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Objective:To explore the significance of plasma homocysteine (Hcy) as a new biomarker for the differential diagnosis of postural tachycardia syndrome (POTS) and suspected myocarditis in children.Methods:A total of 24 children diagnosed with POTS and 21 children diagnosed with suspected myocarditis treated in the Pediatrics Department of the Peking University First Hospital from July to December 2016 were included in the study.Plasma Hcy levels were measured in each subject and compared between children with POTS and suspected myocarditis.The receiver operating characteristic (ROC) curves were depicted for assessing the diagnostic potential of Hcy in distinguishing POTS from suspected myocarditis.Results:Plasma Hcy level in the POTS group was significantly higher than that in the suspected myocarditis group [(14.25±8.09) μmol/L vs.(8.99±3.19) μmol/L], which was also significantly higher than that of the mean levels in Beijing children [(8.82±5.58) μmol/L] (all P<0.05). When the cut-off was 9.36 μmol/L, the area under the ROC curve was 0.76, and the sensitivity and specificity for distinguishing POTS from suspected myocarditis were 71% and 68%, respectively. Conclusions:Plasma Hcy levels are helpful in the differential diagnosis of POTS and suspected myocarditis in children.
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Objective:To investigate the regulatory effects of endogenous nitric oxide (NO) on the activity of superoxide dismutase-1 (SOD1) and apoptosis of human umbilical vein endothelial cells (HUVECs).Methods:HUVECs were taken as the research object.The endothelial NO synthase (eNOS) short hairpin RNA(shRNA) lentivirus was employed to transfect HUVECs to knock down eNOS.HUVECs were divided in 4 groups: the scramble group, the eNOS shRNA group, the eNOS shRNA + sodium nitroprusside(SNP) group and the eNOS shRNA+ SNP+ tris (2-carboxyethyl) phosphine hydrochloride (TCEP) group.The protein expressions of eNOS and SOD1 dimer/monomer in cells were detected by western blot.The activity of SOD was detected by the enzyme-linked immunosorbent assay.The NO content in cells was detected with NO fluorescence probe.The level of superoxide anion in HUVECs was detected with dihydropyridine (DHE). The terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) assay was adopted to detect the apoptosis of HUVECs in situ.Results:Compared with the scramble group, the endogenous NO content (2.690±0.420 vs.15.029±2.193, P<0.01), eNOS protein expression (1.000±0.778 vs.3.141±0.199, P<0.01), SOD1 dimer/monomer ratio (4.6±1.0 vs.7.6±2.0, P<0.05) and SOD activity [(0.432±0.254) Carmen′s unit/10 4 cell vs.(1.000±0.116) Carmen′s unit/10 4 cell, P<0.01] were significantly decreased, while the level of intracellular superoxide anion (11.180±1.560 vs.6.146±1.007, P<0.01) and HUVECs apoptosis [75.0 (55.0, 100.0)% vs.0 (0, 0)%, P<0.01] were significantly increased in the eNOS shRNA group.Compared with the eNOS shRNA group, the content of endogenous NO (16.705±0.116 vs.2.690±0.420, P<0.01), the ratio of SOD1 dimer/monomer (7.3±2.0 vs.4.6±1.0, P<0.05) and the activity of SOD [(0.737±0.060) Carmen′s unit/10 4 cell vs.(0.432±0.254) Carmen′s unit/10 4 cell, P<0.05] were significantly increased, while the level of superoxide anion (6.897±1.648 vs.11.180±1.560, P<0.01) and the HUVECs apoptosis [0 (0, 0)% vs.75.0 (55.0, 100.0)%, P<0.01] were significantly decreased in the eNOS shRNA+ SNP group.Compared with the eNOS shRNA + SNP group, the ratio of SOD1 dimer/monomer (4.4±0.9 vs.7.3±2.0, P<0.05) and the activity of SOD [(0.214±0.084) Carmen′s unit/10 4 cell vs.(0.737±0.060) Carmen′s unit/10 4 cell, P<0.01] were significantly decreased, while the level of superoxide anion (10.917±1.552 vs.6.897±1.640, P<0.01) and the apoptosis level of HUVECs[63.6 (55.0, 90.0)% vs.0 (0, 0)%, P<0.01] were significantly increased in the eNOS shRNA+ SNP+ TCEP group.However, there was no significant difference in the NO content (16.112±0.926 vs.16.705±0.116, P>0.05). Conclusions:Endogenous NO could effectively antagonize the apoptosis of endothelial cells by increasing the cysteine-dependent SOD1 dimer/monomer ratio, enhancing SOD activity and inhibiting the accumulation of reactive oxygen species.
