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1.
Chinese Journal of Contemporary Pediatrics ; (12): 533-535, 2012.
Article in Chinese | WPRIM | ID: wpr-320601

ABSTRACT

<p><b>OBJECTIVE</b>To study the value of high-frequency ultrasound in the diagnosis of duchenne muscular dystrophy diseases (DMD) in children.</p><p><b>METHODS</b>Eight children with DMD were enrolled as DMD group and 10 healthy children as the control group. The echogenicity of the rectus femoris muscle and the gap between the gastrocnemius and soleus muscles in the two groups were detected by high-frequency ultrasound.</p><p><b>RESULTS</b>Compared with the control group, rectus femoris and gastrocnemius muscles in the DMD group showed increased echogenicity and their muscle fibers were arranged irregularly, and the gap between the gastrocnemius and soleus muscles became wilder (P<0.01).</p><p><b>CONCLUSIONS</b>High-frequency ultrasound is valuable in the diagnosis of DMD.</p>


Subject(s)
Child , Child, Preschool , Female , Humans , Male , Muscular Dystrophy, Duchenne , Diagnostic Imaging , Ultrasonography
2.
Acta Physiologica Sinica ; (6): 260-264, 2003.
Article in English | WPRIM | ID: wpr-290975

ABSTRACT

In this study, we observed the levels of adrenomedullin (ADM) and proadrenomedullin N-terminal 20 peptide (PAMP) in myocardium and aorta of spontaneously hypertensive rats (SHRs) in comparison with Wistar-kyoto (WKY) rats. Contents of ADM and PAMP were measured by radioimmunoassay (RIA) in plasma, myocardium and aorta. The amount of Pro-ADM mRNA of myocardium and aorta was determined by competitive quantitative reverse transcription polymerase chain reaction (RT-PCR). In SHRs the amounts of Pro-ADM mRNA of myocardium and aorta were 66.7% (P<0.01) and 73% (P<0.01) higher than those in WKY rat, respectively. In SHRs, the levels of ADM in plasma, myocardium and aorta were 29%, 76.7% and 79% (all P<0.01) higher than those in WKY rats, respectively. The level of PAMP in SHRs was increased by 42.5% in plasma (P<0.01), 47.2% in myocardium (P<0.0.1) and 27.3% in aorta (P<0.05) compared to WKY rats, respectively. In addition, the ratio of ADM content to PAMP content in SHRs group was increased compared with that in WKY group (2.0+/-0.25 vs 1.64+/-0.3 and 2.2+/-0.18 vs 1.56+/-0.28, in myocardium and aorta, respectively, P<0.01). These results suggest that ProADM gene expression is up-regulated and the increase in ADM and PAMP is different in SHRs. The significance of inconsistency of increase in ADM and PAMP in SHRs needs to be further investigated.


Subject(s)
Animals , Female , Male , Rats , Adrenomedullin , Genetics , Metabolism , Aorta , Metabolism , Myocardium , Metabolism , RNA, Messenger , Genetics , Metabolism , Rats, Inbred SHR , Rats, Inbred WKY , Up-Regulation
3.
Chinese Journal of Applied Physiology ; (6): 132-136, 2003.
Article in Chinese | WPRIM | ID: wpr-339660

ABSTRACT

<p><b>AIM</b>To investigate the alterations of taurine transport, and taurine transporter (TAUT) mRNA by hyperglycemia in cultured rat cardiomyocytes.</p><p><b>METHODS</b>3H-taurine measured the amount of taurine uptake. TAUT mRNA consents were measured using quantitative RT-PCR.</p><p><b>RESULTS</b>The cellular uptake amounts of taurine in seven groups increased with incubation time, and near to be saturated after 5 min. The uptake amount of 10, 20, and 30 mmol/L glucose groups was obviously lower than that of the control group (P < 0.05 or P < 0.01). In 30 mmmol/L glucose, taurine release obviously was decreased, as compared with that of the control. Exposure of cells to 10, 20, and 30 mmmol/L glucose decreased taurine uptake in a concentration-dependent fashion. Exposure to hyperglycemia did not affect the Km of the TAUT, but the apparent Vmax were significantly decreased (P < 0.05). In 20 and 30 mmmol/L groups, TAUT mRNA contents of myocardial cells were significantly reduced, as compared with the control group (P < 0.05).</p><p><b>CONCLUSION</b>The data suggests that there are dysfunction of taurine uptake and downregulation of TAUT gene expression by glucose in cultured rat cardiomyocytes.</p>


Subject(s)
Animals , Rats , Cells, Cultured , Glucose , Pharmacology , Hyperglycemia , Metabolism , Membrane Glycoproteins , Genetics , Metabolism , Membrane Transport Proteins , Genetics , Metabolism , Myocytes, Cardiac , Metabolism , RNA, Messenger , Genetics , Rats, Sprague-Dawley , Taurine , Metabolism
4.
Chinese Journal of Applied Physiology ; (6): 51-54, 2002.
Article in Chinese | WPRIM | ID: wpr-319382

