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1.
Int J Legal Med ; 124(2): 155-60, 2010 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-20094724

RESUMO

The objective of this study is to test the validity of sex determination in children and adolescents using lateral radiographic cephalometry and discriminant function analysis. Fifty male and 50 female cephalograms of Taiwanese children were used (males and females with mean age of 15.52 +/- 1.38 and 15.67 +/- 1.54 years, respectively). Twenty-two cephalometric measurements were performed using computerized cephalometry. Statistical analysis shows that all measurements were sexually dimorphic (p < 0.05). Nine measurements, statistically validated and clinically relevant, were used for discriminant function analysis. A stepwise discriminant procedure selected seven of the nine variables, producing 95% accuracy in sex determination. Resubstitution classification reveals the same discriminant rate. Cross-validation classification (the leave-one-out method) reveals that the correct sex determination rate is 91%. However, the combination of four variables using both the stepwise procedure and the resubstitution method achieves a 92% accuracy rate. A cross-validation classification procedure with the same four variables resulted in a 91% accuracy rate. Therefore, this study uses four cephalometric measurements as the minimum number of traits yielding the maximum discriminant effectiveness of sex determination in children and adolescents.


Assuntos
Cefalometria , Análise Discriminante , Determinação do Sexo pelo Esqueleto/métodos , Adolescente , Criança , Pré-Escolar , Feminino , Antropologia Forense , Humanos , Processamento de Imagem Assistida por Computador , Lactente , Masculino , Taiwan
2.
Zhongguo Ying Yong Sheng Li Xue Za Zhi ; 23(3): 347-50, 2007 Aug.
Artigo em Chinês | MEDLINE | ID: mdl-21162282

RESUMO

AIM: To investigate the mechanisms of 17beta-estradiol on the production of endothelin-1 in vascular smooth muscle cells. METHODS: After incubation VSMC with various concentrations of 17beta-estradiol (10(-9) - 10(-7) mol/L) or plus L-NAME(10(- 6) mol/L) for different times, the concentration of endothelin-1 was measured. At the same time, the activity of endothelin converting enzyme-1 was analyzed, and the expression of preproET-1mRNA was measured by RT-PCR. RESULTS: In basal conditions, 17beta-estradiol could inhibit the production of endothelin-1 in VSMC, and the action of 17beta-estradiol had nothing to do with the activity of endothelin converting enzyme-1. L-NAME inhibited the effect of 17-estradiol on the production of endothelin-1 in VSMC. RT-PCR results showed that 17-estradiol inhibited the preproET-1 mRNA expression, and whereas L-NAME reversed this action of 17beta-estradiol. CONCLUSION: In basal conditions, 17beta-estradiol decreases the preproET-1 mRNA expression through NO-pathway to inhibit the production of endothelin-1 in cultured VSMC.


Assuntos
Endotelina-1/biossíntese , Estradiol/farmacologia , Músculo Liso Vascular/citologia , Miócitos de Músculo Liso/metabolismo , Animais , Células Cultivadas , Músculo Liso Vascular/efeitos dos fármacos , Músculo Liso Vascular/metabolismo , Miócitos de Músculo Liso/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Transdução de Sinais/efeitos dos fármacos
3.
Sheng Li Xue Bao ; 55(6): 684-91, 2003 Dec 25.
Artigo em Chinês | MEDLINE | ID: mdl-14695486

RESUMO

Clinical epidemiologic data and animal experimental studies regard estrogen as being protective against the development of cardiovascular diseases. The mechanisms by which estrogen affects the development of vascular diseases are not clear. Recent studies demonstrated that the cardiovascular protective effects of estrogen are closely related to nitric oxide (NO) pathway. Our previous study proved that estrogen inhibited the proliferation and oncogene expression of vascular smooth muscle cells (VSMCs) induced by endothlin 1 (ET-1) and serum,this effect was mediated by NO release. In the present study, we investigated the role of inducible nitric oxide synthase (iNOS) in the VSMCs cycle arrest induced by 17 beta-estradiol (E(2)). The effects of E(2) on iNOS activity and protein expression in cultured rat VSMCs and the influence of NOS inhibitor N(G)-nitro-L-arginine methylester (L-NAME) on the inhibitory effect of E(2) on cell cycle were investigated. NOS assay kit was used to measure the activity of iNOS and protein expression of iNOS was determined by Western-blot. Cell cycle analysis was accessed by flow cytometry. The results obtained showed that E(2) increased iNOS activity of VSMCs but not in a dose-dependent manner. E(2) 10 nmol/L increased the iNOS activity of VSMCs distinctly at two time points: 30 min and 12 h. These effects were significantly inhibited by estrogen receptor (ER) antagonist Tamoxifen (0.1 micromol/L) and NOS inhibitor L-NAME (1 micromol/L). E(2) increased iNOS protein expression of VSMCs in a dose-dependent manner. The effect of E(2) on iNOS protein expression of VSMCs started at 3 h, distinctly increased at 12 h and then decreased. Tamoxifen significantly inhibited the E(2)-induced iNOS protein expression of VSMCs. ET-1 increased cell percentage of S phase and G(2)+S/G(1). This effect was inhibited by E(2). L-NAME significantly attenuated the inhibitory effect of E(2) on cell cycle of VSMCs. The results suggest that E(2) induced G(1) arrest of VSMCs, which was associated with an increase in iNOS activity and protein expression of VSMCs. These effects were at least mediated by estrogen receptor partly.


