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1.
Front Immunol ; 12: 612139, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33679751

RESUMO

Background: Numerous cancer types present the aberrant TANK-binding kinase 1 (TBK1) expression, which plays an important role in driving inflammation and innate immunity. However, the prognostic role of TBK1 and its relationship with immune cell infiltration in hepatocellular carcinoma (HCC) remain unclear. Methods: The expression and prognostic value of TBK1 was analyzed by Tumor Immune Estimation Resource (TIMER), Kaplan-Meier plotter and Gene Expression Profiling Interactive Analysis (GEPIA), Clinical Proteomic Tumor Analysis Consortium (CPTAC) and further confirmed in the present cohort of patients with HCC. The association between TBK1 and HCC immune infiltrates, and its potential mechanism were investigated via analyses of the Tumor Immune Estimation Resource, tumor-immune system interactions database (TISIDB), CIBERSORT, STRING, and Metascape. The effect of TBK1 on immune infiltrates and the therapeutic value of targeting TBK1 were further investigated in a HCC mouse model by treatment with a TBK1 antagonist. Results: The level of TBK1 expression in HCC was higher than that measured in normal tissues, and associated with poorer overall survival (GEPIA: hazard ratio [HR]=1.80, P=0.038; Kaplan-Meier plotter: HR=1.87, P<0.001; CPTAC: HR=2.23, P=0.007; Our cohort: HR=2.92, P=0.002). In addition, high TBK1 expression was found in HCC with advanced TNM stage and identified as an independent poor prognostic factor for overall survival among patients with HCC. In terms of immune infiltration, tumor tissues from HCC patients with high TBK1 expression had a low proportion of CD8+ T cells, and TBK1 expression did not show prognostic value in HCC patients with enriched CD8+ T cells. Furthermore, TBK1 expression was positively correlated with the markers of T cell exhaustion and immunosuppressive cells in the HCC microenvironment. Mechanistically, the promotion of HCC immunosuppression by TBK1 was involved in the regulation of inflammatory cytokines. In vivo experiments revealed that treatment with a TBK1 antagonist delayed HCC growth by increasing the number of tumor-infiltrating CD8+ T cells. Conclusions: The up-regulated expression of TBK1 may be useful in predicting poor prognosis of patients with HCC. In addition, TBK1, which promotes the HCC immunosuppressive microenvironment, may be a potential immunotherapeutic target for patients with HCC.

2.
Hepatology ; 2021 Feb 20.
Artigo em Inglês | MEDLINE | ID: mdl-33609283

RESUMO

Myofibroblasts play a pivotal role in the development and progression of hepatocellular carcinoma (HCC). Here, we aimed to explore the role and mechanism of myofibroblast Musashi RNA binding protein 2 (MSI2) in HCC progression. Myofibroblast infiltration and collagen deposition were detected and assessed in the tissues from 117 HCC patients. Transgenic mice (Msi2ΔCol1a1 ) with floxed Msi2 allele and Col1a1-CreER were constructed to generate a myofibroblast-specific Msi2 knockout model. Mouse HCC cells were orthotopically transplanted into the Msi2ΔCol1a1 or the control mice (Msi2F/F ). We found that the deposition of collagen fibers, the main product of myofibroblasts, predicted a poor prognosis for HCC; meanwhile, we detected high MSI2 expression in the peritumoral infiltrated myofibroblasts. Conditional deletion of Msi2 in myofibroblasts significantly inhibited the growth of orthotopically implanted HCC, reduced both intrahepatic and lung metastasis, and prolonged the overall survival of tumor-bearing mice (P = 0.002). In vitro analysis demonstrated that myofibroblasts promoted cell proliferation, invasion, and epithelial-mesenchymal transformation of HCC cells, whereas Msi2 deletion in myofibroblasts reversed these effects. Mechanically, Msi2 knockout decreased myofibroblast-derived IL6 and IL11 secretion by inhibiting the ERK1/2 pathway, and thus attenuated the cancer stem cell promoting effect of myofibroblasts. Interestingly, we found that the simultaneous knockout of Msi2 in myofibroblasts and knockdown of Msi2 in HCC cells could not further attenuate the implanted HCC progression. CONCLUSION: Myofibroblast-specific Msi2 knockout abrogated the tumor-promoting function of myofibroblasts and inhibited HCC progression in mouse models. Targeting myofibroblast MSI2 expression may thus prove to be a therapeutic strategy for HCC treatment in the future.

