Bacterial Residues in Coprolite of Herbivorous Dinosaurs: Role of Bacteria in Mineralization of Feces

The Cretaceous Two Medicine Formation of northwestern Montana has yielded blocky, calcareous coprolites that contain abundant fragments of conifer wood and were produced by large herbivorous dinosaurs. The coprolites are generally dark gray to black in color due to a dark substance confined chiefly within what originally were the capillaries of tracheid and ray cells of xylem. This substance is a kerogen which consists in part of thin-walled vesicles 0.1-1.3 µm in diameter. Pyrolysis products of this kerogen are diagnostic of a bacterial origin with a possible contribution from terrestrial plants. The vesicular component is interpreted as the residue of bacterial cells, whereas a second filamentous component, closely associated with the vesicles, may be the residue of an extracellular binding material, such as glycocalyx. At least two episodes of calcification of the coprolite are recognized by manganous cathodoluminescence. The earlier of these infilled the capillary channels of the conifer fragments. Wood cell walls, voids, cracks, and small burrows were filled during the later episode. Microprobe data confirm these results and show that phosphate is sequestered in the capillaries. These observations suggest that bacteria within the capillaries induced initial mineralization of the coprolite, and, in so doing, created barriers that protected organic residues from subsequent destruction. Early onset of mineralization is consistent with the degree of preservation of woody xylem found in the coprolites

In situ synthesis of size-controlled, stable silver nanoparticles within ultrashort peptide hydrogels and their anti-bacterial properties

We have developed a silver-releasing biomaterial with promising potential for wound healing applications. The material is made of ultrashort peptides which can self-assemble in water to form hydrogels. Silver nanoparticles (Ag NPs) were synthesized in situ within the biomaterial, using only UV irradiation and no additional chemical reducing agents. The synthetic strategy allows precise control of the nanoparticle size, with the network of peptide fibers preventing aggregation of Ag NPs. The biomaterial shows increased mechanical strength compared to the hydrogel control. We observed a sustained release of Ag NPs over a period of 14 days. This is a crucial prerequisite for effective anti-bacterial therapy. The ability to inhibit bacterial growth was tested using different bacterial strains, namely gram-negative Escherichia coli and Pseudomonas aeruginosa and gram-positive Staphylococcus aureus. Inhibition of bacterial growth was observed for all strains. The best results were obtained for Pseudomonas aeruginosa which is known for exhibiting multidrug resistance. Biocompatibility studies on HDFa cells, using Ag NP-containing hydrogels, did not show any significant influence on cell viability. We propose this silver-releasing hydrogel as an excellent biomaterial with great potential for applications in wound healing due to its low silver content, sustained silver nanoparticle release and biocompatibility

Emerging donors in international development assistance : the China case

This report begins by highlighting the evolution of China’s foreign aid programming. In many respects, current programs stem from the “Eight Principles for China’s Aid to Third World Countries” announced by former Premier Zhou Enlai in 1964. Chinese authorities have tended to focus on projects that achieve maximum impact both in terms of development and foreign policy

Role of Tafazzin in Mitochondrial Function, Development and Disease

Tafazzin, an enzyme associated with the rare inherited x-linked disorder Barth Syndrome, is a nuclear encoded mitochondrial transacylase that is highly conserved across multiple species and plays an important role in mitochondrial function. Numerous studies have elucidated the mechanisms by which Tafazzin affects mitochondrial function, but its effects on development and susceptibility to adult disease are incompletely understood. The purpose of this review is to highlight previous functional studies across a variety of model organisms, introduce recent studies that show an important role in development, and also to provide an update on the role of Tafazzin in human disease. The profound effects of Tafazzin on cardiac development and adult cardiac homeostasis will be emphasized. These studies underscore the importance of mitochondrial function in cardiac development and disease, and also introduce the concept of Tafazzin as a potential therapeutic modality

Hey2 functions in parallel with Hes1 and Hes5 for mammalian auditory sensory organ development

