Effect of Porosity on Dynamic Response of Additive Manufacturing Ti-6Al-4V Alloys.

Additive manufacturing is a rapidly developing manufacturing technology of great potential for applications. One of the merits of AM is that the microstructure of manufactured materials can be actively controlled to meet engineering requirements. In this work, three types of Ti-6Al-4V (TC4) materials with different porosities are manufactured using selective laser melting using different printing parameters. Their dynamic behaviors are then studied by planar impact experiments based on the free-surface velocity measurements and shock-recovery characterizations. Experimental results indicate that the porosity significantly affects their dynamic response, including not only the yield, but also spall behaviors. With the increasing porosity, the Hugoniot elastic limit and spall strength decrease monotonically. In the case of TC4 of a large porosity, it behaves similar to energy-absorbing materials, in which the voids collapse under shock compression and then the spallation takes place.

Metformin protects against insulin resistance induced by high uric acid in cardiomyocytes via AMPK signalling pathways in vitro and in vivo.

High uric acid (HUA) is associated with insulin resistance (IR) in cardiomyocytes. We investigated whether metformin protects against HUA-induced IR in cardiomyocytes. We exposed primary cardiomyocytes to HUA, and cellular glucose uptake was quantified by measuring the uptake of 2-NBDG, a fluorescent glucose analog. Western blot was used to examine the levels of signalling protein. Membrane of glucose transporter type 4 (GLUT4) was analysed by immunofluorescence. We monitored the impact of metformin on HUA-induced IR and in myocardial tissue of an acute hyperuricaemia mouse model established by potassium oxonate treatment. Treatment with metformin protected against HUA-reduced glucose uptake induced by insulin in cardiomyocytes. HUA directly inhibited the phosphorylation of Akt and the translocation of GLUT4 induced by insulin, which was blocked by metformin. Metformin promoted phosphorylation of AMP-activated protein kinase (AMPK) and restored the insulin-stimulated glucose uptake in HUA-induced IR cardiomyocytes. As a result of these effects, in a mouse model of acute hyperuricaemia, metformin improved insulin tolerance and glucose tolerance, accompanied by increased AMPK phosphorylation, Akt phosphorylation and translocation of GLUT4 in myocardial tissues. As expected, AICAR, another AMPK activator, had similar effects to metformin, demonstrating the important role of AMPK activation in protecting against IR induced by HUA in cardiomyocytes. Metformin protects against IR induced by HUA in cardiomyocytes and improves insulin tolerance and glucose tolerance in an acute hyperuricaemic mouse model, along with the activation of AMPK. Consequently, metformin may be an important potential new treatment strategy for hyperuricaemia-related cardiovascular disease.

Correlation of triglycerides with myocardial infarction and analysis of risk factors for myocardial infarction in patients with elevated triglyceride.

BACKGROUND: This study aims to investigate the associations of different (low/medium/high) levels of fasting triglyceride (TG) levels with cardiovascular endpoints. METHODS: This cohort study comprised of in-service and retired employees of the Kailuan Coal Mine Group, who participated in the health examination conducted in 11 hospitals in the Kailuan region from June 2006 to October 2007 (n=100,271). The study population was divided into five groups according to different TG levels. Logistic regression analysis was used to analyze the risk factors for myocardial infarction (MI) in patients with elevated TG, and Cox proportional hazards regression analysis was used to analyze the effects of different TG levels on endpoint events. RESULTS: After a median follow-up of 7 years, 961 patients developed MI and 3,142 subjects died. The multivariate logistic regression analysis revealed that elevated TG, an age of ≥65 years old, body mass index (BMI) >25 kg/m2, fasting blood glucose (FBG) ≥6.1 mmol/L and high density lipoprotein cholesterol (HDL-C) <1.5 mmol/L were all risk factors for MI (P<0.05). Furthermore, Cox proportional hazards regression model revealed that after controlling for gender, age and other factors, with the increase in TG level, the relative risk of MI also increased. Compared to the TG1 group, the risk of MI increased to 1.32 folds in the TG4 group (95% CI: 1.05-1.66, P=0.018) and 1.61 folds in the TG5 group (95% CI: 1.21-1.93, P=0.004). Furthermore, the risk of MI combined with all-cause death and all-cause death also increased, but the differences were not all statistically significant. CONCLUSIONS: In the study population of the Kailuan region, elevated fasting TG increases the risk of MI, particularly in populations with an age of ≥65 years old, BMI >25 kg/m2, FBG ≥6.1 mmol/L and HDL-C <1.5 mmol/L.

