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As more genomes are sequenced, the identification and characterization of the causes of heritable variation within a species will be increasingly important. It is demonstrated that allelic variation in any two isolates of a species can be scanned, mapped, and scored directly and efficiently without allele-specific polymerase chain reaction, without creating new strains or constructs, and without knowing the specific nature of the variation. A total of 3714 biallelic markers, spaced about every 3.5 kilobases, were identified by analyzing the patterns obtained when total genomic DNA from two different strains of yeast was hybridized to high-density oligonucleotide arrays. The markers were then used to simultaneously map a multidrug-resistance locus and four other loci with high resolution (11 to 64 kilobases).

The immunosuppressants cyclosporin A (CsA) and FK506 inhibit the protein phosphatase calcineurin and block T‐cell activation and transplant rejection. Calcineurin is conserved in microorganisms and plays a general role in stress survival. CsA and FK506 are toxic to several fungi, but the common human fungal pathogen Candida albicans is resistant. However, combination of either CsA or FK506 with the antifungal drug fluconazole that perturbs synthesis of the membrane lipid ergosterol results in potent, synergistic fungicidal activity. Here we show that the C.albicans FK506 binding protein FKBP12 homolog is required for FK506 synergistic action with fluconazole. A mutation in the calcineurin B regulatory subunit that confers dominant FK506 resistance ( CNB1‐1/CNB1 ) abolished FK506–fluconazole synergism. Candida albicans mutants lacking calcineurin B ( cnb1/cnb1 ) were found to be viable and markedly hypersensitive to fluconazole or membrane perturbation with SDS. FK506 was synergistic with fluconazole against azole‐resistant C.albicans mutants, against other Candida species, or when combined with different azoles. We propose that calcineurin is part of a membrane stress survival pathway that could be targeted for therapy.

Following 15 years of data collection, field studies, and modeling efforts, the State of Florida in 1987 legislatively mandated the South Florida Water Management District, a regional water management agency, to create and implement a plan to reduce average annual inputs of total phosphorus to Lake Okeechobee by 40 percent. One element of the resulting plan was the creation and implementation of a performance-based regulatory program that set phosphorus discharge limitations for all parcels of land equal to or greater than 1/2 acre in size in almost all of the 1,735,000 acres of the lake's 31 tributary drainage basins. Owners of non-complying parcels are required to take measures to bring the parcels into compliance. This regulatory program, coupled with concurrent cost-share incentive programs and ongoing research efforts, has resulted in a decrease in phosphorus concentrations from individual properties and at some tributary discharge locations to the lake. This effort demonstrates that where there is sufficient historical information, scientific application of state-of-the-art modeling techniques, a political will, and appropriate powers vested in the institutions to take and enforce actions, such programs can be implemented and have positive effects on reducing non-point source pollutants.

A PCR (polymerase chain reaction) assay was developed to distinguish isolates of the sclerotial mycoparasite Coniothyrium minitans. In particular, the assay uniquely identified isolate A69 which was of interest due to its potential as a biocontrol agent for the plant pathogen Sclerotinia sclerotiorum. Random amplification of polymorphic DNA (RAPD) was used to screen isolates of C. minitans for polymorphic products which distinguished A69 from other C. minitans isolates. A 1.4 kb A69-specific RAPD fragment was cloned and sequenced. The sequence was found to contain two tandemly repeated 114 bp units separated by a single base. Southern blot analysis of C. minitans DNA showed that the cloned fragment hybridized to multiple bands in all isolates indicating that it was a dispersed repetitive element. Novel PCR primers were designed from the sequences flanking the tandem repeats. These primers were used to develop a PCR assay which distinguished some isolates of C. minitans and uniquely identified isolate A69. This assay will be used to study the ecology of C. minitans in soil.

