Elastic properties of sand-peat moss mixtures from ultrasonic measurements

Effective remediation of an environmental site requires extensive knowledge of the geologic setting, as well as the amount and distribution of contaminants. Seismic investigations provide a means to examine the subsurface with minimum disturbance, Laboratory measurements are needed to interpret field data. In this experiment, laboratory tests were performed to characterize manufactured soil samples in terms of their elastic properties. The soil samples consisted of small (mass) percentages (1 to 20 percent) of peat moss mixed with pure quartz sand. Sand was chosen as the major component because its elastic properties are well known except at the lowest pressures. The ultrasonic pulse transmission technique was used to collect elastic wave velocity data. These data were analyzed and mathematically processed to calculate the other elastic properties such as the modulus of elasticity. This experiment demonstrates that seismic data are affected by the amount~of peat moss added to pure sand samples. Elastic wave velocities, velocity gradients, and elastic moduli vary with pressure and peat moss amounts. In particular, ultrasonic response changes dramatically when pore space fills with peat. With some further investigation, the information gathered in this experiment could be applied to seismic field research

Linear and Nonlinear Ultrasonic Properties of Granular Soils

The ultrasonic pulse transmission method (100-500 kHz) was adapted to measure compressional (P) and shear (S) wave velocities for synthetic soils fabricated from quartz-clay and quartz-peat mixtures. Velocities were determined as samples were loaded by small (up to 0.1 MPa) uniaxial stress to determine how stress at grain contacts affects ave amplitudes, velocities, and frequency content. Samples were fabricated from quartz sand mixed with either a swelling clay or peat (natural cellulose). P velocities in these dry synthetic soil samples were low, ranging from about 230 to 430 m/s for pure sand, about 91 to 420 m/s for sand-peat mixtures, and about 230 to 470 m/s for dry sand-clay mixtures. S velocities were about half of the P velocity in most cases, about 130 to 250 m/s for pure sand, about 75-220 m/s for sand-peat mixtures, and about 88-220 m/s for dry sand-clay mixtures. These experiments demonstrate that P and S velocities are sensitive to the amount and type of admixed second phase at low concentrations. They found that dramatic increases in all velocities occur with small uniaxial loads, indicating strong nonlinearity of the acoustic properties. Composition and grain packing contribute to the mechanical response at grain contacts and the nonlinear response at low stresses

Towards a map of the Upper Pleistocene loess of the Po Plain Loess Basin (Northern Italy)

Upper Pleistocene (MIS 4-2) loess sequences occur in most of continental Europe and in Northern Italy along the Po Plain Loess Basin. Loess is distributed along the flanks of the Po Plain and was deposited on glacial deposits, fluvial terraces, uplifted isolated hills, karst plateaus, slopes and basins of secondary valleys. Loess bodies are generally tiny and affected by pedogenesis, being locally slightly reworked by slope processes and bioturbation. Notwithstanding, loess in the Po Plain is an important archive of paleoenviron-mental record and its mapping provides new insights in paleoenvironmental and palaeoseismic reconstructions of Northern Italy

Nicotinic Receptor Alpha7 Expression during Tooth Morphogenesis Reveals Functional Pleiotropy

The expression of nicotinic acetylcholine receptor (nAChR) subtype, alpha7, was investigated in the developing teeth of mice that were modified through homologous recombination to express a bi-cistronic IRES-driven tau-enhanced green fluorescent protein (GFP); alpha7GFP) or IRES-Cre (alpha7Cre). The expression of alpha7GFP was detected first in cells of the condensing mesenchyme at embryonic (E) day E13.5 where it intensifies through E14.5. This expression ends abruptly at E15.5, but was again observed in ameloblasts of incisors at E16.5 or molar ameloblasts by E17.5–E18.5. This expression remains detectable until molar enamel deposition is completed or throughout life as in the constantly erupting mouse incisors. The expression of alpha7GFP also identifies all stages of innervation of the tooth organ. Ablation of the alpha7-cell lineage using a conditional alpha7Cre×ROSA26-LoxP(diphtheria toxin A) strategy substantially reduced the mesenchyme and this corresponded with excessive epithelium overgrowth consistent with an instructive role by these cells during ectoderm patterning. However, alpha7knock-out (KO) mice exhibited normal tooth size and shape indicating that under normal conditions alpha7 expression is dispensable to this process. The function of ameloblasts in alpha7KO mice is altered relative to controls. High resolution micro-computed tomography analysis of adult mandibular incisors revealed enamel volume of the alpha7KO was significantly reduced and the organization of enamel rods was altered relative to controls. These results demonstrate distinct and varied spatiotemporal expression of alpha7 during tooth development, and they suggest that dysfunction of this receptor would have diverse impacts upon the adult organ

