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1.
BMC Infect Dis ; 20(1): 961, 2020 Dec 17.
Artículo en Inglés | MEDLINE | ID: mdl-33334317

RESUMEN

BACKGROUND: The clinical characteristics of patients with confirmed 2019 novel coronavirus disease (COVID-19) in Jilin Province, China were investigated. METHODS: Clinical, laboratory, radiology, and treatment data of 41 hospitalized patients with confirmed COVID-19 were retrospectively collected. The population was stratified by disease severity as mild, moderate, or severe, based on guidelines of the National Health and Medical Commission of China. RESULTS: The 41 hospitalized patients with COVID-19 were studied, and the median age was 45 years (interquartile range [IQR], 31-53; range, 10-87 years) and 18 patients (43.9%) were female. All of the patients had recently visited Wuhan or other places (ie, Beijing, Thailand) or had Wuhan-related exposure. Common symptoms included fever (32[78%]) and cough (29[70.7%]). All patients were without hepatitis B/C virus hepatitis. CRP (C-reactive protein, 11.3 mg/L [interquartile range {IQR}, 2.45-35.2]) was elevated in 22 patients (53.7%), and cardiac troponin I (1.5 ng/mL [IQR, 0.8-5.0]) was elevated in 41 patients (100%). Chest computed tomographic scans showed bilateral ground glass opacity (GGO) or GGO with consolidation in the lungs of 27(65.9%) patients. 31(75.6%) patients had an abnormal electrocardiograph (ECG). Comparing the three groups, the levels of CRP and cardiac troponin I, GGO distribution in bilateral lungs, and electrocardiogram changes were statistically significant (p < 0.05). Cardiac troponin I had a strong positive correlation with CRP (r = 0.704, p = 0.042) and LDH (r = 0.738, p = 0.037). CONCLUSION: Significant differences among the groups suggest that several clinical parameters may serve as biomarkers of COVID-19 severity at hospital admission. Elevated cTnI could be considered as a predictor of severe COVID-19, reflecting the prognosis of patients with severe COVID-19. The results warrant further inspection and confirmation.


Asunto(s)
COVID-19/diagnóstico , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Biomarcadores/sangre , COVID-19/epidemiología , COVID-19/patología , COVID-19/fisiopatología , Niño , China/epidemiología , Femenino , Corazón/fisiopatología , Hospitalización , Humanos , Pulmón/diagnóstico por imagen , Pulmón/patología , Masculino , Persona de Mediana Edad , Neumonía Viral/diagnóstico , Neumonía Viral/epidemiología , Neumonía Viral/patología , Neumonía Viral/fisiopatología , Pronóstico , Estudios Retrospectivos , SARS-CoV-2 , Adulto Joven
2.
J Cell Physiol ; 234(7): 10655-10670, 2019 07.
Artículo en Inglés | MEDLINE | ID: mdl-30536889

RESUMEN

The diabetes mellitus (DM)-induced reduction of neurogenesis in the hippocampus is consequently accompanied by cognitive decline. The present study set out to define the critical role played by long noncoding RNA H19 (lncRNA H19) in the apoptosis of hippocampal neurons, as well as oxidative stress (OS) in streptozotocin (STZ)-induced DM mice through regulation of insulin-like growth factor 2 (IGF2) methylation. The expression of lncRNA H19 in the hippocampal neurons and surviving neurons were detected. Hippocampal neurons were cultured and transfected with oe-H19, sh-H19, oe-IGF2, or sh-IGF2, followed by detection of the expressions of IGF2 and apoptosis-related genes. Determination of the lipid peroxide and glutathione levels was conducted, while antioxidant enzyme activity was identified. The IGF2 methylation, the binding of lncRNA H19 to DNA methyltransferase, and the binding of lncRNA H19 to IGF2 promoter region were detected. DM mice exhibited high expressions of H19, as well as a decreased hippocampal neurons survival rate. Higher lncRNA H19 expression was found in DM. Upregulated lncRNA H19 significantly increased the expression of Bax and caspase-3 but decreased that of Bcl-2, thus promoting the apoptosis of hippocampal neuron. Besides, upregulation of lncRNA H19 induced OS. LncRNA H19 was observed to bind specifically to the IGF2 gene promoter region and promote IGF2 methylation by enriching DNA methyltransferase, thereby silencing IGF2 expression. Taken together, downregulated lncRNA H19 reduces IGF2 methylation and enhances its expression, thereby suppressing hippocampal neuron apoptosis and OS in STZ-induced (DM) mice.


