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ABSTRACT Introduction: The human brain controls the body's balance, actinh on the muscle tissues of the body and thus controlling the balance of its center of gravity. Objective: To analyze 6 indicators that affect the brain's ability to control the body's balance and to verify the important muscle areas of the human body and prove that strength training can help improve the body's balance ability. Methods: This article selected young university students with the same physical fitness as sample and analyzed the factors that affect the body's strength and balance using statistical models. Results: Strength training can effectively improve the body›s balance when standing. Conclusion: Training the brain to control the body is mainly to exercise strength, stability, balance, and other abilities of human muscle tissue. Using this kind of exercise method can effectively improve the stability of the human body. Targeted training can also enhance the brain's ability to control the balance of the body. Level of evidence II; Therapeutic studies - investigation of treatment results.
RESUMO Introdução: O cérebro humano controla o equilíbrio do corpo, agindo sobre seus tecidos musculares e, assim, controlando o equilíbrio de seu centro de gravidade. Objetivo: Analisar seis indicadores que afetam a capacidade do cérebro de controlar o equilíbrio do corpo, avaliar áreas musculares relevantes do corpo humano, e provar que atividade física voltada à força pode melhorar o equilíbrio do corpo. Métodos: Esse artigo selecionou como amostra jovens estudantes universitários com preparo físico similar, e analisou quais fatores afetam de maneira relevante a força e o equilíbrio do corpo por meio de modelos estatísticos. Resultados: Treinamentos de força podem efetivamente melhorar o equilíbrio do corpo quando de pé. Conclusão: Treinar o cérebro para controlar o corpo significa, principalmente, treinar a força, a estabilidade, o equilíbrio, e outras capacidades dos tecidos musculares humanos. O uso dessa metodologia de atividade física pode efetivamente aprimorar a estabilidade do corpo humano. O treinamento direcionado também pode melhorar a capacidade do cérebro de controlar o equilíbrio do corpo. Nível de evidência II; Estudos terapêuticos - investigação do resultado de tratamentos.
RESUMEN Introducción: El cerebro humano controla el equilibrio del cuerpo, actuando sobre sus tejidos musculares y, así, controlando el equilibrio de su centro de gravedad. Objetivo: Analizar seis indicadores que afectan la capacidad del cerebro de controlar el equilibrio del cuerpo, evaluar áreas musculares relevantes del cuerpo humano y probar qué actividad física centrada en la fuerza puede mejorar el equilibrio del cuerpo. Métodos: Este artículo seleccionó como muestra jóvenes estudiantes universitarios con preparación física similar y analizó cuáles factores afectan de manera relevante la fuerza y el equilibrio del cuerpo por medio de modelos estadísticos. Resultados: Entrenamientos de fuerza pueden efectivamente mejorar el equilibrio del cuerpo al estar de pie. Conclusión: Entrenar el cerebro para controlar el cuerpo significa, principalmente, entrenar la fuerza, la estabilidad, el equilibrio y otras capacidades de los tejidos musculares humanos. El uso de esta metodología de actividad física puede, efectivamente, mejorar la estabilidad del cuerpo humano. El entrenamiento dirigido también puede optimizar la capacidad del cerebro de controlar el equilibrio del cuerpo. Nivel de evidencia II; Estudios terapéuticos - investigación del resultado de tratamientos.
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<p><b>OBJECTIVE</b>Cytokines such as VEGF and IGF play an important role in maintaining the function of blood vascular endothelium. And Akt1 is an important molecule in the intra-cellular signaling transduction. This study aims to investigate the molecular mechanism of Shugan Yiyang (SGYY) capsule in the treatment of arteriogenic erectile dysfunction (AED) by detecting the expressions and phosphorylation of VEGF, IGF and Akt1 in AED rats.</p><p><b>METHODS</b>We established AED models in 60 three-month-old adult male SD rats by bilateral ligation of the internal iliac artery, and assigned them to a sham operation group, a model control group, a sildenafil group, a low-dose SGYY group (0.5 g/[kg x d]) and a high-dose SGYY group (1 g/[kg x d]). After 30 days of gavage, we assayed the plasma concentrations of VEGF and IGF in the carotid artery of the rats by ELISA, detected the expressions of VEGF and IGF mRNA by real-time PCR and determined the expression and phosphorylation of Aktl protein in the corpus cavernosum penis by Western blot.</p><p><b>RESULTS</b>In the model control group, the expressions of VEGF and IGF mRNA were 0.41 +/- 0.06 and 0.42 +/- 0.06, the plasma concentrations of VEGF and IGF were (28.59 +/- 24.97) pg/ml and (15.82 +/- 4.37) ng/ml, and the expression of p-Aktl/Akt1 was 0.93 +/- 0.14. While in the high-dose SGYY group, the expressions of VEGF and IGF mRNA were 0.77 +/- 0.04 and 0.78 +/- 0.05, the plasma concentrations of VEGF and IGF were (95.83 +/- 37.34) pg/ml and (20.45 +/- 3.83) ng/ml, and the expression of p-Aktl/Aktl was 1.43 +/- 0.50. All the parameters above were significantly higher in the high-dose SGYY than in the model control group (P < 0.05), and so were they in the low-dose SGYY group except the plasma concentration of IGF (P < 0.05).</p><p><b>CONCLUSION</b>SGYY can significantly upregulate the expressions of VEGF, IGF and Akt1 in the corpus cavernosum penis of AED rats, and improve the function of blood vascular endothelium, which is probably an important mechanism of SGYY capsule acting on AED.</p>
Subject(s)
Animals , Male , Rats , Disease Models, Animal , Drugs, Chinese Herbal , Therapeutic Uses , Erectile Dysfunction , Drug Therapy , Metabolism , Insulin-Like Growth Factor I , Metabolism , Phytotherapy , Proto-Oncogene Proteins c-akt , Metabolism , Rats, Sprague-Dawley , Somatomedins , Metabolism , Vascular Endothelial Growth Factor A , MetabolismABSTRACT
According to the knowledge gained from engineering of nisinZ, using plasmid pHJ201 DNA as template, NisinZ was mutated by site-directed mutagenesis, NisinZ mutant T8S contains Serine at position 8 instead of Threonine, NisinZ mutant N27K/H31K contains Lysine at position 27 and 31, respectively, instead of Asparagine and Histidine and NisinZ mutant T2S/ H31K contains dehydrobutyrine and Lysine at position 2 and 31 instead of dehydroalanine and Histidine. They are cloned into pMG36e and expressed in L. Lactis NZ9800, the expression products of these mutants purified by Sephadex CM-25 and Sephadex G-25 chromatography, some properties of NisinZ mutants (T8S, T2S/H31K and N27K/H31K) were studied. The results showed that the spectrum of antimicrobial activity and solubility of these mutants had not been changed, their antimicrobial activities were found to be slightly lower than that of the wild-type NisinZ. but mutants T8S and T2S/H31K showed higher stability, which were significantly more stable than wild-type NisinZ at 55 approximately 100 degrees C and pH7 approximately 9.