Growth of a human mammary tumor cell line is blocked by galangin, a naturally occurring bioflavonoid, and is accompanied by down-regulation of cyclins D3, E, and A

INTRODUCTION: This study was designed to determine if and how a non-toxic, naturally occurring bioflavonoid, galangin, affects proliferation of human mammary tumor cells. Our previous studies demonstrated that, in other cell types, galangin is a potent inhibitor of the aryl hydrocarbon receptor (AhR), an environmental carcinogen-responsive transcription factor implicated in mammary tumor initiation and growth control. Because some current breast cancer therapeutics are ineffective in estrogen receptor (ER) negative tumors and since the AhR may be involved in breast cancer proliferation, the effects of galangin on the proliferation of an ER(-), AhR(high )line, Hs578T, were studied. METHODS: AhR expression and function in the presence or absence of galangin, a second AhR inhibitor, α-naphthoflavone (α-NF), an AhR agonist, indole-3-carbinol, and a transfected AhR repressor-encoding plasmid (FhAhRR) were studied in Hs578T cells by western blotting for nuclear (for instance, constitutively activated) AhR and by transfection of an AhR-driven reporter construct, pGudLuc. The effects of these agents on cell proliferation were studied by (3)H-thymidine incorporation and by flow cytometry. The effects on cyclins implicated in mammary tumorigenesis were evaluated by western blotting. RESULTS: Hs578T cells were shown to express high levels of constitutively active AhR. Constitutive and environmental chemical-induced AhR activity was profoundly suppressed by galangin as was cell proliferation. However, the failure of α-NF or FhAhRR transfection to block proliferation indicated that galangin-mediated AhR inhibition was either insufficient or unrelated to its ability to significantly block cell proliferation at therapeutically relevant doses (IC(50 )= 11 μM). Galangin inhibited transition of cells from the G(0)/G(1 )to the S phases of cell growth, likely through the nearly total elimination of cyclin D3. Expression of cyclins A and E was also suppressed. CONCLUSION: Galangin is a strong inhibitor of Hs578T cell proliferation that likely mediates this effect through a relatively unique mechanism, suppression of cyclin D3, and not through the AhR. The results suggest that this non-toxic bioflavonoid may be useful as a chemotherapeutic, particularly in combination with agents that target other components of the tumor cell cycle and in situations where estrogen receptor-specific therapeutics are ineffective

Cholinergic receptor pathways involved in apoptosis, cell proliferation and neuronal differentiation

Acetylcholine (ACh) has been shown to modulate neuronal differentiation during early development. Both muscarinic and nicotinic acetylcholine receptors (AChRs) regulate a wide variety of physiological responses, including apoptosis, cellular proliferation and neuronal differentiation. However, the intracellular mechanisms underlying these effects of AChR signaling are not fully understood. It is known that activation of AChRs increase cellular proliferation and neurogenesis and that regulation of intracellular calcium through AChRs may underlie the many functions of ACh. Intriguingly, activation of diverse signaling molecules such as Ras-mitogen-activated protein kinase, phosphatidylinositol 3-kinase-Akt, protein kinase C and c-Src is modulated by AChRs. Here we discuss the roles of ACh in neuronal differentiation, cell proliferation and apoptosis. We also discuss the pathways involved in these processes, as well as the effects of novel endogenous AChRs agonists and strategies to enhance neuronal-differentiation of stem and neural progenitor cells. Further understanding of the intracellular mechanisms underlying AChR signaling may provide insights for novel therapeutic strategies, as abnormal AChR activity is present in many diseases