Mineral Carbonation as the Core of an Industrial Symbiosis for Energy‐Intensive Minerals Conversion

The longer term sustainability of the minerals sector may hinge, in large part, on finding innovative solutions to the challenges of energy intensity and carbon dioxide (CO₂) management. This article outlines the need for large‐scale “carbon solutions” that might be shared by several colocated energy‐intensive and carbon‐intensive industries. In particular, it explores the potential for situating a mineral carbonation plant as a carbon sink at the heart of a minerals and energy complex to form an industrial symbiosis. Several resource‐intensive industries can be integrated synergistically in this way, to enable a complex that produces energy and mineral products with low net CO₂ emissions. An illustrative hypothetical case study of such a system within New South Wales, Australia, has been constructed, on the basis of material and energy flows derived from Aspen modeling of a serpentine carbonation process. The synergies and added value created have the potential to significantly offset the energy and emission penalties and direct costs of CO₂ capture and storage. This suggests that greenfield minerals beneficiation and metals refining plants should consider closer integration with the power production and energy provision plants on which they depend, together with a carbon solution, such as mineral carbonation, as a critical element of such integration. Other sustainability considerations are highlighted.     

Development of the ear, hearing capabilities and laterophysic connection in the spotfin butterflyfish (Chaetodon ocellatus)

The ontogeny of the ear, swim bladder and laterophysic connection was investigated in the spotfin butterflyfish, Chaetodon ocellatus in order to determine how the development of the laterophysic connection (a Chaetodon synapomorphy) is correlated with ontogenetic changes in the hearing capabilities in these abundant and ecologically important coral reef fishes. Histological and cleared and stained material revealed that the medial opening in the lateral line canal in the supracleithrum (which defines the laterophysic connection), an inflated physoclistous swim bladder, and the three otolithic organs are already present in the smallest individuals examined (7?C15?mm SL). The medial opening in the supracleithrum increases in size and the cylindrical swim bladder horns form after the loss of the head plates characteristic of the tholichthys stage, in individuals ??29?mm SL. The three sensory maculae of the ear increase in size, and the shape of the sacculus changes most dramatically with fish growth; hair cell density is highest in the utriculus. Physiological analysis of the reponse to sound pressure showed that larval and juvenile C. ocellatus had a hearing sensitivity peak at 100?C200?Hz, which was ~30?C40?dB more sensitive than that measured in larval coral reef fishes (e.g., damselfishes) that lack swim bladder horns. C. ocellatus did not show any ontogenetic changes in sensitivity to sound pressure, which may be explained by the fact that the growth of the swim bladder horns maintains the small distance between the swim bladder and ear that was established earlier during the larval stage. The timing of the development of the swim bladder horns suggests that if the laterophysic connection has a sensory acoustic function, its presence in individuals >29?mm SL suggests that its role is limited to post-settlement, reef-based behaviors.     

CDH1 is essential for endometrial differentiation, gland development, and adult function in the mouse uterus

CDH1 is a cell-cell adhesion molecule expressed in the epithelium to coordinate key morphogenetic processes, establish cell polarity, and regulate epithelial differentiation and proliferation. To determine the role of CDH1 in the mouse uterus, Cdh1 was conditionally ablated by crossing Pgr-Cre and Cdh1-flox mice, and the phenotype was characterized. We found that loss of Cdh1 results in a disorganized cellular structure of the epithelium and ablation of endometrial glands in the neonatal uterus. Cdh1(d/d) mice lost adherens junctions (CTNNB1 and CTNNA1) and tight junctions (claudin, occludin, and ZO-1 proteins) in the neonatal uterus, leading to loss of epithelial cell-cell interaction. Ablation of Cdh1 induced abnormal epithelial proliferation and massive apoptosis, and disrupted Wnt and Hox gene expression in the neonatal uterus. Although the uteri of Cdh1(d/d) mice did not show any myometrial defects, ablation of Cdh1 inhibited expression of epithelial (cytokeratin 8) and stromal (CD10) markers. Cdh1(d/d) mice were infertile because of defects during implantation and decidualization. Furthermore, we showed in the model of conditional ablation of both Cdh1 and Trp53 in the uterus that interrupting cell cycle regulation through the loss of Cdh1 leads to abnormal uterine development. The uteri of Cdh1(d/d) Trp53(d/d) mice exhibited histological features of endometrial carcinomas with myometrial invasion. Collectively, these findings suggest that CDH1 has an important role in structural and functional development of the uterus as well as adult uterine function. CDH1 has a capacity to control cell fate by altering directional cell proliferation and apoptosis.     

N-Ras Forms Dimers at POPC Membranes

Ras is a central regulator of cellular signaling pathways. It is mutated in 20–30% of human tumors. To perform its function, Ras has to be bound to a membrane by a posttranslationally attached lipid anchor. Surprisingly, we identified here dimerization of membrane anchored Ras by combining attenuated total reflectance Fourier transform infrared spectroscopy, biomolecular simulations, and Förster resonance energy transfer experiments. By analyzing x-ray structural models and molecular-dynamics simulations, we propose a dimerization interface between α-helices 4 and 5 and the loop between β2 and β3. This seems to explain why the residues D47, E49, R135, R161, and R164 of this interface are influencing Ras signaling in cellular physiological experiments, although they are not positioned in the catalytic site. Dimerization could catalyze nanoclustering, which is well accepted for membrane-bound Ras. The interface could provide a new target for a seemingly novel type of small molecule interfering with signal transduction in oncogenic Ras mutants.     

