Growth, profits and technological choice: The case of the Lancashire cotton textile industry

Using Lancashire textile industry company case studies and financial records, mainly from the period just before the First World War, the processes of growth and decline are re-examined. These are considered by reference to the nature of Lancashire entrepreneurship and the impact on technological choice. Capital accumulation, associated wealth distributions and the character of Lancashire business organisation were sybiotically linked to the success of the industry before 1914. However, the legacy of that accumulation in later decades, chronic overcapacity, formed a barrier to reconstruction and enhanced the preciptious decline of a once great industry

Quantum corrections to Higher-Dimensional Theories

This is a non-technical summary of the subtleties of quantum corrections on extra-dimensional theories: should one first renormalize and then mode expand, or first expand in four-dimensional modes and then renormalize?Comment: 9 pages, based on a talk at IRGAC 2006, Barcelon

Neck atonia with a focal stimulation-induced seizure arising from the SMA: pathophysiological considerations.

A 28-year-old patient with pharmacoresistant non-lesional right frontal epilepsy underwent extra-operative intracranial EEG recordings and electrical cortical stimulation (ECS) to map eloquent cortex. Right supplementary motor area (SMA) ECS induced a brief seizure with habitual symptoms involving neck tingling followed by asymmetric tonic posturing. An additional feature was neck atonia. During atonia and sensory aura, discharges were seen in the mesial frontal electrodes and precentral gyrus. Besides motor signs, atonia, although rare and not described in the neck muscles, and sensations have been reported with SMA stimulation. The mechanisms underlying neck atonia in seizures arising from the SMA can be explained by supplementary negative motor area (SNMA) - though this was not mapped in electrodes overlying the ictal onset zone in our patient - or primary sensorimotor cortex activation through rapid propagation. Given the broad spectrum of signs elicited by SMA stimulation and rapid spread of seizures arising from the SMA, caution should be taken to not diagnose these as non-epileptic, as had previously occurred in this patient

Direct numerical simulations of statistically steady, homogeneous, isotropic fluid turbulence with polymer additives

We carry out a direct numerical simulation (DNS) study that reveals the effects of polymers on statistically steady, forced, homogeneous, isotropic fluid turbulence. We find clear manifestations of dissipation-reduction phenomena: On the addition of polymers to the turbulent fluid, we obtain a reduction in the energy dissipation rate, a significant modification of the fluid energy spectrum, especially in the deep-dissipation range, a suppression of small-scale intermittency, and a decrease in small-scale vorticity filaments. We also compare our results with recent experiments and earlier DNS studies of decaying fluid turbulence with polymer additives.Comment: consistent with the published versio

Delay of Disorder by Diluted Polymers

We study the effect of diluted flexible polymers on a disordered capillary wave state. The waves are generated at an interface of a dyed water sugar solution and a low viscous silicon oil. This allows for a quantitative measurement of the spatio-temporal Fourier spectrum. The primary pattern after the first bifurcation from the flat interface are squares. With increasing driving strength we observe a melting of the square pattern. It is replaced by a weak turbulent cascade. The addition of a small amount of polymers to the water layer does not affect the critical acceleration but shifts the disorder transition to higher driving strenghs and the short wave length - high frequency fluctuations are suppressed

Cytotoxicity of Cu(II) and Zn(II) 2,2′-Bipyridyl Complexes: Dependence of IC_50 on Recovery Time

We measure the cytotoxicity of three metal complexes containing the 2,2′-bypyridine ligand, Cu(bpy)(NCS)2, 1, [Cu(bpy)2(H2O)](PF6)2, 2, and Zn(bpy)2(NCS)2, 3, toward neuroblastoma cells (SKN- SH) and ovarian cancer cells (OVCAR-3) using two different cell assays. The cells were exposed to various concentrations of the compounds for 1 h and the percent inhibition of cell growth, I, measured for various times after exposure, i.e., as a function of the recovery time t. After developing the theory showing the relationship between I and t, the cytotoxicity data were analyzed to reveal that the two copper complexes, 1 and 2, cause the cells to divide at a slower rate than the controls during the recovery period, but the zinc complex, 3, had little or no effect on cell division during the recovery period. The usual metric for reporting cytotoxicity is IC50, which is the concentration of agent required to inhibit cell growth to 50% of the control population. However, since IC50 can depend on the recovery time, t, as is the case for 1 and 2, reporting IC50 for a single recovery time can hide important information about the long-time effects of a cytotoxic agent on the health of the cell population. Mechanistic studies with the compounds revealed that the copper complexes, 1 and 2, cleave closed circular pBR322 DNA in the presence of ascorbate, while the zinc complex, 3, does not facilitate DNA cleavage under the same conditions. This difference in DNA cleavage activity may be related to the fact that Cu(II) is redox active and can readily change its oxidation state, while Zn(II) is redox inert and cannot participate in a redox cycle with ascorbate to break DNA