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Vasovagal syncope (VVS) and postural tachycardia syndrome (POTS) are the main forms of orthostatic intolerance in pediatrics and both are underlying causes of neurally-mediated syncope. In recent years, increasing attention has been paid to the management of VVS and POTS in children and adolescents. A number of potential mechanisms are involved in their pathophysiology, but the leading cause of symptoms varies among patients. A few studies thus have focused on the individualized treatment of VVS or POTS based on selected hemodynamic parameters or biomarkers that can predict the therapeutic effect of certain therapies and improve their effectiveness. This review summarizes the latest developments in individualized treatment of VVS and POTS in children and indicates directions for further research in this field.
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Kawasaki disease (KD) is an acute, self-limiting, and medium-sized vasculitis, which has been the commonest cause of acquired heart disease in children in developed countries.Without timely diagnosis and treatment, up-to 25% of the affected children may develop coronary artery abnormalities (CAA). Due to the lack of the specific diagnostic method, KD is mainly diagnosed according to the clinical criteria.As a result, typical KD is recognized easily, but it is a big challenge to diagnose KD patients with incomplete or atypical symptoms.The pandemic of novel coronavirus disease 2019 (COVID-19) around the world makes the diagnosis of KD even more complex.In this review, hot issues in diagnosing KD were discussed according to the 2017 guidelines for diagnosis and treatment of KD recently published by the American Heart Association (AHA), expecting to provide help for diagnosis of KD children.
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＂2018 Chinksk Pkdiatric Cardiologe Socikte( CPCS)guidklink for thk diagnosis and trkatmknt of sencopk in childrkn and adolkscknts＂( rkfkrrkd as thk ＂nkw guidklink＂)was publishkd in intkrnational journals. Nkw guidklink in combination with thk rkcknt largk numbkr of clinical rkskarch in this fikld both at homk and abroad,dkvk-lopkd be thk kxpkrts of Pkdiatric Cardiologe Socikte,Chinksk Pkdiatric Socikte,Chinksk Mkdical Lssociation( CML)╱Committkk on Pkdiatric Sencopk,Pkdiatricians Branch,Chinksk Mkdical Doctor Lssociation( CMDL)╱Committkk on Pkdiatric Cardiologe,Chinksk Collkgk of Cardiovascular Phesicians,Chinksk Mkdical Doctor Lssociation( CMDL)╱Pk-diatric Cardiologe Socikte,Bkijing Pkdiatric Socikte,Bkijing Mkdical Lssociation( BML),aftkr rkpkatkd rkskarch and discussion. Thk guidklinks kffkctivkle standardizks thk diagnosis,diffkrkntial diagnosis and prkvkntion stratkgiks of senco-pk diskasks in childrkn and adolkscknts. Baskd on thk kvidknck kvaluation of kvidknck-baskd mkdicink,thk mkthodolo-ge of hkad-up tilt tablk tkst is partialle updatkd,thk prkcautions bkfork thk tkst ark kmphasizkd,and thk charactkristics and safkte of childrkn and adolkscknts ark kvaluatkd. In tkrms of prkvkntion and trkatmknt,thk importanck of hkalthe kducation is kmphasizkd. Thk prognosis of postural tachecardia sendromk is addkd in thk follow-up of kfficace.
