Characterization of Biochars Produced From Peanut Hulls and Pine Wood with Different Pyrolysis Conditions

Background Application of modern biomass pyrolysis methods for production of biofuels and biochar is potentially a significant approach to enable global carbon capture and sequestration. To realize this potential, it is essential to develop methods that produce biochar with the characteristics needed for effective soil amendment. Methods Biochar materials were produced from peanut hulls and pine wood with different pyrolysis conditions, then characterized by cation exchange (CEC) capacity assays, nitrogen adsorption–desorption isotherm measurements, micro/nanostructural imaging, infrared spectra and elemental analyses. Results Under a standard assay condition of pH 8.5, the CEC values of the peanut hull-derived biochar materials, ranging from 6.22 to 66.56 cmol kg−1, are significantly higher than those of the southern yellow pine-derived biochar, which are near zero or negative. The biochar produced from peanut hulls with a steam activation process yielded the highest CEC value of 66.56 cmol kg−1, which is about 5 times higher than the cation exchange capacity (12.51 cmol kg−1) of a reference soil sample. Notably, biochar produced from peanut hulls with batch barrel retort pyrolysis also has a much higher CEC value (60.12 cmol kg−1) than that (12.45 cmol kg−1) from Eprida’s H2-producing continuous steam injection process. The CEC values were shown to correlate well with the ratios of oxygen atoms to carbon atoms (O:C ratios) in the biochar materials. The higher O:C ratio in a biochar material may indicate the presence of more hydroxyl, carboxylate, and carbonyl groups that contribute to a higher CEC value for the biochar product. In addition, the increase in surface area can also play a role in increasing the CEC value of biochar, as in the case of the steam activation char. Conclusion Comparison of characterization results indicated that CEC value is determined not only by the type of the source biomass materials but also by the pyrolysis conditions. Biochar with the desirable characteristics of extremely high surface area (700 m2/g) and cation exchange capacity (\u3e 60 cmol kg) was created through steam activation

Challenges facing airway epithelial cell-based therapy for cystic fibrosis

Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene cause the life-limiting hereditary disease, cystic fibrosis (CF). Decreased or absent functional CFTR protein in airway epithelial cells leads to abnormally viscous mucus and impaired mucociliary transport, resulting in bacterial infections and inflammation causing progressive lung damage. There are more than 2000 known variants in the CFTR gene. A subset of CF individuals with specific CFTR mutations qualify for pharmacotherapies of variable efficacy. These drugs, termed CFTR modulators, address key defects in protein folding, trafficking, abundance, and function at the apical cell membrane resulting from specific CFTR mutations. However, some CFTR mutations result in little or no CFTR mRNA or protein expression for which a pharmaceutical strategy is more challenging and remote. One approach to rescue CFTR function in the airway epithelium is to replace cells that carry a mutant CFTR sequence with cells that express a normal copy of the gene. Cell-based therapy theoretically has the potential to serve as a one-time cure for CF lung disease regardless of the causative CFTR mutation. In this review, we explore major challenges and recent progress toward this ambitious goal. The ideal therapeutic cell would: (1) be autologous to avoid the complications of rejection and immune-suppression; (2) be safely modified to express functional CFTR; (3) be expandable ex vivo to generate sufficient cell quantities to restore CFTR function; and (4) have the capacity to engraft, proliferate and persist long-term in recipient airways without complications. Herein, we explore human bronchial epithelial cells (HBECs) and induced pluripotent stem cells (iPSCs) as candidate cell therapies for CF and explore the challenges facing their delivery to the human airway

Noncommutative Field Theory and Spontaneous Symmetry Breaking

We investigate the noncommutative analogue of the spontaneously broken linear sigma model at the one-loop quantum level. In the commutative case, renormalization of a theory with a spontaneously broken continuous global symmetry depends on cancellations that enable the limited set of counterterms consistent with that symmetry to remove the divergences even after its spontaneous breaking, while preserving the masslessness of the associated Goldstone modes. In the noncommutative case, we find that these cancellations are violated, and the renormalized one-loop correction to the inverse pion propagator explicitly yields a mass shift which depends on the ultraviolet cutoff. Thus, we cannot naively take the ultraviolet cutoff to infinity first, and then take the external momentum to zero to verify Nambu-Goldstone symmetry realization. However, from the Wilsonian perspective where the cutoff is fixed and physical, the zero external momentum limit of the inverse pion propagator still vanishes, and implies the masslessness of the pion fields at one-loop. This is another demonstration of the failure of ultraviolet and infrared limits to commute in noncommutative field theories, and signals the incompatibility of Nambu-Goldstone symmetry realization with the continuum renormalization of these theories.Comment: 17 pages, LaTeX, uses feynmp package; analyzes general case using all orderings of star product in quartic vertices; uses symmetrized Feynman vertex rules; revised combinatorics; reference added; conclusions unaltered; diagrams now appear correctl

