Thermal Desorption Analysis of Hydrogen in Non-hydrogen-Charged Rolling Contact Fatigue-Tested 100Cr6 Steel.

Hydrogen diffusion during rolling contact fatigue (RCF) is considered a potential root cause or accelerator of white etching cracks (WECs) in wind turbine gearbox bearing steels. Hydrogen entry into the bearing steel during operation is thought to occur either through the contact surface itself or through cracks that breach the contact surface, in both cases by the decomposition of lubricant through catalytic reactions and/or tribochemical reactions of water. Thermal desorption analysis (TDA) using two experimental set-ups has been used to measure the hydrogen concentration in non-hydrogen-charged bearings over increasing RCF test durations for the first time. TDA on both instruments revealed that hydrogen diffused into the rolling elements, increasing concentrations being measured for longer test durations, with numerous WECs having formed. On the other hand, across all test durations, negligible concentrations of hydrogen were measured in the raceways, and correspondingly no WECs formed. Evidence for a relationship between hydrogen concentration and either the formation or the acceleration of WECs is shown in the rollers, as WECs increased in number and severity with increasing test duration. It is assumed that hydrogen diffusion occurred at wear-induced nascent surfaces or areas of heterogeneous/patchy tribofilm, since most WECs did not breach the contact surface, and those that did only had very small crack volumes for entry of lubricant to have occurred.

The Evolution of White Etching Cracks (WECs) in Rolling Contact Fatigue-Tested 100Cr6 Steel.

The formation of white etching cracks (WECs) in steel rolling element bearings can lead to the premature rolling contact fatigue (RCF) failure mode called white structure flaking. Driving mechanisms are still debated but are proposed to be combinations of mechanical, tribochemical and electrical effects. A number of studies have been conducted to record and map WECs in RCF-tested samples and bearings failed from the field. For the first time, this study uses serial sectioning metallography techniques on non-hydrogen charged test samples over a range of test durations to capture the evolution of WEC formation from their initiation to final flaking. Clear evidence for subsurface initiation at non-metallic inclusions was observed at the early stages of WEC formation, and with increasing test duration the propagation of these cracks from the subsurface region to the contact surface eventually causing flaking. In addition, an increase in the amount of associated microstructural changes adjacent to the cracks is observed, this being indicative of the crack being a prerequisite of the microstructural alteration.

First-principles mobility calculations and atomic-scale interface roughness in nanoscale structures.

Calculations of mobilities have so far been carried out using approximate methods that suppress atomic-scale detail. Such approaches break down in nanoscale structures. Here we report the development of a method to calculate mobilities using atomic-scale models of the structures and density functional theory at various levels of sophistication and accuracy. The method is used to calculate the effect of atomic-scale roughness on electron mobilities in ultrathin double-gate silicon-on-insulator structures. The results elucidate the origin of the significant reduction in mobility observed in ultrathin structures at low electron densities.

Lip and gum lesions in sheep in two abattoirs in New Zealand.

AIM: To build a profile of the oral lesions that occur in sheep in New Zealand that need to be considered within the differential diagnosis of foot-and-mouth disease. METHODS: Lesions of the anterior lips and gums of sheep were surveyed in two abattoirs, photographed, and described grossly and histopathologically. RESULTS: A sequence of lesions in order of age and stage of healing are described and illustrated, and their pathogenesis discussed. Lesions of the midline of the lips and gums of traumatic or irritant aetiology were common, and the prevalence was higher in adult sheep than in lambs. CONCLUSIONS: The majority of lesions observed appeared to be primarily of traumatic aetiology. They probably arose from the fright/flight response behaviour of sheep, resulting in the mouth impacting against wire fences or yard railings while being handled. A smaller percentage of lesions may have been due to abrasive or irritant feed or soil. The presence of plant material and bacteria in lesions delayed healing and contributed to the formation of ulcers.

Penetration of antibiotics into the surgical wound in a canine model.