Assuntos
Estradiol/farmacologia , Músculo Liso Vascular/citologia , Óxido Nítrico Sintase/metabolismo , Animais , Ciclo Celular/efeitos dos fármacos , Divisão Celular/efeitos dos fármacos , Células Cultivadas , Endotelina-1/metabolismo , Antagonistas de Estrogênios/farmacologia , Feminino , Óxido Nítrico Sintase/fisiologia , Óxido Nítrico Sintase Tipo II , Ratos , Tamoxifeno/farmacologia
4.
Life Sci ; 73(21): 2665-74, 2003 Oct 10.
Artigo em Inglês | MEDLINE | ID: mdl-13679235

RESUMO

In order to clarify the mechanism underlying the possible preventive effect of estrogen on atherogenesis, we investigated the role of 17beta-estradiol (E2) in the regulation of endothelin-1 (ET-1) production in ovariectomized rats, which may contribute to atherogenesis. Female Spragure-Dawly rats were randomly divided into three groups: sham-operated group (sham), ovariectomized group (OVX) and 17beta-estradiol replacement group (OVX + E2, 20 microg(-1).kg.d(-1),s.c.). 4 weeks after operation, the plasma concentration of ET-1, clearance of ET-1, functional ECE activity and preproET-1 mRNA expression in aorta were measured. Concentration of plasma ET-1 change from 107.8 +/- 18.3 pg/ml (sham) and 135.5 +/- 27.6 pg/ml (OVX + E2) to 190.7 +/- 25.5 pg/ml (OVX ) (n = 8, p < 0.05). There was no significant difference in the clearance of 125IET-1 among three groups (p > 0.05). Functional ECE activity was increased in OVX group in comparison to that in sham group (p < 0.05). The OVX increased the preproET-1 mRNA expression in sham, whereas treatment with estrogen reversed these changes (p < 0.05). The present study have shown that estrogen down-regulates plasma ET-1 levels by inhibiting the preproET-1 mRNA expression and functional ECE activity. Clearance of ET-1 was not affected. Inhibition of ET-1 production mediated by modulating ECE activity may be one of the novel mechanisms of the protective of estrogens on the cardiovascular system.


Assuntos
Aorta Torácica/efeitos dos fármacos , Endotelina-1/sangue , Estradiol/farmacologia , Animais , Aorta Torácica/metabolismo , Ácido Aspártico Endopeptidases/sangue , Endotelina-1/genética , Enzimas Conversoras de Endotelina , Estradiol/administração & dosagem , Feminino , Técnicas In Vitro , Injeções Subcutâneas , Metaloendopeptidases , Contração Muscular/efeitos dos fármacos , Músculo Liso Vascular/efeitos dos fármacos , Músculo Liso Vascular/metabolismo , Ovariectomia , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , Reação em Cadeia da Polimerase Via Transcriptase Reversa
5.
Sheng Li Xue Bao ; 55(2): 213-8, 2003 Apr 25.
Artigo em Chinês | MEDLINE | ID: mdl-12715114

RESUMO

In the present study, confluent bovine aortic endothelial cells (BAECs) were used to study the rapid nongenomic effects of 17beta-estradiol and the membrane impermeable conjugated 17beta-estradiol (E(2)BSA) on the activation of endothelial nitric oxide synthase (eNOS) and mitogen activated protein kinase (MAPK). eNOS activation was assessed in whole cells by measuring [(3)H]L-arginine conversion to [(3)H]L-citrulline. MAPK activity was determined by Western blotting. The results obtained show that the addition of various concentrations of E(2) (0.001-1 micromol/L) resulted in 122+/-29, 186+/-17, 83+/-20 and 157+/-29% increases in eNOS activity, respectively, in BAECs within 15 min of exposure to the hormone. E(2) (0.01 mol/L)-stimulated eNOS activity was detectable during 5-, 15- and 30- min incubation which yielded increases of 37+/-6, 56+/-9 and 38+/-8%, respectively. The increase reached a plateau from 15 through 30 min and rapidly declined thereafter. E(2)BSA 17.5 ng/ml also enhanced eNOS activity by an increase of 35+/-9% above the basal activity. The effect of E(2) and E(2)BSA on eNOS activation was unaffected by actinomycin D 25 microg/ml but was obviously inhibited by tamoxifen (0.1 micromol/L) and PD98059 (50 micromol/L). Compared with control E(2) and E(2)BSA stimulation of BAECs for 15 min caused an increase in MAPK activity by 428+/-17 and 360+/-14% respectively. This effect was blocked by tamoxifen. These results suggest that there might be the membrane estrogen receptor localized on BAECs, which mediates the rapid nongenomic effect of estrogen on eNOS activation through MAPK pathways.


