Large heat duty for amine regeneration in absorptionbased CO 2 capture is one of the major drawbacks of this process. Along with a highly endothermic carbamate breakdown reaction in the stripper, the difficulty of proton transfer from protonated amines to water in the amine regeneration process is also considered a basic reason for high heat duty. Transition metal oxide catalysts can play a vital role in decreasing the required thermal energy for amine regeneration in the stripper by providing Bronsted acids and Lewis acids that would help break down the carbamate by direct attack. MEA saturated with CO 2 at 35 °C, with initial loading of 0.56 mole CO 2 /mole amine, was used in this study. The performance of five different transition metal oxide catalysts, V 2 O 5 , MoO 3 , WO 3 , TiO 2 , and Cr 2 O 3 , was studied separately to investigate the effects of these catalysts on amine regeneration in the temperature range of 35−86 °C. It has been observed that MoO 3 performance is much better as it regenerated almost double of the MEA solvent than noncatalytic amine regeneration systems, whereas other catalysts also showed considerable differences in amine regeneration in this temperature range. The amine regeneration performance trend was MoO 3 > V 2 O 5 > Cr 2 O 3 > TiO 2 > WO 3 > blank test. The application of this work would mean that metal oxide catalysts could be used in strippers for a faster CO 2 desorption rate at lower temperature, which would cause a significant reduction of the heat duty.
A MarR-like transcriptional repressor (RcrR) and two predicted ABC efflux pumps (RcrPQ) encoded by a single operon were recently shown to be dominant regulators of stress tolerance and development of genetic competence in the oral pathogen Streptococcus mutans. Here, we focused on polar (⌬rcrR-P) and nonpolar (⌬rcrR-NP) rcrR mutants, which are hyper-and nontransformable, respectively, to dissect the mechanisms by which these mutations impact competence. We discovered two open reading frames (ORFs) in the 3= end of the rcrQ gene that encode peptides of 27 and 42 amino acids (aa) which are also dramatically upregulated in the ⌬rcrR-NP strain. Deletion of, or start codon mutations in, the ORFs for the peptides in the ⌬rcrR-NP background restored competence and sensitivity to competence-stimulating peptide (CSP) to levels seen in the ⌬rcrR-P strain. Overexpression of the peptides adversely affected competence development. Importantly, overexpression of mutant derivatives of the ABC exporters that lacked the peptides also resulted in impaired competence. FLAG-tagged versions of the peptides could be detected in S. mutans, and FLAG tagging of the peptides impaired their function. The competence phenotypes associated with the various mutations, and with overexpression of the peptides and ABC transporters, were correlated with the levels of ComX protein in cells. Collectively, these studies revealed multiple novel mechanisms for regulation of competence development by the components of the rcrRPQ operon. Given their intimate role in competence and stress tolerance, the rcrRPQ-encoded peptides may prove to be useful targets for therapeutics to diminish the virulence of S. mutans.
Identification of active subpopulations who are motivated to talk about, seek out, and select information about organ donation-related issues can improve health communicators' efficacy in increasing awareness of the shortage of organ and health donors. Using the Situational Theory of Problem Solving (STOPS), we segmented the general population into more meaningful subgroups (e.g., active, aware publics about an organ donation issue) and examined whether segmented public profiles could predict their likelihood of active information giving, taking, and selecting about donor shortage. We also tested whether those publics that are more active about the organ donation issue would recognize and be interested in other organ donation issues (e.g., shortage of bone marrow donors). Findings based on two survey data sets (N = 316 and N = 347) suggested that perceptual and motivation variables could predict the likelihood of information behaviors and further donation-related behavioral intentions. In addition, we found some evidence on the problem chain recognition effect-if one becomes active about an organ donation issue, she or he is likely to perceive similar or related issues as problematic. Based on the findings, we discuss the segmentation method and its utility for more strategic planning and practice of health campaigns.