3.
J Bioenerg Biomembr ; 53(2): 129-137, 2021 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-33481135

RESUMO

Sepsis is a life-threatening disease, which can cause the dysfunction of multiple organs, including kidney. Recently, a number of studies found that the long non-coding RNA (lncRNA) is closely associated with the development and progression of sepsis; however, the role of long intergenic non-protein coding RNA 261 (LINC00261) in sepsis-induced acute kidney injury is poorly understood. In this study, we found the expression of LINC00261 was significantly decreased in the serum of patients with sepsis than healthy controls. A similar result was also observed in the mouse model of sepsis induced by lipopolysaccharide (LPS). Further investigations revealed that overexpression of LINC00261 improved the viability, suppressed the apoptosis and reduced the generation of inflammatory cytokines in LPS-treated HK-2 cells. Mechanistically, we confirmed that LINC00261 could function as a sponge to combine with microRNA-654-5p (miR-654-5p) which inhibits nuclear factor-κB (NF-κB) activity by targeting suppressor of cytokine signaling 3 (SOCS3). In conclusion, our results demonstrate that LINC00261 may regulate the progression of sepsis-induced acute kidney injury via the miR-654-5p/SOCS3/NF-κB pathway and therefore provides a new insight into the treatment of this disease.

4.
J Cell Mol Med ; 25(3): 1568-1582, 2021 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-33410581

RESUMO

The pro-inflammatory and pro-fibrotic liver microenvironment facilitates hepatocarcinogenesis. However, the effects and mechanisms by which the hepatic fibroinflammatory microenvironment modulates intrahepatic hepatocellular carcinoma (HCC) progression and its response to systematic therapy remain largely unexplored. We established a syngeneic orthotopic HCC mouse model with a series of persistent liver injury induced by CCl4 gavage, which mimic the dynamic effect of hepatic pathology microenvironment on intrahepatic HCC growth and metastasis. Non-invasive bioluminescence imaging was applied to follow tumour progression over time. The effect of the liver microenvironment modulated by hepatic injury on sorafenib resistance was investigated in vivo and in vitro. We found that the persistent liver injury facilitated HCC growth and metastasis, which was positively correlated with the degree of liver inflammation rather than the extent of liver fibrosis. The inflammatory cytokines in liver tissue were clearly increased after liver injury. The two indicated cytokines, tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6), both promoted intrahepatic HCC progression via STAT3 activation. In addition, the hepatic inflammatory microenvironment contributed to sorafenib resistance through the anti-apoptotic protein mediated by STAT3, and STAT3 inhibitor S3I-201 significantly improved sorafenib efficacy impaired by liver inflammation. Clinically, the increased inflammation of liver tissues was accompanied with the up-regulated STAT3 activation in HCC. Above all, we concluded that the hepatic inflammatory microenvironment promotes intrahepatic HCC growth, metastasis and sorafenib resistance through activation of STAT3.

5.
PLoS One ; 16(1): e0245459, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33465119

RESUMO

BACKGROUND: Although previously published meta-analyses have compared the surgical effects between the methods of Idiopathic epiretinal membrane (iERM) removal with or without ILM peeling, they did not reach an agreement. PURPOSE: We aimed to provide more evidence for the treatment of iERM and whether additional ILM peeling was better or not by analyzing more updated studies and randomized control trials (RCTs). METHOD: The search was conducted in Pubmed, Embase, Cochrane Library, Web of Science and Open Grey without language limitation and the studies included were from inception to December 2019. All studies of iERM with or without ILM peeling showed at least one of outcomes, such as best-corrected visual acuity (BCVA), central macular thickness (CMT) and recurrence of ERM. The pooled results between above groups were showed by the mean differences (MDs) and risk ratios (RR) with corresponding 95% confidence intervals (CIs). RESULT: In total, 1645 eyes of five randomized controlled trials (RCTs) and fifteen retrospective studies were included. The short-term (<12 months) BCVA improvement in both groups showed no significant difference (MD = -0.01; 95% CI = -0.02 to 0.01; P = 0.36). However, the BCVA improvement was significantly better in ILM peeling eyes than in those without ILM peeling when considering the risk bias (MD = -0.04; 95% CI = -0.07 to -0.01; P = 0.008). The short-term (<12 months) CMT had a higher reduction in non ILM peeling group (MD = -9.02; 95% CI = -12.51 to -5.54; P < 0.00001) and the recurrence of ERM in ILM peeling group was lower (P < 0.00001). The long-term (≥12months) BCVA improvement ((MD = -0.00; 95% CI = -0.03 to 0.03; P = 0.97) and reduction of long-term (≥12months) CMT (MD = -1.14; 95% CI = -7.14 to -4.86; P = 0.71) were similar in both groups. CONCLUSION: By considering the risk of bias, we should determine whether ILM peeling is beneficial for short-term changes in BCVA in patients with iERM. Nevertheless, further studies are needed to confirm this. iERM removal without ILM peeling can improve the short-term decrease in CMT and ILM peeling decreases the recurrence of ERM, but the long-term changes in BCVA and CMT are similar with or without ILM peeling. There is a need for a true large scale randomized trial that will also include microperimetry and other functional measures.