Assuntos
Células Endoteliais/metabolismo , Estradiol/farmacologia , Óxido Nítrico Sintase Tipo III/metabolismo , Receptores de Estrogênio/fisiologia , Animais , Aorta/citologia , Bovinos , Membrana Celular/metabolismo , Células Cultivadas , Células Endoteliais/citologia , Proteínas Quinases Ativadas por Mitógeno/metabolismo
6.
Sheng Li Xue Bao ; 55(1): 53-7, 2003 Feb 25.
Artigo em Chinês | MEDLINE | ID: mdl-12598935

RESUMO

We examined the effect of endogenous and exogenous nitric oxide (NO) on protein kinase C (PKC) activity induced by angiotensin II (Ang II) in cultured neonatal rat cardiomyocytes. The results are as follows. The activity of PKC was increased by Ang II (0.01-10 micromol/L) in a dose-dependent manner, but decreased by NO precursor L-arginine (L-Arg) (10 micromol/L-10 mmol/L) in a dose-dependent manner in cultured neonatal rat cardiomyocytes. Pretreatment with L-Arg (100 micromol/L) decreased significantly Ang II -activated PKC activity and PKC activity induced by phorbol 12-myristate 13-acetate (PMA) ( 10 micromol/L), a PKC activator. Pretreatment with N(G)-nitro-L-argingie methyl ester (L-NAME), a nitric oxide synthase (NOS) blocker, may inhibit significantly the role of L-Arg on Ang II - and PMA-activated PKC activity. The activity of PKC was also decreased by NO donor sodium nitroprusside (SNP) (10 micromol/L-1 mmol/L) in a dose-dependent manner in cultured neonatal rat cardiomyocytes. Pretreatment with SNP (10 micromol/L) decreased significantly Ang II - and PMA-activated PKC activity. These results indicate that PKC was controlled by both NO and Ang II. PKC may be a cross talk between Ang II and NO in cardiomyocytes. NO abolished the activity of PKC and impaired PKC downstream signaling transduction pathway cascades.


Assuntos
Angiotensina II/fisiologia , Miócitos Cardíacos/enzimologia , Óxido Nítrico/fisiologia , Proteína Quinase C/metabolismo , Animais , Animais Recém-Nascidos , Células Cultivadas , Feminino , Masculino , Miócitos Cardíacos/citologia , Ratos , Ratos Sprague-Dawley
7.
Sheng Li Xue Bao ; 54(3): 213-8, 2002 Jun 25.
Artigo em Chinês | MEDLINE | ID: mdl-12075467

RESUMO

The aim of this study was to determine the molecular mechanism of nitric oxide (NO) in preventing cardiomyocytes from hypertrophic response induced by angiotensin II (Ang II). Hypertrophic response of neonatal rat cardiomyocytes was assayed by protein synthesis rate and expression of atrial natriuretic peptide (ANP) mRNA. The level of NO was shown by the content of nitrate and nitrite in cardiac myocytes. The protein expression of MKP-1 and the gene expression of eNOS were measured with Western blotting and RT-PCR, respectively. The results are as follows. (1) L-arginine (L-Arg) induced a dose-dependent increase in NO by 16% and 31% at the concentrations of 10 micromol/L and 100 micromol/L, respectively. L-Arg also increased the gene expression of eNOS. However, these effects were inhibited by L-NAME, the inhibitor of NOS. (2) The gene expression and the protein synthesis of ANP induced by Ang II (0.1 micromol/L) were inhibited by L-Arg (100 micromol/L). The inhibitory action of L-Arg was abolished after pretreatment with antisense oligoneucleotide against MKP-1. (3) L-Arg (100 micromol/L) increased the protein expression of MKP-1 by 225%, which was inhibited by L-NAME, an NOS inhibitor, and KT-5823, a cGMP-dependent protein kinase (PKG) inhibitor. However, Ang II enhanced the effect induced by L-Arg. The above results show that NO may activate PKG, and thereby promote the protein expression of MKP-1 and inactivate MAPK, resulting in an inhibition of cardiomyocyte hypertrophic response induced by Ang II.


