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1.
Zhongguo Fei Ai Za Zhi ; 24(3): 141-160, 2021 Mar 20.
Artigo em Chinês | MEDLINE | ID: mdl-33819964

RESUMO

BACKGROUND: Perioperative treatment has become an increasingly important aspect of the management of patients with non-small cell lung cancer (NSCLC). Small-scale clinical studies performed in recent years have shown improvements in the major pathological remission rate after neoadjuvant therapy, suggesting that it will soon become an important part of NSCLC treatment. Nevertheless, neoadjuvant immunotherapy may be accompanied by serious adverse reactions that lead to delay or cancelation of surgery, additional illness, and even death, and have therefore attracted much attention. The purpose of the clinical recommendations is to form a diagnosis and treatment plan suitable for the current domestic medical situation for the immune-related adverse event (irAE). METHODS: This recommendation is composed of experts in thoracic surgery, oncologists, thoracic medicine and irAE related departments (gastroenterology, respirology, cardiology, infectious medicine, hematology, endocrinology, rheumatology, neurology, dermatology, emergency section) to jointly complete the formulation. Experts make full reference to the irAE guidelines, large-scale clinical research data published by thoracic surgery, and the clinical experience of domestic doctors and publicly published cases, and repeated discussions in multiple disciplines to form this recommendation for perioperative irAE. RESULTS: This clinical recommendation covers the whole process of prevention, evaluation, examination, treatment and monitoring related to irAE, so as to guide the clinical work comprehensively and effectively. CONCLUSIONS: Perioperative irAE management is an important part of immune perioperative treatment of lung cancer. With the continuous development of immune perioperative treatment, more research is needed in the future to optimize the diagnosis and treatment of perioperative irAE.

2.
J Mater Chem B ; 2021 Apr 29.
Artigo em Inglês | MEDLINE | ID: mdl-33913461

RESUMO

Tannic acid (TA), a large polyphenolic molecule, has long been known for use in food additives, antioxidants, bio-sorbents, animal feed and adhesives due to its intrinsic properties such as antioxidation, metal chelation, and polymerization. Recently, there has been a renewed interest in fabricating engineered advanced materials with TA modification for novel bio-applications. The modification process involves various interactions/reactions based on its diverse chemical structure, contributed by abundant aromatic rings and hydroxyl groups. In addition, the obtained composites are endowed with retained TA activity and novel enhanced properties. Therefore, the aim of this review is to highlight the recent biomedical application of TA-based metal phenolic networks (TA-MPNs) by focusing on their intrinsic properties and the endowed ability for novel engineered functional composites. The potential contributions of TA-MPNs in "Tumor Theranostics", "Anti-Bacterial Ability", "Wound Repair for Skin Regeneration" and "Bone Tissue Regeneration Applications" are summarized in this paper.

3.
Dev Comp Immunol ; 121: 104093, 2021 Apr 02.
Artigo em Inglês | MEDLINE | ID: mdl-33819544

RESUMO

Beclin 1 and LC3 are important autophagy regulation proteins involved in vesicle nucleation and extension stage, respectively. In the present study, a Beclin 1 and a LC3 were identified from Yesso scallop Patinopecten yessoensis (PyBeclin 1 and PyLC3). The open reading frame (ORF) of PyBeclin 1 was of 1335 bp encoding a putative polypeptide of 444 amino acid residues with an N-terminal BCL-2 homology 3 (BH3) domain, a central coiled-coil domain (CCD), and a C-terminal evolutionarily conserved domain (ECD). The ORF of PyLC3 was of 369 bp encoding a putative polypeptide of 122 amino acid residues with an APG12 domain. The deduced amino acid sequences of PyBeclin 1 and PyLC3 shared 31.92-74.09% and 68.38-79.50% identities with Beclin 1s and LC3s from other species, respectively. The mRNA transcripts of PyBeclin 1 and PyLC3 were found to be expressed in all the examined tissues, including adductor muscle, gonad, gill, haemocytes and mantle, with the highest expression level in gill and haemocytes. The mRNA expression level of PyBeclin 1 in haemocytes increased significantly at 1, 3, 6, 12 and 24 h (2.98-4.07 fold of that in the Blank group, p < 0.05), and returned to normal level at 48 h after acute high temperature stress at 25 °C. Unlike PyBeclin 1, the mRNA transcripts of PyLC3 in haemocytes were significantly up-regulated at1, 3, 6 and 12 h (1.80-2.54 fold of that in the Blank group, p < 0.05), then decreased to blank level at 24 h (p > 0.05), and increased significantly again at 48 h (3.70 fold of that in the Blank group, p < 0.05) after high temperature. PyBeclin 1 and PyLC3 were mainly located in the cytoplasm and a small amount in the nucleus with few puncta, and the numbers of PyBeclin 1 and PyLC3 puncta increased at 3 h after acute high temperature stress. The LC3-II levels in gill and haemocytes were significantly up-regulated at 1 h and 3 h after acute high temperature stress. These results collectively suggested that PyBeclin 1 and PyLC3 were conserved members of Beclin 1 and LC3 family in scallops, and involved in regulating the activation of autophagy in scallops after acute high temperature stress.

