Dry Friction due to Adsorbed Molecules

Using an adiabatic approximation method, which searches for Tomlinson model-like instabilities for a simple but still realistic model for two crystalline surfaces in the extremely light contact limit, with mobile molecules present at the interface, sliding relative to each other, we are able to account for the virtually universal occurrence of "dry friction." The model makes important predictions for the dependence of friction on the strength of the interaction of each surface with the mobile molecules.Comment: four pages of latex, figure provide

Infiltration and short-term movement of nitrogen in a silt-loam soil typical of rice cultivation in Arkansas

Rice production in Arkansas is one of the top three crop commodities in terms of cash receipts. Researchers and farmers report that nitrogen (N) needs to be managed according to a variety of factors with two important ones being soil and fertilizer type. The objectives of this experiment were to determine: 1) the degree to which floodwater-incorporated N applied as urea or as ammonium sulfate infiltrates intact cores (7.2-cm dia., 10-cm depth) containing DeWitt siltloam soil, and 2) the distribution of N during 12 h of ponding. Inorganic-N concentrations were analyzed at 2-cm depth intervals in cores following removal of the flood. Nitrogen from applied fertilizer was recovered as ammonium. Ammonium sulfate-N remained in the top 4 cm of soil with concentrations of 375 µg N g-1 in the surface 2 cm and 300 µg N g-1 at the 2 - 4 cm depth after 12 hr of ponding. At all depth intervals below 4 cm, ammonium sulfate-N remained below 30 µg N g-1. In contrast, after 12 h of ponding, N in soil receiving urea was 105 µg N g-1 in the top 2 cm and 173 µg N g-1 at 2-4 cm. At 4-6, 6-8, and 8-10 cm, N was 109, 108, and 35 µg N g-1, respectively, after 12 h of ponding. These results demonstrate immediate and deeper movement of ammonium into silt loam soil receiving urea as compared to ammonium sulfate, demonstrating how the form of N in fertilizer affects its movement into the soil profile

A novel selective 11b-hydroxysteroid dehydrogenase type 1 inhibitor prevents human adipogenesis.

Glucocorticoid excess increases fat mass, preferentially within omental depots; yet circulating cortisol concentrations are normal in most patients with metabolic syndrome (MS). At a pre-receptor level, 11b-hydroxysteroid dehydrogenase type 1 (11b-HSD1) activates cortisol from cortisone locally within adipose tissue, and inhibition of 11b-HSD1 in liver and adipose tissue has been proposed as a novel therapy to treat MS by reducing hepatic glucose output and adiposity. Using a transformed human subcutaneous preadipocyte cell line (Chub-S7) and human primary preadipocytes, we have defined the role of glucocorticoids and 11b-HSD1 in regulating adipose tissue differentiation. Human cells were differentiated with 1.0 mM cortisol (F), or cortisone (E) with or without 100 nM of a highly selective 11b-HSD1 inhibitor PF-877423. 11b-HSD1 mRNA expression increased across adipocyte differentiation (P!0.001, nZ4), which was paralleled by an increase in 11b-HSD1 oxo-reductase activity (from nil on day 0 to 5.9G1.9 pmol/mg per h on day 16,P!0.01, nZ7). Cortisone enhanced adipocyte differentiation; fatty acid-binding protein 4 expression increased 312-fold (P!0.001) and glycerol-3-phosphate dehydrogenase 47-fold (P!0.001) versus controls. This was abolished by co-incubation with PF-877423. In addition, cellular lipid content decreased significantly. These findings were confirmed in the primary cultures of human subcutaneous preadipocytes. The increase in 11b-HSD1 mRNA expression and activity is essential for the induction of human adipogenesis. Blocking adipogenesis with a novel and specific 11b-HSD1 inhibitor may represent a novel approach to treat obesity in patients with MS

Risk factors for vulnerable youth in urban townships in South Africa: the potential contribution of reactive attachment disorder

Reactive attachment disorder (RAD) is a psychiatric disorder developing in early or middle childhood as a consequence of significant failures in the caregiving environment. RAD results in children failing to relate socially, either by exhibiting markedly inhibited behaviour or by indiscriminate social behaviour and is associated with significant socio-behavioural problems in the longer term. This study examined RAD in South Africa, a setting with high environmental risks. We recruited a sub-sample of 40 10-year-old children from a cohort enrolled during pregnancy for whom early attachment status was known. Children were purposefully selected to represent the four attachment categories using the data available on the strange situation procedure (SSP) at 18 months. The Manchester Child Attachment Story Task (MCAST) assessed current attachment and RAD was diagnosed using a standardised assessment package. A high proportion of the children (5/40% or 12.5%) fulfilled diagnostic criteria for RAD; all were boys and were displaying the disinhibited type. SSP classification at 18 months was not significantly associated with RAD symptoms at age of 10 years, while current MCAST classifications were. This suggests that children in this sample are at much higher risk of RAD than in high-income populations, and despite a fairly typical attachment distribution in this population at 18 months, RAD was evidenced in later childhood and associated with current attachment disorganisation. The strengths of this research include its longitudinal nature and use of diagnostic assessments. Given increasing evidence that RAD is relatively stable over time and introduces longer term socio-behavioural risks; the high rate of RAD in this sample (12.5%) highlights potential developmental threats to children in low- and middle-income countries (LMICs). Our results should be interpreted with caution given sample size and risk of selection bias. Further research is needed to confirm these findings

Mathematical modeling of cell population dynamics in the colonic crypt and in colorectal cancer

Colorectal cancer is initiated in colonic crypts. A succession of genetic mutations or epigenetic changes can lead to homeostasis in the crypt being overcome, and subsequent unbounded growth. We consider the dynamics of a single colorectal crypt by using a compartmental approach [Tomlinson IPM, Bodmer WF (1995) Proc Natl Acad Sci USA 92: 11130-11134], which accounts for populations of stem cells, differential cells, and transit cells. That original model made the simplifying assumptions that each cell popuation divides synchronously, but we relax these assumptions by adopting an age-structured approach that models asynchronous cell division, and by using a continuum model. We discuss two mechanims that could regulate the growth of cell numbers and maintain the equilibrium that is normally observed in the crypt. The first will always maintain an equilibrium for all parameter values, whereas the second can allow unbounded proliferation if the net per capita growth rates are large enough. Results show that an increase in cell renewal, which is equivalent to a failure of programmed cell death or of differentiation, can lead to the growth of cancers. The second model can be used to explain the long lag phases in tumor growth, during which news, higher equilibria are reached, before unlimited growth in cell number ensues