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Objective To explore the effect of different concentrations of endothelin-1 (ET-1)on the en-dogenous nitric oxide (NO)and hydrogen sulfide (H2S)pathways of vascular smooth muscle cells (A7r5 cell lines)in rats.Methods A7r5 cell lines were divided into the control group and the experimental group.ET-1 at a concentra-tion of 10 -8-10 -6 mol/L was added into the experimental group,and as for the control group,the same volume of sterile phosphate buffered saline (PBS)buffer solution was added.The content of NO and H2S in A7r5 cell lines was detected by fluorescent NO probe and H2S probe after ET-1 stimulation for 48 h,respectively.The content of NO in the supernatant was measured by NO assay kit at 48 h of the incubation.The content of H2S in the supernatant was measured by polarographic H2S sensor at 48 h of the incubation. The expressions of inducible nitric oxide synthase (NOS2),endothelial nitric oxide synthase (NOS3),cystathionine -γ -lyase (CSE),cystathionine -β -synthase (CBS)and proliferating cell nuclear antigen (PCNA)were detected by the Western blot method.Results The rela-tive fluorescence intensity of the content of NO in the A7r5 cell lines of ET-1 10 -8,10 -7 and 10 -6mol/L groups (0. 078 ± 0. 080,0.075 ± 0.002,0.056 ± 0.009)was markedly lower than that in the control group(0.094 ± 0. 061), and the differences were statistically significant(F＝15.248,P＜0.05);Compared with the control group[(2. 131 ± 0. 484)μmol/L],the content of NO in the supernatant of the experimental groups [(1.391 ± 0.134 )μmol/L, (1.219 ± 0. 280)μmol/L,(1.116 ± 0.181)μmol/L]was significantly decreased,and the differences were statistically significant(F＝20.833,P＜0.01);NOS2 protein expression(0.457 ± 0.097,0.462 ± 0.116,0.438 ± 0.180)was decreased markedly compared with that of the control group(0.721 ± 0.222),and the differences were statistically sig-nificant(F＝6.196,P＜0.01),but the expression of NOS3 showed no significant differences(F＝2.669,P＞0.05). The relative fluorescence intensity of the content of H2S in the A7r5 cell lines of ET-1 10 -8,10 -7 and 10 -6mol/L groups (0.063 ± 0.002,0.056 ± 0.008,0.042 ± 0.009)was markedly lower than that in the control group (0.082 ± 0. 006),and the differences were statistically significant(F ＝16.297,P＜0.01);Compared with the control group [(29.439 ±4.236)μmol/L],the content of H2S in the supernatant of the experimental groups [(17.516 ±5.144) μmol/L,(14.481 ± 4.885)μmol/L]was significantly decreased,and the differences were statistically significant (F＝12.518,P ＜0.01).CBS protein expression(0.359 ± 0.096,0.270 ± 0.038,0.174 ± 0.051)was decreased markedly compared with that of the control group(0.707 ± 0.107),and the differences were statistically significant (F＝20.833,P＜0.01),and the expression of CSE showed no significant differences(F＝0.708,P＞0.05).The data showed that PCNA protein expression in the 10 -7mol/L ET-1 group(0.686 ± 0.180)significantly increased com-pared with that of the control group(0.437 ± 0.191),and the difference was statistically significant (t＝ -2.840,P＜0.01).Conclusion ET-1 stimulation can lead to the proliferation of vascular smooth muscle cells and down-regu-late its endogenous NO and H2S pathways.
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Objective To explore the effect of endogenous sulfur dioxide (SO2)on the apoptosis induced by cobalt chloride (CoCl2)in the human pulmonary arterial endothelial cells (HPAECs).Methods CoCl2was used in the primary HPAECs to mimize hypoxia-induced cell apoptosis.The aspartate aminotransferase 1(AAT1),and the key enzyme generating endogenous SO2 were over -expressed by transfecting HPAECs with lentivirus containing AAT1 cDNA.HPAECs were divided into 4 groups:vehicle group,vehicle + CoCl2 group,AAT1 group and AAT1 + CoCl2 group.The expressions of AAT1,B-cell lymphoma-2 (bcl-2),bcl-associated X protein (bax),Caspase-3 and activated Caspase-3 (cleaved Caspase-3)in the HPAECs were measured by Western blot.The AAT activity was assessed with colorimetry method.The SO2 content in the HPAECs was in situ observed by SO2-specific fluorescent probe.The HPAECs apoptosis was investigated by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL)assay.Results There were significant differences in the endogenous SO2 content,the expre-ssions of AAT1 and bcl-2,and the ratio of cleaved Caspase-3/Caspase-3 among 4 groups of HPAECs were (F＝147.364,23.738,6.521,64.884,all P＜0.05).However,there was no difference in the expression of bax among 4 groups of HPAECs (F＝1.620,P＞0.05).Compared with vehicle group,AAT activity [(0.96 ± 0.24)Carmen's unit/μg vs.(2.21 ± 0. 60)Carmen's unit/μg],endogenous SO2 content (40.71 ± 7.72 vs.105.60 ± 16.20)and bcl-2 expression (0.59 ± 0.19 vs.1.02 ± 0.20)in the HPAECs of vehicle +CoCl2 group were significantly de-creased,while the cell apoptosis assessed by TUNEL and the ratio of cleaved Caspase-3/Caspase-3 (1.56 ± 0.25 vs.0.95 ± 0.13)were significantly increased (all P＜0.05).However,there were no differences in the expression of AAT1 (0. 50 ± 0.12 vs.0.53 ± 0.11)in the HPAECs between vehicle group and vehicle+CoCl2 group (P＞0.05). The SO2 content (351.50 ± 42.43 vs.105.60 ± 16.20)and AAT1 expression (1.22 ± 0.33 vs.0.53 ± 0.11)in the HPAECs of AAT1 group were higher than those of vehicle group (all P ＜0. 05 ). Compared with AAT1 group, endogenous SO2content (333.50 ± 46.22 vs.351.50 ± 42.43)and the expression of AAT1 (1.26 ± 0.36 vs.1.22 ± 0.33)and bcl-2 (1.14 ± 0.38 vs.1.03 ± 0.27)in the HPAECs of AAT1 +CoCl2group did not change (all P＞0. 05).Moreover,no difference was observed in the HPAECs apoptosis assessed by TUNEL and the ratio of cleaved Caspase-3/Caspase-3 (0.51 ± 0.17 vs.0.50 ± 0.11)between the two AAT1 -overexpressed groups (all P ＞0. 05).Conclusion Endo-genous SO2inhibited the hypoxic HPAECs apoptosis stimulated by the treatment of CoCl2.
