Acidogenic fermentation of blended food‐waste in combination with primary sludge for the production of volatile fatty acids

The performance of a laboratory‐scale anaerobic acidogenic fermenter fed with a mixture of blended kitchen food‐waste and primary sludge from a sewage treatment plant was investigated for the production of volatile fatty acids (VFA). The operating variables for acidogenic fermentation were kitchen food‐waste content (10 and 25 wt %), hydraulic retention time (HRT: 1, 3 and 5 days), temperature (ambient: 18 ± 2 °C, and mesophilic: 35 ± 2 °C) and pH (varied from 5.2 to 6.7). The experimental results indicated that effluent VFA concentrations and VFA production rates were higher at ambient temperature than at mesophilic conditions. The net amount of VFA with 10 wt % food‐waste increased up to 920 mg dm^?3 with an increase of HRT, but contrasting results (a decrease of 2610 mg dm^?3) were found due to the conversion of VFA into biogas in the case of 25 wt % food‐waste, which increased significantly at HRT of 3–5 days. In terms of biogas composition (CO₂ and CH₄), the organic matter was converted into CO₂ through the oxidative pathway by facultative species at low temperature while mesophilic temperature and optimum pH (6.3–7.8) played a pivotal role in increasing rate of conversion of VFA into biogas by methanogenesis. Rates of VFA production and their conversion are dependent on the food‐waste content in the mixture. Yet, the higher concentration of food‐waste (25% compared with 10%) did not produce VFA proportionally due to the increased rate of conversion of VFA into gaseous products. The maximum VFA production rate (0.318 g VFA_produced g^?1 VS_fed day^?1) was achieved in the 10 wt % food‐waste at ambient temperature and at a 5‐day HRT. Copyright © 2005 Society of Chemical Industry     

Stress analysis of a cantilevered fixed partial denture with normal and reduced bone support

A two-dimensional finite element model was constructed to analyze the simulated mechanical behavior of a cantilevered fixed partial denture. The variations of the models were made by altering the degree of bone support, the number of splinted abutments, and the length of the pontics. High stress concentrations were observed around the connectors of the fixed prosthesis and the tooth closest to the cantilever. Reduced bone support increased the deflection and stress concentrations. There was reduction in displacement and stress concentration when the teeth were splinted together. To improve the prognosis of the fixed partial denture cantilever, the number of abutments should be increased and the number of pontics decreased.     

Prolonged recovery of desiccated adenoviral serotypes 5, 8, and 19 from plastic and metal surfaces in vitro

BACKGROUND: Prevention of the spread of epidemic keratoconjunctivitis (EKC) at eye care facilities (doctors' offices, clinics, hospitals) has been a major public health goal for ophthalmology for more than 50 years. The authors explored a potentially contributing attribute of the adenovirus serotypes that cause EKC. Specifically, they investigated the capacity of different clinical and laboratory ocular serotypes (AD8, 19, and 5) to survive for extended periods of time in a desiccated state. METHODS: Twenty microliters containing 2000 plaque-forming units of different ATCC laboratory adenoviral ocular serotypes (AD8, 19, and 5) and clinical isolates (AD8 Cray, AD19 Kowalski, and AD5 McEwen) were inoculated onto 7-mm plastic disks and 6-mm aluminum foil disks and were allowed to completely desiccate. At weekly intervals up to 7 weeks, eight desiccated virus-inoculated plastic or metal disks per serotype were added to tissue culture medium, and the amount of recoverable virus was determined by plaque assay on A549 cells. RESULTS: Ocular adenoviral serotypes AD8, 19, and 5 could be recovered up to 49 days from plastic, and 35 to 49 days from metal. Sufficient virus concentrations (> 100 plaque-forming units/disk) to be clinically infectious were recovered up to 28 days. Differences in recovery among serotypes (AD19 > AD5, AD8) were demonstrated, but laboratory and clinical isolates of the same serotype were usually comparable. CONCLUSIONS: Ocular isolates of adenovirus that cause EKC are much harder than previously suspected, and the capacity to survive in a desiccated state may possibly play some role in office-based mini-epidemics of EKC.     

