Case Western Reserve University

About: Case Western Reserve University is a education organization based out in Cleveland, Ohio, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 54617 authors who have published 106568 publications receiving 5071613 citations. The organization is also known as: Case & Case Western.

Plasma-Engraved Co3 O4 Nanosheets with Oxygen Vacancies and High Surface Area for the Oxygen Evolution Reaction.

Abstract: Co3O4, which is of mixed valences Co2+ and Co3+, has been extensively investigated as an efficient electrocatalyst for the oxygen evolution reaction (OER). The proper control of Co2+/Co3+ ratio in Co3O4 could lead to modifications on its electronic and thus catalytic properties. Herein, we designed an efficient Co3O4-based OER electrocatalyst by a plasma-engraving strategy, which not only produced higher surface area, but also generated oxygen vacancies on Co3O4 surface with more Co2+ formed. The increased surface area ensures the Co3O4 has more sites for OER, and generated oxygen vacancies on Co3O4 surface improve the electronic conductivity and create more active defects for OER. Compared to pristine Co3O4, the engraved Co3O4 exhibits a much higher current density and a lower onset potential. The specific activity of the plasma-engraved Co3O4 nanosheets (0.055 mA cm−2BET at 1.6 V) is 10 times higher than that of pristine Co3O4, which is contributed by the surface oxygen vacancies.

The Genome of the African Trypanosome Trypanosoma brucei

Abstract: African trypanosomes cause human sleeping sickness and livestock trypanosomiasis in sub-Saharan Africa. We present the sequence and analysis of the 11 megabase-sized chromosomes of Trypanosoma brucei. The 26-megabase genome contains 9068 predicted genes, including ∼900 pseudogenes and ∼1700 T. brucei–specific genes. Large subtelomeric arrays contain an archive of 806 variant surface glycoprotein (VSG) genes used by the parasite to evade the mammalian immune system. Most VSG genes are pseudogenes, which may be used to generate expressed mosaic genes by ectopic recombination. Comparisons of the cytoskeleton and endocytic trafficking systems with those of humans and other eukaryotic organisms reveal major differences. A comparison of metabolic pathways encoded by the genomes of T. brucei, T. cruzi, and Leishmania major reveals the least overall metabolic capability in T. brucei and the greatest in L. major. Horizontal transfer of genes of bacterial origin has contributed to some of the metabolic differences in these parasites, and a number of novel potential drug targets have been identified.

Federal Funding for the Study of Antimicrobial Resistance in Nosocomial Pathogens: No ESKAPE

Abstract: The discovery of potent and safe antimicrobial agents is arguably the single greatest health care advance in history. The availability of these agents rapidly reduced the morbidity and mortality associated with a host of formerly fatal diseases. In addition, the confidence that infections could be prevented or treated by antibiotics allowed major leaps forward in the treatment of noninfectious diseases, including serious heart disease, cancers, and organ failure requiring transplants. Medical care, as we now know it, could not exist without the availability of effective antibiotics. The widespread use of antibiotics has been associated with what we now know to be the predictable emergence of resistance. Early confidence that infections would eventually be conquered has given way to a greater appreciation of the genetic flexibility of common human pathogens. Moreover, we have come to appreciate the role played by microorganisms in our homeostasis. Microorganisms are an intrinsic part of us, and we would do well to learn to live with them. Where we cannot live with them is in the hospital, because patients with compromised defenses are particularly vulnerable to bacterial diseases. Although many bacteria remain susceptible to most of our antimicrobial agents, a coterie has emerged that escape the lethal action of antibiotics. In hospitals in both the developed and the developing world, this small group Enterococcus faeciumy Staphylococcus aureusy Klebsiella pneumoniaey Acinetobacter baumanni, Pseudomonas aeruginosa, and Enterobacter species, hereafter referred to as "the ESKAPE bugs" is the same. The ESKAPE bugs are extraordinarily important, not only because they cause the lion's share of nosocomial infections but also because they represent paradigms of pathogenesis, transmission, and resistance. If we learn to control these microorganisms, our hospitals will be immeasurably safer, because the lessons learned could be applied to virtually any species that attempts to take their place. Unfortunately, the ESKAPE bugs are increasingly prevalent in our hospitals and increasingly resistant to many of our antimicrobial agents. In this issue of the Journal Peters et al. [ 1 ] detail the research agenda of the National Institute of Allergy and Infectious Diseases (NIAID) for antimicrobial resistance. As the primary federal agency for conducting and supporting medical research, the National Institutes of Health (NIH) is the standard-bearer for the federal government's commitment to health research. NIAID manages most, but certainly not all, of the work performed by the NIH in the areas of antimicrobial resistance and infectious diseases. As such, the NIAID agenda defines the weight of federal government efforts in the area of infectious diseases. One need look no further than the pivotal role played by NIAID in the enormous success of the AIDS research effort over the past 2 decades to understand the profound impact this institute's agenda can have on the growth and success of individual research areas. Peters et al. indicate that NIAID funding of antimicrobial research has grown considerably over the past decade, now totaling more than $800 million annually. In considering this very large number, it is important to realize that it represents NIAID's total commitment to all areas defined as being related to antimicrobial therapy. This category includes research on antibacterial, antifungal, antiparasitic, and antiviral therapies, whether related to the treatment of diseases or to their prevention through the use of vaccines. It is therefore difficult to get a firm grip on what level of support is devoted to antibacterial therapy and resistance, particularly in reference to the ESKAPE bugs. Regarding research specific to issues involving antimicrobial resistance, Peters Received 26 December 2007; accepted 3 January 2008; electronically published 7 March 2008. Potential conflicts of interest: none reported. Reprints or correspondence: Dr. Louis Rice, Medical Service 111(W), Louis Stokes Cleveland VA Medical Center. 10701 East Blvd.. Cleveland, OH 44106 (louis.rice@va.gov).

Mutations in a member of the ADAMTS gene family cause thrombotic thrombocytopenic purpura

Abstract: Thrombotic thrombocytopenic purpura (TTP) is a life-threatening systemic illness of abrupt onset and unknown cause. Proteolysis of the blood-clotting protein von Willebrand factor (VWF) observed in normal plasma is decreased in TTP patients. However, the identity of the responsible protease and its role in the pathophysiology of TTP remain unknown. We performed genome-wide linkage analysis in four pedigrees of humans with congenital TTP and mapped the responsible genetic locus to chromosome 9q34. A predicted gene in the identified interval corresponds to a segment of a much larger transcript, identifying a new member of the ADAMTS family of zinc metalloproteinase genes (ADAMTS13). Analysis of patients' genomic DNA identified 12 mutations in the ADAMTS13 gene, accounting for 14 of the 15 disease alleles studied. We show that deficiency of ADAMTS13 is the molecular mechanism responsible for TTP, and suggest that physiologic proteolysis of VWF and/or other ADAMTS13 substrates is required for normal vascular homeostasis.