Normal mouse peritoneum contains a large population of Ly-1+ (CD5) B cells that recognize phosphatidyl choline. Relationship to cells that secrete hemolytic antibody specific for autologous erythrocytes

We have found that, in the peritoneums of normal adult mice, 5-15% of lymphocytes bind a fluorescent liposome probe. In ontogeny, cells with this specificity were shown to appear by 8 d after birth, and increase to the adult frequency by 2-3 wk. Some older mice contain an expanded population of these cells. We have shown that liposome binding occurs by cell surface IgM recognizing the common membrane phospholipid, phosphatidyl choline (PtC). Virtually all of these PtC-specific cells bear the cell surface marker Ly-1. Our results indicate that roughly 1 in 10 peritoneal Ly-1+ B cells has this single specificity. We have found that the precursors to all the cells that form plaques on protease-treated autologous erythrocytes (BrMRBC) are included in the PtC-specific population and can be isolated by FACS. We believe this is the first report of sorting large numbers of B cells with a single antigen specificity from normal, unimmunized animals. This method will allow for in vitro and in vivo studies of differentiative and proliferative properties of Ly-1+ B cells, which may help define their role in development and disease

Direct spun aligned carbon nanotube web-reinforced proton exchange membranes for fuel cells

A composite membrane prepared by electrospinning SPEEK and direct spinning of CNTs is more robust than SPEEK alone and outperforms SPEEK and Nafion 212 membranes.</p

On a diffuse interface model for tumour growth with non-local interactions and degenerate mobilities

We study a non-local variant of a diffuse interface model proposed by Hawkins--Darrud et al. (2012) for tumour growth in the presence of a chemical species acting as nutrient. The system consists of a Cahn--Hilliard equation coupled to a reaction-diffusion equation. For non-degenerate mobilities and smooth potentials, we derive well-posedness results, which are the non-local analogue of those obtained in Frigeri et al. (European J. Appl. Math. 2015). Furthermore, we establish existence of weak solutions for the case of degenerate mobilities and singular potentials, which serves to confine the order parameter to its physically relevant interval. Due to the non-local nature of the equations, under additional assumptions continuous dependence on initial data can also be shown.Comment: 28 page

Polymorphisms in the WNK1 gene are asociated with blood pressure variation and urinary potassium excretion

WNK1 - a serine/threonine kinase involved in electrolyte homeostasis and blood pressure (BP) control - is an excellent candidate gene for essential hypertension (EH). We and others have previously reported association between WNK1 and BP variation. Using tag SNPs (tSNPs) that capture 100% of common WNK1 variation in HapMap, we aimed to replicate our findings with BP and to test for association with phenotypes relating to WNK1 function in the British Genetics of Hypertension (BRIGHT) study case-control resource (1700 hypertensive cases and 1700 normotensive controls). We found multiple variants to be associated with systolic blood pressure, SBP (7/28 tSNPs min-p = 0.0005), diastolic blood pressure, DBP (7/28 tSNPs min-p = 0.002) and 24 hour urinary potassium excretion (10/28 tSNPs min-p = 0.0004). Associations with SBP and urine potassium remained significant after correction for multiple testing (p = 0.02 and p = 0.01 respectively). The major allele (A) of rs765250, located in intron 1, demonstrated the strongest evidence for association with SBP, effect size 3.14 mmHg (95%CI:1.23–4.9), DBP 1.9 mmHg (95%CI:0.7–3.2) and hypertension, odds ratio (OR: 1.3 [95%CI: 1.0–1.7]).We genotyped this variant in six independent populations (n = 14,451) and replicated the association between rs765250 and SBP in a meta-analysis (p = 7×10−3, combined with BRIGHT data-set p = 2×10−4, n = 17,851). The associations of WNK1 with DBP and EH were not confirmed. Haplotype analysis revealed striking associations with hypertension and BP variation (global permutation p10 mmHg reduction) and risk for hypertension (OR<0.60). Our data indicates that multiple rare and common WNK1 variants contribute to BP variation and hypertension, and provide compelling evidence to initiate further genetic and functional studies to explore the role of WNK1 in BP regulation and EH