Objective To evaluate the therapeutic efficacy and safety of transcatheter closure of atrial septal defect (ASD) and patent ductus arteriosus (PDA) using Amplatzer occluder. Methods Routine cardiac catheterization and angiography were performed in 50 patients (23 male, 27 female, age ranging from 3 to 64 years old), including 19 cases of ASD and 31 cases of PDA under local or general anesthesia. After balloon sizing of the ASD, the optimal Amplazter septal occluder (ASO) was transmitted into the left atrial, and the left and right disks were released in turn. The Amplatzer occluder was completely released after transthoracic echocardiography confirmed that there was no residual shunts or new onset mitral valve regurgitation. The Amplatzer duct occluder (ADO) size was selected according to the narrowest point of PDA measured by angiography, and the occluder was released after the repeated angiography showed no residual shunts. Results ① The mean diameter of the ASD measured by balloon was 13-31 (23?6) mm and the diameter of ASO was (17-40) mm. The immediate closure rate was 100%. ② Angiography confirmed that closure of the ductus using ADO was achieved in 30 patients, and closure of the large size (12 mm) was achieved in 1 case of PDA patient using ASO (17 mm). No complications were encountered. Conclusion Transcatheter closure of ASD and PDA using Amplatzer device, with the advantages of simple operation, confirmative occlusion efficacy, minimal invasiveness, wide indications, and less complications, has a bright future of clinical application.

BACKGROUNDTo investigate the biological functions of a novel hepatitis B virus e antigen (HbeAg) interacting protein AK026018, and to use cDNA microarray technique to screen genes regulated by the protein.

METHODSThe AK026018 coding DNA fragment was amplified by reverse transcription polymerase chain reaction (RT-PCR) technique from HepG2 cell. The expressive vector of pcDNA3.1-AK was constructed by routine molecular biological methods. The HepG2 cells were transfected with pcDNA3.1 and pcDNA3.1-AK, respectively by using lipofectamine. The total RNA was isolated and reverse transcribed. The cDNA of each sample was subjected to microarray screening with 8,464 cDNA probes and analyzed by bioinformatics.

RESULTSThe expressive vector was constructed and confirmed by DNA sequencing analysis and restriction enzyme digestion. High quality mRNA and cDNA of transfected HepG2 cells had been prepared and successful microarray screening conducted. From the scanning results, there were 122 differential expression genes, of which 36 genes were down-regulated, and 16 genes were up-regulated.

CONCLUSIONMicroarray technique was successfully used to screen the genes trans-regulated by AK026018. The expression of AK026018 protein affects the expression spectrum of HepG2 cells.

Carrier Proteins ; genetics ; metabolism ; physiology ; Cell Line, Tumor ; Computational Biology ; Gene Expression Regulation, Neoplastic ; Hepatitis B e Antigens ; metabolism ; Humans ; Oligonucleotide Array Sequence Analysis ; methods ; Protein Binding ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection

BACKGROUND/OBJECTIVES: The objectives of this study were to investigate the effects of lycopene on the migration, adhesion, tube formation capacity, and p38 mitogen-activated protein kinase (p38 MAPK) activity of endothelial progenitor cells (EPCs) cultivated with high glucose (HG) and as well as explore the mechanism behind the protective effects of lycopene on peripheral blood EPCs. MATERIALS/METHODS: Mononuclear cells were isolated from human peripheral blood by Ficoll density gradient centrifugation. EPCs were identified after induction of cellular differentiation. Third generation EPCs were incubated with HG (33 mmol/L) or 10, 30, and 50 microg/mL of lycopene plus HG. MTT assay and flow cytometry were performed to assess proliferation and apoptosis of EPCs. EPC migration was assessed by MTT assay with a modified boyden chamber. Adhesion assay was performed by replating EPCs on fibronectin-coated dishes, after which adherent cells were counted. In vitro vasculogenesis activity was assayed by Madrigal network formation assay. Western blotting was performed to analyze protein expression of both phosphorylated and non-phosphorylated p38 MAPK. RESULTS: The proliferation, migration, adhesion, and in vitro vasculogenesis capacity of EPCs treated with 10, 30, and 50 microg/mL of lycopene plus HG were all significantly higher comapred to the HG group (P < 0.05). Rates of apoptosis were also significantly lower than that of the HG group. Moreover, lycopene blocked phosphorylation of p38 MAPK in EPCs (P < 0.05). To confirm the causal relationship between MAPK inhibition and the protective effects of lycopene against HG-induced cellular injury, we treated cells with SB203580, a phosphorylation inhibitor. The inhibitor significantly inhibited HG-induced EPC injury. CONCLUSIONS: Lycopene promotes proliferation, migration, adhesion, and in vitro vasculogenesis capacity as well as reduces apoptosis of EPCs. Further, the underlying molecular mechanism of the protective effects of lycopene against HG-induced EPC injury may involve the p38 MAPK signal transduction pathway. Specifically, lycopene was shown to inhibit HG-induced EPC injury by inhibiting p38 MAPKs.
Apoptosis ; Blotting, Western ; Centrifugation, Density Gradient ; Ficoll ; Flow Cytometry ; Glucose* ; Humans ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Protein Kinases ; Signal Transduction ; Stem Cells*