Asunto(s)
Metilación de ADN/genética , Diabetes Mellitus Experimental/genética , Diabetes Mellitus/genética , Factor II del Crecimiento Similar a la Insulina/genética , ARN Largo no Codificante/genética , Animales , Apoptosis/genética , Diabetes Mellitus/patología , Diabetes Mellitus Experimental/patología , Regulación de la Expresión Génica/genética , Impresión Genómica/genética , Hipocampo/metabolismo , Hipocampo/patología , Humanos , Metiltransferasas/genética , Ratones , Neuronas/metabolismo , Neuronas/patología , Estrés Oxidativo/genética , Regiones Promotoras Genéticas/genética , Proteínas Proto-Oncogénicas c-bcl-2/genética , Proteína X Asociada a bcl-2/genética
3.
Cell Physiol Biochem ; 51(3): 1069-1086, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-30476906

RESUMEN

BACKGROUND/AIMS: Cerebral ischemia is considered to be the most common cause of stroke with high mortality. It occurs as a result of the damage of the hippocampal neurons with lymphocyte function-associated antigen (LFA)-1 being emphasized to play a role in the biological functions of hippocampal neurons. This study was conducted in order to investigate the effects of specific knockdown of LFA-1 expression by lentivirus had on the apoptosis of the hippocampal neurons, simulated by rat models of acute cerebral ischemia after cerebral lymphatic blockage. METHODS: A total of 60 Wistar rats were selected as subjects, among which 50 were used to establish models of the acute cerebral ischemia after cerebral lymphatic blockage, while the remaining 10 rats were treated with the sham operation. The underlying regulatory mechanisms regarding LFA-1 were analyzed with the treatment of si-LFA-1 and LFA-1 vector in the hippocampal CA1 area of brain tissues isolated from the rats with acute cerebral ischemia. The brain water content, electrolyte content, and blood-brain barrier permeability located in ischemic area of rats were measured. TUNEL staining and immunochemistry methods were employed in order to determine the apoptosis rate and positive levels of LFA-1, MMP-9, and Caspase-3. The mRNA and protein levels of related genes were also detected by means of RT-qPCR and western blot assay. RESULTS: The brain water content, Na+ and Ca+ contents, blood-brain barrier permeability, apoptosis rate, positive levels of LFA-1, MMP-9, and Caspase-3 were decreased, and the K+ content was increased in ischemic tissues treated with si-LFA-1. The mRNA and protein levels of LFA-1, MMP-9, Caspase-3, and Bax had all decreased, while the mRNA and protein levels of Bcl-2 were elevated in the hippocampal CA1 area of rat brain tissues treated with si-LFA-1. These situations could be reversed through the up-regulation of LFA-1. CONCLUSION: In conclusion, LFA-1 gene silencing could improve the acute cerebral ischemia after cerebral lymphatic blockage by inhibiting apoptosis of the hippocampal neurons in rats.


Asunto(s)
Isquemia Encefálica/genética , Isquemia Encefálica/terapia , Silenciador del Gen , Hipocampo/patología , Antígeno-1 Asociado a Función de Linfocito/genética , Animales , Apoptosis , Isquemia Encefálica/patología , Femenino , Terapia Genética , Hipocampo/citología , Hipocampo/metabolismo , Lentivirus/genética , Sistema Linfático/metabolismo , Sistema Linfático/patología , Masculino , Neuronas/citología , Neuronas/metabolismo , Neuronas/patología , Ratas Wistar
4.
J Cell Biochem ; 118(11): 3875-3882, 2017 11.
Artículo en Inglés | MEDLINE | ID: mdl-28390174