4.
Carbohydr Polym ; 259: 117741, 2021 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-33674001

RESUMO

Polysialic acid (polySia) is a linear polysaccharide comprised of N-acetylneuraminic acid residues and its over-expression in cancer cells has been correlated with poor clinical prognosis. An assay has been developed for quantitative analysis of cellular polySia expression. This was achieved by extracting and purifying released polySia from glycoproteins by mild acid hydrolysis and optimised organic extraction. The polySia was further hydrolysed into Sia monomers, followed by fluorescent labelling and quantitative analysis. The assay was qualified utilising endoneuraminidase-NF to remove polySia from the surface of C6-ST8SiaII cancer cells (EC50 = 2.13 ng/mL). The result was comparable to that obtained in a polySia-specific cellular ELISA assay. Furthermore, the assay proved suitable for evaluation of changes in polySia expression following treatment with a small molecule inhibitor of polysialylation. Given the importance of polySia in multiple disease states, notably cancer, this is a potentially vital tool with applications in the fields of drug discovery and glycobiology.


Assuntos
Cromatografia de Fase Reversa , Ácidos Siálicos/análise , Animais , Linhagem Celular Tumoral , Cromatografia Líquida de Alta Pressão , Cromatografia por Troca Iônica , Inibidores Enzimáticos/química , Inibidores Enzimáticos/metabolismo , Ensaio de Imunoadsorção Enzimática , Glicosídeo Hidrolases/metabolismo , Ratos , Ácidos Siálicos/metabolismo , Sialiltransferases/antagonistas & inibidores , Sialiltransferases/metabolismo
5.
Thorac Cancer ; 12(9): 1469-1488, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-33787090

RESUMO

Perioperative adjuvant treatment has become an increasingly important aspect of the management of patients with non-small cell lung cancer (NSCLC). In particular, the success of immune checkpoint inhibitors, such as antibodies against PD-1 and PD-L1, in patients with lung cancer has increased our expectations for the success of these therapeutics as neoadjuvant immunotherapy. Neoadjuvant therapy is widely used in patients with resectable stage IIIA NSCLC and can reduce primary tumor and lymph node stage, improve the complete resection rate, and eliminate microsatellite foci; however, complete pathological response is rare. Moreover, because the clinical benefit of neoadjuvant therapy is not obvious and may complicate surgery, it has not yet entered the mainstream of clinical treatment. Small-scale clinical studies performed in recent years have shown improvements in the major pathological remission rate after neoadjuvant therapy, suggesting that it will soon become an important part of NSCLC treatment. Nevertheless, neoadjuvant immunotherapy may be accompanied by serious adverse reactions that lead to delay or cancellation of surgery, additional illness, and even death, and have therefore attracted much attention. In this article, we draw on several sources of information, including (i) guidelines on adverse reactions related to immune checkpoint inhibitors, (ii) published data from large-scale clinical studies in thoracic surgery, and (iii) practical experience and published cases, to provide clinical recommendations on adverse events in NSCLC patients induced by perioperative immunotherapy.