6.
Behav Brain Res ; 402: 113087, 2021 Mar 26.
Artigo em Inglês | MEDLINE | ID: mdl-33412228

RESUMO

Brain-derived neurotrophic factor (BDNF) is a biomarker of depression. Recent studies have found adenosine deaminase acting on RNA1 (ADAR1) is a novel target being sensitive to stress at epigenetic level. The epigenetic regulation mechanism of stress-related depression is still unclear so far. To explore the potential regulating mechanism of ADAR1 on BDNF, over and low expression of ADAR1 in PC12 and SH-SY5Y cell lines are prepared. In the meanwhile, chronic unpredictable stress (CUS) mice are treated with ADAR1 inducer (interferon-γ, IFN-γ). ADAR1 regulates BDNF expression, which is proven by that over and low expressions of ADAR1 increase and decrease BDNF mRNA and protein respectively in vitro. Additionally, ADAR1 inducer alleviates the depressive-like behavior of CUS mice by recovering the decreased BDNF protein in brain and serum. Moreover, over and low expressions of ADAR1 reduce and enhance microRNA-432 (miR-432) expression respectively in vitro. Furtherly, over and low miR-432 expressions lead to decreased and increased BDNF and ADAR1 mRNA, protein and immunoreactivity respectively in vitro. The above results demonstrate that ADAR1 is involved in antidepressant action by regulating BDNF via miR-432. Those novel findings can provide a new idea for the study of epigenetic regulation mechanism, early diagnosis, and effective treatment of stress-related depression.

7.
Plast Reconstr Surg ; 147(1): 69-75, 2021 01 01.
Artigo em Inglês | MEDLINE | ID: mdl-33370052

RESUMO

BACKGROUND: Worldwide application of hyaluronic acid has brought about severe complications, including central retinal arterial occlusion, which leads to a deleterious effect on vision. The current study explored the efficacy of superselective arterial hyaluronidase thrombolysis in rabbit retinal artery occlusion induced by hyaluronic acid. METHODS: Occlusion of the internal/external ophthalmic artery in New Zealand White rabbits was induced with superselective injection of hyaluronic acid. Superselective subtraction angiography and fundus examination were conducted to confirm and evaluate the artery embolism. After 30 minutes of embolism, hyaluronidase was injected in the occluded artery through superselective arterial intubation. RESULTS: Compared with preoperative and contralateral eyes, the postoperative eyes showed the symptoms of central retinal arterial occlusion and embolization, confirmed by digital subtraction angiography. After intraarterial hyaluronidase thrombolysis, the embolization failed to dissolve as shown on funduscopic and angiographic examinations. CONCLUSIONS: Superselective ophthalmic artery intervention could accurately and successfully establish the animal models of retinal artery occlusion induced by hyaluronic acid. The precise occlusion site of the retinal artery and complete embolism were confirmed by ophthalmologic examinations. Intraarterial hyaluronidase thrombolysis might not be an effective method to treat retinal artery occlusion induced by hyaluronic acid.


