BACKGROUND: Insulin-like growth factor-1 (IGF-1) has important biological effects on the heart, it can promote cardiac and vascular smooth muscle growth and metabolism.OBJECTIVE: To summarize the biological effects of IGF-1, to clarify the mechanism of exercise-induced cardiac hypertrophy, and make better use of the exercise influence on IGF1 to achieve adaptive cardiac hypertrophy.METHODS: With exercise-induced cardiac hypertrophy, insulin-like growth factor, exercise in English for the search terms,Pubmed database from January 1990 to April 2009 was retrieved; With exercise-induced cardiac hypertrophy, insulin-like growth factor, exercise in Chinese for the search terms, CNKI database from January 1990 to April 2009 was searched. Literatures were limited to English and Chinese languages. Inclusive criteria: animal experimental study and clinical application research closely linked to IGF-1; exclusive criteria: the old literatures and Meta analysis.RESULTS AND CONCLUSION: Totally 41 literatures were screened out by computers, according to the inclusion and exclusion criteria; 31 documents of which were involved for analysis. The IGF coordinates with other growth factors to promote differentiations and maturity of a variety of cells. The current data indicate that the blood serum and the cardiac local IGF-1 play an important role on cardiac hypertrophy. This study used the method of literature to analyze the production and action mechanism of the circulatory and cardiac IGF, discuss the functions of cardiac local IGF and the effect of exercise on it, and bring forward that exercise can alter the IGF expressions, IGF is related to the formation of exercise-induced cardiac hypertrophy.

Objective To investigate the pharmacologic action of the Magnolia biondii Pamp volatile oil nanometer bangosome. MethodsThe pharmacologic action of the Magnolia biondii Pamp volatile oil nanometer bangosome was evaluated by observing its effect on Jimpy mice with swelling ear,capillary permeability and rats with allergic symptoms. Results The Magnolia biondii Pamp volatile oil nanometer bangosome could significantly relieve the degree of swelling in Jimpy mice extended by p-xylene,inhibit the increased capillary permeability in Jimpy mice extended by HAC,and combat the symptoms of rhinocnesmus,sneezing,nasal discharge with a better effect than the Magnolia biondii Pamp volatile oil. Conclusion The Magnolia biondii Pamp Volatile oil nanometer bangosome has a good anti-inflammation and anti-hypersensitiveness effect,which upgrades the effect of the Magnolia biondii Pamp volatile oil.

Child, Preschool ; Chyle ; Female ; Humans ; Infant ; Male ; Mesenteric Cyst ; diagnosis ; surgery

Bronchial asthma is the chronic airway inflammatory disease that characterized by reversible airflow limitation .The presence of airway inflammation could lead to airway remodeling .In recent years , many studies have found that arginase plays an im-portant role in the airway inflammation and airway remodeling of asthma .It not only reduces airway release nitric oxide and increases airway hyperresponsiveness , but also its metabolites such as putrescine , proline, etc can induce cell proliferation and collagen synthe-sis, leading to airway remodeling .In this paper , the arginase and its role in the pathogenesis of asthma are discussed .

Objective To test the reliability and validity of the Chinese Version of the Fatigue severity scale (FSS)in patients with cerebral infarction.Methods The FSS was translated into Chinese language and the reverse translation was done by several experts.Validity,dimensionality,and reliability tests were implemented in 153 cases of cerebral infarction.Results One component was extracted in factor analysis,and the total cumulative contribu- tion was 64.982%.Based on the Mokken Scale analysis for Polytomous items analyses,the scale was found to be u- nidimensional and scale H is 0.6125,Cronbach?of the scale is 0.9287.Conclusion The psychometric proper- ties(reliabilities and validities)of FSS Chinese Version was satisfactory and seemed to be adaptable to Chinese cere- bral infarction patients.