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Objective To explore the changes of Beclin-1,P62/SQSTM1,microtubule-associated protein 1 light chain 3 (LC3)and unc-51 like autophagy activating kinase 1 (ULK-1)in the brains of the rats in the deve-lopmental stage with epilepsy. Methods Seventy-two male Sprague Dawley (SD)rats aged 21 days were randomly divided into the control group and the epilepsy group. The rats in 2 groups were randomly subdivided into 4 groups according to the time intervals (3 h,6 h,12 h and 48 h),respectively,with 9 rats in each group. The rats in the epilep-sy group were injected with kainic acid (12 mg/kg)to induce epilepsy,and the rats in the control group were injected with equal volume of saline. The rats in 2 groups were anaesthetized and sacrificed. Then,the brain tissues of the rats were quickly removed according to the time intervals. The brain damages were determined by adopting Nissl staining method. The apoptotic cells were detected by Terminal - deoxynucleoitidyl transferase mediated nick end labeling (TUNEL)assays. The expressions of Beclin-1,P62/SQSTM1,LC3 and ULK-1 mRNA levels in cortex were mea-sured by using real-time quantitative polymerase chain reaction (qPCR)analysis. Results Nissl staining indicated that many neurons were damaged performing vague outline,irregularly aligned,pyknotic nuclei and shrunken somata in the epilepsy 48 h group. In addition,there was a huge loss of neurons in cortex in the epilepsy 48 h group [(82 ± 8)num-bers],compared with the control group [(122 ± 8)numbers],and the difference was statistically significant (F＝3. 768, P＝0. 01). The apoptotic cells tremendously increased in the epilepsy 48 h group [(13 ± 7)numbers],compared with the control group [(2 ± 1)numbers]by TUNEL analysis,and the diffe-rence was statistically significant (t＝ -3. 821, P＝0. 003). qPCR showed the mRNA levels of Beclin-1,P62/SQSTM1,LC3 and ULK-1 were upregulated in the epi-lepsy 12 h group (1. 70 ± 0. 75,1. 75 ± 0. 77,1. 52 ± 0. 43,7. 48 ± 6. 12)and the epilepsy 48 h group (1. 63 ± 0. 43, 1. 48 ± 0. 74,1. 74 ± 0. 55,7. 69 ± 5. 65),compared with the control group (1. 00,1. 00,1. 00,1. 00),and the differences were statistically significant (F＝2. 820,3. 452,5. 811,5. 002,all P＜0. 05). Conclusion The autophagy activates be-fore apoptosis occurs,and autophagy-related genes probably are involved in epilepsy-induced brain damage.
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Vasovagal syncope(VVS),with its relatively high morbidity,is one of the most common types of au-tonomic-mediated reflex syncope in children,which can seriously affect pediatric patients in their life and study.A se-ries of research have shown that the mechanism for VVS is closely related to autonomic nervous imbalance,neurohor-monal factor,and cerebral blood flow abnormality,and has a certain degree of genetic tendency.Now the progress in the mechanisms for VVS at home and abroad is reviewed,in order to provide certain help for further research.
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Syncope is one of the most common emergencies in the pediatric population,which cause serious in-fluences on the quality of life of children. With the in - depth studies on the pathogenesis mechanism,the evaluation and management level of pediatric syncope has gotten great improvement. The concept of the individualized treatment has been proposed and make the treatment of syncope in children enter a new stage.