The dose and timing of antimicrobial agents given for surgical wound prophylaxis should be based on the concentration-time profile of the drug in tissue at the site of contamination. However, concentrations of antimicrobial agents in surgical wounds are difficult to determine accurately. Since a surgical wound is a unique extravascular compartment with increased vascular permeability and a high surface area/volume ratio, antibiotic concentrations in sera and surgical wounds should be similar. To test this hypothesis, the pharmacokinetics of single intravenous doses of cefazolin (40 mg/kg) and gentamicin (4 mg/kg) in sera and surgical wounds in a clinically relevant surgical model using dogs were compared. Drug concentrations were determined in interstitial fluid in muscle biopsies taken randomly from wound surfaces and serial wound fluid samples collected after the incisions were closed. Protein binding of cefazolin and gentamicin in sera and wound fluids was low (less than or equal to 29 +/- 9%) in this canine model. Cefazolin and gentamicin equilibrated rapidly (less than or equal to 30 min) between serum and the surgical wound, and concentrations in the two sites declined in parallel. Values for the area under the concentration-time curve, mean residence time, and terminal half-life in serum and the surgical site for each drug were similar. Cefazolin concentrations in serum underestimated the time during which concentrations in surgical wounds exceeded the susceptibility breakpoint MIC for important pathogens by an average of 58 min (range, 26 to 109 min; P = 0.036); for gentamicin, the underestimation averaged 30 min (range, 10 to 60 min; P = 0.036). These data support the concept that the concentration-time profiles of antimicrobial agents in serum may prove valuable clinically as guides to determining the and timing of antibiotic administration necessary for effective antimicrobial prophylaxis in surgery. Further studies are needed to determine the surgical wound pharmacokinetics of highly protein-bound antibodies.

Production of pineapple plants in vitro.

In vitro culture of pineapple (Ananas comosus) was studied to determine the efficiency of axillary bud culture for rapid propagation of several cultivars. The technique used maximizes the success rate of various steps in the production of pineapple plants. Rapid mass multiplication of plantlets started 9 months after explanting with a significant log phase. The number of plantlets obtained from the culture of a single bud by the thirteenth month ranged from 210 to 380 for 'Perolera'; 300 to 350 for 'PR-1-67'; and 40 to 85 for 'Smooth Cayenne'. The method permits culture of a range of pineapple cultivars. Little morphological variation was observed in young regenerated plants.

The mechanism of the vagal bradycardia evoked by diencephalic stimulation in the rabbit.

Blood pressure, in the rostral arterial system, was varied in the range 38-122 mm Hg by impeding the flow through the descending thoracic aorta in rabbits, anaesthetized with urethane and chloralose, in whom the spinal cord had been transected at mid-cervical level. Resting heart rate (H.R.) varied inversely with mean rostral arterial blood pressure (B.P.). The linear regression of H.R. on B.P. had a slope that averaged -0.38 beats X min-1 X mm Hg-1. Electrical stimulation in the lateral hypothalamic area, using 10 s trains of 300 microA X 1 ms constant current cathodal pulses at 60 Hz, caused H.R. to slow, provided that B.P. was above a threshold value and that the baroreceptor afferent pathway was intact. The mean threshold pressure was 49.5 mm Hg. Above threshold, the linear regression of the fall in H.R. during stimulation (delta H.R.) on B.P. had a slope that averaged -1.33 beats X min-1 X mm Hg-1. Linearity was good (r = 0.96). The results suggest that an inflow of baroreceptor impulses is essential for electrical stimulation of the cardioinhibitory region in the lateral hypothalamic area of the rabbit to cause bradycardia. This action is brought about by an increase in the gain of the vagal cardiodecelerator limb of the baroreceptor reflex.

An oscilloscope spot intensifier, to improve photographic recordings of action potentials.

