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Cardiovascular diseases (CVDs) are a leading factor driving mortality worldwide. Iron, an essential trace mineral, is important in numerous biological processes, and its role in CVDs has raised broad discussion for decades. Iron-mediated cell death, namely ferroptosis, has attracted much attention due to its critical role in cardiomyocyte damage and CVDs. Furthermore, ferritinophagy is the upstream mechanism that induces ferroptosis, and is closely related to CVDs. This review aims to delineate the processes and mechanisms of ferroptosis and ferritinophagy, and the regulatory pathways and molecular targets involved in ferritinophagy, and to determine their roles in CVDs. Furthermore, we discuss the possibility of targeting ferritinophagy-induced ferroptosis modulators for treating CVDs. Collectively, this review offers some new insights into the pathology of CVDs and identifies possible therapeutic targets.
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Humans , Cardiovascular Diseases , Ferroptosis , Iron , Trace ElementsABSTRACT
OBJECTIVE@#To explore the chronic injury and its possible mechanism of ionizing radiation on multipotent hematopoietic progenitor cells (MPPs) by determining the related indicators of MPPs in bone marrow of mice post-radiation.@*METHODS@#Sixteen C57BL/6 adult mice were randomly divided into normal control and irradiation groups, 8 mice in each group. The mice in irradiation group were exposed to 6 Gy X-ray. The proportion of bone marrow MPPs, their apoptosis and proliferation 2 months after irradiation were detected by flow cytometry. Mitochondrial activity and levels of reactive oxygen species (ROS) in each MPPs population were detected by Mitotracker Red and DCFDA probes, and the senescent state of MPPs in the bone marrow was analyzed.@*RESULTS@#Ionizing radiation could reduce the proportion of MPPs in mouse bone marrow. The proportions and numbers of MPP1, MPP3 and MPP4 in the bone marrow were significantly decreased after whole-body irradiation with 6 Gy X-ray (P<0.05). In addition, radiation significantly reduced the colony-forming capacity of MPPs in bone marrow (P<0.05), the proportions of apoptotic cells in the MPP1 and MPP4 cell populations increased significantly in the bone marrow (P<0.05). The activity of mitochondria was significantly reduced in the bone marrow MPP2, MPP3 and MPP4 cell populations compared with that of the control group (P<0.05). It was also found that the radiation could significantly increase the ROS levels of MPPs in bone marrow, and the content of ROS in the MPP2, MPP3 and MPP4 cell population of the bone marrow was significantly increased(P<0.05). The senescent cells ratios of MPP1, MPP3 and MPP4 cells in the bone marrow after irradiation were significantly higher than those in the control group (P<0.05).@*CONCLUSION@#Ionizing radiation can cause chronic MPPs damage in mice, which is closely associated with persistent oxidative stress, cells apoptosis, and cellular senescence.
Subject(s)
Mice , Animals , Bone Marrow , Reactive Oxygen Species , Mice, Inbred C57BL , Hematopoietic Stem Cells , Whole-Body Irradiation , Radiation, Ionizing , Bone Marrow CellsABSTRACT
OBJECTIVES@#To study the effect of glucose metabolism disorders on the short-term prognosis in neonates with asphyxia.@*METHODS@#A retrospective analysis was performed on the medical data of the neonates with asphyxia who were admitted to 52 hospitals in Hubei Province of China from January to December, 2018 and had blood glucose data within 12 hours after birth. Their blood glucose data at 1, 2, 6, and 12 hours after birth (with an allowable time error of 0.5 hour) were recorded. According to the presence or absence of brain injury and/or death during hospitalization, the neonates were divided into a poor prognosis group with 693 neonates and a good prognosis group with 779 neonates. The two groups were compared in the incidence of glucose metabolism disorders within 12 hours after birth and short-term prognosis.@*RESULTS@#Compared with the good prognosis group, the poor prognosis group had a significantly higher proportion of neonates from secondary hospitals (48.5% vs 42.6%, @*CONCLUSIONS@#Recurrent hyperglycemia in neonates with asphyxia may suggest poor short-term prognosis, and it is necessary to strengthen the early monitoring and management of the nervous system in such neonates.