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Objective To investigate the regulatory effects of endogenous sulfur dioxide (SO2) on collagen accumulation in pulmonary arterial fibroblasts of rats and its mechanisms.Methods Primary rat pulmonary artery fibroblasts were used in the experiment and were divided into 3 groups:the control group,the L-aspartate-beta-hydroxamate(HDX) group and the HDX ± SO2 group.SO2 content of pulmonary artery fibroblasts supernatant was detected by adopting high performance liquid chromatography (HPLC).Collagen type Ⅰ and collagen type Ⅲ in pulmonary artery fibroblasts were determined by using immunofluorescence.Phosphorylation of Smad2/3,protein expression of matrix metalloproteinase (MMP)-13 and tissue inhibitors of MMP (TIMP)-1 were detected by using Western blot.One-way ANOVA was used for multiple group comparisons followed by Bonferroni test for each group.P ＜ 0.05 was considered as significant difference.Results Compared with control group,endogenous SO2 content in HDX group was significantly decreased [(14.30-± 0.48) μmol/L vs.(20.14 ± 0.49) μμmol/L,P ＜ 0.01],the level of Smad2/3 increased (1.03 ±0.31 vs.0.48 ± 0.20,P ＜ 0.01),protein expressions of MMP-13 and TIMP-1 in pulmonary artery fibroblasts were decreased (MMP-13:0.28 ± 0.06 vs.0.75 ± 0.11,P ＜ 0.01;TIMP-1:0.40 ± 0.05 vs.0.66 ± 0.20,P ＜ 0.01),and the ratio of MMP-13/TIMP-1 was decreased (0.71 ± 0.12 vs.1.23 ± 0.45,P ＜0.01).However,contents of collagen Ⅰ and collagen Ⅲ were significantly increased.Compared with HDX group,the level of Smad2/3 phosphorylation in HDX ± SO2 group decreased (0.57 ± 0.16 vs.1.03 ± 0.31,P ＜ 0.01),protein expression of MMP-13 and TIMP-1 upregulated (MMP-13:0.63 ± 0.06 vs.0.28 ± 0.06,P ＜ 0.01;0.59 ± 0.11 vs.0.40 ± 0.05,P =0.015),the ratio of M MP-13/TIMP-1 (1.10 ± 0.22 vs.0.71 ± 0.12,P =0.033) increased,but contents of collagen type Ⅰ and type Ⅲ were reduced obviously.Conclusions SO2 promotes the degradation of collagen and collagen accumulation in pulmonary artery fibroblasts of rats probably by inhibiting Smad2/3 signal pathway,increasing protein expression of MMP-13 and TIMP-1,and upregulating the ratio of MMP-13/TIMP-1.
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Objective To investigate the effects of endogenous sulfur dioxide (SO2) on the oxidative stress induced by cobalt chloride (CoCl2) in the rat pulmonary artery smooth muscle cells (PASMCs).Methods Rat PASMCs were treated with 200 μ mol/L CoCl2 to mimic the hypoxia insult.Endogenous SO2 generating enzyme aspartate aminotransferase 1 (AAT1) expression was upregulated or downregulated (AAT1 sh) by transfection with lentivirus.Rat PASMCs were randomly divided into 8 groups:vehicle group,vehicle + CoCl2 group,AAT1 group,AAT1 + CoCl2 group,scramble group,scramble + SO2 group,AAT1 sh group and AAT1 sh + SO2 group.SO2 donor Na2 SO3/NaHSO3 at concentration of 100 μ mol/L were added in scramble + SO2 group and AAT1sh + SO2 group.The expressions of AAT1,superoxide dismutase 1 (SOD1) and SOD2 in PASMCs were detected by Western blot method.In situ SO2 content in PASMCs was detected by fluorescent probe.The superoxide anions in PASMCs were labeled by dihydroethidium (DHE) probe under fluorescent microscope.Results Compared with the vehicle group,the levels of SO2 and the expressions of AAT1 (0.221 ± 0.002 vs.0.446 ± 0.004),SOD1 (0.076 ± 0.028 vs.0.171 ± 0.019) and SOD2 (0.080 ± 0.031 vs.0.196 ± 0.018) significantly decreased (all P ＜ 0.01),and superoxide anion increased in rat PASMCs of vehicle + CoCl2 group.Meanwhile,compared with vehicle + CoCl2 group,the levels of SO2 and the expressions of AAT1 (0.839 ± 0.056 vs.0.221 ± 0.002),SOD1 (0.177 ± 0.020 vs.0.076 ± 0.028) and SOD2 (0.195 ±0.018 vs.0.080-± 0.031) markedly increased (all P ＜ 0.01),and superoxide anion decreased in rat PASMCs of AAT1 + CoCl2 group.On the contrary,compared with the scramble group,the levels of SO2 and the expressions of AAT1 (0.062 ±0.017 vs.0.354 ±0.034),SOD1 (0.054 ±0.029 vs.0.157 ±0.023) and SOD2(0.180 ±0.100 vs.0.586 ± 0.176)significantly decreased (all P ＜ 0.01),and superoxide anion increased in rat PASMCs of AAT1sh group.Furthermore,compared with the AAT1 sh group,the levels of SO2 and the expressions of SOD1 (0.155 ± 0.022vs.0.054 ± 0.029) and SOD2 (0.578 ± 0.200 vs.0.180 ± 0.100) significantly increased (all P ＜ 0.01),and superoxide anion decreased in rats PASMCs of AAT1sh + SO2 group.Conclusion Endogenous SO2/AAT1 inhibits CoCl2-induced oxidative stress in rat PASMCs.