6.
Sci Rep ; 11(1): 4432, 2021 02 24.
Artigo em Inglês | MEDLINE | ID: mdl-33627696

RESUMO

Cardiac injury is a common complication of the coronavirus disease 2019 (COVID-19), and is associated with adverse clinical outcomes. In this study, we aimed to reveal the association of cardiac injury with coagulation dysfunction. We enrolled 181 consecutive patients who were hospitalized with COVID-19, and studied the clinical characteristics and outcome of these patients. Cardiac biomarkers high-sensitivity troponin I (hs-cTnI), myohemoglobin and creatine kinase-myocardial band (CK-MB) were assessed in all patients. The clinical outcomes were defined as hospital discharge or death. The median age of the study cohort was 55 (IQR, 46-65) years, and 102 (56.4%) were males. Forty-two of the 181 patients (23.2%) had cardiac injury. Old age, high leukocyte count, and high levels of aspartate transaminase (AST), D-dimer and serum ferritin were significantly associated with cardiac injury. Multivariate regression analysis revealed old age and elevated D-dimer levels as being strong risk predictors of in-hospital mortality. Interleukin 6 (IL6) levels were comparable in patients with or without cardiac injury. Serial observations of coagulation parameters demonstrated highly synchronous alterations of D-dimer along with progression to cardiac injury. Cardiac injury is a common complication of COVID-19 and is an independent risk factor for in-hospital mortality. Old age, high leukocyte count, and high levels of AST, D-dimer and serum ferritin are significantly associated with cardiac injury, whereas IL6 are not. Therefore, the pathogenesis of cardiac injury in COVID-19 may be primarily due to coagulation dysfunction along with microvascular injury.


Assuntos
Transtornos da Coagulação Sanguínea/virologia , Traumatismos Cardíacos/virologia , Idoso , Biomarcadores/sangue , Coagulação Sanguínea/fisiologia , Transtornos da Coagulação Sanguínea/sangue , Transtornos da Coagulação Sanguínea/epidemiologia , /fisiopatologia , China/epidemiologia , Estudos de Coortes , Creatina Quinase Forma MB/sangue , Feminino , Produtos de Degradação da Fibrina e do Fibrinogênio/análise , Produtos de Degradação da Fibrina e do Fibrinogênio/metabolismo , Traumatismos Cardíacos/sangue , Traumatismos Cardíacos/epidemiologia , Traumatismos Cardíacos/fisiopatologia , Hemoglobinas/metabolismo , Mortalidade Hospitalar , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Troponina I/sangue
7.
Mol Neurobiol ; 2021 Jan 22.
Artigo em Inglês | MEDLINE | ID: mdl-33481176

RESUMO

Failed neuroprotection leads to the initiation of several diseases. SOX1 plays many roles in embryogenesis, oncogenesis, and male sex determination, and can promote glioma stem cell proliferation, invasion, and migration due to its high expression in glioblastoma cells. The functional versatility of the SOX1 gene in malignancy, epilepsy, and Parkinson's disease, as well as its adverse effects on dopaminergic neurons, makes it an interesting research focus. Hence, we collate the most important discoveries relating to the neuroprotective effects of SOX1 in brain cancer and propose hypothesis worthy of SOX1's role in the survival of senescent neuronal cells, its roles in fibroblast cell proliferation, and cell fat for neuroprotection, and the discharge of electrical impulses for homeostasis. Increase in electrical impulses transmitted by senescent cells affects the synthesis of neurotransmitters, which will modify the brain cell metabolism and microenvironment.