Subject(s)
Anti-Bacterial Agents , Metabolism , Pharmacology , Bacteria , Electrophoresis, Polyacrylamide Gel , Mutagenesis, Site-Directed , Methods , Nisin , Genetics , Metabolism , Pharmacology , Protein Stability , Solubility , TemperatureABSTRACT
Lactic acid bacteria (LAB) are important industrial microorganism used in the production and preservation of food-stuffs. Recently, considerable advances have been made in the genetics and molecular biology of LAB. These have resulted in the construction of food-grade gene expression systems for these bacteria. This paper aims to review the essential features for food-grade systems, food-grade selection markers, food-grade controlled gene expression and food-grade inducible signaling molecule, and recent developments on food-grade cloning and expression systems for LAB. These gene expression systems have great potential for studies on gene expression and regulation in LAB and a variety of bioprocessing application in industrial fermentations.
Subject(s)
Food Industry , Methods , Reference Standards , Food Microbiology , Gene Expression Regulation, Bacterial , Lactococcus lactis , GeneticsABSTRACT
Objective: To elucidate the possible mechanism responsible for the improved protection of terminal warm blood cardioplegia (TWBC) after hypothermic cardiopulmonary bypass (CPB) through analysis of tubulin (TB) components changes in myocardial cells exposed to TWBC. Methods: Stable animal models of CPB were established in cats, which were then randomly divided into 2 groups. Group Ⅰ was subjected to intermittent cold blood cardioplegia (ICBC) whereas group Ⅱ to ICBC followed by TWBC before uncross-clamping. Left ventricular performance was then monitored and evaluated by LVSP, LVEDP, ±dp/dtmax and t-dp/dtmax in both groups and semi-quantitive analysis was conducted with Western blot method as to the content and constitution of TB in myocardial cells at 15 min, 120 min after aortic crossclamping (ACC) and 5 min,15 min, 60 min,120 min after reperfusion. Results: Within 120 min after reperfusion, systolic and diastolic functions decreased significantly in group Ⅰ as compared with group Ⅱ(P<0.05). At 115 min after ACC and 15 min after reperfusion, the content of free and polymerized TB in both groups had no difference (P>0.05). At 120 min after ACC and 5 minutes after reperfusion, there was a significant difference between groupⅠ andⅡ (P<0.01). Conclusion: TWBC accelerates the repolymerization of myocardial TB during hypothermic CPB, which may mediate the improved cardiac performance in the early stage of myocardial reperfusion.
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Objective: To elucidate the possible mechanism responsible for the improved protection of terminal warm blood cardioplegia (TWBC) after hypothermic cardiopulmonary bypass (CPB) through analysis of tubulin (TB) components changes in myocardial cells exposed to TWBC. Methods: Stable animal models of CPB were established in cats, which were then randomly divided into 2 groups. Group Ⅰ was subjected to intermittent cold blood cardioplegia (ICBC) whereas group Ⅱ to ICBC followed by TWBC before uncross-clamping. Left ventricular performance was then monitored and evaluated by LVSP, LVEDP, ±dp/dtmax and t-dp/dtmax in both groups and semi-quantitive analysis was conducted with Western blot method as to the content and constitution of TB in myocardial cells at 15 min, 120 min after aortic crossclamping (ACC) and 5 min,15 min, 60 min,120 min after reperfusion. Results: Within 120 min after reperfusion, systolic and diastolic functions decreased significantly in group Ⅰ as compared with group Ⅱ(P<0.05). At 115 min after ACC and 15 min after reperfusion, the content of free and polymerized TB in both groups had no difference (P>0.05). At 120 min after ACC and 5 minutes after reperfusion, there was a significant difference between groupⅠ andⅡ (P<0.01). Conclusion: TWBC accelerates the repolymerization of myocardial TB during hypothermic CPB, which may mediate the improved cardiac performance in the early stage of myocardial reperfusion.