A panel of national experts was convened by the Infectious Diseases Society of America (IDSA) to update the 2005 guidelines for the treatment of skin and soft tissue infections (SSTIs). The panel's recommendations were developed to be concordant with the recently published IDSA guidelines for the treatment of methicillin-resistant Staphylococcus aureus infections. The focus of this guideline is the diagnosis and appropriate treatment of diverse SSTIs ranging from minor superficial infections to life-threatening infections such as necrotizing fasciitis. In addition, because of an increasing number of immunocompromised hosts worldwide, the guideline addresses the wide array of SSTIs that occur in this population. These guidelines emphasize the importance of clinical skills in promptly diagnosing SSTIs, identifying the pathogen, and administering effective treatments in a timely fashion.

A panel of national experts was convened by the Infectious Diseases Society of America (IDSA) to update the 2005 guidelines for the treatment of skin and soft tissue infections (SSTIs). The panel's recommendations were developed to be concordant with the recently published IDSA guidelines for the treatment of methicillin-resistant Staphylococcus aureus infections. The focus of this guideline is the diagnosis and appropriate treatment of diverse SSTIs ranging from minor superficial infections to life-threatening infections such as necrotizing fasciitis. In addition, because of an increasing number of immunocompromised hosts worldwide, the guideline addresses the wide array of SSTIs that occur in this population. These guidelines emphasize the importance of clinical skills in promptly diagnosing SSTIs, identifying the pathogen, and administering effective treatments in a timely fashion.

Soft-tissue infections are common, generally of mild to modest severity, and are easily treated with a variety of agents. An etiologic diagnosis of simple cellulitis is frequently difficult and generally unnecessary for patients with mild signs and symptoms of illness. Here, Stevens et al present details of a study on practice guidelines for the diagnosis and management of Skin and Soft-Tissue Infections.

Biosilicification (the formation of biological structures from silica) occurs in diverse eukaryotic lineages, plays a major role in global biogeochemical cycles, and has significant biotechnological applications. Silicon (Si) uptake is crucial for biosilicification, yet the evolutionary history of the transporters involved remains poorly known. Recent evidence suggests that the SIT family of Si transporters, initially identified in diatoms, may be widely distributed, with an extended family of related transporters (SIT-Ls) present in some nonsilicified organisms. Here, we identify SITs and SIT-Ls in a range of eukaryotes, including major silicified lineages (radiolarians and chrysophytes) and also bacterial SIT-Ls. Our evidence suggests that the symmetrical 10-transmembrane-domain SIT structure has independently evolved multiple times via duplication and fusion of 5-transmembrane-domain SIT-Ls. We also identify a second gene family, similar to the active Si transporter Lsi2, that is broadly distributed amongst siliceous and nonsiliceous eukaryotes. Our analyses resolve a distinct group of Lsi2-like genes, including plant and diatom Si-responsive genes, and sequences unique to siliceous sponges and choanoflagellates. The SIT/SIT-L and Lsi2 transporter families likely contribute to biosilicification in diverse lineages, indicating an ancient role for Si transport in eukaryotes. We propose that these Si transporters may have arisen initially to prevent Si toxicity in the high Si Precambrian oceans, with subsequent biologically induced reductions in Si concentrations of Phanerozoic seas leading to widespread losses of SIT, SIT-L, and Lsi2-like genes in diverse lineages. Thus, the origin and diversification of two independent Si transporter families both drove and were driven by ancient ocean Si levels.

Among patients with severe ischemic mitral regurgitation who were assigned to mitral-valve repair or replacement, there were no significant between-group differences in left ventricular remodeling or mortality at 2 years. Mitral regurgitation recurred more frequently in the repair group. Ischemic mitral regurgitation is a serious consequence of coronary artery disease that carries a substantial risk of death from cardiovascular causes in proportion to its severity. 1 , 2 Ischemic mitral regurgitation is anatomically characterized by remodeling or distortion of left ventricular geometry that ultimately results in papillary-muscle displacement, leaflet tethering, and impaired coaptation. For the subgroup of patients with severe ischemic mitral regurgitation, the prognosis is grave, with rates of death ranging from 15 to 40% at 1 year. 2 – 4 For patients with severe ischemic mitral regurgitation, the benefit of surgical revascularization is undisputed, provided that the patient has suitable coronary . . .