BACKGROUND/OBJECTIVES: The objectives of this study were to investigate the effects of lycopene on the migration, adhesion, tube formation capacity, and p38 mitogen-activated protein kinase (p38 MAPK) activity of endothelial progenitor cells (EPCs) cultivated with high glucose (HG) and as well as explore the mechanism behind the protective effects of lycopene on peripheral blood EPCs. MATERIALS/METHODS: Mononuclear cells were isolated from human peripheral blood by Ficoll density gradient centrifugation. EPCs were identified after induction of cellular differentiation. Third generation EPCs were incubated with HG (33 mmol/L) or 10, 30, and 50 microg/mL of lycopene plus HG. MTT assay and flow cytometry were performed to assess proliferation and apoptosis of EPCs. EPC migration was assessed by MTT assay with a modified boyden chamber. Adhesion assay was performed by replating EPCs on fibronectin-coated dishes, after which adherent cells were counted. In vitro vasculogenesis activity was assayed by Madrigal network formation assay. Western blotting was performed to analyze protein expression of both phosphorylated and non-phosphorylated p38 MAPK. RESULTS: The proliferation, migration, adhesion, and in vitro vasculogenesis capacity of EPCs treated with 10, 30, and 50 microg/mL of lycopene plus HG were all significantly higher comapred to the HG group (P < 0.05). Rates of apoptosis were also significantly lower than that of the HG group. Moreover, lycopene blocked phosphorylation of p38 MAPK in EPCs (P < 0.05). To confirm the causal relationship between MAPK inhibition and the protective effects of lycopene against HG-induced cellular injury, we treated cells with SB203580, a phosphorylation inhibitor. The inhibitor significantly inhibited HG-induced EPC injury. CONCLUSIONS: Lycopene promotes proliferation, migration, adhesion, and in vitro vasculogenesis capacity as well as reduces apoptosis of EPCs. Further, the underlying molecular mechanism of the protective effects of lycopene against HG-induced EPC injury may involve the p38 MAPK signal transduction pathway. Specifically, lycopene was shown to inhibit HG-induced EPC injury by inhibiting p38 MAPKs.
Apoptosis ; Blotting, Western ; Centrifugation, Density Gradient ; Ficoll ; Flow Cytometry ; Glucose* ; Humans ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Protein Kinases ; Signal Transduction ; Stem Cells*

OBJECTIVETest the cytokines secretion by peripheral blood mononuclear cells (PBMC) from hepatitis C patients after stimulation with highly variable region (HVR1) synthetic peptides.

METHODSELISA was used to test the cytokines secretion, flow cytometry to group the proliferated cells, and the antigenicity of synthetic peptide was predicted by the computer modeling.

RESULTS(1)There were PBMC proliferation when stimulated by HVR1 antigen synthetic peptides. (2) There was a rise of IFN-gamma, IL-4 and IL-10. But no rise of IL-2 and TNF-gamma was found. (3) The proliferated cells were mainly CD4+ lymphocytes.

CONCLUSIONPMBC from hepatitis C patients tend to secret Th2 cytokines after stimulation with HVR1 designed by the authors.