A circuit diagram is shown for a semiconductor device to intensify the brightness of an oscilloscope during the rapidly rising and falling phases of signals such as action potentials. Brightening pulses proportional in amplitude to the rate of change in the Y-axis are available for connection to an oscilloscope with an external intensity ('Z') modulation input. The circuit requires one transistor, one dual operational amplifier and two single fast operational amplifiers.

Effects of some alpha-adrenoceptor antagonists on central cardio-decelerator mechanisms in the rabbit.

Bradycardia was evoked in rabbits anaesthetized with chloralose-urethane by electrical stimulation (200 or 300 microA, 1 ms, 60 s-1 for 9 s, repeated every 5 min) of a selected point in the caudal hypothalamus 1.5 mm from the midline dorsal to the mammillary bodies. Phenoxybenzamine, prazosin and yohimbine solutions were infused intracerebroventricularly at a rate of 20 microliters min-1. Phenoxybenzamine did not cause any effects additional to those attributable to the solvent alone. Prazosin attenuated the evoked bradycardia at all doses (40 to 300 micrograms) and altered resting heart rate (HR) and arterial blood pressure (BP) after the higher doses. Yohimbine (200 + 300 micrograms) attenuated the bradycardia with negligible effects on HR and BP. Prazosin and yohimbine were given intravenously. Both caused dose-related attenuation of evoked bradycardia but prazosin also lowered BP sufficiently for this action alone to account for almost all the loss of bradycardia. The weaker hypotensive action of yohimbine was insufficient to account for the attenuation, a conclusion confirmed in animals whose BP was maintained constant by noradrenaline infusion after cervical spinal transection. In this preparation yohimbine caused dose-related attenuation of the bradycardia. The experiments have shown that yohimbine and probably prazosin also, can prevent hypothalamic stimulation from evoking bradycardia. The results suggest the presence of an alpha-adrenergic pathway from this region of the hypothalamus which projects caudally to increase the gain of the cardio-decelerator baroreceptor reflex in the rabbit.

Bradycardia evoked by hypothalamic stimulation in the rabbit: dependence upon the arterial blood pressure.

The spinal cord was transected in adult New Zealand White rabbits anaesthetized with urethane plus chloralose. The level of transection was in the mid-cervical region. The animals were than ventilated mechanically and the arterial blood pressure was maintained with an intravenous infusion of noradrenaline solution. Stimulation of the hypothalamus 1-2 mm lateral to the third ventricle and 1.5-3 mm dorsal to the mammillary nuclei, in a region known to evoke pressor responses and bradycardia in normal anaesthetized rabbits, never evoked pressor responses in the spinally transected rabbits. Bradycardia was evoked only when the mean arterial blood pressure was maintained above 44-49 mmHg. At higher pressures stimulation evoked a greater bradycardia and the relationship between bradycardia and pressure was approximately linear over much of the range of pressures tested (up to 116 mmHg). Because the threshold mean arterial blood pressure at which hypothalamic stimulation evoked bradycardia was similar to the threshold pressures reported in the literature for baroreceptor activation in the rabbit and because the curve of bradycardia:pressure was similar to published curves of baroreceptor and baroreflex activity against blood pressure, it is concluded that the bradycardia evoked by hypothalamic stimulation in the rabbit is mediated by a neural pathway in the hypothalamus that can increase the gain of the cardio-inhibitory baroreceptor reflex.

Endogenous prostaglandin synthesis and glucose-induced insulin secretion from the adult rat pancreatic islet.