8.
Int J Clin Oncol ; 26(3): 461-484, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-33387088

RESUMO

Cryoablation (CA), high-intensity focused ultrasound (HIFU), irreversible electroporation (IRE), and vascular-targeted photodynamic therapy (VTP) have been evaluated as novel strategies for selected patients with prostate cancer (PCa). We aim to determine the current status of literature regarding the clinical outcomes among these minimally invasive therapies. A systematic search of PubMed, EMBASE, and the Cochrane Library for all English literature published from January 2001 to December 2019 was conducted to identify studies evaluating outcomes of CA, HIFU, IRE or VTP on PCa. Proportionality with 95% confidence intervals (CIs) was performed using STATA version 14.0. 56 studies consisting of 7383 participants were found to report data of interest and fulfilled the inclusion criteria in the final meta-analysis. The pooled proportions of positive biopsy after procedure were 20.0%, 24.3%, 24.2%, and 36.2% in CA, HIFU, IRE and VTP, respectively. The pooled proportions of BRFS were 75.7% for CA and 74.4% for HIFU. The pooled proportions of CSS were 96.1%, 98.2%, and 97.9% for CA, HIFU, and IRE, respectively. The pooled proportions of OS were 92.8% for CA and 85.2% for HIFU. The pooled proportions of FFS were 64.7%, 90.4%, and 76.7% for CA, IRE and VTP, respectively. The pooled proportions of MFS were 92.8% for HIFU and 99.1% for IRE. This meta-analysis shows that CA, HIFU, IRE, and VTP are promising therapies for PCa patients with similar clinical outcomes. However, further larger, well-designed randomized controlled trials are required to confirm this assertion.


Assuntos
Criocirurgia , Fotoquimioterapia , Neoplasias da Próstata , Biópsia , Eletroporação , Humanos , Masculino , Neoplasias da Próstata/tratamento farmacológico , Neoplasias da Próstata/cirurgia , Resultado do Tratamento
9.
Hypertension ; 77(1): 59-71, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33249863

RESUMO

Right ventricular (RV) failure is a major cause of death in patients with pulmonary arterial hypertension, and the mechanism of RV failure remains unclear. While the malfunction of RyR2 (ryanodine receptor type 2) on sarcoplasmic reticulum (SR) and aberrant Ca2+ cycling in cardiomyocytes have been recognized in some cardiovascular diseases, their roles in RV failure secondary to pulmonary arterial hypertension require further investigation. In a monocrotaline-induced rat model of pulmonary arterial hypertension, the RV remodeling process was divided into normal, compensated, and decompensated stages according to the hemodynamic and morphological parameters. In both compensated and decompensated stages, significant diastolic SR Ca2+ leakage was detected along with reduced intracellular Ca2+ transient amplitude and SR Ca2+ contents in RV myocytes. RyR2 protein levels decreased progressively during the process, and the thiol oxidation proportions of RyR2 were higher in compensated and decompensated stages than in normal stage. Inhibition of RyR2 oxidation by dithiothreitol or repairing RyR2 directly by dantrolene could restore Ca2+ homeostasis in RV myocytes. Daily intraperitoneal injection of dantrolene delayed decompensation progression and significantly improved the survival rate of pulmonary hypertension rats in decompensated stage (79.3% versus 55.9%; P=0.026). Our findings suggest that diastolic SR Ca2+ leakage via oxidized RyR2 facilitates the development of RV failure. Dantrolene can inhibit diastolic SR Ca2+ leakage in RV cardiomyocytes, delay right cardiac dysfunction, and improve the survival of rats with pulmonary arterial hypertension.

10.
J Mol Cell Cardiol ; 2020 Dec 07.
Artigo em Inglês | MEDLINE | ID: mdl-33301800

RESUMO

Pathological cardiac remodeling, characterized by excessive deposition of extracellular matrix proteins and cardiac hypertrophy, leads to the development of heart failure. Meprin α (Mep1a), a zinc metalloprotease, previously reported to participate in the regulation of inflammatory response and fibrosis, may also contribute to cardiac remodeling, although whether and how it participates in this process remains unknown. Here, in this work, we investigated the role of Mep1a in pathological cardiac remodeling, as well as the effects of the Mep1a inhibitor actinonin on cardiac remodeling-associated phenotypes. We found that Mep1a deficiency or chemical inhibition both significantly alleviated TAC- and Ang II-induced cardiac remodeling and dysfunction. Mep1a deletion and blocking both attenuated TAC- and Ang II-induced heart enlargement and increases in the thickness of the left ventricle anterior and posterior walls, and reduced expression of pro-hypertrophic markers, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and myosin heavy chain beta (ß-MHC). In addition, Mep1a deletion and blocking significantly inhibited TAC- and Ang II-induced cardiac fibroblast activation and production of extracellular matrix (ECM). Moreover, in Mep1a-/- mice and treatment with actinonin significantly reduced Ang II-induced infiltration of macrophages and proinflammatory cytokines. Notably, we found that in vitro, Mep1a is expressed in cardiac myocytes and fibroblasts and that Mep1a deletion or chemical inhibition both markedly suppressed Ang II-induced hypertrophy of rat or mouse cardiac myocytes and activation of rat or mouse cardiac fibroblasts. In addition, blocking Mep1a in macrophages reduced Ang II-induced expression of interleukin (IL)-6 and IL-1ß, strongly suggesting that Mep1a participates in cardiac remodeling processes through regulation of inflammatory cytokine expression. Mechanism studies revealed that Mep1a mediated ERK1/2 activation in cardiac myocytes, fibroblasts and macrophages and contributed to cardiac remodeling. In light of our findings that blocking Mep1a can ameliorate cardiac remodeling via inhibition of cardiac hypertrophy, fibrosis, and inflammation, Mep1a may therefore serve as a strong potential candidate for therapeutic targeting to prevent cardiac remodeling.

