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Laser treatment of an aluminum composite surface was carried out to improve tribological properties and corrosion resistance at the surface. The workpiece consists of 15% SiC and pure aluminum, and it is produced by hot pressing. The characteristics of the laser-treated surface were examined using optical and scanning electron microscopes, energy dispersive spectroscopy, X-ray diffraction, a micro-tribometer, and a potentiostat. Laser treatment was carried out by following a spiral scanning track at the surface. This provides a self-annealing effect of the lately formed laser tracks on the initially formed tracks while lowering the cooling rates at the surface. It was found that laser-treated surfaces are free from asperities such as large-scale cracks and voids. Laser treatment improves the hardness of the surface because of the dense layer formation in the surface region. The friction coefficient of the laser-treated surface attains lower values than that corresponding to the untreated surface. Laser treatment improves the corrosion resistance of the surface.

This article focuses on a study that compares poorer short term outcome in indo-asians and Caucasians after percutaneous coronary intervention (PCI) for ethnicity as an independent risk factor. Despite the complex nature of this patient group there is a low incidence of tropinin elevation and myocardial necrosis following PCI. Coronary artery disease tends to be more extensive and diffuse in Indo-Asians (IA) as compared with Caucasians. There are, however, few data relating to ethnicity and outcome after revoscularisation. Ethnicity in relation to lAs emerged as an independent risk factor for poor short term outcome following PCI.

Hydrogen generation through the hydrolysis of aluminum alloys has attracted significant attention because it generates hydrogen directly from alkaline water without the need for hydrogen storage technology. The hydrogen generation rate from the hydrolysis of aluminum in alkaline water is linearly proportional to its corrosion rate. To accelerate the corrosion rate of the aluminum alloy, we designed Al-Ni alloys by continuously precipitating an electrochemically noble Al 3 Ni phase along the grain boundaries. The Al-0.5~1 wt.% Ni alloys showed an excellent hydrogen generation rate of 16.6 mL/cm2·min, which is about 6.4 times faster than that of pure Al (2.58 mL/cm2·min). This excellent performance was achieved through the synergistic effects of galvanic and intergranular corrosion on the hydrolysis of Al. By raising the solution temperature to 50 °C, the optimal rate of hydrogen generation of Al-1 wt.% Ni in 10 wt.% NaOH solutions at 30 °C can be further increased to 54.5 mL/cm2·min.

A technology based on velocity ratio indices is described for application in the myocardium. Angle-independent Doppler indices, such as the pulsatility index, which employ velocity ratios, can be measured even if the ultrasound beam vector at the moving target and the motion vector are not in a known plane. The unknown plane situation is often encountered when an ultrasound beam interrogates sites in the myocardium. The velocities employed in an index calculation must be close to the same or opposite directions. The Doppler velocity ratio indices are independent of angle in 3D space as are ratio indices based on 1D strain and 1D speckle tracking. Angle-independent results with spectral Doppler methods are discussed. Possible future imaging techniques based on velocity ratios are presented. By using indices that involve ratios, several other sources of error cancel in addition to that of angular dependence for example errors due to less than optimum gain settings and beam distortion. This makes the indices reliable as research or clinical tools. Ratio techniques can be readily implemented with current commercial blood flow pulsed wave duplex Doppler equipment or with pulsed wave tissue Doppler equipment. In 70 patients where the quality of the real-time B-mode looked suitable for the Doppler velocity ratio technique, there was only one case where clear spectra could not be obtained for both the LV wall and the septum. A reproducibility study of spectra from the septum of the heart shows a 12% difference in velocity ratios in the repeat measurements., (© 2019 The authors)

The vast majority of what is considered fact about adult neurogenesis comes from research on laboratory mice and rats: where it happens, how it works, what it does. However, this relative exclusive focus on two rodent species has resulted in a bias on how we think about adult neurogenesis. While it might not prevent us from making conclusions about the evolutionary significance of the process or even prevent us from generalizing to diverse mammals, it certainly does not help us achieve these outcomes. Here, we argue that there is every reason to expect striking species differences in adult neurogenesis: where it happens, how it works, what it does. Species-specific adaptations in brain and behavior are paramount to survival and reproduction in diverse ecological niches and it is naive to think adult neurogenesis escaped these evolutionary pressures. A neuroethological approach to the study of adult neurogenesis is essential for a comprehensive understanding of the phenomenon. Furthermore, most of us are guilty of making strong assertions about our data in order to have impact yet this ultimately creates bias in how work is performed, interpreted, and applied. By taking a step back and actually placing our results in a much larger, non-biomedical context, we can help to reduce dogmatic thinking and create a framework for discovery.

Background: Preclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans., Methods and Results: Overall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P<0.0001) and plasma C-reactive protein concentrations (6.50 [2.00 to 12.75] versus 2.00 [0.50 to 4.00] mg/dL, P=0.0005) despite having similar aortic (P=0.12) and less coronary (P=0.006) atherosclerotic burden and similar paraspinal muscular 18F-fluorodeoxyglucose uptake (P=0.52). Patients with ST-segment elevation MI had larger infarcts (peak plasma troponin 32 300 [10 200 to >50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non-ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI., Conclusions: The presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization: MI begets MI., Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01749254., (© 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

Accurately assessing an individual's risk of myocardial infarction or stroke using currently available risk stratification tools remains a challenge, even in patients with symptomatic disease. Inflammation, micro-calcification and intra-plaque angiogenesis occur during the development and ultimate rupture of vulnerable plaques. Molecular imaging techniques such as combined positron emission tomography and computed tomography (PET/CT) offer the opportunity to target these key cellular processes within atheroma and identify high-risk lesions. In this review we will set out the studies that have demonstrated the feasibility of PET/CT imaging in assessing atherosclerotic plaque inflammation, micro-calcification and angiogenesis. We will also discuss the potential of PET/CT molecular imaging as both a screening tool for novel therapeutic interventions and as a means of improving cardiovascular risk stratification.

Neutralizing injurious stimuli, proinflammatory mediator catabolism, and polymorphonuclear leukocyte (PMN) clearance are determinants of inflammatory resolution. To this, we recently added innate-type lymphocyte repopulation as being central for restoring postinflammation tissue homeostasis with a role in controlling innate immune-mediated responses to secondary infection. However, although macrophages dominate resolution, their phenotype and role in restoring tissue physiology once inflammation abates are unknown. Therefore, we isolated macrophages from the resolving phase of acute inflammation and found that compared with classically activated proinflammatory M1 cells, resolution-phase macrophages (rMs) possess weaker bactericidal properties and express an alternatively activated phenotype but with elevated markers of M1 cells including inducible cyclooxygenase (COX 2) and nitric oxide synthase (iNOS). This phenotype is controlled by cAMP, which, when inhibited, transforms rM to M1 cells. Conversely, elevating cAMP in M1 cells transforms them to rMs, with implications for cAMP in the resolution of systemic inflammation. It transpires that although rMs are dispensable for clearing PMNs during self-limiting inflammation, they are essential for signaling postresolution lymphocyte repopulation via COX 2 lipids. Thus, rM macrophages are neither classically nor alternatively activated but a hybrid of both, with a role in mediating postresolution innate-lymphocyte repopulation and restoring tissue homeostasis.