Although exogenous prostaglandins are recognized modulators of insulin secretion, the relationship between their endogenous synthesis and insulin secretion has not been rigorously studied in isolated adult rat islets. Using 3H-arachidonic acid as a tracer, we evaluated the effect of glucose stimulation upon the incorporation of this fatty acid into islet phospholipids and prostaglandins (separated by extraction and sequential silicic acid, thin-layer and paper chromatography). We observed that 3H-arachidonic acid was incorporated into islet phospholipids and prostaglandins under basal conditions (0.3 mg/ml glucose). Furthermore, exposure of islets to a stimulatory glucose concentration led to significant increases in the recovery of 3H-arachidonic acid-derived radioactivity in islet phosphatidylethanolamine, phosphatidylserine, sphingomyelin, and phosphatidylinositol as well as into all of the measured prostaglandins (A2, B2, D2, E2, and F2 alpha). The most marked increases in recovered radioactivity resulting from a stimulatory glucose concentration were in islet phosphatidylethanolamine and prostaglandin A2 (which we believe to be derived, in large part, from endogenously synthesized prostaglandin E2). These glucose-induced increases in 3H-arachidonic acid-derived radioactivity in both the phospholipid and the prostaglandin fractions were eliminated by the inhibition of phospholipase A2 activity with mepacrine or by the inhibition of cyclooxygenase activity with sodium salicylate. When islets prelabeled with 3H-arachidonic acid were exposed to a high glucose concentration in a perifusion system, there was a brisk extracellular release of radioactivity (presumably representing unidentified prostaglandins) that began within 1 min and that peaked slightly before the peak of the first phase of insulin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence for central alpha-adrenergic transmission in a cardio-inhibitory response from the rabbit hypothalamus.

The heart rate of the anaesthetized rabbit was slowed by electrical stimulation of the hypothalamus with 7-9 sec trains of 250-330 microA pulses, duration 1 msec, frequency 60 Hz. This vagally-mediated cardio-decelerator response was attenuated in a dose-dependent manner after intravenous administration of phenoxybenzamine (0.01-5 mg/kg), phentolamine (0.01-3 mg/kg) or yohimbine (0.1-5 mg/kg). The attenuation of the cardio-decelerator response was not due to any vagolytic action of these drugs nor to block of the baroreceptor reflex, but appeared to be due to a central block of pathways descending from the hypothalamus. Propranolol, haloperidol, pimozide and spiperone did not show this central blocking action except in very large doses when there was evidence of some alpha-adrenoceptor blockade.

Effects of methysergide on some cardiovascular responses in the anaesthetized rabbit.

Methysergide (0.1-5 mg/kg i.v.) caused dose-dependent reductions in the resting heart rate of anaesthetized rabbits. Resting mean arterial blood pressure was reduced only after the maximum dose. Methysergide 5 mg/kg significantly enhanced the pressor responses to i.v. phenylephrine and enhanced the accompanying bradycardia disproportionately. There was no evidence for a central increase in baroreflex gain, so an action of methysergide on baroreceptor sensory endings is suggested as a possible explanation.

Substrate requirements for the phosphoinositide response in rat pancreatic islets.

The relationship between phosphatidylinositol hydrolysis and the first phase of insulin secretion has been investigated by briefly exposing rat pancreatic islets that had been prelabelled with myo-[2-3H]inositol to various agonists and antagonists of insulin secretion. The recovery of lipid-bound radioactivity progressively decreased as the D-glucose concentration of the incubation medium was increased. Those carbohydrates that stimulated insulin secretion evoked a phosphoinositide response, whereas non-stimulatory carbohydrates did not. With the notable exception of amino acids, non-carbohydrate secretagogues were also found to decrease the islet lipid-bound radioactivity. Inhibition of islet glucose metabolism was found to decrease the recovery of lipid-bound radioactivity, largely as a result of impaired de novo phosphoinositide synthesis. The phosphoinositide response to glucose was not affected by inhibition of microtubular function, but was dependent upon the availability of extracellular calcium ions. We conclude that the phosphoinositide response in carbohydrate-stimulated islets is not directly related to the activation of membrane-associated glucose receptors, but may occur as a consequence of the subsequent transmembrane movement of calcium ions. Finally, the observation that stimulatory amino acids did not evoke a phosphoinositide response suggests that, under certain circumstances, this phenomenon can be dissociated from insulin secretion.

An effect of hypothalamic stimulation on cardiac output in the rabbit.

