In Situ Recalibration of Ion Selective Electrodes

Reference electrode drift resulting from the exchange of ions at the solution/reference electrode chamber interface is the number one reason why ion selective electrodes and pH sensors in particular require...

Volumetric fusion of graphite-doped nylon 12 powder with radio frequency radiation

Purpose Additive manufacturing (AM) of thermoplastic polymers for powder bed fusion processes typically requires each layer to be fused before the next can be deposited. The purpose of this paper is to present a volumetric AM method in the form of deeply penetrating radio frequency (RF) radiation to improve the speed of the process and the mechanical properties of the polymer parts. Design/methodology/approach The focus of this study was to demonstrate the volumetric fusion of composite mixtures containing polyamide (nylon) 12 and graphite powders using RF radiation as the sole energy source to establish the feasibility of a volumetric AM process for thermoplastic polymers. Impedance spectroscopy was used to measure the dielectric properties of the mixtures as a function of increasing graphite content and identify the percolation limit. The mixtures were then tested in a parallel plate electrode chamber connected to an RF generator to measure the heating effectiveness of different graphite concentrations. During the experiments, the surface temperature of the doped mixtures was monitored. Findings Nylon 12 mixtures containing between 10% and 60% graphite by weight were created, and the loss tangent reached a maximum of 35%. Selective RF heating was shown through the formation of fused composite parts within the powder beds. Originality/value The feasibility of a novel volumetric AM process for thermoplastic polymers was demonstrated in this study, in which RF radiation was used to achieve fusion in graphite-doped nylon powders.

Effects of 5-bromo-2′-deoxyuridine on Friend erythroleukaemia cells. II. Oxidative metabolism and enzyme content of whole cells and isolated mitochondria

Untreated or bromodeoxyuridine (BrdUrd)-treated Friend erythroleukaemia (EL) cells from 15- and 72-h-cultures were harvested and the mitochondria were isolated by homogenization and differential centrifugation. Aliquots of the original cell suspensions or the final mitochondrial suspensions were either fixed for electron microscopy, assayed for enzyme activities, or introduced into a 1-ml Clarke oxygen electrode chamber. Whole BrdUrd-treated cells exhibited notable morphological alterations (see accompanying paper) but no effect was observed on whole-cell respiration. Morphologically, isolated mitochondria exhibited a highly condensed matrix and a greatly expanded outer compartment. Functionally, these mitochondria oxidized a variety of substrates at high state-3 (ADP-stimulated) rates (60-210 ng atoms O/min per mg protein) and displayed adequate respiratory control and ADP/O ratios. In the mitochondria isolated from BrdUrd-treated EL cells (both 15- and 72-h cultures), the state-3 oxygen consumption rates, respiratory control ratios, and ADP/O ratios generally decreased compared to their matched controls. These functional deficiencies coincided with in situ increases in the volume of the mitochondrial compartment and conspicuous (30-100%) increases in the specific and total activities of several mitochondrial enzymes. In addition, the mitochondria isolated from the 72-h group (treated and untreated) displayed immediate alterations when BrdUrd was added to the electrode chamber. Oxygen consumption rates dropped, respiratory control ratios changed moderately, and ADP/O ratios increased. BrdUrd may act both as an inhibitor of oxidative phosphorylation and perhaps as a sink for some of the high energy phosphate that is being generated. Thus, BrdUrd may exert its inhibitory effect on cell differentiation by interfering with mitochondrial function.

Slow postcapillary pH changes in blood in anesthetized animals

To investigate the hypothesis that blood pH and PCO2 continue to change after the blood leaves an exchange capillary, we used a rapidly responding, pressure-insensitive, stopped-flow pH electrode apparatus. Arterial blood from an anesthetized dog or cat is drawn through the apparatus into a syringe. Syringe movement is then suddenly stopped. Temperature and pH of the blood in the electrode assembly are continuously monitored, both before and after blood withdrawal ceases. Hemolysis was reduced by coating all blood contact surfaces with silicone and fasting the animal overnight, anesthetizing it with crystalline pentobarbital sodium, and allowing it to ventilate spontaneously. After stopping withdrawal, pH of blood in the electrode chamber continued to change, rising 0.01 unit with t1/2 of 4.4 s. After lysed blood was returned to the animal to provide carbonic anhydrase to the plasma, no pH change was seen after stopping the flow. The small pH rise occurring in arterial blood in vivo is probably due in large part to disequilibrium of [H+] between red blood cells and plasma at the end of the pulmonary capillary, the equilibration process being rate-limited by the extracellular CO2 hydration-dehydration reaction.

Slow postcapillary changes in blood pH in vivo: titration with acetazolamide

A stopped-flow pH electrode apparatus was used to investigate the mechanisms underlying slow changes in plasma pH (pHO) after blood leaves the pulmonary capillaries in carbonic anhydrase-inhibited animals. After acetazolamide was administered to an anesthetized dog or cat, arterial blood was withdrawn through the electrode apparatus into a syringe. Syringe movement was then suddenly stopped. Temperature and pHO of the blood in the electrode chamber were monitored both before and after blood withdrawal ceased. After stopping flow, pHO of the blood in the electrode chamber a) rose 0.02 after a dose of about 1 mg/kg acetazolamide; b) did not change after a dose of about 2 mg/kg acetazolamide; and c) fell 0.10 after a dose greater than about 5 mg/kg acetazolamide. With reasonable red cell and plasma carbonic anhydrase activities assumed for each dose level of acetazolamide, a computer model of the reaction and transport processes occurring in blood after gas exchange in the lung yielded predicted time courses of pHo that were in good agreement with the experimental results. The observed slow pHo changes are largely a result of disequilibrium of [H+] between red blood cells and plasma as blood leaves the pulmonary capillaries.