Amygdalin and exercise training exert a synergistic effect in improving cardiac performance and ameliorating cardiac inflammation and fibrosis in a rat model of myocardial infarction.

This study investigated the effects of amygdalin (AMY, a cyanogenic glycoside widely distributed in the fruits and seeds of Rosaceae plants) on cardiac performance and ventricular remodeling in a rat model of myocardial infarction (MI). We also investigated whether the combination of AMY with exercise training (ExT) has a beneficial synergistic effect in treating MI rats. MI was induced by the ligation of the left anterior descending coronary artery in male SD rats. ExT or AMY treatment was started 1 week after MI and continued for 1 week (short-term) or 8 weeks (long-term). Cardiac function was evaluated by echocardiographic and hemodynamic parameters. Heart tissues were harvested and subjected to 2,3,5-triphenyl-tetrazolium chloride, Masson's trichrome, hematoxylin-eosin, and immunohistochemical staining. Gene expression was determined by quantitative polymerase chain reaction. Western blot gave a qualitative assessment of protein levels. AMY or ExT improved cardiac function and reduced infarct size in MI rats. AMY or ExT also suppressed myocardial fibrosis and attenuated inflammation in the infarct border zone of hearts from MI rats, as evidenced by inhibition of collagen deposition, inflammatory cell infiltration, and pro-inflammatory markers (interleukin 1ß, interleukin 6, tumor necrosis factor-α, and cyclooxygenase 2). Notably, the effects of AMY combined with ExT were superior to those of AMY alone or ExT alone. Mechanistically, these beneficial functions were correlated with the inhibition of MI-induced activation of the transforming growth factor-ß/Smad pathway. Collectively, AMY and ExT exert a synergistic effect on improving cardiac performance and ameliorating cardiac inflammation and fibrosis after MI, and the effects of long-term intervention were better than short-term intervention.

[Effects of gender on treatment strategies for elderly patients with acute coronary syndrome].

OBJECTIVE: To explore the effects of gender on treatment strategies for elderly patients with acute coronary syndrome (ACS). METHODS: March 2009 to March 2012, consecutive 619 aged ACS patients undergoing coronary angiography (CA) were screened at our hospital. There were 273 females and 346 males. Risk factors, ACS diagnosis, CA results, treatments and prognosis were compared between female and male groups. RESULTS: The risk factors of body mass index, stroke history, smoking history, hemoglobin (Hb), serum cholesterol (TC), low density lipoprotein (LDL-C) and blood uric acid (UA) levels were significantly lower in female group than those in male group (P < 0.05). The morbidity of diabetes in female group was obviously higher than that in male group (27.8% vs 18.5%, P < 0.05). The prevalence of myocardial infarction history, percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) history in male group were significantly greater than that in female group (48.0% vs 39.9%, P < 0.05; 30.6% vs 22.3%, P < 0.05; 19.9% vs 10.3%, P < 0.01). The rate of combined multiple risk factors (3 or higher) increased significantly in female group (41.8% vs 29.8%, P < 0.05). The incidence of unstable angina pectoris (UAP) and non-ST segment elevation myocardial infarction (NSTEMI) in female group was greater, but there was no statistical significance. The rate of 3-vessel and calcification lesions in female group was significantly elevated compared with male group (36.26% vs 28.61%, P < 0.05). Regarding the choice of treatment strategy, conservative treatment was common in females, but there was no statistical significance between them. PCI, emergency PCI and selective CABG operation were performed more frequently in female group compared with male group (26.0% vs 14.2%, P < 0.01; 14.7% vs 6.6%, P < 0.01; 19.1% vs 7.7%, P < 0.01). The prognosis had no statistical significance between two groups. CONCLUSION: The treatment strategies have certain limitations for female ACS patients. And an more aggressive treatment should be offered to improve the prognosis.

Transient increased expression of VEGF and MMP-1 in a rat liver tumor model after hepatic arterial occlusion.

BACKGROUND/AIMS: This study investigates the influence of hepatic arterial occlusion (HAO) on blood perfusion of transplanted cancer in rat's liver, and the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinase-1 (MMP-1) and explores the mechanisms involved in transcatheter arterial embolization (TAE)-induced metastasis of liver cancer preliminarily. METHODOLOGY: Walker 256 carcinosarcoma was transplanted into rat's liver to create the liver cancer model. Hepatic arterial ligation (HAL) was used to block the hepatic arterial blood supply and simulate TAE. Rats bearing tumor were divided into three groups: control, laparotomy control, and HAL groups. Blood perfusion of tumor was analyzed by a Hoechst 33342 labeling assay. The level of serum VEGF was assayed by ELISA; and the expression of VEGF and MMP-1 mRNA was detected by in situ hybridization. RESULTS: Two days after HAL, the number of Hoechst 33342 labeled cells which represent the blood perfusion of the tumor directly and hypoxia of tumor indirectly in the HAL group decreased significantly compared with that in the control group (329.1+/-29.3 vs. 383.6+/-19.2, P<0.01). The level of serum VEGF in the HAL group increased significantly compared with that of the control group (92.5+/-43.9 pg/mL vs. 54.9+/-19.3 pg/mL, P<0.05). The expression of VEGF and MMP-1 mRNA in the tumor tissue of the HAL group increased significantly compared with that of the control and the laparotomy control groups (P<0.05). The blood perfusion data of the tumor, represented by number of Hoechst 33342 labeled cells, showed an inverse correlation with the expression of VEGF mRNA in tumor tissue (P<0.05). While 6 days after HAL, the blood perfusion of tumor in HAL group decreased and the expression of VEGF and MMP-1 increased only slightly, not significantly, compared with that in the control group. CONCLUSIONS: In conclusion, blockage of hepatic arterial blood supply results in transient decreased blood perfusion and increased expression of metastasis-associated genes VEGF and MMP-1 of transplanted liver cancer in rats. Decreased blood perfusion and hypoxia may be the major reason for up-regulated expression of VEGF. Better understanding of the mechanisms involved with TAE-induced metastasis may lead to the enhancement of the long-term effects of TAE for liver cancer.

[Resting energy expenditure in healthy newborn infants].

OBJECTIVE: To establish the value of the resting energy expenditure (REE) in healthy newborns and evaluate relative factors of REE. METHODS: One hundred and fifty-four healthy newborns (75 boys, 79 girls; birth-weight 2,500-3,999 g) were enrolled in this study. The Apgar score at the 5th minute was equal to or more than 8; the postnatal age was equal to or more than 5 days. The newborns had no apparent defect. The mothers had no history of metabolic and endocrine diseases. REE was measured by Deltatrac II in child canopy mode for 30-45 minutes during asleep or quiet awake status. RESULTS: The average REE was (201.8 +/- 25.4) kJ/(kg.d), which was significantly lower than the predicted REE by Schofield formula[(226.1 +/- 4.8) kJ/(kg.d), P = 0.000], the predicted REE was 12.04% higher than the measured REE. There were no differences in sex and ways of delivery. The newborns whose birth-weight was between 2,500-2,999 g were measured in two modes: baby and child mode, and the REE values were significantly higher (122.6 +/- 25.0) kJ/(kg.d) and (208.8 +/- 26.4) kJ/(kg.d), respectively (P = 0.000). CONCLUSIONS: The prediction formula might be improper for calculating the REE in newborn infants. The indirect calorimetry was the better way to know the actual REE of newborns. The authors recommended that in child mode the measurement of REE in newborns would be the indirect calorimetry, and the REE in healthy newborns was (201.8 +/- 25.4) kJ/(kg.d).