6.66 kPa),30 cases of light degree pulmonary artery hypertension group (3.99 kPa

Aim To evaluate the effects of aspirin on the expression of inflammatory proteins induced by oxidized low-density lipoprotein(ox-LDL) in human vascular endothelial cells (HUVECs). Methods HUVECs were stimulated with different concentrations of ox-LDL. The expression of inflammatory proteins was detected by Western blot.Intracellular ROS generation was measured by flow cytometry using perexide-sensitive flurscent probe 2′, 7′-dichrofluorescein diacetate(DCFH-DA).Results ① Aspirin inhibited COX-2 expression induced by ox-LDL. Cells were preincubated with 2.5 mmol?L-1, 5 mmol?L-1 of aspirin or without any treatment for 30 min and then stimulated by 0.3 g?L-1 ox-LDL for 16 h, COX-2 expression was reduced by treating of aspirin.COX-2 expression was enhanced after the stimulation with ox-LDL, and aspirin inhibited the increasing.② Aspirin suppressed ICAM-1 expression induced by ox-LDL in HUVECs. ICAM-1 expression was increased by ox-LDL stimulation for 16 h, and aspirin significantly down-regulated the expression. Similar results were obtained by immunofluorescence.③ Aspirin partially reduced ROS production induced by ox-LDL in HUVECs. After stimulation with 0.3 g?L-1 ox-LDL for 16 h, the intracellular level of ROS was increased, however, aspirin failed to fully inhibit the phenomenon.Conclusion Nonsteroidal anti-inflammatory drugs (NSAID) aspirin significantly down-regulated the expression of COX-2 and ICAM-1 induced by ox-LDL.The results suggested that aspirin could reduce the inflammation responses mediated by ox-LDL on HUVECs in atherosclerosis.

Objective To investigate the diagnosis of a case with 7p15.3p22.1 microdeletion by applying array-based comparative genomic hybridization (array-CGH) and to analyze the relationship between the clinical manifestations and 7p15.3p22.1 microdeletion. Method Array-CGH technique was used to detect genomic copy number variations (CNVs) in an infant with normal karyotype after conventional chromosomal karyotyping. Results Array-CGH detected 7p15.3p22.1 deletion (chr7: 6777262-23981753), which was confirmed as pathogenic CNV after comparative analysis with database. Conclusion Array-CGH could serve as a useful complement for G-banding to be used in the clinical cytogenetic diagnosis.

AIM: To investigate the effects of advanced glycation end products (AGEs) on protein and mRNA expression of macrophage inflammatory protein-1? (MIP-1?) in cultured human umbilical vein endothelial cells(HUVECs). METHODS: HUVECs were cultured with AGEs at different concentrations for 24 h and at a concentration of 400 mg/L for different time.The levels of mRNA and protein expression of MIP-1? in cultured HUVEC were detected by in situ hybridization and Western blot, respectively. RESULTS: In situ hybridization showed that after exposure of HUVECs to AGEs at different concentrations (100 mg/L, 200 mg/L, 400 mg/L) for 24 h, the average integrated optical density values (18.76?3.17, 26.58?1.61, 34.23?2.25) of MIP-1? mRNA expression in HUVECs were higher than that in control group (13.83?1.24, P

Two patients with neonatal diabetes tested as V59A and V59M mutations were chosen for the study. Clinical data were analyzed retrospectively. The results showed that the patient with V59A mutation was characteristic of spasm and hyperglycemia at the age of three month, and treated with insulin for a long time as unresponsive to the glibenclamide at the beginning. Myasthenia and delay of development were observed during the follow-up. At the age of two years, glibenclamide was tried for the second time with a high dose and fairly-controlled glucose level. The patient with V59M mutation was diagnosed with diarrhea, hyperglycemia, and ketosis at the age of two month, and was responsive to glibenclamide at a relatively low dose with well-controlled glucose level. These results suggest that KCNJ11 V59M mutation would show some milder clinical manifestations and better glibenclamide efficacy as compared with V59A mutation.