In the dental caries pathogen Streptococcus mutans, phosphotransacetylase (Pta) catalyzes the conversion of acetyl coenzyme A (acetyl-CoA) to acetyl phosphate (AcP), which can be converted to acetate by acetate kinase (Ack), with the concomitant generation of ATP. A ⌬ackA mutant displayed enhanced accumulation of AcP under aerobic conditions, whereas little or no AcP was observed in the ⌬pta or ⌬pta ⌬ackA mutant. The ⌬pta and ⌬pta ⌬ackA mutants also had diminished ATP pools compared to the size of the ATP pool for the parental or ⌬ackA strain. Surprisingly, when exposed to oxidative stress, the ⌬pta ⌬ackA strain appeared to regain the capacity to produce AcP, with a concurrent increase in the size of the ATP pool compared to that for the parental strain. The ⌬ackA and ⌬pta ⌬ackA mutants exhibited enhanced (p)ppGpp accumulation, whereas the strain lacking Pta produced less (p)ppGpp than the wild-type strain. The ⌬ackA and ⌬pta ⌬ackA mutants displayed global changes in gene expression, as assessed by microarrays. All strains lacking Pta, which had defects in AcP production under aerobic conditions, were impaired in their abilities to form biofilms when glucose was the growth carbohydrate. Collectively, these data demonstrate the complex regulation of the Pta-Ack pathway and critical roles for these enzymes in processes that appear to be essential for the persistence and pathogenesis of S. mutans. Streptococcus mutans is a facultatively anaerobic, Gram-positive bacterium with fermentative metabolism. Human dental caries is associated with increased proportions of multiple acid-tolerant species in tooth biofilms, but S. mutans shows a particularly strong association with the initiation and progression of this common infectious disease (1, 2). The pathogenic potential of S. mutans is highly dependent on its ability to form biofilms, to use a variety of carbohydrates to produce organic acids that dissolve tooth mineral, and to tolerate stresses commonly encountered in oral biofilms. In particular, tolerance of a variety of reactive oxygen species (ROS), including superoxide ions and hydrogen peroxide, is considered critical for S. mutans to overcome antagonism by oral commensals and host defenses (3, 4).S. mutans has a partial tricarboxylic acid (TCA) cycle and lacks cytochromes, so the primary route for ATP generation by this organism is through the Embden-Meyerhof-Parnas pathway (4-7). Under anaerobic conditions and with growth in the presence of an excess of a preferred carbohydrate, the pyruvate generated by glycolysis is acted on by lactate dehydrogenase (LDH), which is allosterically activated by fructose-1,6-bisphosphate (F-1,6-BP), to produce lactate and regenerate NAD (4, 8). If carbohydrate is limiting, S. mutans produces a pyruvate formate lyase enzyme, which converts pyruvate to acetyl coenzyme A (acetyl-CoA) and formate (Fig. 1). However, the pyruvate formate lyase (PFL) enzyme of S. mutans is inactivated by oxygen, so under aerobic conditions and if catabolite repression is alleviated (M. Watts and R. A....
Nonalcoholic fatty liver disease (NAFLD) is an important health concern worldwide and progresses into nonalcoholic steatohepatitis (NASH). Although prevalence and severity of NAFLD/NASH are higher in men than premenopausal women, it remains unclear how sex affects NAFLD/NASH pathophysiology. Formyl peptide receptor 2 (FPR2) modulates inflammatory responses in several organs; however, its role in the liver is unknown. Here we show that FPR2 mediates sex-specific responses to diet-induced NAFLD/NASH. NASH-like liver injury was induced in both sexes during choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) feeding, but compared with females, male mice had more severe hepatic damage. Fpr2 was more highly expressed in hepatocytes and healthy livers from females than males, and FPR2 deletion exacerbated liver damage in CDAHFD-fed female mice. Estradiol induced Fpr2 expression, which protected hepatocytes and the liver from damage. In conclusion, our results demonstrate that FPR2 mediates sex-specific responses to diet-induced NAFLD/NASH, suggesting a novel therapeutic target for NAFLD/NASH.
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