Assuntos
Técnicas Cosméticas/efeitos adversos , Preenchedores Dérmicos/efeitos adversos , Hialuronoglucosaminidase/administração & dosagem , Oclusão da Artéria Retiniana/tratamento farmacológico , Terapia Trombolítica/métodos , Angiografia Digital , Animais , Preenchedores Dérmicos/administração & dosagem , Modelos Animais de Doenças , Humanos , Ácido Hialurônico/administração & dosagem , Ácido Hialurônico/efeitos adversos , Injeções Intra-Arteriais , Injeções Subcutâneas/efeitos adversos , Artéria Oftálmica/diagnóstico por imagem , Artéria Oftálmica/efeitos dos fármacos , Coelhos , Oclusão da Artéria Retiniana/induzido quimicamente , Oclusão da Artéria Retiniana/diagnóstico , Terapia Trombolítica/efeitos adversos , Resultado do Tratamento , Ativador de Plasminogênio Tipo Uroquinase
8.
Eur J Ophthalmol ; : 1120672120970401, 2020 Nov 11.
Artigo em Inglês | MEDLINE | ID: mdl-33176497

RESUMO

Diabetic retinopathy (DR), which is known as a severe complication of type 2 diabetes mellitus, can cause varying degrees of damage to visual acuity. The pathogenesis of DR is multifactorial and not fully understood. Many previous research studies have revealed that an aberrant level of some long non-coding RNAs (lncRNAs) may accelerate the development of DR. These lncRNAs are regulatory factors and research related to them is always underway. In this review, we will update several types of lncRNAs based on the previous studies which are related to the development of DR and discuss its potential mechanisms of action and connections. Generally, the review will help us know more about lncRNAs and provide directions for future research related to DR.

9.
Cell Death Dis ; 11(10): 830, 2020 Oct 06.
Artigo em Inglês | MEDLINE | ID: mdl-33024090

RESUMO

Elongation factor Tu GTP binding domain containing 2 (EFTUD2), a spliceosomal GTPase, plays a pivotal role in multiple organ development and innate immune. It has been reported that EFTUD2 is a new host factor with activity against HCV infection. However, the role of EFTUD2 in solid tumors, including hepatocellular carcinoma (HCC), remains unexplored. In this study, we investigated the molecular function of EFTUD2 in HCC. Data from The Cancer Genome Atlas (TCGA) indicated an upregulation of EFTUD2 in HCC tissues compared to that in nontumor liver tissues. Immunohistochemical analysis performed on two independent HCC cohorts confirmed the upregulation of EFTUD2 in HCC tissues and further suggested that a high level of EFTUD2 expression predicted shorter overall and recurrence-free survival in HCC patients. Functional studies suggested that siRNA interference with EFTUD2 expression significantly suppressed cell viability, blocked cell cycle progression, facilitated tumor cell apoptosis, and inhibited metastasis, while the enhancement of EFTUD2 expression promoted the proliferation and migration of HCC cells both in vitro and in vivo. Surprisingly, we also found that the stable knockdown of EFTUD2 expression via lentivirus infection was lethal for HCC cells. This finding suggested that EFTUD2 was essential for maintaining the survival of HCC cells. Mechanistically, RNA sequencing and gene set enrichment analysis (GSEA) suggested that the gene sets of epithelial-mesenchymal transition (EMT) and the JAK/STAT3 pathway were enriched in EFTUD2-overexpressing cells. Further verification indicated that EFTUD2-overexpressing cells exhibited an EMT-like phenotype and had enhanced STAT3 activation, while the STAT3 inhibitor S3I-201 partially blocked these pro-malignant effects of EFTUD2 overexpression. In summary, we report EFTUD2 as a novel oncogene that helps to maintain the survival of HCC cells and promotes HCC progression through the activation of STAT3. The high level of expression of EFTUD2 in HCC tissues indicates shorter overall and recurrence-free survival in HCC patients.

10.
Int J Mol Sci ; 21(20)2020 Oct 19.
Artigo em Inglês | MEDLINE | ID: mdl-33086620

RESUMO

Perinatal stem cells have been regarded as an attractive and available cell source for medical research and clinical trials in recent years. Multiple stem cell types have been identified in the human placenta. Recent advances in knowledge on placental stem cells have revealed that human amniotic epithelial stem cells (hAESCs) have obvious advantages and can be used as a novel potential cell source for cellular therapy and clinical application. hAESCs are known to possess stem-cell-like plasticity, immune-privilege, and paracrine properties. In addition, non-tumorigenicity and a lack of ethical concerns are two major advantages compared with embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs). All of the characteristics mentioned above and other additional advantages, including easy accessibility and a non-invasive application procedure, make hAESCs a potential ideal cell type for use in both research and regenerative medicine in the near future. This review article summarizes current knowledge on the characteristics, therapeutic potential, clinical advances and future challenges of hAESCs in detail.