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AIM: To explore the regulatory effect of adrenomedullin (ADM) on pulmonary oxidative stress in the rats with pulmonary hypertension induced by high blood flow.METHODS: Healthy male SD rats (n=22) were randomly divided into control group, shunt group and shunt with ADM group.Abdominal aorta and inferior vena cava shunting was produced in the rats in shunt group and shunt with ADM group.After 8 weeks, ADM (1.5 μg·kg-1·h-1) was administered into the rats in shunt with ADM group subcutaneously by mini-osmotic pump for 2 weeks.Mean pulmonary artery pressure (mPAP) was evaluated by a right cardiac catheterization procedure.The ratio of right ventricular mass to left ventricular plus interventricular septal mass [RV/(LV+SP)] and relative medial thickness (RMT) in pulmonary muscularized arteries were calculated.The content of malonaldehyde (MDA), total antioxidative capacity (T-AOC), and activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in lung tissues were detected by colorimetry.The expression of NADPH oxidase 4 (NOX4) in the lung tissue was analyzed by Western blot.RESULTS: Compared with control group, the mPAP, RV/(LV+SP) and RMT in pulmonary muscularized arteries in shunt group were all significantly increased.The content of MDA and the expression of NOX4 in the lung tissues were significantly increased.The T-AOC, and activity of SOD and GSH-Px in the lung tissues were significantly decreased.However, mPAP, RV/(LV+SP) and RMT in pulmonary muscularized arteries in shunt with ADM group were significantly decreased as compared with shunt group.Meanwhile, ADM decreased the content of MDA and the expression of NOX4 in the lung tissues, but increased the T-AOC, and activity of SOD and GSH-Px in the lung tissue of shunt rats.CONCLUSION: ADM inhibits oxidative stress response in the development of pulmonary hypertension and pulmonary vascular structural remodeling induced by high pulmonary blood flow in the rats by down-regulating the NOX4 expression and strengthening the anti-oxidation response.
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Objective@#To explore the relationship between venous blood routine test parameters and syncopal recurrence of children with vasovagal syncope (VVS).@*Method@#Sixty-three children (male 32, female 31) diagnosed as VVS in Department of Pediatrics, Peking University First Hospital from November 2010 to October 2015 were included in a case observational study.Their mean age was (11.2±2.7) years and basic treatment such as predisposing causes avoiding, standing training, autonomic nervous function exercise and oral rehydration salts were advised to them.The clinical data were obtained by out-patient visit and over telephone from December 2015 to January 2016, with a median follow-up period of 10 (4, 26) months. The effects of baseline venous blood routine test parameters, gender, age, and body mass index (BMI) on syncopal recurrence were studied via univariate and multivariate Cox regression analysis.Kaplan-Meier curve was used to evaluate the long-term prognosis.@*Result@#Among the 63 VVS children in this study, 31 cases were diagnosed as VVS vasodepressor type, 4 cases as VVS cardioinhibitory type and 28 cases as VVS mixed type, 16 cases (25%) had experienced recurrence of syncope while 47 cases (75%) had not.The result of univariate analysis of Cox regression showed that baseline platelet count (PLT) (HR=1.012, 95%CI: 1.003-1.022) had a marked impact on the survival rate.And the result of multivariate analysis of Cox regression showed that baseline hemoglobin concentration (HGB) (HR=1.055, 95%CI: 1.007-1.105), mean corpuscular hemoglobin (MCH) (HR=0.612, 95%CI: 0.423-0.884) and PLT(HR=1.015, 95%CI: 1.006-1.024) had significant effects on survival rate of VVS children.In this study, the one-year, two-year, and three-year survival rate were 83% (52/63), 79% (50/63) and 75% (47/63), respectively.@*Conclusion@#The baseline venous blood routine test parameters HGB, MCH and PLT might be the influencing factors of the syncopal recurrence of VVS children.
