University of Maryland Biotechnology Institute

About: University of Maryland Biotechnology Institute is a based out in . It is known for research contribution in the topics: Gene & Population. The organization has 1565 authors who have published 2458 publications receiving 171434 citations. The organization is also known as: UMBI.

Synthesis and characterization of human alpha-defensins 4-6.

Abstract: Human alpha-defensins are small, Cys-rich, cationic proteins expressed predominantly in neutrophils and intestinal epithelia. They play important roles in innate and adaptive immunity against infection. Progress in studying these molecules can be accelerated by access to large quantities of high-quality materials, which have been obtained mainly from natural sources. Here, we report total synthesis of human alpha-defensins 4, 5, and 6, also known as HNP4, HD5, and HD6, using the optimized N,N-diisopropylethylamine (DIEA) in situ neutralization/2-(1 H-benzotriazolyl)-1,1,3,3-tetramethyluroniumhexafluorophosphate (HBTU) activation protocol for solid-phase Boc chemistry. Oxidative folding/disulfide formation was achieved directly using crude peptides, resulting in an overall synthetic yield of 10-16% with high purity. Antimicrobial activity assays were performed with Escherichia coli ATCC 25922 and Staphylococcus aureus ATCC 29213, using colony-counting methods, and the results demonstrated differential activity against these strains. Our report describes a highly efficient synthetic approach that enables thorough structural and functional studies of these three important immunologic molecules.

The Ca2+ leak paradox and “rogue ryanodine receptors”: SR Ca2+ efflux theory and practice

Abstract: Ca 2+ efflux from the sarcoplasmic reticulum (SR) is routed primarily through SR Ca 2+ release channels (ryanodine receptors, RyRs). When clusters of RyRs are activated by trigger Ca 2+ influx through L-type Ca 2+ channels (dihydropyridine receptors, DHPR), Ca 2+ sparks are observed. Close spatial coupling between DHPRs and RyR clusters and the relative insensitivity of RyRs to be triggered by Ca 2+ together ensure the stability of this positive-feedback system of Ca 2+ amplification. Despite evidence from single channel RyR gating experiments that phosphorylation of RyRs by protein kinase A (PKA) or calcium-calmodulin dependent protein kinase II (CAMK II) causes an increase in the sensitivity of the RyR to be triggered by [Ca 2+ ] i there is little clear evidence to date showing an increase in Ca 2+ spark rate. Indeed, there is some evidence that the SR Ca 2+ content may be decreased in hyperadrenergic disease states. The question is whether or not these observations are compatible with each other and with the development of arrhythmogenic extrasystoles that can occur under these conditions. Furthermore, the appearance of an increase in the SR Ca 2+ “leak” under these conditions is perplexing. These and related complexities are analyzed and discussed in this report. Using simple mathematical modeling discussed in the context of recent experimental findings, a possible resolution to this paradox is proposed. The resolution depends upon two features of SR function that have not been confirmed directly but are broadly consistent with several lines of indirect evidence: (1) the existence of unclustered or “rogue” RyRs that may respond differently to local [Ca 2+ ] i in diastole and during the [Ca 2+ ] i transient; and (2) a decrease in cooperative or coupled gating between clustered RyRs in response to physiologic phosphorylation or hyper-phosphorylation of RyRs in disease states such as heart failure. Taken together, these two features may provide a framework that allows for an improved understanding of cardiac Ca 2+ signaling.

Sequential Reductive Dechlorination of meta-Chlorinated Polychlorinated Biphenyl Congeners in Sediment Microcosms by Two Different Chloroflexi Phylotypes

Abstract: Three species within a deeply branching cluster of the Chloroflexi are the only microorganisms currently known to anaerobically transform polychlorinated biphenyls (PCBs) by the mechanism of reductive dechlorination. A selective PCR primer set was designed that amplifies the 16S rRNA genes of a monophyletic group within the Chloroflexi including Dehalococcoides spp. and the o-17/DF-1 group. Assays for both qualitative and quantitative analyses by denaturing gradient gel electrophoresis and most probable number-PCR, respectively, were developed to assess sediment microcosm enrichments that reductively dechlorinated PCBs 101 (2,2′,4,5,5′-CB) and 132 (2,2′,3,3′,4,6′-CB). PCB 101 was reductively dechlorinated at the para-flanked meta position to PCB 49 (2,2′,4,5′-CB) by phylotype DEH10, which belongs to the Dehalococcoides group. This same species reductively dechlorinated the para- and ortho-flanked meta-chlorine of PCB 132 to PCB 91 (2,2′,3′,4,6′-CB). However, another phylotype designated SF1, which is more closely related to the o-17/DF-1 group, was responsible for the subsequent dechlorination of PCB 91 to PCB 51 (2,2′,4,6′-CB). Using the selective primer set, an increase in 16S rRNA gene copies was observed only with actively dechlorinating cultures, indicating that PCB-dechlorinating activities by both phylotype DEH10 and SF1 were linked to growth. The results suggest that individual species within the Chloroflexi exhibit a limited range of congener specificities and that a relatively diverse community of species within a deeply branching group of Chloroflexi with complementary congener specificities is likely required for the reductive dechlorination of different PCBs congeners in the environment.

Steroid regulation of programmed cell death during Drosophila development

Abstract: Steroid hormones play an important role in the regulation of numerous physiological responses, but the mechanisms that enable these systemic signals to trigger specific cell changes remain poorly characterized. Recent studies of Drosophila illustrate several important features of steroid-regulated programmed cell death. A single steroid hormone activates both cell differentiation and cell death in different tissues and at multiple stages during development. While several steroid-regulated genes are required for cell execution, most of these genes function in both cell differentiation and cell death, and require more specific factors to kill cells. Genes that regulate apoptosis during Drosophila embryogenesis are induced by steroids in dying cells later in development. These apoptosis genes likely function downstream of hormone-induced factors to serve a more direct role in the death response. This article reviews the current knowledge of steroid signaling and the regulation of programmed cell death during development of Drosophila. Cell Death and Differentiation (2000) 7, 1057–1062

Microbial diversity : the importance of exploration and conservation

Abstract: Microbial diversity is fundamental to maintenance and conservation of global genetic resources. As extreme environments are explored, the richness of microbial diversity is increasingly evident. Measures must be taken to estimate, record, and conserve microbial diversity, not only to sustain human health but also to enrich the human condition globally through wise use and conservation of genetic resources of the microbial world.