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As a result of medical advancement and increasing requirements for the physiological reconstruction of the spine, various kinds of artificial lumbar prostheses have flourished.The first-generation Charité prosthesis, the second-generation ProDisc-L prosthesis and the third-generation Activ-L Systems prosthesis have all been applied widely in clinic.In addition, Acroflex, Maverick, XL TDR, M6-L and other products have also been approved for clinical application.This article reviews the literature on application of artificial lumbar intervertebral disc prostheses to conduct a comprehensive analysis of the surgical complications related to the different design features of the prostheses like unconstrained, semiconstrained, constrained, one elastomeric piece, constrained plus elastic core and integral lateral implantation, hoping to provide references for subsequent improvement in design and application of the prosthesis.
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Objective:To explore the feasibility of simultaneous combined operation for congenital heart disease with other malformations and to summarize the experience of operation and the ways to avoid risks.Methods:From May 2015 to December 2019, the clinical data of 44 children undergoing simultaneous combined operation in our hospital were collected, and the data of 44 children who were matched with the children undergoing combined operation in the same period were collected as the research objects, which were divided into high-risk group(17 cases)and low-risk group(27 cases). To compare and analyze the early hemodynamic indexes and other hospitalization indexes of different groups of children undergoing simultaneous operation and staged operation, so as to evaluate whether the scheme of simultaneous combined operation is more optimized.Results:All the children in the same period successfully underwent combined operation, among which 4 cases had postoperative complications and 1 case died out of hospital, all of them were children in high-risk group, and the other children were cured and discharged. Compared with the staging group, there was no significant difference in general data and early postoperative hemodynamic indexes of children in the same period group, but the cost of operation and anesthesia was lower, and the average hospitalization time was shortened by about 5 days for each person, with statistical significance. Compared with the low-risk group, the children in the high-risk group were significantly lower in age and weight, complicated in deformity, longer in operation time, lower in early postoperative cardiac output, stable in hemodynamics after operation, but higher in inotropicscore score(IS). Postoperative endotracheal intubation time, ICU time and overall hospitalization time were prolonged, and the overall cost was more( P<0.05) The incidence of postoperative adverse events was higher. Conclusion:Simultaneous combined operation for children with congenital heart disease with other malformations is generally safe and feasible., Staging is safe for children in high-risk group, and if simultaneous combined surgery is unavoidable, the condition must be assessed individually and a detailed treatment plan must be developed to avoid surgical risks.
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Objective@#Recent studies have shown the important influence of various micro factors on the general biological activity and function of endothelial cells (ECs). Vascular endothelial growth factor (VEGF) and angiogenin (ANG) are classic micro factors that promote proliferation, differentiation, and migration of ECs. The underlying pathophysiological mechanisms and related pathways of these micro factors remain the focus of current research.@*Data sources@#An extensive search was undertaken in the PubMed database by using keywords including "micro factors" and "endothelial cell." This search covered relevant research articles published between January 1, 2007 and December 31, 2018.@*Study selection@#Original articles, reviews, and other articles were searched and reviewed for content on micro factors of ECs. Results: VEGF and ANG have critical functions in the occurrence, development, and status of the physiological pathology of ECs. Other EC-associated micro factors include interleukin 10, tumor protein P53, nuclear factor kappa B subunit, interleukin 6, and tumor necrosis factor. The results of Gene Ontology analysis revealed that variations were mainly enriched in positive regulation of transcription by the RNA polymerase II promoter, cellular response to lipopolysaccharides, negative regulation of apoptotic processes, external side of the plasma membrane, cytoplasm, extracellular regions, cytokine activity, growth factor activity, and identical protein binding. The results of the Kyoto Encyclopedia of Genes and Genomes analysis revealed that micro factors were predominantly enriched in inflammatory diseases.@*Conclusions@#In summary, the main mediators, factors, or genes associated with ECs include VEGF and ANG. The effect of micro factors on ECs is complex and multifaceted. This review summarizes the correlation between ECs and several micro factors.
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OBJECTIVE@#Recent studies have shown the important influence of various micro factors on the general biological activity and function of endothelial cells (ECs). Vascular endothelial growth factor (VEGF) and angiogenin (ANG) are classic micro factors that promote proliferation, differentiation, and migration of ECs. The underlying pathophysiological mechanisms and related pathways of these micro factors remain the focus of current research.@*DATA SOURCES@#An extensive search was undertaken in the PubMed database by using keywords including "micro factors" and "endothelial cell." This search covered relevant research articles published between January 1, 2007 and December 31, 2018.@*STUDY SELECTION@#Original articles, reviews, and other articles were searched and reviewed for content on micro factors of ECs.@*RESULTS@#VEGF and ANG have critical functions in the occurrence, development, and status of the physiological pathology of ECs. Other EC-associated micro factors include interleukin 10, tumor protein P53, nuclear factor kappa B subunit, interleukin 6, and tumor necrosis factor. The results of Gene Ontology analysis revealed that variations were mainly enriched in positive regulation of transcription by the RNA polymerase II promoter, cellular response to lipopolysaccharides, negative regulation of apoptotic processes, external side of the plasma membrane, cytoplasm, extracellular regions, cytokine activity, growth factor activity, and identical protein binding. The results of the Kyoto Encyclopedia of Genes and Genomes analysis revealed that micro factors were predominantly enriched in inflammatory diseases.@*CONCLUSIONS@#In summary, the main mediators, factors, or genes associated with ECs include VEGF and ANG. The effect of micro factors on ECs is complex and multifaceted. This review summarizes the correlation between ECs and several micro factors.