Cytotoxicity of Cu(II) and Zn(II) 2,2′-Bipyridyl Complexes: Dependence of IC 50 on Recovery Time

We measure the cytotoxicity of three metal complexes containing the 2,2′-bypyridine ligand, Cu(bpy)(NCS) 2, 1, [Cu(bpy) 2(H 2O)](PF 6) 2, 2, and Zn(bpy) 2(NCS) 2, 3, toward neuroblastoma cells (SK-N-SH) and ovarian cancer cells (OVCAR-3) using two different cell assays. The cells were exposed to various concentrations of the compounds for 1 h and the percent inhibition of cell growth, I, measured for various times after exposure, i.e., as a function of the recovery time t. After developing the theory showing the relationship between I and t, the cytotoxicity data were analyzed to reveal that the two copper complexes, 1 and 2, cause the cells to divide at a slower rate than the controls during the recovery period, but the zinc complex, 3, had little or no effect on cell division during the recovery period. The usual metric for reporting cytotoxicity is IC 50, which is the concentration of agent required to inhibit cell growth to 50% of the control population. However, since IC 50 can depend on the recovery time, t, as is the case for 1 and 2, reporting IC 50 for a single recovery time can hide important information about the long-time effects of a cytotoxic agent on the health of the cell population. Mechanistic studies with the compounds revealed that the copper complexes, 1 and 2, cleave closed circular pBR322 DNA in the presence of ascorbate, while the zinc complex, 3, does not facilitate DNA cleavage under the same conditions. This difference in DNA cleavage activity may be related to the fact that Cu(II) is redox active and can readily change its oxidation state, while Zn(II) is redox inert and cannot participate in a redox cycle with ascorbate to break DNA

Nonlinear Diffusion Through Large Complex Networks Containing Regular Subgraphs

Transport through generalized trees is considered. Trees contain the simple nodes and supernodes, either well-structured regular subgraphs or those with many triangles. We observe a superdiffusion for the highly connected nodes while it is Brownian for the rest of the nodes. Transport within a supernode is affected by the finite size effects vanishing as $N\to\infty.$ For the even dimensions of space, $d=2,4,6,...$, the finite size effects break down the perturbation theory at small scales and can be regularized by using the heat-kernel expansion.Comment: 21 pages, 2 figures include

New Extracellular Resistance Mechanism for Cisplatin

The HSQC NMR spectrum of 15N-cisplatin in cell growth media shows resonances corresponding to the monocarbonato complex, cis-[Pt(NH3)2(CO3)Cl]-, 4, and the dicarbonato complex, cis-[Pt(NH3)2(CO3)2]-2, 5, in addition to cisplatin itself, cis-[Pt(NH3)2Cl2], 1. The presence of Jurkat cells reduces the amount of detectable carbonato species by (2.8 ± 0.7) fmol per cell and has little effect on species 1. Jurkat cells made resistant to cisplatin reduce the amount of detectable carbonato species by (7.9 ± 5.6) fmol per cell and also reduce the amount of 1 by (3.4 ± 0.9) fmol per cell. The amount of detectable carbonato species is also reduced by addition of the drug to medium that has previously been in contact with normal Jurkat cells (cells removed); the reduction is greater when drug is added to medium previously in contact with resistant Jurkat cells (cells removed). This shows that the platinum species are modified by a cell-produced substance that is released to the medium. Since the modified species have been shown not to enter or bind to cells, and since resistant cells modify more than non-resistant cells, the modification constitutes a new extracellular mechanism for cisplatin resistance which merits further attention