The elastically equivalent softening zone size for an elastic-softening material: II. A simple piece-wise softening law

The paper determines the elastically equivalent softening zone size R_E for an elastic-softening material when there is a semi-infinite crack in a remotely loaded infinite solid; the parameter R_E plays a central role in size effect expressions that are used to correlate the maximum loads that can be sustained by solids having different dimensions. The stress (p) versus displacement (v) softening law considered is that for which P = p_c for oc and P = ; qp_c = p_* for λδ_c< v <δ_c. Particular attention is focussed on the case where the parameters λ and q are both small. Such a softening law simulates the softening behaviour of plain concrete, where there is an initially rapid softening to a low stress value at a small displacement, followed by a long tail that is associated with a low stress. The paper shows that the behaviour of a material with such a softening law can be conveniently analysed by assuming that there is a non-zero stress intensity (K_IC) at the crack tip followed by a constant stress p_* within the softening zone; , where E_o is the reduced modulus and G_{I = λpcδc} is the contribution to the specific fracture energy arising from the initially rapid softening region. Analysis of a specific model demonstrates the viability of this approach by showing that there is consistency with the proposed size effect expressions based on R_E.     

Abdominal vagotomy alters the structure of the ingestive behavior of rats ingesting liquid diets.

A microstructural analysis of the licking behavior of the rat was used to investigate the effects of total abdominal vagotomy on ingestive behavior. Vagotomy decreased the meal size of milk and 3 concentrations of sucrose. The decrease was due to an increase in the decline in the rate of licking during the meal, suggesting that negative feedback from the gastrointestinal tract was enhanced by vagotomy, perhaps because of accelerated clearance of fluid from the stomach to the intestine. No evidence was found for motor dysfunction of licking or alterations in gustatory sensitivity to the test solution. The results suggest that vagotomy enhanced the strength of an extravagally mediated negative feedback signal from the intestine and that the vagus nerve normally prevents this from occurring by regulating gastric clearance. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Damage to cochlear efferents following AF64A intoxication

Damage to cochlear efferents in chinchillas was assessed using transmission electron microscopy following unilateral treatment with the cholinotoxin ethylcholine mustard aziridinium ion (AF64A). AF64A was diluted in artificial perilymph to concentrations ranging from 0.5 to 100 microM. Survival times ranged from 1 to 12 weeks. At concentrations above 10 microM, widespread damage was noted to efferent fibers within the inner spiral bundle (ISB), tunnel spiral bundle (TSB), tunnel radial fibers (TRF) and efferent terminals at the base of OHCs. This damage included degeneration of fibers and terminals, delamination of mitochondria, vacuolization, and loss of cell membrane. However, at high concentrations, non-specific damage was also noted as thinnings or discontinuities of the membrane of OHCs and afferent fibers. At concentrations between 3 and 10 microM, selective damage was observed to efferent fibers within the ISB, TSB, TRF, and to terminals at the base of the OHCs, with all other structures appearing normal. At concentrations of 0.5 and 1 microM, damage was limited to efferent fibers within the TSB and ISB below the inner hair cells. In general, insult was greatest to middle- and basal-turn efferents, and longer survival times did not produce greater damage to, or loss of, efferents. These data suggest that at low concentrations, AF64A produces a partial yet selective degeneration of cochlear efferents within both the medial and lateral tracts, and that at the lowest concentrations used in these studies, AF64A produces a preferential insult on lateral olivocochlear efferents.     

FDTD simulation of microwave sintering of ceramics in multimodecavities

Microwave sintering of ceramics in multimode cavities, particularly the use of picket-fence arrangements, has recently received considerable attention. Various types of ceramics have been successfully sintered and, in some cases, a desirable and unique “microwave effect” has been observed. At present, various aspects of the sintering profess such as preparation of sample sizes and shapes, types of insulations, and the desirability of including a process stimulus such as SiC rods are considered forms of art and highly dependent on human expertise. The simulation of realistic sintering experiments in a multimode cavity may provide an improved understanding of critical parameters involved and allow for the development of guidelines towards the optimization of the sintering process. In this paper, we utilize the FDTD technique to model various geometrical arrangements and material compatibility aspects in multimode microwave cavities and to simulate realistic sintering experiments. The FDTD procedure starts with the simulation of a field distribution in multimode microwave cavities that resembles a set of measured data using liquid crystal sheets. Also included in the simulation is the waveguide feed as well as a ceramic loading plate placed at the base of the cavity     

Magnetic resonance staging of neoplasms of the uterus

The treatment of patients with uterine neoplasms may be significantly altered by the stage of disease at the time of diagnosis. A noninvasive and accurate means of staging these tumors is therefore desirable. This article discusses the magnetic resonance imaging techniques and findings that are essential for the accurate staging of uterine neoplasms. The imaging findings are presented following a discussion of the histopathologic findings, clinical presentation, diagnosis and staging, pathways of tumor spread, and treatment of each neoplasm. A comparison of magnetic resonance and other imaging techniques is also provided.     

