Microfiltration of yeast suspensions with self-cleaning spiral vortices: possibilities for a new membrane module design

A novel method of producing controlled vortices was used to reduce both concentration polarization and membrane fouling during microfiltration of Saccharomyces cerevisiae broth suspensions. The method involves flow around a curved channel at a sufficient rate so as to produce centrifugal instabilities (called Dean vortices). These vortices depolarize the build-up of suspended particles such as yeast cells at the membrane-solution interface and allow for increased membrane permeation rates. Various operating conditions under which such vortices effectively reduced cake build-up of suspended particles such as yeast cells at the membrane-solution interface and allow for increased membrane permeation rates. Various operating conditions under which such vortices effectively reduced cake build-up during microfiltration of 0 to 0.55 dry wt% yeast broth were investigated. Flux improvements of over 60% for 0.25 dry wt% yeast broth for flow with over that without Dean vortices were observed. This beneficial effect increased with increasing retentate flow rate and increasing transmembrane pressure and decreased with increasing concentration of suspended matter. Similar behavior was observed whether the cells were viable of killed. the improvement in flux in the presence over that in the absence of vortices correlated well with centrifugal force or azimuthal velocity squared. The relative cake resistances increased with reservoir yeast concentration. These values with vortices increased from 62% to 75% of that without vortices with increasing yeast concentration. The ratio of the cake thicknesses in the limiting case (at high feed concentration) was 3.25. These results suggest that self-cleaning spiral vortices could be effective in maintaining good and steady microfiltration performance with cell suspensions other than those tested. (c) 1995 John Wiley & Sons, Inc.     

Semen alloantigens and lymphocytotoxic antibodies in AIDS and ICL

More than 90% of people with AIDS develop circulating immune complexes (CICs) and lymphocytotoxic antibodies (LCTAs). Animals infected with HIV, however, never display CICs or LCTAs, and remain healthy. Similarly, HIV-infected people who do not develop CICs or LCTAs also do not progress to AIDS. The appearance of CICs and LCTAs is, however, highly prognostic for AIDS and death. Since HIV infection does not,per se, lead to the development of CICs and LCTAs, other causes are likely. One such cause, for which both epidemiologic and experimental evidence exists, is semen. Semen components include sperm, seminal fluid, lymphocytes, and sometimes infectious agents, including HIV, mycoplasmas, and herpes and hepatitis viruses, all of which independently cause immune suppression. Extensive evidence demonstrates sperm (and various viruses) contains many proteins mimicking the CD4 protein of T-helper cells, while HIV, mycoplasmas, and seminal fluid mimic class II MHC proteins of other lymphocytes. We identify a large number of protein sequences that display such mimicry using computer homology searching, and demonstrate experimentally that sperm antibodies specifically precipitate antibodies against class II MHC mimics such as mycoplasmas, which in turn precipitate antibodies to lymphocyte antigens. These data prove that immunologic exposure to sperm and lymphocytes (as may occur in receptive anal intercourse, needle sharing, or blood transfusions) is theoretically capable of initiating lymphocytotoxic autoimmunity. Such autoimmunity may play a significant role in the pathogenesis of AIDS, and will need to be addressed clinically in high risk individuals regardless of HIV status and regardless of the success of anti-HIV prophylaxis and treatment.     

Latent Transforming Growth Factor-β Binding Protein Domains Involved in Activation and Transglutaminase-dependent Cross-Linking of Latent Transforming Growth Factor-β

Transforming growth factor-β (TGF-β) is secreted by many cell types as part of a large latent complex composed of three subunits: TGF-β, the TGF-β propeptide, and the latent TGF-β binding protein (LTBP). To interact with its cell surface receptors, TGF-β must be released from the latent complex by disrupting noncovalent interactions between mature TGF-β and its propeptide. Previously, we identified LTBP-1 and transglutaminase, a cross-linking enzyme, as reactants involved in the formation of TGF-β. In this study, we demonstrate that LTBP-1 and large latent complex are substrates for transglutaminase. Furthermore, we show that the covalent association between LTBP-1 and the extracellular matrix is transglutaminase dependent, as little LTBP-1 is recovered from matrix digests prepared from cultures treated with transglutaminase inhibitors. Three polyclonal antisera to glutathione S–transferase fusion proteins containing amino, middle, or carboxyl regions of LTBP-1S were used to identify domains of LTBP-1 involved in crosslinking and formation of TGF-β by transglutaminase. Antibodies to the amino and carboxyl regions of LTBP-1S abrogate TGF-β generation by vascular cell cocultures or macrophages. However, only antibodies to the amino-terminal region of LTBP-1 block transglutaminase-dependent cross-linking of large latent complex or LTBP-1. To further identify transglutaminase-reactive domains within the amino-terminal region of LTBP-1S, mutants of LTBP-1S with deletions of either the amino-terminal 293 (ΔN293) or 441 (ΔN441) amino acids were expressed transiently in CHO cells. Analysis of the LTBP-1S content in matrices of transfected CHO cultures revealed that ΔN293 LTBP-1S was matrix associated via a transglutaminasedependent reaction, whereas ΔN441 LTBP-1S was not. This suggests that residues 294–441 are critical to the transglutaminase reactivity of LTBP-1S.     

