This paper presents a new three-dimensional elastic viscoplastic (3D EVP) constitutive model for the time-dependent stress–strain behaviour of both normally consolidated and overconsolidated clays. There are two major new developments in the 3D EVP model: (i) incorporation of a nonlinear creep function with a limit for the creep volume strain under isotropic stressing conditions; (ii) adoption of a new loading surface function with a smooth shape on the π plane. Based on the "equivalent time" concept of Yin and Graham, the formulation of the new 3D EVP model is derived using the new nonlinear creep function and loading surface function. A new approach to determining all model parameters is presented. The 3D EVP model is calibrated using data from one conventional isotropic stress creep test and consolidated-undrained triaxial tests on soft Hong Kong marine deposits (HKMD). The model is verified by comparing model results with those from both normally and overconsolidated triaxial tests on HKMD and a mixture of kaolin and bentonite.Key words: creep, time-dependent, viscoplastic, equivalent time, stress–strain, constitutive model, verification, clay.

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Monocyte chemoattractant protein 1 (MCP-1) is a member of the chemokine superfamily of genes that induces chemotaxis of monocytes in inflammatory processes. The effects of interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), transforming growth factor beta (TGF-beta), platelet-derived growth factor (PDGF-BB), parathyroid hormone (PTH), and 1,25(OH)2D3 on MCP-1 expression in human osteoblastic cells were compared. Inflammatory or proinflammatory cytokines stimulated the production of MCP-1 in normal human osteoblastic cells as determined by RIA. The osteotrophic mediators PTH and 1,25(OH)2D3 and PDGF-BB had no effect on MCP-1 expression. In further studies, the steady-state mRNA and MCP-1 protein levels in two human osteoblastic cell lines, MG-63 and SaOS-2, were examined. MCP-1 expression at both the protein and mRNA levels was greatly increased by IL-1 beta and TNF-alpha. At the mRNA level, IL-1 beta and TNF-alpha strongly induced MCP-1 expression; TGF-beta and IL-6 induced MCP-1 but to a lesser extent. No significant changes in MCP-1 mRNA or MCP-1 protein secretion were observed when cells were treated with PDGF-BB, PTH, and 1,25(OH)2D3. When tested on preosteoclasts, MCP-1 was shown to have no effect on the formation of multinucleated, tartrate-resistant acid phosphatase (TRAP)-positive osteoclastic cells.

Migration of monocytes to sites of inflammation involves a series of attachments and detachments to extracellular matrix proteins. We examined the capacity of a chemokine, monocyte chemoattractant protein-1 (MCP-1), to regulate attachment of human monocytes to laminin, collagen I, collagen IV, or fibronectin. MCP-1 increased monocyte attachment to laminin in a dose- and time-dependent manner and stimulated a lesser increase to the other matrix proteins. Function-blocking monoclonal antibodies (MAbs) to the integrin beta 2-subunit (CD18), including Fab' fragments and alpha M (CD11b) blocked > 70% of attachment, whereas MAbs to the beta 1-integrin subunit reduced attachment by < 30%. This suggests that the CD11b/CD18 integrin is the predominant molecule involved in adhesion of MCP-1-stimulated monocytes to laminin. The association of CD11b with F-actin illustrated by confocal microscopy further supports this concept. In contrast, when monocytes were stimulated with the beta 1-stimulatory MAb TS2/16, monocyte adhesion to laminin occurred through beta 1-integrins. Thus MCP-1 can stimulate monocyte attachment to laminin, and this process is mediated through beta 2-integrins, principally CD11b/CD18.

The study was undertaken to characterize the microbiology of dental abscesses in children and to compare clindamycin and ampicillin/sulbactam in the treatment of facial cellulitis of odontogenic origin. Sixty children with acute facial cellulitis of dental origin underwent surgery (extraction or root canal procedure) within 24 hours of presentation. Pus samples were cultured aerobically and anaerobically. Patients were randomized (1:1) to receive intravenous ampicillin/sulbactam or clindamycin for 48 hours followed by oral amoxicillin/clavulanate or clindamycin for 7 days. A total of 211 bacterial isolates were recovered from 54 samples. The most common aerobic and facultative organisms were viridans streptococci, Neisseria, and Eikenella species. Among anaerobes, Prevotella and Peptostreptococcus species were the most frequent. No treatment failure occurred in either group. Dental abscesses in children are polymicrobial aerobic/anaerobic infections. Treatment of complicated dental infections with ampicillin plus a beta-lactamase inhibitor or clindamycin in combination with surgical drainage is very effective.