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Hypertensive crisis is defined as significantly elevated blood pressure accompanied by heart,kidney and central nervous system and other target organ damage. Hypertensive crisis is rare but often occult in children. It acts as a serious threatening to children′s health. At different ages,there are different eti-ologies of composition. So the hypertensive children need to be monitored closely,and given targeted individ-ualized treatment. Venous anti-hypertensive drugs are recommended to be used under monitoring as initial treatment to control the blood pressure decline speed precisely,and then gradually changed to oral anti-hyper-tensive drugs,to maximize the protection of target organs and avoid permanent damage caused by fluctuation of the blood pressure.
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Hypertensive crisis is defined as significantly elevated blood pressure accompanied by heart,kidney and central nervous system and other target organ damage. Hypertensive crisis is rare but often occult in children. It acts as a serious threatening to children′s health. At different ages,there are different eti-ologies of composition. So the hypertensive children need to be monitored closely,and given targeted individ-ualized treatment. Venous anti-hypertensive drugs are recommended to be used under monitoring as initial treatment to control the blood pressure decline speed precisely,and then gradually changed to oral anti-hyper-tensive drugs,to maximize the protection of target organs and avoid permanent damage caused by fluctuation of the blood pressure.
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Postural tachycardia syndrome (POTS) is one type of orthostatic intolerance.The treatment for POTS including non-drug treatment and medications,such as α-receptor agonists,β-recepter blockers and oral rehydration salts.The prognostic meaning of biomarkers and hemodynamic parameters in the POTS children treated with midodrine hydrochloride are discussed in this paper.
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Objective To explore the changes in the endogenous sulfur dioxide (SO2) pathway in the myocardial hypertrophy induced by the angiotensin Ⅱ (Ang Ⅱ) in mice.Methods Fourteen healthy C57BL mice,9 weeks old,were randomly divided into control group(n =7) and Ang Ⅱ group(n =7),and capsule osmotic pump with pre loaded 9 g/L saline and Ang Ⅱ was implanted into the back of each mouse subcutaneously.Mter 2 weeks,the mice were executed.The heart weight/body weight (HW/BW) and the left heart weight/full heart weight (LVW/HW) of the mice were measured.The microstructure of the cardiac myocyte was observed by hematoxylin-eosin (HE) staining under the microscope.The expression of myocardial alpha myosin heavy chain (α-MHC) was detected by immunohistochemistry and Western blot methods.SO2 enzymes aspartate aminotransferase 1 (AAT1) and AAT2 protein expression were detected by Western blot method.Myocardial SO2 content and AAT activity were measured by high performance liquid chromatography with fluorimetric detection and colometric method.Results Compared with control group,the HW/BW and LVW/HW in mice of Ang Ⅱ group were significantly increased (all P ＜ 0.O1),the cardiac myocytes were hypertrophy,and α-MHC positive staining in the cytoplasm of myocardium was weakened.Moreover,Western blot data showed that α-MHC protein expression in heart tissue of Ang Ⅱ-treated mice was decreased significantly (allP ＜ 0.05).Simultaneously,the data showed that AAT2 protein expression,SO2 content and AAT activity in heart tissue of Ang Ⅱ-treated mice were also decreased markedly[(1.093 ±0.131) μ mol/g protein vs.(0.737 ±0.233) μmol/g protein,P ＜ 0.05;(7.979 ± 1.317) U/rmg protein vs.(6.470 ± O.516) U/mg protein,P ＜ 0.01].Furthermore,there was a negative correlation between LVW/HW and cardiac SO2 content in heart tissue (r =-0.56,P ＜ 0.05).Conclusions Myocardial endogenous SO2/AAT2 pathway is down-regulated in the development of myocardial hypertrophy induced by Ang Ⅱ in mice.