Clinical analysis of acute myocardial infarction caused by coronary embolism.

BACKGROUND: This study aims to investigate the clinical and angiographic features in patients with acute myocardial infarction (AMI) induced by coronary artery embolism. METHODS: Clinical data of five patients with AMI induced by coronary artery embolism were analyzed retrospectively. RESULTS: One patient had left atrial myxoma, one patient had non-valvular atrial fibrillation, and three patients had rheumatic heart disease. Furthermore, one patient had mitral mechanical valve prostheses, two patients had atrial fibrillation. Coronary angiography showed the absence of significant atherosclerostic lesions in the coronary arteries except infarct related artery in five patients. Angiography suggested the presence of IRA occlusion caused by embolism. CONCLUSIONS: The status for AMI due to coronary artery embolism usually expresses embolic material originating from the left heart chambers. Rheumatic heart disease and atrial fibrillation are the common reasons for coronary artery embolism. Coronary artery occlusion is the common performance in the results of primary coronary artery angiography. Sometimes it expresses visible signs of embolism.

Masquerading bundle branch block as a presenting manifestation of complete atrioventricular block that caused syncope.

A 59-year-old male patient was admitted with the main complaints of stuffiness and shortness of breath. An ECG from precordial leads on admission showed masquerading bundle branch block. Syncope frequently occurred after admission. During syncope episodes, ECG telemetry showed that the syncope was caused by intermittent complete atrioventricular block, with the longest RR interval lasting for 4.36 s. At the gap of syncope, ECG showed complete right bundle branch block accompanied by alternation of left anterior fascicular block and left posterior fascicular block. The patient was implanted with a dual-chamber permanent pacemaker. Follow-up of 9 months showed no reoccurrence of syncope.

Downregulation of microRNA-19b contributes to angiotensin II-induced overexpression of connective tissue growth factor in cardiomyocytes.

OBJECTIVES: The present study was designed to decipher the molecular mechanisms underlying angiotensin (Ang) II-induced overexpression of connective tissue growth factor (CTGF) in cultured cardiomyocytes. METHODS: Cardiomyocytes isolated from 1- to 3-day-old neonatal rats were cultured and treated with 100 nM Ang II with or without pretreatment with 10 nM telmisartan, an Ang II type 1 receptor antagonist. The role of microRNA (miR)-19b in the regulation of Ang II-induced CTGF expression was evaluated in cultured cardiomyocytes with quantitative real-time reverse transcription polymerase chain reaction and Western blot analysis. RESULTS: We provide several lines of evidence to show that miR-19b contributes to the Ang II-induced overexpression of CTGF in cultured cardiomyocytes. Firstly, administration of Ang II decreased the level of miR-19b dramatically (p < 0.05 vs. control), which was abolished by telmisartan. Secondly, Ang II increased the level of CTGF significantly (p < 0.05 vs. control), which was also prevented by pretreatment with telmisartan. Thirdly, overexpression of miR-19b decreased CTGF levels (p < 0.05 vs. control). Finally, transfection of miR-19b into cardiomyocytes prevented the upregulation of CTGF induced by Ang II. CONCLUSION: Downregulation of miR-19b contributes to Ang II-induced overexpression of CTGF in cultured cardiomyocytes.