11.
Brain Res Bull ; 2020 Dec 02.
Artigo em Inglês | MEDLINE | ID: mdl-33278485

RESUMO

BACKGROUND: Glial cell line-derived neurotrophic factor (GDNF) is expressed in both astrocytes and glioblastoma (GBM) cells. GDNF expression is significantly increased in GBM, and inhibiting its expression can retard GBM progression. However, there is no known method for specific inhibition of GDNF in GBM cells. METHODS: Promoter-targeted dsRNA-induced transcriptional gene silencing or activation was recently achieved in human cells. This approach has the potential to specifically regulate gene transcription via epigenetic modifications. In this study, we designed six candidate dsRNAs targeting the enhancer or silencer in GDNF gene promoter II to check their effects on GDNF transcription and GBM progression. RESULTS: Among these dsRNAs, enhancer II-targeted dsRNA significantly inhibited U251 GBM progression by downregulating GDNF (P < 0.05), while silencer II-targeted dsRNA exerted an opposite effect. Moreover, enhancer II-targeted dsRNA did not significantly change GDNF expression in human astrocytes (HA) and the proliferation and migration of HA cells (P > 0.05). Bisulfate PCR and chromatin immunoprecipitation analyses revealed that both DNA methylation and trimethylation of histone 3 at lysine 9 (H3K9me3) at silencer II-targeted region significantly increased, and H3K9me3 at enhancer II-targeted region significantly decreased, in U251 cells compared with HA cells in non-intervention condition (P < 0.05). Both enhancer II- and silencer II-targeted dsRNA significantly increased H3K9me3 methylation rather than DNA at the targeted site in U251 cells (P < 0.05). The expression and activity of histone methyltransferase SETDB1 increased dramatically in U251 cells compared with HA cells, and it was recruited to enhancer II targeting region after enhancer II-targeted dsRNA treatment in U251 cells (P < 0.05). CONCLUSIONS: Our results demonstrate that a promoter-targeted dsRNA can silence or promote gene transcription depending on its targeted site in different cis-acting elements in the gene promoter. Targeted inhibition of GDNF by enhancer II-targeted dsRNA may be explored as a novel treatment for GBM.