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<p><b>Objective</b>Endothelial cells (ECs) are important metabolic and endocrinal organs which play a significant role in regulating vascular function. Vascular ECs, located between the blood and vascular tissues, can not only complete the metabolism of blood and interstitial fluid but also synthesize and secrete a variety of biologically active substances to maintain vascular tension and keep a normal flow of blood and long-term patency. Therefore, this article presents a systematic review of common injuries and healing mechanisms for the vascular endothelium.</p><p><b>Data Sources</b>An extensive search in the PubMed database was undertaken, focusing on research published after 2003 with keywords including endothelium, vascular, wounds and injuries, and wound healing.</p><p><b>Study Selection</b>Several types of articles, including original studies and literature reviews, were identified and reviewed to summarize common injury and repair processes of the endothelial lining.</p><p><b>Results</b>Endothelial injury is closely related to the development of multiple cardiovascular and cerebrovascular diseases. However, the mechanism of vascular endothelial injury is not fully understood. Numerous studies have shown that the mechanisms of EC injury mainly involve inflammatory reactions, physical stimulation, chemical poisons, concurrency of related diseases, and molecular changes. Endothelial progenitor cells play an important role during the process of endothelial repair after such injuries. What's more, a variety of restorative cells, changes in cytokines and molecules, chemical drugs, certain RNAs, regulation of blood pressure, and physical fitness training protect the endothelial lining by reducing the inducing factors, inhibiting inflammation and oxidative stress reactions, and delaying endothelial caducity.</p><p><b>Conclusions</b>ECs are always in the process of being damaged. Several therapeutic targets and drugs were seeked to protect the endothelium and promote repair.</p>
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Humans , Biological Transport , Endothelial Cells , Endothelium, Vascular , Wounds and Injuries , Inflammation , TherapeuticsABSTRACT
Objective: To study the relationship between CXCL12/CXCR4 expression and the neural invasion of salivary adenoid cystic carcinoma (SACC). Methods: Totally 41 SACC specimens, 30 tongue cancer specimens, 20 pleomorphic adenoma specimens and 20 normal nerve specimens were included in the present study. The specimens were made into sections of 4 μm and EnVision method was used to detect the expression of the chemokine receptor CXCR4 in SACC sections and the expression of the chemokine CXCL12 in the peripheral nerve tissue sections. Results: The chemokine receptor was highly expressed in ACC cells. The positive rate of CXCR4 was 63.41% in the SACC sections, which was significantly higher than those in the tongue cancer group (36.67%) and the pleomorphic adenoma parotid group (35%) (P<0.05). The expression of CXCL12 was not significantly different between the nerve tissues of SACC, tongue cancer and the normal nerve tissues. Conclusion: The cbemokine CXCL12 is elevated in the SACC cells and its receptor CXCR4 is elevated in the peripheral nerve tissues, indicating a role of the biological axis of CXCL12/CXCR4 in the neural invasion of salivary adenoid cystic carcinoma.
