) both involve inflammation. Patients with asthma have an increased risk of developing AAA or experiencing aortic rupture. This study tests the development of one disease on the progression of the other. APPROACH AND RESULTS: Ovalbumin sensitization and challenge in mice led to the development of allergic lung inflammation (ALI). Subcutaneous infusion of angiotensin II into mice produced AAA. Simultaneous production of ALI in AAA mice doubled abdominal aortic diameter and increased macrophage and mast cell content, arterial media smooth muscle cell loss, cell proliferation, and angiogenesis in AAA lesions. ALI also increased plasma IgE, reduced plasma interleukin-5, and increased bronchioalveolar total inflammatory cell and eosinophil accumulation. Intraperitoneal administration of an anti-IgE antibody suppressed AAA lesion formation and reduced lesion inflammation, plasma IgE, and bronchioalveolar inflammation. Pre-establishment of ALI also increased AAA lesion size, lesion accumulation of macrophages and mast cells, media smooth muscle cell loss, and plasma IgE, reduced plasma interleukin-5, interleukin-13, and transforming growth factor-ß, and increased bronchioalveolar inflammation. Consequent production of ALI also doubled lesion size of pre-established AAA and increased lesion mast cell and T-cell accumulation, media smooth muscle cell loss, lesion cell proliferation and apoptosis, plasma IgE, and bronchioalveolar inflammation. In periaortic CaCl2 injury-induced AAA in mice, production of ALI also increased AAA formation, lesion inflammation, plasma IgE, and bronchioalveolar inflammatory cell accumulation. CONCLUSIONS: This study suggests a pathological link between airway allergic disease and AAA. Production of one disease aggravates the progression of the other.


Assuntos
Angiotensina II , Aorta Abdominal/patologia , Aneurisma da Aorta Abdominal/induzido quimicamente , Pneumonia/complicações , Hipersensibilidade Respiratória/complicações , Animais , Antialérgicos/farmacologia , Anticorpos Monoclonais/farmacologia , Aorta Abdominal/efeitos dos fármacos , Aorta Abdominal/imunologia , Aorta Abdominal/metabolismo , Aneurisma da Aorta Abdominal/imunologia , Aneurisma da Aorta Abdominal/metabolismo , Aneurisma da Aorta Abdominal/patologia , Aneurisma da Aorta Abdominal/prevenção & controle , Apolipoproteínas E/deficiência , Apolipoproteínas E/genética , Cloreto de Cálcio , Dilatação Patológica , Modelos Animais de Doenças , Progressão da Doença , Imunoglobulina E/sangue , Imunoglobulina E/imunologia , Mediadores da Inflamação/imunologia , Mediadores da Inflamação/metabolismo , Pulmão/imunologia , Pulmão/metabolismo , Macrófagos/imunologia , Macrófagos/metabolismo , Masculino , Mastócitos/imunologia , Mastócitos/metabolismo , Camundongos Endogâmicos C57BL , Camundongos Knockout , Ovalbumina , Pneumonia/induzido quimicamente , Pneumonia/imunologia , Pneumonia/metabolismo , Pneumonia/prevenção & controle , Hipersensibilidade Respiratória/induzido quimicamente , Hipersensibilidade Respiratória/imunologia , Hipersensibilidade Respiratória/metabolismo , Hipersensibilidade Respiratória/prevenção & controle , Fatores de Risco , Transdução de Sinais , Remodelação Vascular
16.
Artigo em Chinês | MEDLINE | ID: mdl-26930919

RESUMO

A case of a papillary thyroid carcinoma in a patient with situs inversus with associated bronchiectasis and chronic sinusitis (Kartagener's syndrome) is reported. A 61-year-old male patient has the symptoms of nasal obstruction. nasal purulent discharge and headache for 2 years. Physical examination: right nasal purulent in right nasal cavity and multiple lychee-like opaque mass in right middle meatus. A nodule, one centimeter in diameter, locates in the upper pole of right thyroid. Evidence of full situs inversus viscerum can be confirmmed by chest radiographs and ultrasound doppler. Pathology: right nasal polyps, the right small papillary thyroid cancer. TEM Tip primary ciliary dyskinesia. Clinical diagnosis: Kartagener syndrome, papillary thyroid carcinoma (T1a N0 M0, I period), chronic sinusitis-nasal polyps.


Assuntos
Carcinoma/complicações , Carcinoma/diagnóstico , Síndrome de Kartagener/complicações , Síndrome de Kartagener/diagnóstico , Neoplasias da Glândula Tireoide/complicações , Neoplasias da Glândula Tireoide/diagnóstico , Carcinoma Papilar , Doença Crônica , Humanos , Masculino , Pessoa de Meia-Idade , Obstrução Nasal/patologia , Pólipos Nasais/patologia , Radiografia Torácica , Rinite/patologia , Sinusite/patologia , Situs Inversus/patologia , Câncer Papilífero da Tireoide
17.
Am J Pathol ; 182(1): 64-70, 2013 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-23141928

RESUMO

Homeobox (HOX) transcript antisense RNA (HOTAIR) is a long intergenic noncoding RNA (lincRNA) that is significantly overexpressed in breast and hepatocellular cancers. It remains unclear, however, whether HOTAIR plays an oncogenic role in human laryngeal squamous cell cancer (LSCC). We therefore investigated the expression and functional role of HOTAIR in LSCC. HOTAIR levels were significantly higher in LSCC than in corresponding adjacent non-neoplastic tissues, and patients with poor histological grade or advanced clinical stage had higher HOTAIR expression. Log-rank test showed a significant association between high levels of HOTAIR and poor prognosis in LSCC patients. Multivariate Cox analysis suggested that HOTAIR is an independent prognostic factor of LSCC. siRNA-mediated knockdown of HOTAIR led to reduced invasion and increased apoptosis of Hep-2 cells in vitro and significantly reduced growth of LSCC xenograft tumors in mice. Moreover, PTEN methylation was significantly reduced in Hep-2 cells depleted of HOTAIR. Taken together, these results suggest that the oncogenic role of HOTAIR in LSCC is related to promotion of PTEN methylation. HOTAIR could serve as a marker for LSCC prognosis and a potential target for therapeutic intervention.