12.
Circulation ; 2020 Dec 11.
Artigo em Inglês | MEDLINE | ID: mdl-33305586

RESUMO

Background: Immunoglobulin E (IgE) belongs to a class of immunoglobulins involved in immune response to specific allergens. However, the roles of IgE and IgE receptor (FcεR1) in pathological cardiac remodeling and heart failure (HF) are unknown. Methods: Serum IgE levels and cardiac IgE receptor (FcεR1) expression were assessed in diseased hearts from human and mouse. The role of FcεR1 signaling in pathological cardiac remodeling was explored in vivo by FcεR1 genetic depletion, anti-IgE antibodies, and bone-marrow (BM) transplantation. The roles of IgE-FcεR1 pathway were further evaluated in vitro in primary cultured rat cardiomyocytes (CMs) and cardiac fibroblasts (CFs). RNA-seq and bioinformatic analyses were used to identify biochemical changes and signaling pathways that are regulated by IgE/FcεR1. Results: Serum IgE levels were significantly elevated in patients with HF as well as in two mouse cardiac disease models induced by chronic pressure overload via transverse aortic contraction (TAC) and chronic angiotensin II (Ang II) infusion. Interestingly, FcεR1 expression levels were also significantly up-regulated in failing hearts from human and mouse. Blockade of the IgE-FcεR1 pathway by FcεR1 knockout alleviated TAC- or Ang II-induced pathological cardiac remodeling and/or dysfunction. Anti-IgE antibodies (including the clinical drug, omalizumab) also significantly alleviated Ang II-induced cardiac remodeling. BM transplantation experiments indicated that IgE-induced cardiac remodeling was mediated through non-BM-derived cells. FcεR1 was found to be expressed in both CMs and CFs. In cultured rat CMs, IgE-induced CM hypertrophy and hypertrophic marker expression were abolished by depleting FcεR1. In cultured rat CFs, IgE-induced CF activation and matrix protein production were also blocked by FcεR1 deficiency. RNA-seq and signaling pathway analyses revealed that transforming growth factor-ß (TGF-ß) may be a critical mediator and blocking TGF-ß indeed alleviated IgE-induced cardiomyocyte hypertrophy and cardiac fibroblast activation in vitro. Conclusions: Our findings suggest that IgE induction plays a causative role in pathological cardiac remodeling, at least partially via the activation of IgE-FcεR1 signaling in CMs and CFs. Therapeutic strategies targeting the IgE-FcεR1 axis may be effective for managing IgE-mediated cardiac remodeling.

13.
Artigo em Inglês | MEDLINE | ID: mdl-33369674

RESUMO

OBJECTIVE: Myocardial involvement (MCI) is known to increase morbidity and mortality in polymyositis (PM) and dermatomyositis (DM). This study aims to investigate whether complicating with ventricular arrhythmia (VA) predicts poor outcomes in patients with PM/DM-related myocardial involvement (PM/DM-MCI). METHODS: We reviewed all PM/DM-MCI patients admitted in Peking Union Medical College Hospital from October 1997 to April 2019. VA and the other possible risk factors for the composite end point, including death from any cause and rehospitalization for cardiac causes, were analysed. RESULTS: A total of 75 PM/DM-MCI patients (44 PM and 31 DM) were enrolled, of which 27 (36%) met the composite end point during a median follow-up of 24 months. Independent prognostic factors for the composite end point includes VA (HR 4.215, 95% CI [1.737, 10.230]), NT-proBNP > 3415 pg/ml (HR 2.606, 95% CI [1.203, 5.646]), interstitial lung disease (HR 2.688, 95% CI [1.209, 5.978]), and anti-cardiac remodelling therapy (HR 0.302, 95% CI [0.115, 0.792]). The 3-year event-free survival rate of patients without VA was significantly higher than that of patients with VA (63.3% vs 40.7%, p = 0.034). Skin lesions (OR 0.163, 95% CI [0.051, 0.523]) and positive antimitochondrial antibody (OR 3.484, 95% CI [1.192, 10.183]) were independent predictors of VA. CONCLUSION: VA provides prognostic insights for PM/DM-MCI patients and predicts poor outcome. Polymyositis and positive antimitochondrial antibody are closely associated with the presence of VA in PM/DM-MCI.

14.
Can J Cardiol ; 2020 Dec 11.
Artigo em Inglês | MEDLINE | ID: mdl-33310144

RESUMO

BACKGROUND: Coronary artery involvement is a severe but uncommon manifestation of polyarteritis nodosa (PAN), so clinicians have little knowledge of it. Our aim was to investigate the clinical characteristics, risk factors and outcomes of patients with PAN complicated with coronary artery lesions. METHODS: Data from 145 patients with PAN who were admitted to Peking Union Medical College Hospital from January 2000 to September 2019 were retrospectively collected. RESULTS: Nineteen patients (13.1%) had coronary artery lesions due to PAN. The age at the onset of PAN was 32.3 ± 11.8 years. There were no significant differences in common risk factors for coronary arterial atherosclerosis between the patients with coronary artery involvement and those without. Affected branches of the coronary arteries were left anterior descending branch (15 patients), right coronary artery (14 patients), and left circumflex branch (9 patients). Eleven of the 19 patients exhibited multivessel lesions. Multivariate logistic regression analysis showed that celiac artery involvement (odds ratio [OR] 3.722, 95% confidence interval [CI] 1.115-12.427; P = 0.033) and new-onset hypertension (OR 6.668, 95% CI 1.936-22.961; P = 0.003) were risk factors for coronary artery involvement in patients with PAN. Stent placement was performed for 2 patients, and in-stent restenosis occurred in 1 of those patients a year later. CONCLUSIONS: PAN with coronary artery involvement exhibits more combined involvement of arteries of other organs and more severe diseases. PAN should be considered when treating young adults with an unknown origin of coronary artery lesions. In addition to systemic immunosuppressive treatment, other measures including antiplatelet and anticoagulation therapy should be initiated; however, determining the optimal time to perform procedures such as intervention or surgery is still challenging.