RESUMEN

This study is designed to investigate the role of basic fibroblast growth factor (bFGF) antisense oligonucleotide (ASODN) on the proliferation and differentiation of neural stem cells (NSCs) in rat models with focal cerebral infarction (CI). Seventy-five Sprague-Dawlay (SD) rats were randomly divided into the control, sham, middle cerebral artery occlusion (MCAO), MCAO + nonsense oligonucleotide (NODN), and MCAO + ASODN groups. Proliferation and differentiation of NSCs were detected by bromodeoxyuridine (BrdU) and immunofluorescence staining, respectively. ELISA was performed to detect the expressions of endogenous factors that include insulin-like growth factor 1 (IGF-1), glial cell line derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF), transforming growth factor-α1 (TGF-α1), bFGF, and nerve growth factor (NGF). Results show significant neurological deficits and focal CI in the MCAO and MCAO + NODN groups. An obvious increase of NSC proliferation, reactive proliferation of astrocytes in CI areas, differentiation of newly proliferated NSCs into mature neuronal cells, and expressions of endogenous growth factors exhibited in the MCAO, MCAO + NODN and MCAO + ASODN groups. Compared to the MCAO and MACO + NODN groups, the MCAO + ASODN group showed a significant decrease NSC proliferation and differentiation in CI areas as well as decrease expressions of endogenous growth factors. These findings may offer insight to help us understand more as to how bFGF ASODN can effectively suppress the proliferation and differentiation of NSCs. These findings are expected to help contribute to research for new targets in the treatment of focal CI. J. Cell. Biochem. 118: 3875-3882, 2017. © 2017 Wiley Periodicals, Inc.


Asunto(s)
Diferenciación Celular/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Infarto Cerebral/metabolismo , Factor 2 de Crecimiento de Fibroblastos/antagonistas & inhibidores , Regulación de la Expresión Génica/efectos de los fármacos , Células-Madre Neurales/metabolismo , Oligodesoxirribonucleótidos Antisentido/farmacología , Animales , Infarto Cerebral/patología , Factor 2 de Crecimiento de Fibroblastos/biosíntesis , Células-Madre Neurales/patología , Ratas , Ratas Sprague-Dawley
5.
Zhonghua Yi Xue Za Zhi ; 92(1): 50-4, 2012 Jan 03.
Artículo en Zh | MEDLINE | ID: mdl-22490659

RESUMEN

OBJECTIVE: To construct TRX-ABAD-DP-TRX (T-A-T) fusion gene of a novel ABAD-DP aptamer through the insertion of ABAD-DP into the modified human thioredoxin (hTRX) and exploit the possibility of further applications for the gene therapy of Alzheimer's disease. METHODS: According to the designed sequence, the target fragments of TRX1, TRX2 and ABAD-DP were created by PCR (polymerase chain reaction) and then inserted into the multiple clone site of adeno-associated virus shuttle plasmid pSSHG-CMV with gene cloning technique. The corresponding fusion gene TRX1-ABAD-DP-TRX2 was identified by restriction enzymes digestion with EcoRI and BamHI. The recombinant adeno-associated virus (AAV/T-A-T) was produced in HeLa cells with linear polyethylenimine. The expression of T-A-T fusion gene and co-localization between T-A-T and Aß peptide in NIH 3T3 cells were examined by fluorescent immunohistochemistry. RESULTS: The size of fusogenic fragment TRX1-ABAD-DP-TRX2 was approximately 435 bp. And it was consistent with our design. T-A-T fusion gene was expressed in NIH 3T3 cells. Through co-expression, T-A-T aptamer and intracellular Aß peptide were co-localized. It indicated that T-A-T aptamer could bind Aß within NIH 3T3 cells. CONCLUSION: The TRX1-ABAD-DP-TRX2 fusion gene is successfully cloned and expressed. And it may provide rationales for further applications in the gene therapy of Alzheimer's disease's.