Amino Acid Sequence ; Cells, Cultured ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Hepatitis C ; blood ; virology ; Humans ; Interferon-gamma ; metabolism ; Interleukin-10 ; metabolism ; Interleukin-4 ; metabolism ; Leukocytes, Mononuclear ; cytology ; drug effects ; metabolism ; Oligopeptides ; chemical synthesis ; chemistry ; pharmacology ; Time Factors

Objective To evaluate interventional therapy for biliary stricture (BS) after orthotopic liver transplantation (OLT). Methods The efficacy of interventional therapy for BS after OLT from Oct 2003 to Jan 2006 was analyzed retrospectively. Fifty-three patients received 107 times of interventional therapy through endoscopic retrograde cholangiography ( ERC) which included 68 nasobiliary catheter placements,26 biliary balloon dilatations and stent placements and 13 ERC. Nine patients received 11 times of interventional therapy through percutaneous transhepatic cholangiography ( PTC) including 2 PTC, 7 percutaneous drainages,3 biliary balloon dilatations and 1 biliary stent replacement. One patient received bile drainage through T tube. Results The success rate of ERC was 88. 8% (95/107) , that of nasobiliary catheter placement 94% (64/68) , biliary stent placement 88. 5% (23/26). The success rate of PTC was 81. 8% (9/11) , that of percutaneous drainage was 100% (7/7) , biliary stent replacement 100% (1/1). The curative rate of interventional therapy for 53 patients with BS was 28. 3% (15/53) ,the improvement rate was 41. 5% (22/53). The curative rate of interventional therapy for anastomotic, extrahepatic, intrahepatic hilar and diffuse BS was respectively 66. 7% (4/6)、66. 7% (10/15)、50% (1/2)、0 (0/7) and 0 (0/22). Conclusions The efficacy of interventional therapy for BS after OLT was not satisfactory. The result relates to the type of BS, for anastomotic, extrahepatic and solitary intrahepatic BS this therapy was effective, while that for hilar and diffuse BS the prognosis was poor.

Purpose: During the COVID-19 pandemic, nurses have faced many professional and ethical dilemmas and challenges along with bearing physical, mental, and emotional stress resulting from worrying about themselves or their family being infected and stigmatized. This stress can potentially lead to burnout and resignation. Professional resilience is crucial for nurses to cope with these adverse situations. This study aimed to investigate the process by which nurses adapt, change, and overcome challenges during the COVID-19 pandemic and ultimately demonstrate professional resilience. Methods: Descriptive phenomenology was applied. Semi-structured interviews were conducted with 11 nurses working in COVID-19 wards and intensive care units to collect data. Giorgi's phenomenological analysis method was employed. Results: Based on the interview responses, four major themes were identified: 1) balancing patient care, self-protection, and passing on experience; 2) providing timely pandemic team resources and social support; 3) nurses' perseverance amid social discourse and constrained lives; and 4) selfless dedication shaping nursing's pinnacle experiences. Conclusions In the face of a sudden pandemic, frontline nurses play a critical role in maintaining medical capacity. Consequently, they must balance their families, lives, and work while adapting to the impact of the pandemic and changing practices and procedures based on the development of the pandemic and policy demands. The study findings provide insights into the challenges and emotional experiences encountered by nurses during a sudden pandemic outbreak and can serve as a reference for developing strategies to help nurses overcome these challenges and enhance their professional resilience.

BACKGROUNDCholesterol-lowering therapy with statins has been reported to reduce the morbidity and mortality of cardiovascular diseases. This study aimed to investigate the effects of combined application of extended-release niacin and atorvastatin on lipid profile modification and the risks of adverse events in patients with coronary artery disease.

METHODSConsecutive 108 patients with coronary artery disease and serum total cholesterol (TC) > or = 3.5 mmol/L were randomized into two groups: group A using atorvastatin and group B using extended-release niacin (niacin ER) and atorvastatin. Plasma lipid profile, glucose, and adverse events were assessed at the hospitalization, and 6 and 12 months after treatment. In addition, clinical cardiovascular events were evaluated after 12 months of treatment.

RESULTSThe levels of TC, low density lipoprotein cholesterol (LDL-C) were significantly decreased (P < 0.05) in groups A and B, but the levels of high density lipoprotein cholesterol (HDL-C) and ApoA increased by 29.36% and 40.81% respectively after 12 months of treatment in group B (P < 0.01). The medications were generally well tolerated in the two groups. No significant difference of adverse events was found between the two groups (group A: 3.2% vs group B 5.1%, P > 0.05).

CONCLUSIONSCombined use of extended-release niacin with atorvastatin was superior to atorvastatin monotherapy alone in lipid profile regulation. Combination therapy with niacin ER and atorvastatin was well tolerated and safe in patients with coronary artery disease.