<p>Abstract</p> <p>Background</p> <p>During mouse development, the precursor cells that give rise to the auditory sensory organ, the organ of Corti, are specified prior to embryonic day 14.5 (E14.5). Subsequently, the sensory domain is patterned precisely into one row of inner and three rows of outer sensory hair cells interdigitated with supporting cells. Both the restriction of the sensory domain and the patterning of the sensory mosaic of the organ of Corti involve Notch-mediated lateral inhibition and cellular rearrangement characteristic of convergent extension. This study explores the expression and function of a putative Notch target gene.</p> <p>Results</p> <p>We report that a putative Notch target gene, hairy-related basic helix-loop-helix (bHLH) transcriptional factor Hey2, is expressed in the cochlear epithelium prior to terminal differentiation. Its expression is subsequently restricted to supporting cells, overlapping with the expression domains of two known Notch target genes, <it>Hairy </it>and enhancer of split homolog genes <it>Hes1 </it>and <it>Hes5</it>. In combination with the loss of <it>Hes1 </it>or <it>Hes5</it>, genetic inactivation of <it>Hey2 </it>leads to increased numbers of mis-patterned inner or outer hair cells, respectively. Surprisingly, the ectopic hair cells in <it>Hey2 </it>mutants are accompanied by ectopic supporting cells. Furthermore, <it>Hey2</it>^-/-<it>;Hes1</it>^-/-and <it>Hey2</it>^-/-<it>;Hes1</it>^+/-mutants show a complete penetrance of early embryonic lethality.</p> <p>Conclusion</p> <p>Our results indicate that <it>Hey2 </it>functions in parallel with <it>Hes1 </it>and <it>Hes5 </it>in patterning the organ of Corti, and interacts genetically with <it>Hes1 </it>for early embryonic development and survival. Our data implicates expansion of the progenitor pool and/or the boundaries of the developing sensory organ to account for patterning defects observed in <it>Hey2 </it>mutants.</p

Very low resistance nonalloyed ohmic contacts using low-temperature molecular beam epitaxy of GaAs

Ex situ nonalloyed ohmic contacts were made to n- and p‐type GaAs using low‐temperature molecular beam epitaxy. For n‐type GaAs, Ag, and Ti/Au nonalloyed contacts displayed specific contact resistitivities of mid 10-7 ohm cm2. For p‐type GaAs, nonalloyed Ti/Au contacts with specific contact resistivities of about 10-7 ohm cm2 were obtained

A novel αB-crystallin R123W variant drives hypertrophic cardiomyopathy by promoting maladaptive calcium-dependent signal transduction

Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiovascular disorder affecting 1 in 500 people in the general population. Characterized by asymmetric left ventricular hypertrophy, cardiomyocyte disarray and cardiac fibrosis, HCM is a highly complex disease with heterogenous clinical presentation, onset and complication. While mutations in sarcomere genes can account for a substantial proportion of familial cases of HCM, 40%–50% of HCM patients do not carry such sarcomere variants and the causal mutations for their diseases remain elusive. Recently, we identified a novel variant of the alpha-crystallin B chain (CRYABR123W) in a pair of monozygotic twins who developed concordant HCM phenotypes that manifested over a nearly identical time course. Yet, how CRYABR123W promotes the HCM phenotype remains unclear. Here, we generated mice carrying the CryabR123W knock-in allele and demonstrated that hearts from these animals exhibit increased maximal elastance at young age but reduced diastolic function with aging. Upon transverse aortic constriction, mice carrying the CryabR123W allele developed pathogenic left ventricular hypertrophy with substantial cardiac fibrosis and progressively decreased ejection fraction. Crossing of mice with a Mybpc3 frame-shift model of HCM did not potentiate pathological hypertrophy in compound heterozygotes, indicating that the pathological mechanisms in the CryabR123W model are independent of the sarcomere. In contrast to another well-characterized CRYAB variant (R120G) which induced Desmin aggregation, no evidence of protein aggregation was observed in hearts expressing CRYABR123W despite its potent effect on driving cellular hypertrophy. Mechanistically, we uncovered an unexpected protein-protein interaction between CRYAB and calcineurin. Whereas CRYAB suppresses maladaptive calcium signaling in response to pressure-overload, the R123W mutation abolished this effect and instead drove pathologic NFAT activation. Thus, our data establish the CryabR123W allele as a novel genetic model of HCM and unveiled additional sarcomere-independent mechanisms of cardiac pathological hypertrophy

Characterization of regional left ventricular function in nonhuman primates using magnetic resonance imaging biomarkers: A test-retest repeatability and inter-subject variability study

10.1371/journal.pone.0127947PLoS ONE105e012794