The mismatch of narratives and local ecologies in the everyday governance of water access and mosquito control in an urbanizing community.

Mosquito-borne disease presents a significant threat to urban populations, but risk can be uneven across a city due to underlying environmental patterns. Urban residents rely on social and economic processes to control the environment and mediate disease risk, a phenomenon known as everyday governance. We studied how households employed everyday governance of urban infrastructure relevant to mosquito-borne disease in Bengaluru, India to examine if and how inequalities in everyday governance manifest in differences in mosquito control. We found that governance mechanisms differed for water access and mosquitoes. Economic and social capital served different roles for each, influenced by global narratives of water and vector control.

Recovery from Mosaic Caused by Sorghum Mosaic Virus in Sugarcane and Impact on Yield.

Mosaic is a historically important viral disease of sugarcane in Louisiana caused by Sugarcane mosaic virus and, currently, by Sorghum mosaic virus (SrMV). Sugarcane clones can have variable responses to mosaic for different traits, including susceptibility to infection and yield loss. Disease incidence and rate of increase within a multiple-year crop cycle is affected by susceptibility and other epidemiological factors, possibly including recovery from symptom expression and virus infection. Recovery (defined as the emergence of asymptomatic plants from buds on planted symptomatic stalks) and the impact of mosaic on yield components were evaluated in two sugarcane cultivars, HoCP 09-804 and L 10-147. Recovery varied between the two cultivars. Across two experiments, L 10-147 had a higher frequency of recovery (range 9.4 to 19.8%) than HoCP 09-804 (range 0.9 to 2.3%). A reverse-transcription PCR assay did not detect SrMV in 96.5% of 143 L 10-147 leaf samples and 83.3% of 6 HoCP 09-804 leaf samples collected from recovered plants. When comparing symptomatic and asymptomatic plantings, mosaic reduced cane and sucrose yield in HoCP 09-804 but not L 10-147, suggesting a possible association between recovery and tolerance to virus infection.

Sugarcane Mosaic Distribution, Incidence, Increase, and Spatial Pattern in Louisiana.

Sugarcane mosaic is a historically important disease in Louisiana currently caused by sorghum mosaic virus (SrMV). Successful breeding for resistance reduced the disease to low incidence in commercial cultivars. However, mosaic was detected in experimental clone evaluations at multiple locations, leading to uncertainty concerning the current distribution and incidence in the state. Field surveys were conducted from 2016 to 2018 in breeding program yield trials and experimental clone seed cane increase fields. Mosaic symptomatic plants were observed in a newly released cultivar, HoCP 09-804, in three of five production areas, with incidences ranging from 0 to 10%. Mosaic also was observed in nine additional experimental clones. Single leaf samples were tested for SrMV using reverse transcription PCR. All symptomatic samples and a low percentage (0.3%) of asymptomatic samples tested positive for SrMV, confirming that it continues to be the causal species. Runs analysis detected aggregation of infected plants within at least 70% of rows in 94% of surveyed fields. The spatial pattern and geographical distribution of disease incidence suggested that infected seed cane was the source of the disease. Surveys conducted in the same fields of HoCP 09-804 through two subsequent crops detected disease incidence increases in some fields and decreases in the others in first ratoon, but observed incidence was lower compared with plant cane in all fields in second ratoon. The results indicated that disease increase owing to aphid transmission did not occur under the prevailing conditions.

PTTG1 Levels Are Predictive of Saracatinib Sensitivity in Ovarian Cancer Cell Lines.

Src kinase is recognized as a key target for molecular cancer therapy. However, methods to efficiently select patients responsive to Src inhibitors are lacking. We explored the sensitivity of ovarian cancer cell lines to the Src kinase inhibitor saracatinib to identify predictive markers of drug sensitivity using gene microarrays. Pituitary tumor transforming gene 1 (PTTG1) was selected as a potential biomarker as mRNA levels were correlated with saracatinib resistance, as well as higher PTTG1 protein expression. PTTG1 expression was correlated with proliferation, cell division, and mitosis in ovarian cancer tissues data sets. In sensitive cell lines, saracatinib treatment decreased PTTG1 and fibroblast growth factor 2 (FGF2) protein levels. Downregulating PTTG1 by siRNAs increased saracatinib sensitivity in two resistant cell lines. Our results indicate PTTG1 may be a valuable biomarker in ovarian cancer to predict sensitivity to saracatinib, and could form the basis of a targeted prospective saracatinib trial for ovarian cancer.