Subject(s)
Humans , Infant, Newborn , Asphyxia , Asphyxia Neonatorum/epidemiology , Hyperglycemia , Prognosis , Retrospective StudiesABSTRACT
:Traditional apical or atrial appendage pacing have adverse impact on myocardial function ,while atrial sep‐tum is a relatively physiological pacing site .M3830 electrode is a kind of active fixing ,bipolar and hormone‐relea‐sing electrode ,which can effectively reduce diameter of pacing wire up to 40%,and effectively reduce incidence of complications .The present article made a review on application of 3830 pacing electrode in atrial septal pacing .
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While receiving cardiac resynchronization therapy (CRT) ,traditional left ventricular lead implantation may fail due to anatomical abnormality of heart vein ,poor left ventricular pacing threshold ,lead dislocation and ra-dial nerve stimulation etc .So left ventricular quadripolar leads rise in response to the proper time and condition .The present article made a brief review on research progress of application of left ventricular quadripolar leads in clinic .
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Cardiac pacemaker is a critical therapeutic option for patients with bradyarrhythmias,but traditional wired pacemakers have many shortcomings.Current efforts to develop leadless cardiac pacemakers(LCP)have two primary goals,namely to reduce lead-associated complications and to avoid surgical scar associated with placement. The present article reviewed related researches on LCP in recent years,and explored the limitations and future de-velopment of different LCP currently under study.
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Paroxysmal supraventricular tachycardia (PSVT) is one of the frequent cardiovascular diseases.In recent years, cryoablation has become a research hot spot for PSVT treatment.Theoretically, its operability and safety are both better than those of radiofrequency ablation.Cryoablation can significantly reduce risk of ablation complications, but how to reduce recurrent rate after cryoablation is still a problem in the future.The present article made a review on main therapeutic methods of PSVT, especially application of cryoablation.
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Objective To investigate the situation of Pseudomonas aeruginosa strains carrying metallo-β-lactamases and inte-grases in the Second Affiliated Hospital of Harbin Medical University.Methods The phenotype of metallo-β-lactamases were detected by modified Hodge test,double-disc synergy and combination paper method,respectvily.PCR method was used to detecte metallo-β-lactamases genotypes and the integrationⅠ,Ⅱ and Ⅲ.The PCR products of the whole length bla-IMP gene were purified,sequenced and analyzed by Blast.Results Among 62 Pseudomonas aeruginosa strains,metallo-β-lactamases phenotype of 3 by modified hodge test,4 by double-disc synergy test,4 by combination paper method and were all positive 4 of IMP-1 type metallo-β-lactamases of Pseudomonasaeruginosa strains (10%,4/40)were positives by PCR.Inte-grase Ⅰ of 16(40 %,16/40)strains were positives by PCR method in IMP-resistant Pseudomonasaeruginosa,and integraseⅠ of 22.73 %(5/22)were positives in IMP-sensitive Pseudomonasaeruginosa.No other metallo-β-lactamases,integraseⅡandⅢ were detected in this study.Conclusion IMP-type metallo-β-lactamase existed in IMP-resistant Pseudomonasaerugi-nosa isolates of the Second Affiliated Hospital of Harbin Medical University.Most strains carried integraseⅠ,and other re-sistance mechanisms may be associated with multi-drug resistance,so it is important to prevent the Pseudomonasaeruginosa strains which carried metallo-β-lactamases and integrons widely spread in the hospital.
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Objective To construct mutant strains of Klebsiella pneumoniae with ampG gene dele-tion by homologous recombination and to evaluate the role of ampG gene in inducing the expression of AmpC enzyme.Methods Polymerase chain reaction ( PCR) was used to amplify the upstream and downstream fragments of ampG gene.The gene splicing by overlap extension PCR ( SOE-PCR) technique was used to construct the fusion fragment , which was then ligated into the temperature sensitive suicide vector pKO 3-km after enzyme digestion as pKO3-km-ΔampG.To achieve allelic exchange , the plasmid pKO3-km-ΔampG was introduced into Kp1 and Kp NTUH-K2044 strains by electroporation .The mutant strains of Klebsiella pneu-moniae with ampG gene deletion were screened out .The plasmid pACYC184-ampCR was introduced into the Kp NTUH-K2044 wild-type strain and its mutant strain with ampG gene deletion to make them harbor the gene encoding AmpC enzyme .The disk diffusion method was used to evaluate the effects of ampG gene on the expression of AmpC enzyme in Klebsiella pneumoniae strains with cefoxitin as the inducer .Results The recombinant plasmid pKO3-km-ΔampG was constructed successfully .The mutant strains of Klebsiella pneu-moniae with ampG gene deletion were constructed as verified by PCR and DNA sequencing .Compared with the Kp1 wild type strain, no AmpC enzyme was produced by the ampG gene knock-out Kp1 strain.The Kp NTUH-K2044 strain could produce AmpC enzyme , while the mutant strain of Kp NTUH-K2044 with ampG gene deletion could not after introduced the pACYC 184-ampCR plasmid .Conclusion The mutant strain of Klebsiella pneumoniae with ampG gene deletion was successfully constructed .The Klebsiella pneumonia strain without the ampG gene could not produce the AmpC enzyme .
