Axle whine phenomenon in light trucks: a combined numerical and experimental investigation

Axle whine is a continuous, steady state tonal sound, emitted from the differential unit’s hypoid gears. It is essentially induced by torque variations. This can be as a result of resonant conditions or torque fluctuations caused by engine order vibrations, compounded by gear transmission error. The principal mechanism of gear whine noise generation is, therefore, through transmission of vibration from the gear shafts and bearings to the differential housing, which is radiated as noise. Furthermore, interactions between the differential unit, axles and driveshafts often generate excessive tonal noises, which are the result of coupled bending and torsional resonances of assembled components. These resonances induce a magnification effect upon the noise source itself through exciting the gear shafts and distorting the alignment of the gear sets. Axle whine noise has become an important Noise, Vibration and Harshness (NVH) concern, because of the nature of the noise, further compounded by the human aural system, which is highly sensitive in tonal memory. The result is a continuously increasing warranty costs or use of expensive palliatives to mitigate the phenomenon. In this paper, a combined experimental and numerical investigation of axle whine in a rear wheel drive light truck is presented. The aim is to reveal some root causes of the drivetrain’s NVH behaviour, which can be related to the amplification/reduction of axle whine vibration and noise. Correlation of the experimental results with the vibration modes of the drivetrain has shown that for vehicle coasting conditions a number of modes are excited, which can interact with the vibrations of the hypoid gear pair. Finally, some light is shed on the role that differential bulk oil temperature plays in the severity of the ensuing vibration

Pseudohyperkalemia in Serum: A New Insight into an Old Phenomenon

Pseudohyperkalemia, a rise in serum potassium concentration with concurrently normal plasma potassium concentration, is an in vitro phenomenon that was first described 50 years ago. It was originally attributed to the release of potassium from platelets during platelet aggregation and degranulation, and a significant correlation between pseudohyperkalemia and platelet count was established. During the last decade, new data were added to this phenomenon. In particular, pseudohyperkalemia was defined when serum potassium concentration exceeded that of plasma by more than 0.4 mmol/L provided that samples are collected under strict techniques, remain at room temperature and are tested within 1 hour from blood specimen collection. Moreover, it is positively correlated to (1) thrombocytosis due to the release of potassium from platelet granules during coagulation, (2) erythrocytosis due to the dilution of the released potassium in smaller volumes of serum, and (3) the presence of activated platelets, which have the capability of aggregation at a higher speed and release more potassium during degranulation. However, pseudohyperkalemia may be “masked” when in a state of hypokalemia because potassium moves back into the intracellular space in vitro, and the phenomenon is ameliorated or even not detected

Immunosuppression for acquired hemophilia A: results from the European Acquired Haemophilia Registry (EACH2)

Acquired hemophilia A (AHA) is an autoimmune disease caused by an autoantibody to factor VIII. Patients are at risk of severe and fatal hemorrhage until the inhibitor is eradicated, and guidelines recommend immunosuppression as soon as the diagnosis has been made. The optimal immunosuppressive regimen is unclear; therefore, data from 331 patients entered into the prospective EACH2 registry were analyzed. Steroids combined with cyclophosphamide resulted in more stable complete remission (70%), defined as inhibitor undetectable, factor VIII more than 70 IU/dL and immunosuppression stopped, than steroids alone (48%) or rituximab-based regimens (59%). Propensity score-matched analysis controlling for age, sex, factor VIII level, inhibitor titer, and underlying etiology confirmed that stable remission was more likely with steroids and cyclophosphamide than steroids alone (odds ratio = 3.25; 95% CI, 1.51-6.96; P <.003). The median time to complete remission was approximately 5 weeks for steroids with or without cyclo-phosphamide; rituximab-based regimens required approximately twice as long. Immunoglobulin administration did not improve outcome. Second-line therapy was successful in approximately 60% of cases that failed first- line therapy. Outcome was not affected by the choice of first-line therapy. The likelihood of achieving stable remission was not affected by underlying etiology but was influenced by the presenting inhibitor titer and FVIII level. (Blood. 2012;120(1):47-55