Aged ; Anticholesteremic Agents ; pharmacology ; therapeutic use ; Apolipoproteins A ; blood ; Atorvastatin Calcium ; Cholesterol ; blood ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Coronary Artery Disease ; drug therapy ; Female ; Heptanoic Acids ; pharmacology ; therapeutic use ; Humans ; Lipid Metabolism ; drug effects ; Male ; Middle Aged ; Niacin ; pharmacology ; therapeutic use ; Pyrroles ; pharmacology ; therapeutic use

BACKGROUNDThere remains significant debate as to the relationship between fragmented QRS (fQRS) complexes on electrocardiogram (ECG) and acute myocardial infarction (AMI). Few studies have reported on this relationship in non-ST elevated AMI (NSTEMI), and thus, we attempt to assess this relationship and its potential short-term prognostic value.

METHODSThis was a single-center, observational, retrospective cohort study. A total of 513 consecutive patients (399 men, 114 women) with NSTEMI within 24 h who underwent coronary angiography at our department, between January 1, 2014, and December 31, 2014. Patients were divided into 2 groups according to the presence or absence of fQRS complex on the admission ECG. fQRS complexes were defined as the existence of an additional R' or crochetage wave, notching in the nadir of the S wave, RS fragmentation, or QS complexes on 2 contiguous leads. All patients were followed up for 6 months, and all major adverse cardiac events (MACE) were recorded.

RESULTSIn this study, there were 285 patients with fQRS ECG in the 513 patients with NSTEMI. The number of patients with 0-2 coronary arteries narrowed by ≥50% in fQRS group were less while patients with 3 narrowed arteries were more than in the non-fQRS group (P = 0.042). There were fewer Killip Class I patients in the fQRS group (P = 0.019), while Killip Class II, III, and IV patients were more in the fQRS group than in the non-fQRS group (P = 0.019). Left ventricular ejection fraction levels were significantly lower in the fQRS group (P = 0.021). Baseline total cholesterol, low-density lipoprotein, creatinine, creatine kinase, homocysteine, high-sensitivity C-reactive protein (CRP), and red blood cells distribution width levels were significantly higher in the fQRS group. Total MACE (MACE, P = 0.028), revascularization (P = 0.005), and recurrent angina (P = 0.005) were also significantly greater in the fQRS group. On final logistic regression analysis, after adjusting for baseline variables, the following variables were independent predictors of fQRS: Coronary artery narrowing (P = 0.035), Killip classification (P = 0.026), and total cholesterol (P = 0.002). The following variables were found to be independent predictors of preoperative MACE: Hemoglobin (P = 0.000), gender (P = 0.026), fQRS (P = 0.016), and time from myocardial infarction to balloon or coronary artery bypasses grafting (P = 0.013).

CONCLUSIONSThe fQRS complexes are commonly present in NSTEMI and the fQRS complexes are an independent predictor of MACE in NSTEMI patients. The number of narrowed coronary arteries, Killip classification, and total cholesterol are all independent predictors of the fQRS complexes.

Aged ; C-Reactive Protein ; analysis ; Electrocardiography ; Female ; Humans ; Logistic Models ; Male ; Middle Aged ; Myocardial Infarction ; blood ; physiopathology ; Prognosis ; Retrospective Studies

OBJECTIVETo investigate the mechanism of the development of cisplatin resistance in a human esophageal squamous carcinoma cell line.

METHODSThe cytotoxicity of cisplatin in the cisplatin-resistant resistant cell line EC109/CDDP and its parental cell line EC109 was measured by MTT assay. Whole-cell cisplatin accumulation and Pt-DNA adduct formation were determined by inductively coupled plasma mass spectrometry (ICP-MS). Western blotting was used to investigate the protein expression of full length PARP, cleaved PARP, and copper transporter 1 (CTR1).

RESULTSEC109/CDDP cells was more resistant to cisplatin-induced cytotoxicity and apoptosis than EC109 cells. Compared with EC109 cells, EC109/CDDP cells exhibited less cisplatin accumulation and Pt-DNA adduct formation with also decreased CTR1 protein expression.

CONCLUSIONCisplatin induces drug resistant phenotype by decreasing the protein level of CTR1, which controls cell accumulation and cytotoxic effect of cisplatin.

Carcinoma, Squamous Cell ; metabolism ; Cation Transport Proteins ; metabolism ; Cell Line, Tumor ; Cisplatin ; pharmacology ; Down-Regulation ; Drug Resistance, Neoplasm ; drug effects ; Esophageal Neoplasms ; metabolism ; Humans