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Cardiac pacing site has an important impact on the activation sequence and systolic synchrony of heart , which is an important factor determining clinical effect of cardiac pacing .Along with expanding and use of active fixed electrode in clinic ,especially adjustable bending delivery sheath ,it makes right atrial pacing of non -tradition‐al site possible .But whether changing atrial pacing site can reduce atrial fibrillation load after pacemaker implanta‐tion is still controversial .Now the present article made a simple review about research progress of interatrial septum pacing .
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Many studies have shown that changes in ion channels,abnormal regulation of neurotransmitters and their receptors,blood-brain barrier damage,inflammation,oxidative stress etc,are all related with seizures.Animal models of epilepsy,focusing on autopsy of patients with epilepsy or pathological changes of epileptic,have found that there is a certain relationship between astrocytes and epilepsy,but the cause has remained unclear.At present,most of antiepilepfic drugs work on the target of neurons,which have certain impact on the patient's congnitive and brain function.Therefore,to investigate the pathogenesis of epilepsy from the perspective of astcytes,it might help to identify new intervention targets for new antiepileptic drugs.
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<p><b>OBJECTIVE</b>To investigate the effects of B7H4 on human bone marrow mesenchymal stem cells (HBMSC) mediating immune suppression.</p><p><b>METHODS</b>The expression of the negative immunoregulatory factor B7H4 on HBMSC were analyzed by RT-PCR and flow cytometry (FCM), respectively. The blocking experiment was used to detect the effects of B7H4 on HBMSC mediating suppression on PHA induced T cell activation, proliferation and cell cycle. HBMSC inhibiting T cell proliferation was examined by transwell cell culture system.</p><p><b>RESULTS</b>B7H4 was highly expressed on HBMSC. Blocking the B7H4 expression by B7H4mAb significantly attenuated the inhibitory effects of HBMSC on T cell proliferation. Compared with that of the unblocking group, T cell stimulator index (SI) of the B7H4 blocked group was significantly increased (53 +/- 5 vs 15 +/- 8, P < 0.01) and the inhibitory effects of HBMSC on T cell cycle were weakened significantly through down-regulating the cell number in G(0)/G(1) phase \[(85.6 +/- 9.9)% vs (95.8 +/- 9.9)%\] and up-regulating those in S phase\[(5.8 +/- 3.2)% vs (2.3 +/- 2.2)%, P < 0.05\]. The suppressive effects of HBMSC on T cell proliferation were significantly weakened after separating HBMSC from T cells by transwell cell culture system. Compared with the cell to cell contact group, T cell SI was significantly increased (27 +/- 17 vs 15 +/- 3, P < 0.01).</p><p><b>CONCLUSION</b>HBMSC highly express B7H4, which plays an important role in the suppressive effects of HBMSC on T cell proliferation.</p>
Subject(s)
Humans , B7-1 Antigen , Metabolism , Physiology , Bone Marrow Cells , Allergy and Immunology , Metabolism , Cell Cycle , Allergy and Immunology , Cell Proliferation , Cells, Cultured , Lymphocyte Activation , Allergy and Immunology , Mesenchymal Stem Cells , Allergy and Immunology , Metabolism , Phytohemagglutinins , Pharmacology , T-Lymphocytes , Cell Biology , Allergy and Immunology , V-Set Domain-Containing T-Cell Activation Inhibitor 1ABSTRACT
D-Serine has recently been identified as a major gliotransmitter in the mammal central nervous system (CNS). The distribution of D-serine is analogous to the N-methyl-D-aspartate (NMDA)-type glutamate receptors in the brain. D-Serine is as potent as glycine as a coagonist at the glycine-binding site of NMDA receptors. Thus, D-serine has been considered as an endogenous ligand of the NMDA receptors in the brain. D-Serine is synthesized by serine racemase (SR) from L-serine. Both D-serine and SR have been enriched to astrocytes which are the dynamic partners of neurons at synapses and participate in controlling synaptic transmission, synaptic plasticity and synaptogenesis. The present review highlights the most recent findings on the molecular mechanisms of controlling D-serine metabolism in the CNS, the physiological role of D-serine in synaptic plasticity, and the pathological relevance of D-serine to schizophrenia, excitotoxicity- and neuroinflammation-induced neuronal death as well as neuropathic pain. Finally, as we have recently established SR knockout mouse strain with pure C57BL/6 genetic background, this novel mouse model will contribute the analysis of physiological and pathophysiological role of D-serine in vivo.