Asunto(s)
Alcohol Deshidrogenasa/genética , Péptidos beta-Amiloides/genética , Aptámeros de Péptidos/genética , Fusión Artificial Génica , Animales , Dependovirus/genética , Células HeLa , Humanos , Ratones , Células 3T3 NIH , Tiorredoxinas/genética
6.
Int J Infect Dis ; 89: 66-71, 2019 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-31521852

RESUMEN

OBJECTIVES: To determine blood Brucella DNA loads between brucellosis patients and those without brucellosis. METHODS: The patient group included 350 brucellosis patients. The control was composed of 200 subjects without brucellosis. The extracted DNA from blood was tested by quantitative polymerase chain reaction (qPCR). The cutoff value was determined by receiver operating characteristic curve analysis. A portion of the brucellosis patients were monitored by qPCR during therapy. RESULTS: The detection limit of qPCR was between 1E+01cfu/µL and 1E+08cfu/µL. The standard curve R2 reached 0.998. The cutoff value was 4E+01cfu/µL, which was determined by comparison of the patient group and the control. The qPCR assay had a specificity of 100% and a sensitivity of 93.14%. The monitoring results showed that the Brucella DNA load decreased in most patients during the first 4 weeks of treatment. One patient with bad treatment compliance showed a rebound. CONCLUSIONS: The qPCR results were in accordance with the course of brucellosis in the clinic. The DNA load often reflects the situation of the Brucella-infected patient. The cutoff value provides an important reference of infection. This qPCR-based method can be used to assist in the diagnosis of brucellosis and to adjust the therapy.


Asunto(s)
Brucella/aislamiento & purificación , Brucelosis/diagnóstico , ADN Bacteriano/sangre , Adulto , Pruebas de Aglutinación , Médula Ósea/microbiología , Brucella/efectos de los fármacos , Brucella/genética , Brucelosis/tratamiento farmacológico , Brucelosis/microbiología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Reacción en Cadena en Tiempo Real de la Polimerasa , Sensibilidad y Especificidad
7.
Sci Rep ; 7: 43834, 2017 03 08.
Artículo en Inglés | MEDLINE | ID: mdl-28272417

RESUMEN

This study aims to explore the effects of the TLR4 signaling pathway on the apoptosis of neuronal cells in rats with diabetes mellitus complicated with cerebral infarction (DMCI). A DMCI model was established with 40 Sprague Dawley rats, which were assigned into blank, sham, DM + middle cerebral artery occlusion (MCAO) and DM + MCAO + TAK242 groups. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured. A TUNEL assay was applied for detecting cell apoptosis, and Western blotting was used for detecting the expression of TLR4, TNF-α, IL-1ß and apoptosis-related proteins. Compared with the blank and sham groups, there was an increase in cell apoptosis, expression of Bcl-2, Bax, cleaved caspase-3, TNF-α, IL-1ß and TLR4 proteins and MDA content and a decrease in SOD activity in the DM + MCAO and DM + MCAO + TAK242 groups. Compared with those in the DM + MCAO group, rats in the DM + MCAO + TAK242 group exhibited an increase in SOD activity and a decrease in cell apoptosis, expression of Bcl-2, Bax, cleaved caspase-3, TNF-α, IL-1ß and TLR4 proteins and MDA content. Inhibition of the TLR4 signaling pathway reduces neuronal cell apoptosis and nerve injury to protect the brain.


Asunto(s)
Apoptosis , Diabetes Mellitus Experimental/metabolismo , Infarto de la Arteria Cerebral Media/metabolismo , Neuronas/metabolismo , Transducción de Señal , Receptor Toll-Like 4/metabolismo , Animales , Proteínas Reguladoras de la Apoptosis/metabolismo , Encéfalo/metabolismo , Encéfalo/patología , Diabetes Mellitus Experimental/complicaciones , Infarto de la Arteria Cerebral Media/complicaciones , Interleucina-1beta/metabolismo , Masculino , Malondialdehído/metabolismo , Ratas Sprague-Dawley , Superóxido Dismutasa/metabolismo , Factor de Necrosis Tumoral alfa/metabolismo
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