15.
J Am Heart Assoc ; 9(19): e017939, 2020 Oct 20.
Artigo em Inglês | MEDLINE | ID: mdl-32990132

RESUMO

Background Moderate hypothermic circulatory arrest (MHCA) has been widely used in aortic arch surgery. However, the renal function after MHCA remains controversial. We performed a systematic review and meta-analysis direct comparison of the postoperative renal function of MHCA versus deep hypothermic circulatory arrest (DHCA) in aortic arch surgery. Methods and Results We searched PubMed, Embase, and the Cochrane Library for postoperative renal function after aortic arch surgery with using MHCA and DHCA, published from inception to January 31, 2020. The primary outcome was renal failure. Secondary outcomes were the need for renal therapy and other major postoperative outcomes. The random-effects model was used for all comparisons to pool the estimates. A total of 14 observational studies with 4142 patients were included. Compared with DHCA, MHCA significantly reduced the incidence of renal failure (odds ratio [OR], 0.76; 95% CI, 0.61-0.94; P=0.011; I2=0.0%) and the need of renal replacement (OR, 0.68; 95% CI, 0.48-0.97; P=0.034; I2=0.0%). Subgroup analysis showed that when the hypothermic circulatory arrest time was <30 minutes, the incidence of renal failure in MHCA group was significantly lower than that in DHCA group (OR, 0.73; 95% CI, 0.54-0.99; P=0.040; I2=1.1%), whereas an insignificant difference between 2 groups when hypothermic circulatory arrest time was >30 minutes (OR, 0.76; 95% CI, 0.51-1.13; P=0.169; I2=17.3%). Conclusions MHCA compared with DHCA reduces the incidence of renal failure and the need for renal replacement. Registration URL: https://www.crd.york.ac.uk/prospero; Unique identifier: CRD42020169348.

16.
Front Oncol ; 10: 1489, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32983986

RESUMO

Purpose: To compare the oncologic outcomes of cryoablation (CA) and radical prostatectomy (RP) in patients with low- and intermediate-risk localized prostate cancer (PCa). Materials and Methods: PCa patients who received CA or RP between 2004 and 2015 were identified from the Surveillance, Epidemiology, and End Results database. Multivariable Cox proportional hazard analysis was used to compare the prostate cancer-specific survival (CSS) and overall survival (OS). We conducted 1:3 propensity score matching and adjusted standardized mortality ratio weighting (SMRW) to balance the clinicopathological characteristics. Results: Ninety-seven thousand seven hundred eighty-three patients were identified after preliminary screening. After matching, the CA and RP groups included 1,942 and 5,826 patients and had median follow-up periods of 85 and 72 months, respectively. CA had lower CSS and OS rates (hazard ratio [HR], 2.07; P = 0.007; HR, 2.09; P < 0.001, respectively) than did RP, which was consistent in the SMRW model (CSM: HR, 2.66; P < 0.001; OS: HR, 2.29; P < 0.001). The 10-years CSS and OS for CA vs. RP were 98.1 vs. 99.2% and 61.3 vs. 79.9%, respectively. Conclusions: In patients with low- to intermediate-risk localized PCa, CA had lower CSS rates than did RP. However, the high 10-years CSS rates indicated that CA could be an option for those who are not RP candidates. Further high-quality trials are needed to confirm and expand our findings.

