Characterizing Multiscale Mechanical Properties of Brain Tissue Using Atomic Force Microscopy, Impact Indentation, and Rheometry

To design and engineer materials inspired by the properties of the brain, whether for mechanical simulants or for tissue regeneration studies, the brain tissue itself must be well characterized at various length and time scales. Like many biological tissues, brain tissue exhibits a complex, hierarchical structure. However, in contrast to most other tissues, brain is of very low mechanical stiffness, with Young's elastic moduli E on the order of 100s of Pa. This low stiffness can present challenges to experimental characterization of key mechanical properties. Here, we demonstrate several mechanical characterization techniques that have been adapted to measure the elastic and viscoelastic properties of hydrated, compliant biological materials such as brain tissue, at different length scales and loading rates. At the microscale, we conduct creep-compliance and force relaxation experiments using atomic force microscope-enabled indentation. At the mesoscale, we perform impact indentation experiments using a pendulum-based instrumented indenter. At the macroscale, we conduct parallel plate rheometry to quantify the frequency dependent shear elastic moduli. We also discuss the challenges and limitations associated with each method. Together these techniques enable an in-depth mechanical characterization of brain tissue that can be used to better understand the structure of brain and to engineer bio-inspired materials

Hemolytic-uremic syndrome: Etiopathogenesis, diagnostics and basic principles of treatment

© 2015, Serbian Medical Society. All Rights Reserved. Hemolytic uremic syndrome (HUS) is a clinical syndrome that is manifested by thrombocytopenia, hemolytic anemia and acute renal failure. A typical HUS is caused by the action of verotoxin on endothelial cells of small blood vessels of the kidneys and the brain. The disorder of regulation of the alternative pathway of the complement system (mutations of genes for proteins that regulate the activity of the alternative complement system, antibodies to the complement factor H) plays the main role in the pathogenesis of atypical HUS. The disease is clinically manifested by symptoms and signs of damage to the kidneys and brain. The diagnosis of HUS is set on the basis of the reduced number of platelets, microangiopathic hemolytic anemia (negative Coombs test, decreased haptoglobin concentration, increased serum total bilirubin and lactate dehydrogenase, the number of schizonts in peripheral blood smear) and increased creatinine concentration in serum. To distinguish the typical from the atypical HUS it is necessary to perform microbiological examination chairs, measured titer anti-verotoxin antibodies and anti-lipopolysaccharide-antibodies and determine the activity of the enzyme ADAMTS13 (mutations in ADAMTS13, anti-ADAMTS13 antibody) and examine the activity of the alternative pathway of the complement system (C3 component of complement, the complement factor H. I, B, expression of MCP on mononuclear cells from peripheral blood. anti-CFH-antibodies). Patients with typical HUS infection are treated with solutions for infusion, antibiotics that do not increase the release of verotoxin dialysis and supportive therapy. In patients with atypical HUS, a therapeutic plasmapheresis is a first-line process, while in patients where there is resistance or dependence of applied plasmapheresis the blocker of the C5 component of complement (eculizumab) is used

Acute kidney damage: Definition, classification and optimal time of hemodialysis

© 2019, University of Kragujevac, Faculty of Science. All rights reserved. Acute damage to the kidney is a serious complication in patients in intensive care units. The causes of acute kidney damage in these patients may be prerenal, renal and postrenal. Sepsis is the most common cause of the development of acute kidney damage in intensive care units. For the definition and classification of acute kidney damage in clinical practice, the RIFLE, AKIN and KDIGO classifications are used. There is a complex link between acute kidney damage and other organs. Acute kidney damage is induced by complex pathophysiological mechanisms that cause acute damage and functional disorders of the heart (acute heart failure, acute coronary syndrome and cardiac arrhythmias), brain (whole body cramps, ischaemic stroke and coma), lung (acute damage to the lung and acute respiratory distress syndrome) and liver (hypoxic hepatitis and acute hepatic insufficiency). New biomarkers, colour Doppler ultrasound diagnosis and kidney biopsy have significant roles in the diagnosis of acute kidney damage. Prevention of the development of acute kidney damage in intensive care units includes maintaining an adequate haemodynamic status in patients and avoiding nephrotoxic drugs and agents (radiocontrast agents). The complications of acute kidney damage (hyperkalaemia, metabolic acidosis, hypervolaemia and azotaemia) are treated with medications, intravenous solutions, and therapies for renal function replacement. Absolute indications for acute haemodialysis include resistant hyperkalaemia, severe metabolic acidosis, resistant hypervolaemia and complications of high azotaemia. In the absence of an absolute indication, dialysis is indicated for patients in intensive care units at stage 3 of the AKIN/KDIGO classification and in some patients with stage 2. Intermittent haemodialysis is applied for haemodynamically stable patients with severe hyperkalaemia and hypervolaemia. In patients who are haemodynamically unstable and have liver insufficiency or brain damage, continuous modalities of treatment for renal replacement are indicated

