Modeling flotation separation in a semi-batch process

A model for a semi-batch flotation separation process has been developed, based on available microprocess probabilities, and compared to experimental data obtained using a WEMCO laboratory flotation cell. In general, the model predicts the correct experimental trends. In many cases, the model also predicts removal efficiency very well. Parametric studies reveal that the model predictions are sensitive to a stability parameter, the turbulent energy density in the flotation cell, the contact angle between the solid particle and fluid, and the ratio of initial-to-critical film thickness.     

Reply to Silverman.

Responds to commentary by I. Silverman (see record 2007-08963-001) entitled "Review of Pure types are rare": Comment on book review. I do not think that either one of us will change his position, and therefore it is up to the interested (yet disinterested) reader to adjudicate our dispute by checking Professor Silverman's book and his references. In the process, the reader will be forced to consider the thought-provoking implications for our mental health system of some of the incidents which the author describes so vividly, and that will not be a bad thing. There is one point, however, which is worth pursuing further here, for Professor Silverman persists in an elementary statistical fallacy. Let us take the situation which he cites, where the base rate for diagnosing schizophrenia is 50%. Suppose with the same base rate the degree of agreement is in fact 53%; this is far above chance level. It must be emphasized, however, that the 53% agreement under discussion came not from a study where the base rate for diagnosing schizophrenia was 50%, but from one where the conditions were far more stringent since the base rate for diagnosing schizophrenia was around 20%. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Identification of N,N'-dicyclohexylcarbodiimide-reactive glutamic and aspartic acid residues in Escherichia coli transhydrogenase and the exchange of these by site-specific mutagenesis

Pyridine nucleotide transhydrogenase (EC 1.6.1.1) from Escherichia coli was investigated with respect to the role of glutamic and aspartic acid residues reactive to N,N'-dicyclohexylcarbodiimide (DCCD) and potentially involved in the proton-pumping mechanism of the enzyme. The E. coli transhydrogenase consists of an alpha (510 residues) and a beta (462 residues) subunit. DCCD reacts with the enzyme to inhibit catalytic activity and proton pumping. This reagent modifies Asp alpha 232, Glu alpha 238, and Glu alpha 240 as well as amino acid residue(s) in the beta subunit. Using the cloned and overexpressed E. coli transhydrogenase genes (Clarke, D. M., and Bragg, P. D. (1985) J. Bacteriol. 162, 367-373), Asp alpha 232 and Glu alpha 238 were replaced independently by site-specific mutagenesis. In addition, Asp alpha 232, Glu alpha 238, and Glu alpha 240 were replaced to generate triple mutants. The specific catalytic activities of the mutant transhydrogenases alpha D232N, alpha D232E, alpha D232K, alpha D232H, alpha E238K, and alpha E238Q as well as of the triple mutants alpha D232N, alpha E238Q, alpha E240Q and alpha D232H, alpha E238Q, alpha E240Q were in the range of 40-90% of the wild-type activity. Proton-pumping activity was present in all mutants. Examination of the extent of subunit modification by [14C]DCCD revealed that the label was still incorporated into both alpha and beta subunits in the Asp alpha 232 mutants, but that the alpha subunit was not labeled in the triple mutants. Catalytic and proton-pumping activities were nearly insensitive to DCCD in the triple mutants. This suggests that loss of catalytic and proton-pumping activities is associated with modification of the aspartic and glutamic acid residues of the alpha subunit. In the presence of the substrate NADPH, the rate of modification of the beta subunit by [14C]DCCD was increased, and there was a greater extent of enzyme inactivation. By contrast, NADH and 3-acetylpyridine-NAD+ protected the catalytic activity of the transhydrogenase from inhibition by DCCD. The protection was particularly marked in the E238Q and E238K mutants. It is concluded that the Asp alpha 232, Glu alpha 238, and Glu alpha 240 residues are not essential for catalytic activity or proton pumping. The inactivation by DCCD is likely due to the introduction of a sterically hindering group that reacts with the identified acidic residues close to the NAD(H)-binding site.     

The use of low-osmolar contrast agents: technological change and defensive medicine

The escalating cost of medical care in the United States, especially in the past decade, has resulted in efforts to identify the factors contributing to rising costs. One factor often assumed to cause higher medical costs is the physician's fear of liability for not using the latest available technology. In this article, we report the results of a case study we conducted to better understand the relationship between the introduction and use of one particular technology, low-osmolar contrast agents, and liability concerns. Our study suggests that both clinicians and administrators are primarily guided by the medical benefits of low-osmolar contrast agents, and that liability concerns, although widespread, are of secondary importance. The inability to control this and similar technologies is likely to put a far greater strain on the nation's health care resources than is the practice of defensive medicine. These findings may be helpful to health policy makers, physicians, administrators, and legislators considering choices for health care reform in general and for medical liability reform in particular.     

Characterization of mutated transforming growth factor-beta s which possess unique biological properties

Transforming growth factor-beta (TGF-beta) is a potent regulator of cell growth and differentiation. On the basis of the crystal structure of TGF-beta 2, we have designed and synthesized two mutant TGF-beta s, TGF-beta 1 (71 Trp) and TGF-beta 1 (delta 69-73). Although both of these molecules inhibited the growth of Mv1Lu mink lung epithelial cells and LS1034 colorectal cancer cells, which are affected equally by TGF-beta 1 and TGF-beta 2, TGF-beta 1 (delta 69-73) was much less potent than TGF-beta 1 or TGF-beta 1 (71 Trp) at inhibiting the growth of LS513 colorectal cancer cells which are growth-inhibited by TGF-beta 1 but not TGF-beta 2. Both TGF-beta 1 (71 Trp) and TGF-beta 1 (delta 69-73) increased levels of mRNAs for fibronectin and plasminogen activator inhibitor with Mv1Lu cells, whereas only TGF-beta 1 (71 Trp) and not TGF-beta 1 (delta 69-73) up-regulated the mRNA level of carcinoembryonic antigen in LS513 cells. The expression level of carcinoembryonic antigen mRNA in LS1034 cells was not altered by either wild-type or mutant TGF-beta s. Receptor labeling experiments demonstrated that TGF-beta 1 (71 Trp) bound with high affinity to the cell-surface receptors of Mv1Lu, LS1034, and LS513 cells while TGF-beta 1 (delta 69-73) bound effectively to the receptors of Mv1Lu and LS1034 cells but much less to the receptors on LS513 cells.(ABSTRACT TRUNCATED AT 250 WORDS)