Over-expression of stress protein-encoding genes helps Clostridium acetobutylicum to rapidly adapt to butanol stress

The toxicity of n-butanol in microbial fermentations limits its formation. The stress response of Clostridium acetobutylicum involves various stress proteins and therefore, over-expression of genes encoding stress proteins constitutes an option to improve solvent tolerance. Over-expression of groESL, grpE and htpG, significantly improved butanol tolerance of C. acetobutylicum. Whereas the wild type and vector control strain did not survive 2?% (v/v) butanol for 2?h, the recombinant strains showed 45?% (groESL), 25?% (grpE) and 56?% (htpG), respectively, of the initial c.f.u. after 2?h of butanol exposure. As previously, over-expression of groESL led to higher butanol production rates, but the novel strains over-expressing grpE or htpG produced only 51 and 68?%, respectively, of the wild type butanol concentrations after 72?h clearly differentiating butanol tolerance and production. Not only butanol tolerance but also the adaptation to butanol in successive stress experiments was significantly facilitated by increased levels of GroESL, GrpE and HtpG. Re-transformation and sequence analyses of the plasmids confirmed that not the plasmids, but the host cells evolved to a more robust phenotype.     

Overexpression of miR156 in switchgrass (Panicum virgatum L.) results in various morphological alterations and leads to improved biomass production

Switchgrass (Panicum virgatum L.) has been developed into a dedicated herbaceous bioenergy crop. Biomass yield is a major target trait for genetic improvement of switchgrass. microRNAs have emerged as a prominent class of gene regulatory factors that has the potential to improve complex traits such as biomass yield. A miR156b precursor was overexpressed in switchgrass. The effects of miR156 overexpression on SQUAMOSA PROMOTER BINDING PROTEIN LIKE (SPL) genes were revealed by microarray and quantitative RT-PCR analyses. Morphological alterations, biomass yield, saccharification efficiency and forage digestibility of the transgenic plants were characterized. miR156 controls apical dominance and floral transition in switchgrass by suppressing its target SPL genes. Relatively low levels of miR156 overexpression were sufficient to increase biomass yield while producing plants with normal flowering time. Moderate levels of miR156 led to improved biomass but the plants were non-flowering. These two groups of plants produced 58%-101% more biomass yield compared with the control. However, high miR156 levels resulted in severely stunted growth. The degree of morphological alterations of the transgenic switchgrass depends on miR156 level. Compared with floral transition, a lower miR156 level is required to disrupt apical dominance. The improvement in biomass yield was mainly because of the increase in tiller number. Targeted overexpression of miR156 also improved solubilized sugar yield and forage digestibility, and offered an effective approach for transgene containment.     

NFL-225 Test to Predict 1RM Bench Press in NCAA Division I Football Players

ABSTRACT: Mann, JB, Stoner, JD, and Mayhew, JL. NFL-225 test to predict 1RM bench press in NCAA Division I football players. J Strength Cond Res 26(10): 2623-2631, 2012-The National Football League (NFL)-225 test has gained popularity for assessing muscular performance among college football programs. Although the test is a measure of absolute muscular endurance, it was reputed to be highly correlated with maximum muscular strength. The purposes of this study were to assess the predictive potential of the NFL-225 test for estimating 1 repetition maximum (1RM) bench press performance in National Collegiate Athletic Association Division I college football players and to evaluate the accuracy of previous NFL-225 prediction equations. Players (n = 289) in a successful Division I program were assessed over a period of 5 years for 1RM bench press and repetitions completed with 102.3 kg (225 lb). Test sessions occurred within 1 week of each other during the off-season training period. In a validation group (n = 202), repetitions were significantly correlated with 1RM (r = 0.95), producing a prediction equation (1RM [kg] = 103.5 + 3.08 Reps) with a standard error of estimate = 6.4 kg (coefficient of variation = 4.3%). In a randomly selected cross-validation group (n = 87), the new equation nonsignificantly underpredicted by 0.9 ± 7.2 kg produced a high correlation with actual 1RM (intraclass correlation coefficient [ICC] = 0.967), had a limit of agreement of -15.0 to 13.2 kg, and predicted 69% of the group within ±4.5 kg of their actual 1RM. The best previous equation was that of Slovak et al., which was nonsignificantly underpredicted by -0.5 ± 6.7 kg, produced a high correlation with actual 1RM (ICC = 0.975), and predicted 68% of the group within ±4.5 kg of their actual 1RM. The new NFL-225 test seems to be a reasonable predictor of 1RM bench press in Division I players but should be further assessed on players from other high-level programs.     

Differential regulation of the cyclin-dependent kinase inhibitors p21(Cip1) and p27(Kip1) by phosphorylation directed by the cyclin encoded by Murine Herpesvirus 68

Members of the gamma2-herpesvirus family encode cyclin-like proteins that have the ability to deregulate mammalian cell cycle control. Here we report the key features of the viral cyclin encoded by Murine Herpesvirus 68, M cyclin. M cyclin preferentially associated with and activated cdk2; the M cyclin/cdk2 holoenzyme displayed a strong reliance on phosphorylation of the cdk T loop for activity. cdk2 associated with M cyclin exhibited substantial resistance to the cdk inhibitor proteins p21(Cip) and p27(Kip). Furthermore, M cyclin directed cdk2 to phosphorylate p27(Kip1) on threonine 187 (T187) and cellular expression of M cyclin led to down-regulation of p27(Kip1) and the partial subversion of the associated G1 arrest. Mutation of T187 to a non-phosphorylatable alanine rendered the p27(Kip1)-imposed G1 arrest resistant to M cyclin expression. Unlike the related K cyclin, M cyclin was unable to circumvent the G1 arrest associated with p21(Cip1) and was unable to direct its associated catalytic subunit to phosphorylate this cdk inhibitor. These results imply that M cyclin has properties that are distinct from other viral cyclins and that M cyclin expression alone is insufficient for S phase entry.