Subject(s)
Brain/physiology , Serine/physiology , Animals , Astrocytes/physiology , Brain/metabolism , Cell Death , Mice , Neuronal Plasticity , Neurotransmitter Agents/physiology , Pain/etiology , Racemases and Epimerases/physiology , Receptors, N-Methyl-D-Aspartate/physiology , Schizophrenia/etiology , Serine/biosynthesis , Serine/metabolism , Synapses/physiology , Synaptic TransmissionABSTRACT
<p><b>OBJECTIVE</b>To evaluate the prognostic value of ST resolution (STR) measured in a single ECG lead obtained early after primary PCI in patients with ST-elevation myocardial infarction (STEMI).</p><p><b>METHODS</b>In this retrospective study, STR, MACE and factors contributed to STR were analyzed in 964 patients underwent primary PCI post STEMI. The ECGs analysis was made by technicians blinded to the clinical data. MACE was compared between the STR (n = 662) and the non-STR (n = 302) groups. Factors associated with non-STR were analyzed by logistic regression method.</p><p><b>RESULTS</b>Although TIMI grade III flow was achieved after PCI, non-STR was shown in nearly 1/3 patients and these patients were older, dominant with anterior myocardial infarction, cardiac dysfunction, diabetes and was associated with a higher MACE ratio (25.5% vs. 4.4%, P < 0.001). Cox regression showed that non-STR was one of the independent predictors of in-hospital MACE (RR = 3.33, P < 0.001). Logistic regression showed that anterior myocardial infarction, the pain to balloon time, cardiac dysfunction and white blood cell count on admission were predictive factors of non-STR.</p><p><b>CONCLUSIONS</b>STR obtained in a single ECG lead is an easy and important prognosticator of MACE post PCI in patients with STEMI. It could therefore be used to identify low- and high-risk STEMI patients post primary PCI.</p>
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Angioplasty, Balloon, Coronary , Electrocardiography , Emergency Treatment , Myocardial Infarction , Therapeutics , Prognosis , Retrospective Studies , Treatment OutcomeABSTRACT
OBJECTIVE To investigate the occurrence and the genotype character of AmpC ?-lactamases-producing Escherichia coli isolated from the Second Hospital affiliated to Harbin Medical University.METHODS K-B disk diffusion test and FOX(≤17mm) test were used as initial screen tests to detect the clinical isolates;AmpC ?-lactamases were confirmed by three-dimentional extract tests;multiple-PCR was used for detecting plasmid-mediated AmpC gene and their genotypes were determined by DNA sequencing;the regulator genes of high producing AmpC isolates of E.coli were cloned to pUCm vectors and sequenced,the difference among them was analyzed by blast method.RESULTS Among total 586 E.coli clinical isolates,10 isolates(1.70%) resisted to cefoxitin;three-dimensional extract tests were positive for all 10 isolates;4 isolates of E.coli were plasmid-mediated DHA-1 type AmpC ?-lactamases by using multiplex PCR and DNA sequencing;6 isolates of chromosomal high level AmpC ?-lactamases-producing E.coli were sequenced and contrasted to that of E.coli K12,showed that they were gene polymorphism.CONCLUSIONS E.coli clinical isolates producing high level AmpC ?-lactamases not only acquire plasmid-mediated DHA-1 AmpC ?-lactamases but also cause by chromosomal ampC promotor or attenuator gene mutations in our hostiptal.
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The immunoregulatory effects of mescenchymal stem cell (MSC) and its application have become a hot research topic in recent years. This article reviews the up-to-dated research advances in the features and mechanisms of immune regulation of MSC and its application.