ABSTRACT
Arrhythmia-induced cardiomyopathy (AIC) is a myocardial disease condition in which left ventricular dysfunction and cardiomegaly are induced or mediated by atrial or ventricular arrhythmias.The pathophysiological mechanisms remain unclear.Early recognition of AIC and provision of prompt treatment with pharmacological or ablative techniques could result in symptom resolution and recovery of ventricular function.But,the long-term prognosis of these patients is not clear and needs further observation and research.
ABSTRACT
Objective:To investigate whether endogenous hydrogen sulfide (H2 S)was involved in the pathogenesis of osteoarthritis (OA)and its underlying mechanism,to detect H2 S and its synthases ex-pression in knee cartilage in patients diagnosed with different severity of OA,and to explore the transcrip-tion and expression of gene MMP-13 in chondrocytes treated with IL-1βor H2S.Methods:Synovial fluids of the in-patients with different severity of OA hospitalized in Peking University First Hospital were collected for measurement of H2 S content using methylene blue assay.Articular cartilages of the patients who underwent knee arthroplasty were collected for the cell culture of relatively normal chondrocytes.The chondrocytes were cultured to the P3 generation and H2 S molecular probes were used for detection of endogenous H2 S generation in the chondrocytes.Immunocytochemistry was used to detect the localization of H2 S synthases including cystathionine β-synthase (CBS),cystathionine-γ-lyase (CSE),and mercap-topyruvate sulfurtransferase (MPST)in OA chondrocytes.Western blot was used to quantify the protein expressions of CSE,MPST,and CBS in cartilage tissues of the patients who were diagnosed with OA and underwent knee arthroplasty.The relatively normal human chondrocytes were cultured to passage 3 and then divided into 4 groups for different treatments:(1 )the normal control group,no reagent was added;(2)the IL-1βgroup,5 μg/L of IL-1βwas added;(3)the IL-1β+H2S group,200 μmol/L of NaHS was added 30 min before adding 5 μg/L of IL-1β;(4)the H2 S group,200 μmol/L of NaHS was added. The transcription and expression of gene MMP-13 in chondrocytes of each group were determined with Real-time PCR and Western blot,respectively.And the total NF-κB p65 and phosphorylated NF-κB p65 in chondrocytes were detected with Western blot.Results:The content of H2 S in the synovial fluid of degenerative knee was (14.3 ±3.3)μmol/L.Expressions of endogenous H2 S and its synthases including CBS,CSE and MPST were present in the cytoplasm of chondrocytes.CSE protein expression in Grade 3 (defined by outerbridge grading)cartilage tissues was significantly increased as compared with that of Grade 1 cartilage tissues (1.67 ±0.09 vs.1.26 ±0.11,P<0.05).However,no significant difference of CBS or MPST expression among the different groups was observed.The expression of MMP-13 protein in the IL-1βgroup was significantly higher than that in the normal chondrocytes (1 .87 ±0.67 vs.0.22 ± 0.10,P<0.05 ),and that in the IL-1β+H2 S group was significantly decreased than that in the IL-1βgroup (0.55 ±0.11 vs.1.87 ±0.67,P<0.05),and that in the H2S group had no significant difference compared with that in the normal control group.The transcription of MMP-13 protein in the IL-1βgroup was significantly higher than that in the normal chondrocytes (31.40 ±0.31 vs.1.00 ±0.00,P<0.05), and that in the IL-1β+H2 S group was significantly decreased than that in the IL-1βgroup (24.41 ± 1.28 vs.31.40 ±0.31,P<0.05),and that in the H2S group had no significant difference compared with that in the normal control group.The total NF-κB p65 in the IL-1βgroup was significantly higher than that in the normal chondrocytes (2.13 ±0.08 vs.0.73 ±0.08,P<0.05),and that in the IL-1β+H2S group was significantly decreased than that in the IL-1βgroup (1 .24 ±0.13 vs.2.13 ±0.08,P<0.05 ),and that in the H2 S group had no significant difference compared with that in the normal control group.The phosphorylated NF-κB p65 in IL-1βgroup was significantly higher than that in the normal chondrocytes (1.30 ±0.13 vs.0.19 ±0.04,P<0.05),and that in IL-1β+H2S group was significantly decreased than that in the IL-1βgroup (0.92 ±0.26 vs.1.30 ±0.13,P<0.05),and that in the H2S group had no significant difference compared with that in the normal control group.Conclusion:H2 S affected the cartilage degeneration by partly inhibiting the degradation of extracellular matrix.