Diversity of oxygenase genes from Methane- and Ammonia-oxidizing bacteria in the Eastern Snake River Plain aquifier

PCR amplification, restriction fragment length polymorphism, and phylogenetic analysis of oxygenase genes were used for the characterization of in situ methane- and ammonia-oxidizing bacteria from free-living and attached communities in the Eastern Snake River Plain aquifer. The following three methane monooxygenase (MMO) PCR primer sets were used: A189-A682, which amplifies an internal region of both the pmoA gene of the MMO particulate form and the amoA gene of ammonia monooxygenase; A189-mb661, which specifically targets the pmoA gene; and mmoXA-mmoXB, which amplifies the mmoX gene of the MMO soluble form (sMMO). Whole-genome amplification (WGA) was used to amplify metagenomic DNA from each community to assess its applicability for generating unbiased metagenomic template DNA. The majority of sequences in each archive were related to oxygenases of type II-like methanotrophs of the genus Methylocystis. A small subset of type I sequences found only in free-living communities possessed oxygenase genes that grouped nearest to Methylobacter and Methylomonas spp. Sequences similar to that of the amoA gene associated with ammoniaoxidizing bacteria (AOB) most closely matched a sequence from the uncultured bacterium BS870 but showed no substantial alignment to known cultured AOB. Based on these functional gene analyses, bacteria related to the type II methanotroph Methylocystis sp. were found to dominate both free-living and attached communities. Metagenomic DNA amplified by WGA showed characteristics similar to those of unamplified samples. Overall, numerous sMMO-like gene sequences that have been previously associated with high rates of trichloroethylene cometabolism were observed in both free-living and attached communities in this basaltic aquifer.Copyrighted by American Society for Microbiology

Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008

SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Diversity of Oxygenase Genes from Methane- and Ammonia-Oxidizing Bacteria in the Eastern Snake River Plain Aquifer

PCR amplification, restriction fragment length polymorphism, and phylogenetic analysis of oxygenase genes were used for the characterization of in situ methane- and ammonia-oxidizing bacteria from free-living and attached communities in the Eastern Snake River Plain aquifer. The following three methane monooxygenase (MMO) PCR primer sets were used: A189-A682, which amplifies an internal region of both the pmoA gene of the MMO particulate form and the amoA gene of ammonia monooxygenase; A189-mb661, which specifically targets the pmoA gene; and mmoXA-mmoXB, which amplifies the mmoX gene of the MMO soluble form (sMMO). Whole-genome amplification (WGA) was used to amplify metagenomic DNA from each community to assess its applicability for generating unbiased metagenomic template DNA. The majority of sequences in each archive were related to oxygenases of type II-like methanotrophs of the genus Methylocystis. A small subset of type I sequences found only in free-living communities possessed oxygenase genes that grouped nearest to Methylobacter and Methylomonas spp. Sequences similar to that of the amoA gene associated with ammonia-oxidizing bacteria (AOB) most closely matched a sequence from the uncultured bacterium BS870 but showed no substantial alignment to known cultured AOB. Based on these functional gene analyses, bacteria related to the type II methanotroph Methylocystis sp. were found to dominate both free-living and attached communities. Metagenomic DNA amplified by WGA showed characteristics similar to those of unamplified samples. Overall, numerous sMMO-like gene sequences that have been previously associated with high rates of trichloroethylene cometabolism were observed in both free-living and attached communities in this basaltic aquifer

Moisture-Associated Skin Damage: Overview and Pathophysiology

Moisture-associated skin damage (MASD) is caused by prolonged exposure to various sources of moisture, including urine or stool, perspiration, wound exudate, mucus, saliva, and their contents. MASD is characterized by inflammation of the skin, occurring with or without erosion or secondary cutaneous infection. Multiple conditions may result in MASD; 4 of the most common forms are incontinence-associated dermatitis, intertriginous dermatitis, periwound moisture-associated dermatitis, and peristomal moisture-associated dermatitis. Although evidence is lacking, clinical experience suggests that MASD requires more than moisture alone. Instead, skin damage is attributable to multiple factors, including chemical irritants within the moisture source, its pH, mechanical factors such as friction, and associated microorganisms. To prevent MASD, clinicians need to be vigilant both in maintaining optimal skin conditions and in diagnosing and treating minor cases of MASD prior to progression and skin breakdown

MASD Part 2: Incontinence-Associated Dermatitis and Intertriginous Dermatitis: A Consensus

A consensus panel was convened to review current knowledge of moisture-associated skin damage (MASD) and to provide recommendations for prevention and management. This article provides a summary of the discussion and the recommendations in regards to 2 types of MASD: incontinence-associated dermatitis (IAD) and intertriginous dermatitis (ITD). A focused history and physical assessment are essential for diagnosing IAD or ITD and distinguishing these forms of skin damage from other types of skin damage. Panel members recommend cleansing, moisturizing, and applying a skin protectant to skin affected by IAD and to the perineal skin of persons with urinary or fecal incontinence deemed at risk for IAD. Prevention and treatment of ITD includes measures to ensure that skin folds are dry and free from friction; however, panel members do not recommend use of bed linens, paper towels, or dressings for separating skin folds. Individuals with ITD are at risk for fungal and bacterial infections and these infections should be treated appropriately; for example, candidal infections should be treated with antifungal therapies

MASD Part 3: Peristomal Moisture-Associated Dermatitis and Periwound Moisture-Associated Dermatitis: A Consensus

Moisture-associated skin damage (MASD) occurs when excessive moisture in urine, stool, and wound exudate leads to inflammation of the skin, with or without erosion or secondary cutaneous infection. This article, produced by a panel of clinical experts who met to discuss moisture as an etiologic factor in skin damage, focuses on peristomal moisture-associated dermatitis and periwound moisture-associated dermatitis. The principles outlined here address assessment, prevention, and treatment of MASD affecting the peristomal or periwound skin

Disrupted Circadian Rhythms in a Mouse Model of Schizophrenia

Sleep and circadian rhythm disruption has been widely observed in neuropsychiatric disorders including schizophrenia [1] and often precedes related symptoms [2]. However, mechanistic basis for this association remains unknown. Therefore, we investigated the circadian phenotype of blind-drunk (Bdr), a mouse model of synaptosomal-associated protein (Snap)-25 exocytotic disruption that displays schizophrenic endophenotypes modulated by prenatal factors and reversible by antipsychotic treatment [3, 4]. Notably, SNAP-25 has been implicated in schizophrenia from genetic [5–8], pathological [9–13], and functional studies [14–16]. We show here that the rest and activity rhythms of Bdr mice are phase advanced and fragmented under a light/dark cycle, reminiscent of the disturbed sleep patterns observed in schizophrenia. Retinal inputs appear normal in mutants, and clock gene rhythms within the suprachiasmatic nucleus (SCN) are normally phased both in vitro and in vivo. However, the 24 hr rhythms of arginine vasopressin within the SCN and plasma corticosterone are both markedly phase advanced in Bdr mice. We suggest that the Bdr circadian phenotype arises from a disruption of synaptic connectivity within the SCN that alters critical output signals. Collectively, our data provide a link between disruption of circadian activity cycles and synaptic dysfunction in a model of neuropsychiatric disease