11.
Front Pediatr ; 8: 543, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33014937

RESUMO

Mutations that affect the STING1 (TMEM173) gene cause a rare autoinflammatory syndrome, which is known as STING-associated vasculopathy with onset in infancy (SAVI) and which was initially described in 2014 (1). Thus far, only four reports have been conducted regarding families affected with SAVI in the literature. In this article, the clinical, laboratory, and genetic characteristics of two generations (three cases) of SAVI are described. Unlike previously reported cases that were caused by STING1 mutation, the initial and major clinical manifestations of the mentioned cases are largely identified in the lungs with interstitial lung disease (ILD), and the evidence of typical extrapulmonary symptoms of early-onset systemic inflammation (e.g., cutaneous vasculopathy) were minimal except for the proband, who was diagnosed with arthritis 8 years after onset. In addition, a younger sibling showed no symptoms. Such reports are rarely related to mutations in STING1. The proband was examined with bronchoscopy and alveolar lavage to determine the cause. This study emphasizes that, in the clinical assessment of interstitial pneumonia in children, the possibility of STING1 mutation should be considered, especially in patients with arthritis in addition.

12.
Am J Pathol ; 190(11): 2267-2281, 2020 11.
Artigo em Inglês | MEDLINE | ID: mdl-32805235

RESUMO

Liver fibrosis is an increasing health problem worldwide, for which no effective antifibrosis drugs are available. Although the involvement of aerobic glycolysis in hepatic stellate cell (HSC) activation has been reported, the role of pyruvate kinase M2 (PKM2) in liver fibrogenesis still remains unknown. We examined PKM2 expression and location in liver tissues and primary hepatic cells. The in vitro and in vivo effects of a PKM2 antagonist (shikonin) and its allosteric agent (TEPP-46) on liver fibrosis were investigated in HSCs and liver fibrosis mouse model. Chromatin immunoprecipitation sequencing and immunoprecipitation were performed to identify the relevant molecular mechanisms. PKM2 expression was significantly up-regulated in both mouse and human fibrotic livers compared with normal livers, and mainly detected in activated, rather than quiescent, HSCs. PKM2 knockdown markedly inhibited the activation and proliferation of HSCs in vitro. Interestingly, the PKM2 dimer, rather than the tetramer, induced HSC activation. PKM2 tetramerization induced by TEPP-46 effectively inhibited HSC activation, reduced aerobic glycolysis, and decreased MYC and CCND1 expression via regulating histone H3K9 acetylation in activated HSCs. TEPP-46 and shikonin dramatically attenuated liver fibrosis in vivo. Our findings demonstrate a nonmetabolic role of PKM2 in liver fibrosis. PKM2 tetramerization or suppression could prevent HSC activation and protects against liver fibrosis.


Assuntos
Células Estreladas do Fígado/enzimologia , Cirrose Hepática/enzimologia , Multimerização Proteica , Piruvato Quinase/metabolismo , Acetilação , Animais , Ciclina D1/metabolismo , Feminino , Células Estreladas do Fígado/patologia , Histonas/metabolismo , Humanos , Cirrose Hepática/patologia , Masculino , Camundongos , Compostos Orgânicos/farmacologia , Proteínas Proto-Oncogênicas c-myc/metabolismo
13.
J Environ Manage ; 268: 110650, 2020 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-32510427