Oxidation Behaviour of Sanicro 25 (42Fe22Cr25NiWCuNbN) in O-2/H2O Mixture at 600 degrees C

The present study investigates oxidation at 600 A degrees C of alloy Sanicro 25 (42Fe22Cr25NiWCuNbN) in dry and wet O-2 environments. The exposure time was 1-168 h. The oxidized samples were analyzed by grazing incidence X-ray diffraction, glow discharge optical emission spectroscopy, scanning electron microscopy, transmission electron microscopy and energy dispersive X-ray spectroscopy. Alloy Sanicro 25 showed protective oxidation behaviour under the present conditions. Initially, a thin and smooth corundum-type single layer base oxide formed, featuring a Cr-rich bottom part and a Fe-rich top. With time, double-layered oxide nodules form consisting of inward- and outward-growing parts. Below the oxide scale a 100-200 nm thick oxidation-affected zone formed in the alloy, which was depleted in Cr and enriched in Ni. In this region the chromium carbides and copper-rich particles present in the bulk alloy were dissolved. In O-2 + H2O environment, chromium volatilized from the surface, causing the chromium content of the oxide to be lower than after oxidation in dry O-2. However, under present experimental conditions, the Cr depletion of the scale was not enough to trigger accelerated corrosion of the alloy

Oxidation Behaviour of Sanicro 25 (42Fe22Cr25NiWCuNbN) in O-2/H2O Mixture at 600 degrees C

The present study investigates oxidation at 600 A degrees C of alloy Sanicro 25 (42Fe22Cr25NiWCuNbN) in dry and wet O-2 environments. The exposure time was 1-168 h. The oxidized samples were analyzed by grazing incidence X-ray diffraction, glow discharge optical emission spectroscopy, scanning electron microscopy, transmission electron microscopy and energy dispersive X-ray spectroscopy. Alloy Sanicro 25 showed protective oxidation behaviour under the present conditions. Initially, a thin and smooth corundum-type single layer base oxide formed, featuring a Cr-rich bottom part and a Fe-rich top. With time, double-layered oxide nodules form consisting of inward- and outward-growing parts. Below the oxide scale a 100-200 nm thick oxidation-affected zone formed in the alloy, which was depleted in Cr and enriched in Ni. In this region the chromium carbides and copper-rich particles present in the bulk alloy were dissolved. In O-2 + H2O environment, chromium volatilized from the surface, causing the chromium content of the oxide to be lower than after oxidation in dry O-2. However, under present experimental conditions, the Cr depletion of the scale was not enough to trigger accelerated corrosion of the alloy

Oxidation of a Dispersion-Strengthened Powder Metallurgical FeCrAl Alloy in the Presence of O2

The oxidation behaviour of the FeCrAl alloy Kanthal(A (R)) APMT in O-2 + N-2 and O-2 + N-2 + H2O environments at 1,100 A degrees C was investigated using thermogravimetry and detailed analyses of the scale morphology with SEM/EDX and STEM/EDX. Wrought FeCrAl alloy Kanthal(A (R)) AF was used as a reference. Exposure time was up to 168 h. Water vapour influenced the early oxide growth kinetics. This effect is explained in terms of water acting as an oxidant, simultaneously with O-2. During later stages of the exposures, H2O had no effect on the kinetics of oxidation