Catecholamine and MHPG plasma levels,platelet MAO activity,and3H-imipramine binding in heroin and cocaine addicts

This work evaluated in a population of heroin and heroin plus cocaine human addicts:

1. Norepinephrine (NE), epinephrine (Epi), and 3-methoxy-4-hydroxyphenylglycol (MHPG) (the principal metabolite of brain NE) plasma levels;
2. Monoamine oxidase (MAO) activity; and
3. ³H-imipramine specific binding to the amine carrier in platelets.

NE plasma levels were significantly lower in the short-term heroin user groups (1–3 and 4–6 yr), a finding not observed in both the long-term heroin user (>6 yr) and heroin plus cocaine user (>6 yr) groups. Epi levels changed in a similar manner, except that a significant increase was noted in heroin plus cocaine abusers. Conversely, dopamine and MHPG plasma levels increased with the duration of heroin use, and even more with cocaine abuse. Platelet MAO activity increased in all groups. Specific³H-imipramine binding sites showed an increase after 3 yr of heroin abuse and in all heroin plus cocaine addicts. In conclusion, short-term use of heroin decreases NE or Epi release, but with prolonged use, a slow adpatation occurs. In contrast, cocaine inhibits the neuronal Epi uptake, even in a situation of long duration of abuse. Probably the amine levels additionally regulate the amine carrier, resulting in changes that show a different pattern from major depression. These drugs of abuse may also influence directly or indirectly related enzymatic systems.     

Photoperiodic time measurement in the spider mite Tetranychus urticae: A novel concept

To explain photoperiodic induction of diapause in the spider mite Tetranychus urticae a new theoretical model was developed which took into account both the hourglass and rhythmic elements shown to be present in the photoperiodic reaction of these mites. It is emphasized that photoperiodic induction is the result of time measurement as well as the summation and integration of a number of successive photoperiodic cycles: the model, therefore, consists of separate ‘clock’ and ‘counter’ mechanisms. In current views involvement of the circadian system in photoperiodism is interpreted in terms of the hypothesis that the photoperiodic clock itself is based on one or more circadian oscillators. Here a different approach has been chosen as regards the role of the circadian system in photoperiodism: the possibility, previously put forward by other authors, that some aspect of the photoperiodic induction mechanism other than the clock is controlled by the circadian system was investigated by assuming a circadian influence on the photoperiodic counter mechanism. The derivation of this ‘hourglass timer oscillator counter’ model of photoperiodic induction in T. urticae is described and its operation demonstrated on the basis of a number of diel and nondiel photoperiods, with and without light interruptions.     

Inhibition of parasympathetic axonal sprouting in the cat submandibular gland by sympathetic axons

Summary The sprouting of parasympathetic axons into the submandibular sympathetic nerve trunk following sympathetic denervation has been investigated. It was found that a permanent sympathetic denervation was necessary in order for the sprouting to develop and be maintained: if reinnervation by adrenergic nerves was delayed, the sprouting developed but was reduced at longer survival times when the original innervation was reestablished. The evidence for suppression of the cholinergic sprouting by the adrenergic axons is discussed, as is the evidence that these sprouts arise from the submandibular gland.     

Inhibition of dihydropteridine reductase by dopamine

Dihydropteridine reductase has been purified 900-fold from rat liver. Dopamine inhibited the enzyme up to 50% at a concentration of 0.11mm. In the presence of dopamine the enzyme gave non-hyperbolic v-against-[S] plots. This enzyme may have a role in control of dopamine biosynthesis.     

Phenotypic instability in a tif-1 mutant of Escherichia coli

Summary A recent study showed that in E. coli T44 () carrying the tif-1 mutation, elevated temperature and adenine can interfere with the translation process. The present study shows that the expression of tif phenotypes (thermoinduction and filamentation) is suppressed by factors which affect ribosomal function. Ethanol suppresses thermoinduction and, in some spc ^r mutants, both thermoinduction and filamentation are suppressed. An unknown factor(s) in yeast extract suppresses both thermoinduction and filamentation. In thermoresistant revertant (ts⁺), the expression of the ts⁺ phenotype is suppressed by yeast extract, ethanol, guanosine+cytidine and by the addition of a spc ^r mutation. This indicates that this phenotype could be due to suppressor mutations, and the interaction between factors affecting ribosomal function and the ts⁺ phenotype suggests that the suppression of tif in the ts⁺ strains could operate on the ribosomal level. In vitro studies show that in extracts from either spc ^r or ts⁺ strains, or in the presence of ethanol, translational restriction is relieved, suggesting that the suppression of tif phenotypes could involve the translation process.