Assuntos
Carcinoma de Células Escamosas/genética , Neoplasias Laríngeas/genética , PTEN Fosfo-Hidrolase/genética , RNA Longo não Codificante/biossíntese , Animais , Apoptose/genética , Biomarcadores Tumorais/biossíntese , Biomarcadores Tumorais/genética , Carcinoma de Células Escamosas/metabolismo , Carcinoma de Células Escamosas/patologia , Metilação de DNA/genética , DNA de Neoplasias/genética , Feminino , Regulação Neoplásica da Expressão Gênica/genética , Técnicas de Silenciamento de Genes , Genes Neoplásicos , Humanos , Neoplasias Laríngeas/metabolismo , Neoplasias Laríngeas/patologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Pessoa de Meia-Idade , Invasividade Neoplásica , Transplante de Neoplasias , PTEN Fosfo-Hidrolase/metabolismo , Prognóstico , RNA Longo não Codificante/genética , RNA Neoplásico/genética , Transplante Heterólogo , Células Tumorais Cultivadas
19.
Am J Hypertens ; 24(6): 701-7, 2011 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-21436792

RESUMO

BACKGROUND: Angiotensin II (Ang II)-induced cardiac remodeling with the underlying mechanisms involving inflammation and fibrosis has been well documented. Cytosolic adaptor caspase recruitment domain 9 (CARD9) has been implicated in the innate immune response. We aimed to examine the role of CARD9 in inflammation and cardiac fibrosis induced by Ang II. METHODS: Two-month-old CARD9-deficient (CARD9(-/-)) and wild-type (WT) male mice were infused with Ang II (1,500 ng/kg/min) or saline for 7 days. Heart sections were stained with hematoxylin and eosin and Masson trichrome and examined by immunohistochemistry; and activity and protein levels were measured in macrophages obtained from mice. RESULTS: WT mice with Ang II infusion showed a marked increase in CARD9(+) macrophages in the heart, but CARD9(-/-) mice showed significantly suppressed macrophage infiltration and expression of proinflammatory cytokines, including interleukin-1ß (IL-1ß) and connective tissue growth factor (CTGF). Importantly, Ang II-induced cardiac fibrosis (extracellular matrix and collagen I deposition) was diminished in CARD9(-/-) hearts, as was the expression of transforming growth factor-ß (TGF-ß) and level of myofibroblasts positive for α-smooth muscle actin (α-SMA). Furthermore, Ang II activation of nuclear factor-κB (NF-κB), JNK and p38 mitogen-activated protein kinases (MAPKs) in WT macrophages was reduced in CARD9(-/-) macrophages. CONCLUSION: CARD9 plays an important role in regulating cardiac inflammation and fibrosis in response to elevated Ang II.


Assuntos
Proteínas Adaptadoras de Sinalização CARD/fisiologia , Miocárdio/patologia , Angiotensina II/efeitos adversos , Animais , Proteínas Adaptadoras de Sinalização CARD/deficiência , Fibrose , Inflamação/fisiopatologia , Interleucina-1beta/metabolismo , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases/fisiologia , Macrófagos/fisiologia , Masculino , Camundongos , Camundongos Knockout , Miofibroblastos/fisiologia , NF-kappa B/metabolismo , Fator de Crescimento Transformador beta/biossíntese
20.
Eur J Cancer ; 46(18): 3409-16, 2010 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-20801640

RESUMO

MiRNAs are small, noncoding RNA molecules that emerge as important regulators of cancer-related processes. The miR-21 microRNA is overexpressed in a wide variety of cancers and has been causally related to cellular proliferation and apoptosis. In this study, we found that miR-21 is overexpressed in Laryngeal squamous cell carcinoma (LSCC) and correlated with advanced stage. Inhibition of miR-21 by antisense oligonucleotides (ASO) led to decreased protein level of Ras and profound suppression of cell proliferation and invasion. Hep-2 cells exposed to miR-21 ASO exhibited cell cycle arrest at G1 phase and increased apoptosis. Furthermore, growth of LSCC xenograft tumours was significantly suppressed by repeated injection of ASO-miR-21 lentivirus and the Ras protein expression in LSCC xenograft tumours was also downregulate by ASO-miR-21. Taken together, our data suggest that miR-21 may play an oncogenic role in the cellular processes of LSCC and represent a novel target for effective therapies.


Assuntos
Apoptose/fisiologia , Carcinoma de Células Escamosas/metabolismo , Neoplasias Laríngeas/metabolismo , MicroRNAs/metabolismo , Proteínas de Neoplasias/metabolismo , Proteínas Proto-Oncogênicas p21(ras)/metabolismo , Animais , Carcinoma de Células Escamosas/patologia , Regulação para Baixo , Feminino , Humanos , Neoplasias Laríngeas/patologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Pessoa de Meia-Idade , Invasividade Neoplásica/fisiopatologia , Células Tumorais Cultivadas
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