Response of piles subjected to progressive soil movement

Model tests were conducted to investigate the behavior of vertically loaded, free head piles undergoing lateral soil movement using an experimental apparatus developed in house. This paper presents ten new tests on an instrumented model pile in dry sand, which provide the profiles of bending moment, shear force and pile deflection along the pile, the development of maximum bending moment Mmax, maximum shear force Tmax, and pile deflection y0 at the ground surface with soil movement. The tests reveal the effects of axial load P (at pile head), the distance between the tested pile and source of free soil movement Sb, sliding depths, and angle of soil movement (via loading angle) on the pile response. For instance, the axial loading P leads to extra bending moment and deflection in the passive pile; the Mmax reduces with increase in Sb; and the Mmax is proportional to the angle of soil movement. The elastic solution by Guo and Qin [Guo, W. D., Qin, H. Y., 2010, Thrust and Bending Moment of Rigid Piles Subjected to Moving Soil, Can. Geotech. J., Vol. 47, No. 2, pp. 180-196] was used to predict the development of Mmax and Tmax observed in the current tests, a boundary element analysis, and an in situ pile test, respectively. It provides satisfactory predictions for all cases against the measured data

3-(2-Bromo­benz­yl)-1-methyl-1H-imidazol-3-ium bromide

In the title compound, C11H12BrN2 +·Br−, the imidazole and phenyl rings are nearly perpendicular, making a dihedral angle of 87.71 (7)°. The crystal structure is stabilized by non-classical inter­molecular C—H⋯Br hydrogen bonds and inversion-related mol­ecules are linked through π–π inter­actions between the imidazole ring systems [centroid–centroid distance = 3.472 (6) Å]

Enhanced excitability of small dorsal root ganglion neurons in rats with bone cancer pain

<p>Abstract</p> <p>Background</p> <p>Primary and metastatic cancers that affect bone are frequently associated with severe and intractable pain. The mechanisms underlying the development of bone cancer pain are largely unknown. The aim of this study was to determine whether enhanced excitability of primary sensory neurons contributed to peripheral sensitization and tumor-induced hyperalgesia during cancer condition. In this study, using techniques of whole-cell patch-clamp recording associated with immunofluorescent staining, single-cell reverse-transcriptase PCR and behavioral test, we investigated whether the intrinsic membrane properties and the excitability of small-sized dorsal root ganglion (DRG) neurons altered in a rat model of bone cancer pain, and whether suppression of DRG neurons activity inhibited the bone cancer-induced pain.</p> <p>Results</p> <p>Our present study showed that implantation of MRMT-1 tumor cells into the tibial canal in rats produced significant mechanical and thermal hyperalgesia in the ipsilateral hind paw. Moreover, implantation of tumor cells provoked spontaneous discharges and tonic excitatory discharges evoked by a depolarizing current pulse in small-sized DRG neurons. In line with these findings, alterations in intrinsic membrane properties that reflect the enhanced neuronal excitability were observed in small DRG neurons in bone cancer rats, of which including: 1) depolarized resting membrane potential (RMP); 2) decreased input resistance (R_in); 3) a marked reduction in current threshold (CT) and voltage threshold (TP) of action potential (AP); 4) a dramatic decrease in amplitude, overshot, and duration of evoked action potentials as well as in amplitude and duration of afterhyperpolarization (AHP); and 5) a significant increase in the firing frequency of evoked action potentials. Here, the decreased AP threshold and increased firing frequency of evoked action potentials implicate the occurrence of hyperexcitability in small-sized DRG neurons in bone cancer rats. In addiotion, immunofluorescent staining and single-cell reverse-transcriptase PCR revealed that in isolated small DRG neurons, most neurons were IB4-positive, or expressed TRPV1 or CGRP, indicating that most recorded small DRG neurons were nociceptive neurons. Finally, using in vivo behavioral test, we found that blockade of DRG neurons activity by TTX inhibited the tumor-evoked mechanical allodynia and thermal hyperalgesia in bone cancer rats, implicating that the enhanced excitability of primary sensory neurons underlied the development of bone cancer pain.</p> <p>Conclusions</p> <p>Our present results suggest that implantation of tumor cells into the tibial canal in rats induces an enhanced excitability of small-sized DRG neurons that is probably as results of alterations in intrinsic electrogenic properties of these neurons. Therefore, alterations in intrinsic membrane properties associated with the hyperexcitability of primary sensory neurons likely contribute to the peripheral sensitization and tumor-induced hyperalgesia under cancer condition.</p