Surface phagocytosis and host defence in the peritoneal cavity during continuous ambulatory peritoneal dialysis.

Since patients on continuous ambulatory peritoneal dialysis are at high risk for peritonitis, the opsonins in peritoneal dialysis effluent responsible for phagocytosis and a neutrophil chemiluminescence response to surface-adherent Staphylococcus epidermidis were examined. In surface phagocytosis assays uninfected dialysate was as opsonic as 1% serum. The opsonic activity was heat stable and equal to that of purified IgG at the same concentration (0.1 mg/ml). In contrast, optimal chemiluminescence to surface-adherent Staphylococcus epidermidis was dependent on complement. C3 deposition on Staphylococcus epidermidis opsonized in dialysate was quantitated by an enzyme immunoassay (EIA) and represented 13% of control C3 deposited with opsonization in 10% serum. Unused dialysate was found to be inhibitory to neutrophil phagocytosis and complement deposition. A combination of the low pH and high dextrose concentration of dialysate was responsible, but restoration of the pH to 7.4 largely restored both indices. During peritonitis there was a parallel increase in IgG levels and C3 deposition (r = 0.8), and surface phagocytosis was also enhanced. On further analysis, subjects with a single episode of peritonitis had a significantly more opsonic peritoneal effluent than those who had two infections during the study. This latter group had a poor IgG response to infection. This study demonstrates the relative deficiencies of host defence in the peritoneal cavity and indicates that measures to improve opsonin delivery and reduce the inhibitory effects of dialysate would be beneficial.

Surface phagocytosis of Staphylococcus epidermidis and Escherichia coli by human neutrophils: serum requirements for opsonization and chemiluminescence.

We examined the serum requirements for surface phagocytosis of Staphylococcus epidermidis and Escherichia coli and for the subsequent chemiluminescent response of human neutrophils. Substantial surface phagocytosis of S. epidermidis occurred in the absence of opsonins, although the presence of 10% pooled or heat-inactivated serum significantly increased phagocytosis. There was no significant difference between these opsonins, indicating that surface phagocytosis of S. epidermidis did not require complement. Unopsonized E. coli were not as readily phagocytized as S. epidermidis (33% versus 57%). In contrast to S. epidermidis optimal phagocytosis of E. coli required complement as 10% heat inactivated donor serum (HHS) was significantly less effective as an opsonin than 10% pooled healthy donor serum (PHS). The time kinetics for phagocytosis of each organism were similar, with most of the phagocytosis occurring in the first 10 min. The chemiluminescent response of neutrophils produced discrepant results. Maximal chemiluminescence was observed when neutrophils were stimulated with bacteria opsonized in PHS. The response to HHS-opsonized bacteria was less, and chemiluminescence to unopsonized bacteria was only marginally higher than the control, even though there was relatively good phagocytosis. These results define the opsonic requirements for surface phagocytosis of S. epidermidis and E. coli and indicate that although complement may not be required for phagocytosis, it is necessary for generation of a maximal oxidative burst, and thus may be essential for efficient intracellular killing.

Regulation of human neutrophil type 3 complement receptor (iC3b receptor) expression during phagocytosis of Staphylococcus aureus and Escherichia coli.

Human neutrophils (PMN) express a receptor for iC3b, a cleavage product of C3b. CR3 is an important receptor for phagocytosis of opsonized bacteria and its expression is enhanced by cell activation. We examined PMN CR3 expression during phagocytosis using flow cytometry and a CR3-specific monoclonal antibody. After 30 min phagocytosis of opsonized S. aureus and E. coli, CR3 expression increased to 151% and 221% of controls, respectively. Unopsonized S. aureus had no effect on CR3; however, unopsonized E. coli enhanced CR3 expression despite not being phagocytosed. Time-kinetic studies indicated a rapid initial fall in CR3 after addition of bacteria to PMN, followed by enhanced expression within 5-10 min. The initial fall in CR3 probably represented CR3 internalization rather than receptor destruction, as superoxide dismutase, catalase and protease inhibitors had no effect on this. Correlation of CR3 expression with the PMN oxidative response, measured with the intracellular fluorescent probe DCF-DA, demonstrated a dichotomy. Opsonized S. aureus and E. coli caused an oxidative response from PMN but unopsonized E. coli, which caused significant CR3 up-regulation, did not. CR3 up-regulation with unopsonized and opsonized E. coli was markedly inhibited by Polymyxin B, suggesting a role for endotoxin. These experiments indicate that CR3 expression can be regulated during phagocytosis, and the mechanisms responsible are distinct from those involved in the oxidative burst. CR3 up-regulation following exposure to bacteria in vivo may enhance neutrophil function at sites of infection.