RESUMO

The nonlinear response of O3 to nitrogen oxides (NOx) and volatile organic compounds (VOC) is not conducive to accurately identify the various source contributions and O3-NOx-VOC relationships. An enhanced meta-modeling approach, polynomial functions based response surface modeling coupled with the sectoral linear fitting technique (pf-ERSM-SL), integrating a new differential method (DM), was proposed to break through the limitation. The pf-ERSM-SL with DM was applied for analysis of O3 formation regime and real-time source contributions in July and October 2015 over the Pearl River Delta Region (PRD) of Mainland China. According to evaluations, the pf-ERSM-SL with DM was proven to be effective in source apportionment when the traditional sensitivity analysis was unsuitable for deriving the source contributions in the nonlinear system. After diagnosing the O3-NOx-VOC relationships, O3 formation in most regions of the PRD was identified as a distinctive NOx-limited regime in July; in October, the initial VOC-limited regime was found at small emission reductions (less than 22-44%), but it will transit to NOx-limited when further reductions were implemented. Investigation of the source contributions suggested that NOx emissions were the dominated contributor when turning-off the anthropogenic emissions, occupying 85.41-94.90% and 52.60-75.37% of the peak O3 responses in July and October respectively in the receptor regions of the PRD; NOx emissions from the on-road mobile source (NOx_ORM) in Guangzhou (GZ), Dongguan&Shenzhen (DG&SZ) and Zhongshan (ZS) were identified as the main contributors. Consequently, the reinforced control of NOx_ORM is highly recommended to lower the ambient O3 in the PRD effectively.


Assuntos
Poluentes Atmosféricos , Ozônio , China , Monitoramento Ambiental , Rios
14.
Brain Res ; 1746: 146945, 2020 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-32531223

RESUMO

Currently, there is no efficacious pharmacological treatment for traumatic brain injury (TBI). Previous studies revealed that L-lactate preconditioning has shown rich neuroprotective effects against cerebral ischemia, and therefore has the potential to improve neurological outcomes after TBI. L-lactate played a neuroprotective role by activating GPR81 in diseases of the central nervous system (CNS) such as TBI and cerebral ischemia. In this study we investigated the effects of L-lactate preconditioning on TBI and explored the underlying mechanisms. In this study, the mNSS test revealed that L-lactate preconditioning alleviates the neurological deficit caused by TBI in rats. L-lactate preconditioning significantly increased the expression of GPR81, PSD95, GAP43, BDNF, and MCT2 24 h after TBI in the cortex and hippocampus compared with the sham group. Taken together, these data suggested that L-lactate preconditioning is an effective method with which to recover neurological function after TBI. This reveals the mechanism of L-lactate preconditioning on TBI and provides a potential therapeutic method for TBI in humans.

15.
PLoS One ; 15(6): e0234016, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32480401

RESUMO

PURPOSE: We propose a new method to calculate proptosis by using the simple Heron's formula and analyze its feasibility. METHOD: It was a none-inferiority trial. The registration number was ChiCTR1900026490. The absolute value of proptosis in 120 eyes, 60 patients without eye injury or diseases, was measured by computed tomography (CT) and simple Heron's formula. We did regression analysis and analyzed the differences between the two methods with Medcalc software version 19.0.4. The result was showed by Passing-Bablok regression analysis diagram and Bland and Altman plot. RESULTS: The Passing-Bablok showed that the result of proptosis measured by CT and simple Heron's formula showed good positive correlation. A 95% limit of agreement in proptosis between CT and Heron's formula method was -0.46 to 0.54 mm in right eye and -0.45 to 0.46 mm in left eye. 1.66% (1/60) point was outside 95% LoA in both eyes. Moreover, a 95% limit of agreement between CT and Heron's formula method was -0.42 to 0.56 mm in difference of both eyes. 3.33% (2/60) points were outside 95% LoA. The points in all Bland and Altman plots were lower than 5%. It means that the results of comparison between the two methods had a good consistency in the measurement of proptosis. CONCLUSIONS: Heron's formula could be applied to calculate proptosis and has a good consistency compared with computed tomography (CT). This method is practical in proptosis assessment because of its accuracy, reliability and simplicity.


Assuntos
Antropometria/métodos , Exoftalmia/diagnóstico , Adulto , Antropometria/instrumentação , Olho/diagnóstico por imagem , Estudos de Viabilidade , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Reprodutibilidade dos Testes , Tomografia Computadorizada por Raios X , Adulto Jovem
16.
BMC Ophthalmol ; 20(1): 127, 2020 Apr 03.
Artigo em Inglês | MEDLINE | ID: mdl-32245437

RESUMO

BACKGROUND: To report a case of conjunctival sac fistula after cosmetic lateral canthoplasty which is rare. CASE PRESENTATION: A young women who underwent bilateral canthoplasty appeared with lacrimation of the right eye. We found there was a skin fistula with transparent tears at 2 mm lateral to the right canthus ligament and the liquid containing fluorescein was seen to overflow at the fistula after using fluorescein sodium eye drops. The number 7 lacrimal duct probe was visible under the temporal conjunctiva when exploring the fistula, and the fistula was about 4 mm. The patient was diagnosed with conjunctival sac fistula and fistula excision was performed. The patient did not tear abnormally after observation 3 months later and the incision healed well. CONCLUSIONS: The case report illustrates an uncommon post-lateral canthoplasty complication. We suggested that surgeons who perform this kind of surgery should ask about epiphora and look for conjunctival sac fistula at follow-up assessment.