ABSTRACT

<p><b>AIM AND METHODS</b>To observe the effect of myocardial mitochondrial L-arginine (L-Arg)/nitric oxide (NO) system on mitochondrial Ca2+ transport by using purified rat mitochondria and incubation of them in vitro.</p><p><b>RESULTS</b>Compared with control group, incubation of mitochondria with L-Arg (10(-4) mol/L, NO substrate) or sodium nitroprusside (5 x 10(-7) mol/L, the donor of exogenous NO, SNP) increased significantly mitochondrial NO2- (66% and 89%, P < 0.01), respectively, and decreased the Ca2+ content (40% and 54%, P < 0.01). After L-Arg or SNP treatment, mitochondrial Ca2+ uptake were decreased by 67% and 85%, respectively (P < 0.01), vs control. The rate of mitochondrial Ca2+ release decreased by 11% and 8%, respectively (P < 0.01). When L-NAME (NO synthase inhibitor) was incubated with mitochondria and the L-Arg together, it inhibited the effects of L-Arg, NO2 on the mitochondrial NO2 formation, Ca2+ content descending, and decrease of Ca2+ uptake and release.</p><p><b>CONCLUSION</b>The data suggest that myocardial mitochondrial L-Arg /NO systems take part in the regulation of cardiomyocytes Ca2+ transportation.</p>


Subject(s)
Animals , Female , Male , Rats , Arginine , Metabolism , Biological Transport , Calcium , Metabolism , Mitochondria, Heart , Metabolism , Myocytes, Cardiac , Metabolism , Nitric Oxide , Metabolism , Nitric Oxide Synthase , Metabolism , Rats, Wistar
5.
Acta Physiologica Sinica ; (6): 337-341, 2002.
Article in Chinese | WPRIM | ID: wpr-318989

ABSTRACT

To explore the changes in adrenomedullin (ADM) and receptor activity-modifying protein 2 (RAMP2) mRNA in myocardium and vessels in hypertension, a hypertensive rat model was prepared by administering L-NNA. Contents of ADM in plasma, myocardium and vessels were measured by radioimmunoassay (RIA). The levels of pro-ADM mRNA of myocardium and vessels were determined by competitive quantitative RT-PCR. The results showed that L-NNA induced hypertension and cardiomegaly. The ratio of heart to body weight increased by 35.5% (P<0.01). In hypertensive rats the ir-ADM in plasma, myocardium and vessels was increased by 80%, 72% and 57% (P<0.01), respectively compared with the control. The amounts of ADM mRNA in myocardium and vessels were increased by 50% and 109.2% (P<0.05), respectively, and the amounts of RAMP2 mRNA was increased by 132% and 87% (P<0.01), respectively, compared with control. The levels of ADM in myocardium and vessels were positively correlated with RAMP2 mRNA, the correlation coefficients were 0.741 and 0.885 (P<0.01), respectively. The results obtained indicate that in hypertensive rats, ADM is elevated in plasma, myocardium and ves-myocardium and vessel, and ADM and RAMP2 mRNA are up-regulated in myocardium and vessel. The ADM/RAMP2 system may play an important role in the pathogenesis of hypertension.


Subject(s)
Animals , Rats , Adrenomedullin , Metabolism , Cardiomegaly , Metabolism , Hypertension , Metabolism , Myocardium , Metabolism , Nitroarginine , Pharmacology , RNA, Messenger , Receptor Activity-Modifying Protein 2 , Metabolism , Reverse Transcriptase Polymerase Chain Reaction , Up-Regulation
6.
Acta Physiologica Sinica ; (6): 359-364, 2002.
Article in English | WPRIM | ID: wpr-318985

ABSTRACT

The alterations of taurine transport and the expression of taurine transporter (TAUT) mRNA in myocardium and aortic wall were investigated in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. It was demonstrated that plasma taurine concentration and taurine release from myocardium and aortic wall in SHR were higher than those in WKY rats, whereas taurine content, taurine uptake and TAUT mRNA in myocardium and aortic wall of SHR were lower than those of WKY rats. In SHR, the maximal velocity (V(max)) of taurine transportation in myocardium and aortic wall was lower by 24% (P<0.05) and 35% (P<0.05) than that in WKY, their michaelis constants (Km) values were higher by 16% (P<0.05) and 39% (P<0.05), respectively. The results suggest that there is dysfunction of taurine transport in myocardium and aortic wall in SHR, which may be partly resulted from the decrease of TAUT activity and affinity, and down-regulation of TAUT gene expression.


Subject(s)
Animals , Male , Rats , Blood Vessels , Metabolism , Carrier Proteins , Metabolism , Heart , In Vitro Techniques , Myocardium , Metabolism , Rats, Inbred SHR , Rats, Inbred WKY , Taurine , Metabolism
7.
Acta Academiae Medicinae Sinicae ; (6): 359-363, 2002.
Article in Chinese | WPRIM | ID: wpr-278165

ABSTRACT

<p><b>OBJECTIVE</b>To observe the alterations of taurine transport, taurine transporter (TAUT) and cysteine sulfinate decarboxylase (CSD) mRNA in the calcification of myocardial cells in vitro.</p><p><b>METHODS</b>3H-taurine measured the amount of taurine uptake. TAUT and CSD mRNA consents were measured using competitive quantitative RT-PCR in cultured and calcified myocardial cells.</p><p><b>RESULTS</b>In calcification of myocardial cells, taurine concentration was decreased by 27% (P < 0.05), taurine uptake was markedly reduced, Vmax reduced by 39% (P < 0.01), there were no statistical significance of Km values between the two groups. TAUT mRNA decreased by 45% (P < 0.01), but CSD mRNA increased by 25% (P < 0.05).</p><p><b>CONCLUSIONS</b>The data suggest that there were impediment of taurine transport in calcification of myocardial cells, as TAUT mRNA level was decreased, but CSD mRNA concentration was improved.</p>


Subject(s)
Animals , Rats , Biological Transport , Calcinosis , Metabolism , Pathology , Calcium , Metabolism , Carboxy-Lyases , Metabolism , Cells, Cultured , Myocytes, Cardiac , Metabolism , Pathology , RNA, Messenger , Metabolism , Taurine , Genetics , Metabolism
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