Opsonin-dependent and independent surface phagocytosis of S. aureus proceeds independently of complement and complement receptors.

We examined the mechanism of surface phagocytosis of Staphylococcus aureus by human polymorphonuclear leucocytes (PMN). Surface phagocytosis of unopsonized bacteria occurred, but was significantly enhanced by the presence of serum. The serum requirement was low, and a maximal effect occurred with serum concentrations of 0.25-0.5%. The opsonic effect of serum was not removed by heat inactivation of complement but was adsorbed, at low serum concentrations, by protein A, indicating that opsonin-dependent surface phagocytosis requires IgG but not C3. The requirement of opsonin-dependent surface phagocytosis for IgG was demonstrated further with purified IgG preparations as the sole opsonin. Activation of PMN by N-formyl-methionyl-leucyl-phenylalanine (FMLP) or phorbol myristate acetate (PMA) increased opsonin-independent surface phagocytosis by 47% and 66%, respectively, but had no effect on opsonin-dependent surface phagocytosis. Blockade of the PMN iC3b receptor (CR3), which has lectin-like properties, by a panel of monoclonal antibodies against the alpha- and beta-chains of CR3 did not inhibit the surface phagocytosis of opsonized or unopsonized S. aureus, and one antibody (NIMP-R10) enhanced opsonin-independent surface phagocytosis. These results indicate that the mechanism of surface phagocytosis is quite different to that observed in suspension assays. Opsonin-independent surface phagocytosis occurs and is enhanced by PMN activation, opsonin-dependent surface phagocytosis is dependent on IgG and not complement, and neither opsonin-independent nor -dependent surface phagocytosis proceeds through CR3.

Infection in experimental arthroplasties.

Experimental bacterial infection following implant arthroplasties was investigated in rabbits. Bone cement and a stainless steel head and stem prosthesis were inserted after reaming of the femoral neck and shaft. Measured doses of Staphylococcus aureus were injected either into the femoral medullary cavity or intravenously. Intravenous challenge required high inocula to establish arthroplasty infection, whereas infection around the prosthesis was consistently established after inoculation of 10(3) bacteria into the femoral medulla. The erythrocyte sedimentation rate (ESR) proved the most reliable clinical test of infection. Hematogenous infection was difficult to reproduce. Three weeks after operation, the arthroplasty was as resistant as the normal hip. Antibiotics were administered in doses equivalent to doses used in the treatment of infections in humans. When gentamicin-impregnated cement was used, 60 times the number of organisms were required to establish infection. Flucloxacillin and Imipenem gave similar protection. Rifampicin gave protection to a level exceeding the lethal dose of organisms for the model.

Infection in experimental hip arthroplasties.

The relationship between the route of inoculation, the dose of inoculum and the development of infection after prosthetic replacement has been determined in an animal model. The rabbit hip served as the model and a Staphylococcus aureus isolated from an infected human hip arthroplasty was introduced using different protocols. The 50% infective dose (ID50) was determined for comparative purposes. Contamination of the wound site with only a few bacteria was likely to result in infection. It was considerably more difficult to induce infection when the operation was performed without inserting the prosthesis, which suggests that the implant inhibits the body's mechanism for dealing with the insult. It was difficult to produce infection by inoculating the organisms into the bloodstream: if this inoculation was delayed till three weeks after operation the animals were often grossly septicaemic by the time the arthroplasty was infected. The results emphasise the importance of minimising intra-operative contamination and the efficacy of antibiotic cover.