Subject(s)
Animals , Humans , Lymphocyte Subsets , Allergy and Immunology , Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells , Physiology , T-Lymphocytes, Regulatory , Allergy and ImmunologyABSTRACT
Objective To test the timeliness of newly developed electronic medical tag system.Methods According to a standardized logistical process of medical tag in battlefield,timeliness tests of electronic medical tag and paper-based medical tag in two different echelons: battalion-company and medical battalion were completed,and the data of two groups were compared.Results It showed that the consumed time in the electronic medical tag system was 3/10 and 1/11 of the consumed time in paper-based medical tag respectively.Conclusion The timeliness of the electronic medical tag system is much better than that of the paper-based medical tag and meets the timeliness requirements of treatment in battlefield.
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Objective To select a electronic medical tag system suitable for modern war. Methods The active radio frequency identification technology was surveyed, modeled, and improved. Results It was demonstrated be tests that active radio frequency identification technology met the requirements of electronic medical tag system. Conclusion The electronic medical tag system based on radio frequency identification technology changes the traditional working mode and enhances integral capability of field first aid.
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The non-receptor-type Src tyrosine kinases are key components of intracellular signal transduction that are expressed at high levels in the nervous system. To improve understanding of the cascades of molecular events underlying peripheral nerve regeneration, we analyzed active Src expression in the crushed or cut rat sciatic nerves using a monoclonal antibody (clone 28) that recognizes the active form of Src tyrosine kinases, including c-Src and c-Fyn. Western blots showed that active Src expressed in the normal sciatic nerve transiently increased up to threefolds after both types of injury. Immunohistochemistry using clone 28 showed that axonal components are the primary sites of active Src expression in the normal sciatic nerve. Soon after both types of injury, active Src was abundantly expressed in Schwann cells of the segments distal to the injury site. The expression of active Src in the cells decreased with restoration of the axon-Schwann cell relationship and eventually became depleted to very low levels after crushing, but was sustained at high levels in the cut model until the end of the experiment. Regenerated axons consistently expressed active Src throughout nerve regeneration and these eventually became the major sites of active Src expression in the crushed nerve. Among the Src tyrosine kinases, active c-Src selectively increased after crushing according to immunoprecipitation and immunoblotting analyses. Due to its potent biological activity, the increased amounts of the active form of Src probably enhance axonal regrowth, the Schwann cell response, and axon-Schwann cell contact for peripheral nerve regeneration.
Subject(s)
Axons/metabolism , Nerve Regeneration/physiology , Schwann Cells/metabolism , Sciatic Neuropathy/metabolism , Up-Regulation/physiology , src-Family Kinases/metabolism , Animals , Axotomy , Cell Communication/physiology , Disease Models, Animal , Ectodysplasins , GAP-43 Protein/metabolism , Immunohistochemistry , Male , Membrane Proteins/metabolism , Nerve Crush , Neurofilament Proteins/metabolism , Proto-Oncogene Proteins/metabolism , Proto-Oncogene Proteins c-fyn , Rats , Rats, Sprague-Dawley , S100 Proteins/metabolism , Sciatic Neuropathy/pathology , Sciatic Neuropathy/physiopathology , Signal Transduction/physiology , Wallerian Degeneration/metabolism , Wallerian Degeneration/pathology , Wallerian Degeneration/physiopathologyABSTRACT
Schwann cells are crucially important for peripheral nerve regeneration. These cells synthesize several factors that are supposed to enhance axonal regeneration when injured. Platelet-derived growth factor (PDGF) B-chain and its beta-receptor are expressed in Schwann cells in both normal peripheral nerves and culture. To elucidate the role of PDGF-B in peripheral nerve regeneration, we investigated its expression in cut or crush-injured rat sciatic nerves for up to 28 days. Northern blotting identified substantial increase of PDGF B-chain transcripts in injured nerves. Immunohistochemistry demonstrated that protein products of the transcripts were augmented at the distal tip of swollen axons in proximal nerve segments and in regenerating axons. Soon after both types of injury, considerable amounts of PDGF-B accumulated in numerous Schwann cells in distal segments of both models. With restoration of the axon-Schwann cell relationship in the crush model, levels of PDGF-B tended to decrease, eventually returning to normal. In the cut model in which the relationship cannot be restored, the PDGF-B was depleted to a very low level. The spatiotemporal correlation between PDGF-B and cell proliferation was very close throughout the study. These results differed strikingly from those of our previous study of rat optic nerve transection, in which PDGF-B was expressed only in a few recruited macrophages and glial cells. Augmented PDGF-B expression after sciatic nerve injury might contribute to peripheral nerve regeneration because PDGF-B is a mitogen and survival factor for Schwann cells and because it has trophic activity on neurons.