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<p><b>OBJECTIVE</b>Cardiotonic steroids (CTS) can bind to Na+, K+ -ATPase to activate complex intracellular signaling cascades regulating the proliferation and apoptosis of cells. The aim of this study was to investigate the effects of ouabain at different concentrations on growth regulation in various kinds of leukemia cell lines and explore the pathogenesis of leukemia, the functions of Na+, K+ -ATPase as a signal transduction conductor and its effects on cell growth.</p><p><b>METHODS</b>Using the MTT assay, the survival rates of leukemia cell lines were observed 6, 12 and 24 hrs after treatment with 1 or 10 nmol/L ouabain. The expression of Na+, K+ -ATPase alpha1 subunit of leukemia cells was detected by Western blot.</p><p><b>RESULTS</b>The MTT results showed that ouabain at 1 nmol/L or 10 nmol/L induced proliferation of lymphocytic leukemia B95 and Jhhan cell lines, as well as megakaryocytic leukemia M07e and Meg01 cell lines. Ouabain at 1 nmol/L or 10 nmol/L increased the expression of Na+, K+ -ATPase alpha1 subunit. There were significant differences in the proliferation and the expression of Na+, K+ -ATPase alpha1 subunit of the leukemia cell lines between the ouabain treatment and the blank control groups 24 hrs after ouabain treatment (P<0.05). The proliferation effect of leukemia cell lines was in a direct proportion with the ouabain concentration and incubation time.</p><p><b>CONCLUSIONS</b>Na+, K+ -ATPase plays an important role in signal transductions. Through binding to ouabain, Na+, K+ -ATPase may regulate proliferation of leukemia cell lines of different origins. Ouabain at 1 nmol/L or 10 nmol/L may induce proliferation of lymphocytic leukemia cell lines (B95, Jhhan) and megakaryocytic leukemia cell lines (M07e, Meg01), and the proliferation effect was in a direct proportion with the concentration and incubation time of ouabain.</p>
Subject(s)
Humans , Cell Proliferation , Dose-Response Relationship, Drug , Leukemia , Pathology , Ouabain , Pharmacology , Signal Transduction , Sodium-Potassium-Exchanging ATPase , Genetics , PhysiologyABSTRACT
The aim of this study was to investigate the effects of ouabain and some specific signal pathway inhibitors on growth regulation in various kinds of leukemia cell lines and to explore the role of signal pathways participating in proliferation or apoptosis of leukemia cells induced by ouabain. By using MTT, the survival rates of leukemia cell lines were observed after utilizing ouabain and the specific signal pathway inhibitors. The expressions of Na(+), K(+)-ATPase alpha1 subunit of leukemia cells were evaluated by RT-PCR and Western blot. The results showed that low concentration of ouabain (10 nmol/L) could increase the survival rates of lymphocytic leukemia Jhhan cell line and megakaryocytic leukemia M07e cell line, and could up-regulate the expression of Na(+), K(+)-ATPase alpha1 subunit. Proliferation of these leukemia cells induced by ouabain could be inhibited by PP2 and PD98059 with different extents. It is concluded that Na(+), K(+)-ATPase plays an important role in signal transductions through binding to CTS (ouabain), and they can activate complex signal pathways regulating the growth of leukemia cells. The proliferation effects of cells promoted by ouabain are mediated by activation of Src kinase and ERK1/2 dependent signaling pathway.
Subject(s)
Humans , Cell Line, Tumor , Cell Proliferation , Leukemia , Metabolism , Ouabain , Pharmacology , Signal Transduction , Sodium-Potassium-Exchanging ATPase , MetabolismABSTRACT
This study was aimed to investigate the effects of ouabain at low concentrations on growth regulation in various leukemia cell lines and to determine the therapeutic potential of ouabain in leukemia. By using MTT, flow cytometry (FCM), the changes in cell growth and cell cycle of leukemia cell lines were observed after treating with ouabain at low concentrations (<or=10 nmol/L). The expression of sodium pump alpha1 subunit was evaluated by Western blot. The results showed that in megakaryocytic leukemia M07e and Meg-01 cell lines, the low concentrations of ouabain (<or=10 nmol/L) inhibited the cell growth, blocked the cell cycle at G1 phase, and decreased the protein expression of sodium pump alpha1 subunit. The same concentrations of ouabain induced the proliferation of lymphocytic leukemia B95 and Jhhan cell lines, increased the percentage of cells at S phase and G2/M phase and up-regulated the expression of sodium pump alpha1 subunit. The basic expression of the sodium pump alpha1 subunit in M07e and Meg-01 was lower than that in B95 and Jhhan. It is concluded that the low concentrations of ouabain inhibit the cell growth of the megakaryocytic leukemia cell lines M07e and Meg-0, which may be related with the low expression of sodium pump alpha1 subunit of that cell lines and the negative regulation of the protein induced by ouabain.
Subject(s)
Humans , Cell Line, Tumor , Cell Proliferation , Dose-Response Relationship, Drug , Leukemia , Pathology , Leukemia, Megakaryoblastic, Acute , Pathology , Ouabain , Pharmacology , Sodium-Potassium-Exchanging ATPase , MetabolismABSTRACT
<p><b>AIM</b>Probe into protective action of taurine against exercise-induced myocardial damage in rats after exhaustive exercise.</p><p><b>METHODS</b>Using the model of exhaustive exercise, the present study researches into effects of taurine on the content of triiodothyronine (T3) and tetraiodothyronine (T4) in serum and myocardium as well as the activity of T(4) 5' deiodinase (T(4)5'-DI) and second messenger cAMP in myocardium of rats.</p><p><b>RESULTS</b>The content of T3 in serum and myocardium, T(4)5'-DI activity, second messenger cAMP in myocardium increased significantly (P < 0.01) while that of T4 in serum and myocardium did not change significantly after exhaustive swimming. The supplement of taurine might significantly inhibit above changes caused by exhaustive exercise.</p><p><b>CONCLUSION</b>Taurine could protect myocardium from exhaustive exercise induced damage by inhibiting hypermetabolism of thyroid hormone and change of second messenger.</p>
Subject(s)
Animals , Male , Rats , Myocardium , Metabolism , Physical Conditioning, Animal , Rats, Sprague-Dawley , Second Messenger Systems , Taurine , Pharmacology , Thyroid Hormones , BloodABSTRACT
0.05).However,phosphor-ERK and phosphor-STAT3,NF-?B were higher in CVB_3 group than those in control groups(P