Modification of the third phase in the framework for vertebrate species persistence in urban mosaic environments.

Urbanisation is rapidly transforming natural landscapes with consequences for biodiversity. Little is documented on the response of African wildlife to urbanisation. We reviewed case studies of vertebrate species' responses to urbanisation in KwaZulu-Natal, South Africa to determine trends. Connected habitat mosaics of natural and anthropogenic green spaces are critical for urban wildlife persistence. We present a novel modification to the final of three phases of the framework described by Evans et al. (2010), which documents this sequence for vertebrate species persistence, based on the perspective of our research. Species in suburbia exhibit an initial phase where behavioural and ecological flexibility, life-history traits and phenotypic plasticity either contribute to their success, or they stay at low numbers. Where successful, the next phase is a rapid increase in populations and distribution; anthropogenic food resources and alternate breeding sites are effectively exploited. The modified third phase either continues to spread, plateau or decline.

Salmeterol, a Long-Acting ß2-Adrenergic Receptor Agonist, Inhibits Macrophage Activation by Lipopolysaccharide From Porphyromonas gingivalis.

BACKGROUND: Salmeterol is a long-acting ß2-adrenergic receptor agonist used to treat chronic obstructive pulmonary disease. The authors of the current study previously showed that preincubation of primary microglial-enriched cells with salmeterol could inhibit the inflammatory response induced by Escherichia coli lipopolysaccharide (LPS), a Toll-like receptor (TLR)-4 agonist. In this study, the authors sought to determine if salmeterol had a similar inhibitory effect on the inflammatory response of the murine macrophage cell line RAW264.7 and human monocyte THP-1 to LPS from Porphyromonas gingivalis (PgLPS), an oral microbe implicated in the pathogenesis of periodontal disease. METHODS: RAW264.7 and THP-1 cells were pretreated with salmeterol, followed by PgLPS, and monitored for production of inflammatory mediators by enzyme-linked immunosorbent assay. The nitric oxide concentration and nuclear factor-kappa B (NF-κB) activity were measured by Griess method and secretory alkaline phosphatase reporter activity assay, respectively. Reverse-transcriptase polymerase chain reaction and immunoblot analysis were used to measure messenger RNA and protein levels. Nuclear translocation of NF-κB was detected by immunofluorescence. RESULTS: Pretreatment with salmeterol significantly inhibited production of proinflammatory mediators by RAW264.7 and THP-1 cells. Salmeterol downregulated PgLPS-mediated phosphorylation of the extracellular signal-regulated kinase 1/2 and c-Jun N-terminal kinase but not p38 mitogen-activated protein kinases (MAPKs). Salmeterol also attenuated activation of NF-κB via inhibition of nuclear translocation of p65-NFκB, the transcriptional activity of NF-κB and IκBα phosphorylation. CONCLUSION: Salmeterol can significantly inhibit activation of macrophage-mediated inflammation by PgLPS, suggesting that use of salmeterol may be an effective treatment in inhibiting or lessening the inflammatory response mediated through TLR pathway activation.

Recent Canadian experience with targeted hepatitis C virus lookback.

BACKGROUND: Targeted hepatitis C virus (HCV) lookback studies have been performed in Canada since 1995. The yield of HCV lookback has not been reassessed since the introduction of improved HCV screening tests. STUDY DESIGN AND METHODS: Data were combined from the two Canadian blood suppliers to determine the yield of targeted HCV lookback performed on donors found to be HCV-positive by antibody screening and/or nucleic acid testing (NAT) from the introduction of NAT in 1999 until January 1, 2005. RESULTS: Lookback was performed on 498 donations from 176 HCV-seropositive and two NAT-only-positive donors; 494 components had been transfused, and 160 components were traced to living recipients who underwent HCV testing. Seventy-two percent of recipients of components derived from donations given before the introduction of second-generation enzyme immunoassay (EIA) testing were HCV-seropositive. Four recipients of components derived from donations tested by second- or third-generation EIA, with or without NAT, were HCV-seropositive. Two of these recipients tested HCV-seropositive before transfusion, and a third was probably infected by transfusions before the introduction of HCV testing. The fourth recipient likely received a noninfectious transfusion, since five other recipients of components from subsequent donations made by this donor were seronegative. CONCLUSION: When previous donations had been tested by second- or third-generation EIA, the yield of HCV lookback was likely zero. Because HCV infection is relatively common in the general population and patients in Canada do not undergo pretransfusion testing, coincident infections in recipients may be erroneously attributed to transfusion. The regulatory requirement for HCV lookback should be reassessed.