Lysosomal enzyme and inhibitor levels in the human trabecular meshwork

PURPOSE: To examine in the human trabecular meshwork lysosomal enzymes and one inhibitor of serine proteases that actively participate in the degradation of macromolecules into low molecular weight constituents. METHODS: Using an avidin-biotin-peroxidase technique, lysosomal proteases and alpha 1-proteinase inhibitor were examined in the trabecular meshwork of 23 human eyes with donor ages ranging from 2 to 90 years. These eyes were categorized into three age groups (< or = 20, 21 to 49, and > or = 50 years). Histochemical staining for lysosomal hydrolases was also performed on frozen sections of 20 human eyes. The staining was analyzed by an image analyzer and the levels of lysosomal proteases were further measured by biochemical assays. RESULTS: The trabecular meshwork from all the eyes stained intensely against antibodies to cathepsins B and G and alpha 1-proteinase inhibitor. The staining for elastase was weaker but evident. Image analyses revealed that the staining intensity for each protease or inhibitor was similar in all age groups. The staining in the uveal meshwork appeared to be the strongest among all the trabecular meshwork regions. Biochemical assays of tissue extracts confirmed that the enzyme and inhibitor levels were comparable among the three donor age groups. Activities of two lysosomal hydrolases, acid phosphatase and acid esterase, were also found in trabecular meshwork cells of 20 eyes. No apparent difference in enzyme activities was found with increasing age, and variation related to region was not observed. CONCLUSIONS: This study demonstrated the age-independent distribution of a variety of lysosomal enzymes and a protease inhibitor in the human trabecular meshwork. The presence of these proteins suggests a possible role in the metabolic operation of the trabecular meshwork.     

Polymerase chain reaction amplification analyses of clonality in T-cell malignancy including peripheral T-cell lymphoma

Clonality in T-cell malignancy was investigated using T-cell receptor (TcR) V beta 1-20 family primers and polymerase chain reaction amplification (PCR) of cDNA prepared from tissue biopsies and blood involved with tumour. Secondary PCR amplification of the VDJ joints of primary PCR products was performed to distinguish clonal from polyclonal products, and clonal V beta gene products were confirmed by direct PCR sequencing in the majority of cases. In eight T-cell malignancies including T-cell acute lymphoblastic leukaemia (T-ALL) and T-cell chronic lymphocytic leukaemia (T-CLL) shown to be clonal by Southern blot analysis, one or two primary PCR products were identified and shown to be clonal. In five cases of peripheral T-cell lymphoma (PTCL) all V beta 1-20 families were identified after primary PCR amplification, and clonal products were identified in two cases after secondary amplification; TcR V beta clonal families could not be demonstrated in the remaining three cases. These data were in agreement with previous Southern blot analysis of these cases, and confirmed the presence of reactive T cells in PTCL as well as providing further evidence for the genotypic heterogeneity of this entity. In the remaining case, a blood lymphocytosis, primary PCR amplification produced predominant TcR V beta 6 and V beta 12 family products, of which the V beta 6 family proved clonal after secondary PCR amplification. There was no evidence for overrepresentation of TCR V beta families by the tumour populations in this study, furthermore the data confirm the involvement of reactive cells in T-cell malignancy and the genetic heterogeneity of PTCL.     

Accommodation of a D-Phe residue into a right-handed 3(10)-helix: structure of Boc-D-Phe-(Aib)4-Gly-L-Leu-(Aib)2-OMe, an analogue of the amino terminal segment of antiamoebins and emerimicins

Recently an unstable trinucleotide CTG repeat, located within the 3' untranslated region of a gene on 19q13.3 was discovered in kindreds with myotonic dystrophy (DM). The age-of-onset/severity of DM shows a good correlation with CTG repeat size, and pedigrees and data reported to date have shown a striking trend toward amplification of the size of the CTG repeat during transmission from parent to child. The amplification has been accepted as the biological explanation for anticipation in the clinical severity observed in many families with DM. In this paper we report on 3 families where CTG amplification decreased during transmission from parent to child. In one case there was a gene conversion event, while in the remaining 2 there was a simpler reduction in the size of the repeat length. The changes appear to have been accompanied by a reduction in clinical severity in the child when compared to the parent. These observations are discussed in terms of their clinical implications and the biases that may exist in much of the reported data.