18.
Thorac Cancer ; 11(10): 3047-3052, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32893490

RESUMO

Immune checkpoint inhibitors (ICIs) activate host antitumor immunity to kill tumor cells. However, ICI therapy may be accompanied by a series of immunotherapy-related adverse effects (irAEs) caused by activated autoreactive T cells. Glucocorticoids are the mainstream therapy for irAEs. However, the usage, dosage and course of treatment of irAEs with glucocorticoids differs from those used in classic autoimmune diseases. Furthermore, the long-term use of large doses of glucocorticoids may cause serious adverse effects. In this article, the mechanism, dosage forms, adverse effects and management of glucocorticoids are described in detail, providing references and suggestions for oncologists to use glucocorticoids in the treatment of irAEs.

19.
ESC Heart Fail ; 2020 Sep 08.
Artigo em Inglês | MEDLINE | ID: mdl-32898341

RESUMO

AIMS: The coronavirus disease 2019 (COVID-19) has spread rapidly around the globe, causing significant morbidity and mortality. This study aims to describe electrocardiographic (ECG) characteristics of COVID-19 patients and to identify ECG parameters that are associated with cardiac involvement. METHODS AND RESULTS: The study included patients who were hospitalized with COVID-19 diagnosis and had cardiac biomarker assessments and simultaneous 12-lead surface ECGs. Sixty-three hospitalized patients (median 53 [inter-quartile range, 43-65] years, 76.2% male) were enrolled, including patients with (n = 23) and without (n = 40) cardiac injury. Patients with cardiac injury were older, had more pre-existing co-morbidities, and had higher mortality than those without cardiac injury. They also had prolonged QTc intervals and more T wave changes. Logistic regression model identified that the number of abnormal T waves (odds ratio (OR), 2.36 [95% confidence interval (CI), 1.38-4.04], P = 0.002) and QTc interval (OR, 1.31 [95% CI, 1.03-1.66], P = 0.027) were independent indicators for cardiac injury. The combination model of these two parameters along with age could well discriminate cardiac injury (area the under curve 0.881, P < 0.001) by receiver operating characteristic analysis. Cox regression model identified that the presence of T wave changes was an independent predictor of mortality (hazard ratio, 3.57 [1.40, 9.11], P = 0.008) after adjustment for age. CONCLUSIONS: In COVID-19 patients, presence of cardiac injury at admission is associated with poor clinical outcomes. Repolarization abnormalities on surface ECG such as abnormal T waves and prolonged QTc intervals are more common in patients with cardiac involvement and can help in further risk stratification.

20.
Int J Ophthalmol ; 13(8): 1272-1280, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32821682

RESUMO

AIM: To investigate the affecting factors of parapapillary gamma and delta zones and other fundus morphological features in high myopia. METHODS: Seventy high myopia patients were included in this retrospective observational study and 47 patients were female. Patients were divided into three groups: no posterior staphyloma (no PS), PS with myopic traction maculopathy (PS with MTM), and PS without MTM using 3-dimensional magnetic resonance imaging and optical coherence tomography. MTM patients were further classified into three types [epiretinal membrane, macular hole, and macular retinoschisis (MRS)]. Diameters of the gamma and delta zones were measured among other morphometric variables using fundus photographs. RESULTS: Of the 70 individuals (127 eyes), the mean age was 57.46±13.56y. In univariate analysis, morphological features changed most dramatically in PS with MTM patients, who had the largest gamma zone diameters, the largest disk-fovea distance (DFD) and disk-fovea angle, and the smallest angle kappa and vertical distance of temporal arterial arcade. However, their horizontal delta zone diameter was smaller than in the patients with PS yet without MTM. In multivariate analysis, with axial length (AL) and age adjusted, the horizontal diameter in the delta zone of the PS without MTM group was still significantly larger than in the PS with MTM group (P=0.024). Comparing the three subtypes of MTM patients, the diameters of the gamma zone and DFD in MRS group were the largest. CONCLUSION: The characteristics of the gamma and delta zones change inconsistently in different stages of high myopia. These changes may be associated with anatomical changes caused by local traction. Factors such as PS, AL and age play an important role. These findings may provide a hint about the pathogenesis of traction in high myopia.

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