Electrical stimulation of a discrete region of the rabbit brainstem, in the lateral hypothalamic area near the mammillothalamic tract, caused an increase in arterial blood pressure accompanied by bradycardia in anaesthetized animals. The cardiac output, measured by a thermodilution technique, was found to fall when the stimulus strength was great enough to evoke strong bradycardia. Threshold current for this effect varied in different animals in the range: 50-350 microA (1 msec pulse duration and 60 pulses/sec repetition rate). Bilateral vagotomy eliminated almost all the negative chronotropic effects of hypothalamic stimulation, but reversed only about one-third of the fall in cardiac output during strong stimulation. It is suggested that negative chronotropic, and possibly inotropic, vagal effects on the heart play a relatively minor role in reducing cardiac output. The major factor in causing output to fall may be left ventricular overload during the widespread peripheral vasoconstriction that accompanies stimulation of this region of the rabbit hypothalamus.

Responses evoked by stimulation of points in the diencephalon of unrestrained rabbits.

Behavioural responses were obtained from unanaesthetized rabbits by stimulating the diencephalon through implanted electrodes (10--250 micro A, 1 msec, 60 Hz). Mild arousal and related effects were evoked from widespread sites between stereotaxic planes P 1.5--P 4.5 and 0.1--3.5 mm from the midline. Stimulation readily evoked vigorous running responses, together with other responses suggestive of agitation with escape and concealment behaviour, at sites in the hypothalamus within 2 mm of the midline near or just caudal to the mammillothalamic tracts. Signs of rage or aggression were infrequently seen. When the centre of this hypothalamic zone was stimulated after re-anaesthetizing the animals, bradycardia was obtained. The results are interpreted as suggesting that stimulation in this area, which is known to evoke cardiovascular responses different from the carnivore, also evokes a modified form of "Defence Reaction" appropriate to a species that is preyed upon.

Vasoactive sites in the diencephalon of the rabbit.

Stimulation of the brain stem of the anaesthetized rabbit, in the lateral hypothalamic area and the zona incerta 0.5-3 mm from the midline and a similar distance dorsal to the lateral mammillary nucleus, evoked vasoconstriction in the skin of the ear and of the hindpaw. Only weak and inconstant effects on muscle blood flow were evoked from this region of the brain stem. Muscle vasodilatation was obtained by stimulation of more medial regions of the brain stem, extending almost all the way from the supramammillary nucleus to the dorsal surface. This vasodilatation was not diminished by atropine. Alpha-adrenergic blocking agents diminished the cutaneous vasoconstrictor responses and also reduced or even reversed the bradycardia that could be evoked by hypothalamic stimulation.

Potentiation of a cardioinhibitory reflex by hypothalamic stimulation in the rabbit.

Repetitive stimulation of an area within the lateral hypothalamus, near the mammillothalamic tract, evoked pressor responses with bradycardia in anaesthetized rabbits. With weak stimulation (cathodal pulses below 75--150 microamperemeter, 1 msec duration, 60--100 per sec for 5--9 sec) the pressor responses were accompanied by bradycardia similar in intensity to that evoked by i.v. administration of noradrenaline. Stronger stimulating currents evoked an intense bradycardia that could not have arisen solely through the baroreceptor reflex. With these stronger currents the heart rate sometimes fell, transiently, to less than 20% of the resting rate. After denervation of the 4 main buffer nerves (sinus and aortic nerves), hypothalamic stimulation could not readily evoke bradycardia, although the pressor, respiratory and other effects remained. When the baroreceptor afferents were activated, either by evoked pressor responses in rabbits whose buffer nerves were intact or by electrical stimulation of the central ends of divided aortic nerves, strong hypothalamic stimulation augmented the bradycardia evoked reflexly from these baroreceptor afferents. This evidence suggests that electrical stimulation of this area in the hypothalamus may facilitate the cardioinhibitory component of the baroreceptor reflex in the rabbit.