No abstract

This article describes the mechanism of precursor events; the mechanism was determined through an experiment and simulation by considering non-uniform normal loading. In the experiment, real-time observations of a contact zone were performed using a longitudinal line contact of PMMA specimens (i.e., a slider on a stationary base block) under a total normal load of 400 N. Partial propagations of the detachment front were considered as precursor events, and it was found that non-uniform normal loading influences the occurrence frequency of the precursor events and the increasing rate of the propagation length. In the simulation, the time evolution of a multidegree-of-freedom system with Coulomb friction was studied. The model considered in the simulation comprised multiple masses serially connected by linear springs on a stationary rigid plane. By regarding the precursor in the experiment to correspond to a partial slip (i.e., simultaneous slip of some of the masses) in the simulation, the influence of non-uniform normal loading on the precursor events can be explained to a certain extent. Additionally, it was found that the apparent static friction coefficient (i.e., the ratio of the maximum tangential load to the total normal load) could be lesser than the real static friction coefficient due to the residual strain in the slider.

No abstract

Late-onset Alzheimer’s disease (AD) remains a medical mystery. Recent studies have linked it to impaired repair of aged neurons. Potential involvement of interleukin33 (IL33) in AD has been reported. Here we show that IL33, which was expressed by up to 75% astrocytes in the aged brains, was critical for repair of aged neurons. Mice lacking Il33 gene (Il33−/−) developed AD-like disease after 60–80 weeks, which was characterized by tau abnormality and a heavy loss of neurons/neurites in the cerebral cortex and hippocampus accompanied with cognition/memory impairment. We detected an abrupt aging surge in the cortical and hippocampal neurons at middle age (40 weeks). To counter the aging surge, wild-type mice rapidly upregulated repair of DNA double-strand breaks (DSBs) and autophagic clearance of cellular wastes in these neurons. Il33−/− mice failed to do so, but instead went on to develop rapid accumulation of abnormal tau, massive DSBs and abnormal autophagic vacuoles in these neurons. Thus, uncontrolled neuronal aging surge at middle age due to lack of IL33 resulted in neurodegeneration and late-onset AD-like symptome in Il33−/− mice. Our study also suggests that the aging surge is a time to search for biomarkers for early diagnosis of AD before massive neuron loss.

The composition of myofiber types varies within thigh muscles of chickens. The present study was designed to determine whether or not myofiber types were distributed uniformly across the diameter of the thigh muscles of chickens. Cross sections from middle portions of muscles were used histochemically to examine differences in distribution and composition of myofiber types in the muscles. Myofibers that reacted moderately (M) or strongly (S) for myosin adenosine triphosphatase (ATPase) after preincubation at pH 4.3 were classified as type I. Type I myofibers reacted weakly (W), moderately (M), or strongly (S) for ATPase after preincubation at pH 10.6; these type I myofibers were subclassified into four types (I , I , I , and I ). Myofibers that reacted negatively for acid-stable ATPase and strongly for alkali-stable ATPase were classified into two types: type IIA, with strong NADH tetrazolium reductase (NADH-TR), and type IIB, with weak NADH-TR activity. The M. pubo-ischio-femoralis pars lateralis had numerous type IIA myofibers and very few type I myofibers, whereas the pars medialis had many type I myofibers and few type I and IIA myofibers. The type I group of myofibers did not exceed about 50% in the other muscles, which had one to three types of type I , I , and I myofibers. The Mm. femorotibiales had more type I , and I myofibers in the deep regions near the femur than in the superficial regions. The M. iliotibialis cranialis, M. iliofibularis, and M. flexor cruris medialis had more type I , I , or I myofibers in the medial regions than in the lateral regions. A few type I myofibers were scattered in the cranial part of M. iliotibialis and in the M. ambiens. The M. flexor cruris lateralis pars pelvica had type IIA and IIB myofibers exclusively. All the muscles had type IIA myofibers. Type IIB myofibers existed in the muscles except the M. puboischio-femoralis. Type IIA and IIB myofibers differed in proportion in different muscles and in their different regions. The type I group of myofibers was generally concentrated more in the deep regions near the femur and in the medial regions than in the superficial and lateral regions of the thigh muscles. The distribution of type IIA myofibers resembled that of type I group. Type IIB myofibers showed a distribution opposite to that of type I group and IIA myofibers. The spatial distribution of myofiber types within individual muscles can account for the various locomotory and postural requirements of the thigh.