Assuntos
Angiotensina II/farmacologia , Cardiomegalia/metabolismo , Miócitos Cardíacos/metabolismo , Óxido Nítrico/fisiologia , Transdução de Sinais , Animais , Animais Recém-Nascidos , Arginina/farmacologia , Cardiomegalia/fisiopatologia , Proteínas Fúngicas , Técnicas In Vitro , Proteínas Quinases Ativadas por Mitógeno/biossíntese , Ratos , Ratos Sprague-Dawley
9.
Sheng Li Xue Bao ; 54(1): 17-22, 2002 Feb 25.
Artigo em Inglês | MEDLINE | ID: mdl-11930235

RESUMO

Rat vascular smooth muscle cells (VSMC) were used to study the effect of 17beta -estradiol (E(2)) on cellular proliferation (cell counting), DNA synthesis ((3)H thymidine incorporation), MTT, c -fos mRNA expression and nitric oxide (NO) release. The results obtained showed that E(2) (10(-12) 10(-8) mol/L) induced NO release from VSMC in a concentration-dependent manner; 10(-8) mol/L E (2)significantly inhibited VSMC cellular proliferation and DNA synthesis induced by 10% FCS and 10(-7) mol/L ET-1, which was obviously reversed by 10(-7)mol/L tamoxifen and 10(-6) mol/L L-NAME; after a pretreatment for 24 hours, 10(-8)mol/L E(2) significantly inhibited VSMC c -fos mRNA expression induced by 10(-7)mol/L ET-1, which was also obviously reversed by 10(-6) mol/L L-NAME. These results suggest that the inhibitory effects of E(2) on VSMC cellular proliferation and c -fos mRNA expression are closely related with NO release in VSMC, which is, at least, partly medicated by ER.


Assuntos
Estradiol/farmacologia , Músculo Liso Vascular/metabolismo , Óxido Nítrico/fisiologia , Proteínas Proto-Oncogênicas c-fos/biossíntese , Animais , Divisão Celular/efeitos dos fármacos , Células Cultivadas , Feminino , Músculo Liso Vascular/citologia , Óxido Nítrico/metabolismo , RNA Mensageiro/biossíntese , Ratos , Ratos Sprague-Dawley
10.
Sheng Li Xue Bao ; 54(2): 175-8, 2002 Apr 25.
Artigo em Chinês | MEDLINE | ID: mdl-11973601

RESUMO

Experiments were performed in male Sprague-Dawley rats (150-200 g). A silver clip (0.2 mm internal diameter) was placed on the left renal artery of rats. After operation the rats were divided into 4 groups sham group, 2K1C (two-kidney one clip) group, 2K1C+Arg (2K1C and L-Arg 150 mg/kg x d(-1) by drinking) group, and 2K1C+NAME (2K1C and L-NAME 10 mg/kg x d(-1) i.p.) group. The animals were studied at two time points (4 and 7 weeks after operation) corresponding to phases I and II of Goldblatt hypertension. The animals were deeply anesthetized with pentobarbital and perfused by the cardiac route with saline (100 ml) and freshly prepared 4% paraformaldehyde in phosphate buffer (300 ml). The caudal medulla was removed, then placed in 25% sucrose in PB for 12 h in a 4 degrees C fridge. The 40 microm coronal slices of brainstems were cut with cryostat, collected in PBS for nNOS study by immunohistochemistry. The results showed that (1) only a few neuronal nitric oxide synthase (nNOS) positive neurones were found in caudal medulla, including the depressor area of the ventral surface of medulla oblongata (VSMd) and the caudal pressor area (CPA) of the sham operated animals. The number of nNOS positive neurons in caudal medulla was significantly increased in 2K1C Goldblatt hypertension rats at 4 and 7 weeks. (2) The number of nNOS positive neurons in VSMd and CPA were 2K1C+Arg > 2K1C >2K1C +NAME > sham. (3) L-Arg enhanced the expression of nNOS whereas L-NAME inhibited the expression of nNOS in caudal medulla. (4) The character of nNOS expression was similar in Goldblatt hypertension rats at 4 weeks with that of the rats at 7 weeks.


Assuntos
Hipertensão Renovascular/enzimologia , Bulbo/enzimologia , Óxido Nítrico Sintase/biossíntese , Animais , Hipertensão Renovascular/fisiopatologia , Masculino , Bulbo/metabolismo , Ratos , Ratos Sprague-Dawley
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