17.
Front Pharmacol ; 11: 367, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32292345

RESUMO

Berberine (BBR) has a variety of pharmacological activities and is widely used in Asian countries. However, the clinical application of BBR still lacks scientific basis, what protective mechanism of BBR against myocardial ischemia-reperfusion injury (MIRI). In vitro experiments, BBR pretreatment regulated autophagy-related protein expression, induced cell proliferation and autophagosome formation, and reduced the mitochondrial membrane potential (ΔΨm) increase in H9C2 cells. In vivo experiments, BBR reduced the myocardial infarct size, decreased cardiomyocyte apoptosis, and markedly decreased myocardial enzyme (CK-MB, LDH, and AST) activity-induced I/R. In addition, upon BNIP3 knockdown, the regulatory effects of BBR on the above indicators were weakened both in H9C2 cells and in vivo. Luciferase reporter and ChIP assays indicated that BBR mediated BNIP3 expression by enhancing the binding of HIF-1α to the BNIP3 promoter. BBR protects against myocardial I/R injury by inducing cardiomyocytes proliferation, inhibiting cardiomyocytes apoptosis, and inducing the mitophagy-mediated HIF-1α/BNIP3 pathway. Thus, BBR may serve as a novel therapeutic drug for myocardial I/R injury.

19.
J Cataract Refract Surg ; 46(3): 465-473, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-32142042

RESUMO

To analyze the visual acuity and complications between primary intraocular lens (IOL) implantation and contact lens wearing, this literature search was performed with data on patients with congenital cataract younger than 2 years published in March 2019. Seven identified studies enrolling 675 eyes were selected for analysis. Patients with primary IOL implantation owned better visual acuity than those with aphakia who wore the contact lens (weighted mean difference = 0.161; 95% CI, 0.108-0.214). For visual axis opacification (VAO), primary IOL implantation increases the incidence of VAO compared with contact lens wearing (relative risk = 0.23; 95% CI, 0.13-0.42). No statistically significant difference was found between the 2 groups about the prevalence of glaucoma and strabismus. Primary IOL implantation achieved better visual outcomes after cataract extraction in patients younger than 2 years. In addition, no higher risk for complications among primary IOL implantation compared with contact lens wearing was noted. Therefore, implanting a primary IOL during congenital cataract surgery is a better therapy for children younger than 2 years than wearing a contact lens.

20.
Int J Nurs Pract ; 26(3): e12823, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32012398

RESUMO

BACKGROUND: Education for asthmatic children in the outpatient department is insufficient. AIM: To evaluate the efficacy of a nurse-led education pathway, a standard education programme, on children with asthma. METHODS: One hundred and eighty participants enrolled and were randomly assigned to either the control group or the intervention group. The intervention group received predetermined step-by-step education sessions based on the self-designed education pathway, while the control group received usual care. Asthma control, health-related quality of life, and health-care utilization measures were taken at baseline and at follow-up visits between February 2016 and May 2018. RESULTS: Significantly higher scores for health-related quality of life and inhaler technique at the third-month visit and asthma control test at the sixth-month visit were seen in the intervention group. The numbers of unscheduled physician visits and school absences were lower in the intervention group than in the control group within 6 months. However, no significant differences were observed in emergency department visits and hospitalizations. CONCLUSION: The nurse-led education pathway could be considered effective for children with asthma visiting the outpatient department.


Assuntos
Asma/enfermagem , Continuidade da Assistência ao Paciente , Relações Enfermeiro-Paciente , Pacientes Ambulatoriais , Asma/fisiopatologia , Criança , Serviço Hospitalar de Emergência , Feminino , Hospitalização , Humanos , Masculino , Qualidade de Vida
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