Monoclonal antibody-based competitive ELISA for simultaneous detection of rinderpest virus and peste des petits ruminants virus antibodies

An experimental competitive enzyme-linked immunosorbent assay (morbillivirus cELISA) using a recombinant N antigen (rRPV N) expressed in a baculovirus and a ruminant morbillivirus (RPV and PPRV)-specific monoclonal antibody (P-13A9) was developed for simultaneous detection of rinderpest virus (RPV) and peste des petits ruminants virus (PPRV) antibodies and its diagnostic performance was evaluated. A set of known reference antisera against RPV and PPRV belonging to different lineages, experimental sera from cattle vaccinated for a RPV of Asian lineage, and field sera from cattle and sheep/goat populations known to be positive (West Africa) and negative (Korea) for RPV and PPRV were used for the evaluation. Morbillivirus cELISA results on the panel of experimental RPV and PPRV antisera showed high correlation (r=0.97) between the whole virus and the rRPV N antigens, suggesting that the rRPV N contains a ruminant morbillivirus-specific antigenic determinant recognized by the P-13A9 and it may be suitable as an ELISA antigen in place of the whole virus. Morbillivirus cELISA detected anti-RPV and anti-PPRV antibodies in all reference RPV and PPRV antisera containing VN titers >/=1:8, suggesting that the assay can simultaneously detect antibodies against RPV and PPRV. Anti-RPV antibody was detected by morbillivirus cELISA in vaccinated cattle as early as the VNT and continued to be detectable by both the cELISA and the VNT until termination of the study. When applied to field samples from Africa, morbillivirus cELISA showed good agreement with a RP cELISA kit (kappa value of 0.86) in bovine sera and with a peste des petits ruminant cELISA kit (kappa value of 0.81) in caprine/ovine sera. Usefulness of morbillivirus cELISA using the rRPV N protein was discussed.     

Pulmonary vasoconstrictor effects of prostacyclin in rats: potential role of thromboxane receptors

Endogenous prostacyclin (PGI2; epoprostenol) is a potent endothelium-derived pulmonary vasodilator. However, the effects of exogenous PGI2 on isolated arteries could be either relaxant or contractile, depending on the species and organ studied. The present study investigated the distal pathways involved in the PGI2-induced contraction in rat intrapulmonary artery (PA) and relaxation in lamb PA. When vessels were precontracted with 30 mM K+, PGI2 (1 microM) induced relaxation in lamb PA but caused contraction in rat PA. Use of 30 mM K+, phenylephrine, serotonin, angiotensin II, or hypoxia to precontract the vessels did not alter the contractile effect of PGI2 in rat PA. Nevertheless, PGI2 produced a mild relaxation in rat PA precontracted by U-46619, a thromboxane A2 (TxA2)-receptor agonist, whereas the TxA2-receptor blocker SQ-29548 (0.1-0.5 microM) abolished the contractile response in rat PA. These data suggest that PGI2-induced contraction is mediated by activation of TxA2 receptors. The PGI2-induced modest relaxation in rat PA, which was only observed when TxA2 receptors were blocked by SQ-29548, suggests that the PGI2-mediated vasorelaxant pathway is diminished in these vessels. Simultaneous application of forskolin, an adenylate cyclase activator, and rolipram, a phosphodiesterase inhibitor, caused similar relaxation in both rat and lamb PA. This suggests that the adenosine 3',5'-cyclic monophosphate-dependent relaxing pathway is intact in rat PA and is comparable to that in lamb PA. On the basis of these data, we conclude that the pathways responsible for the paradoxical effects of PGI2 on rat and lamb PA are located upstream of the adenosine 3',5'-cyclic monophosphate-dependent relaxing pathway and that a paucity of PGI2 receptors in rat PA may be responsible.     

Cross-specialty linkage and extrapolation of resource-based relative value scales

We used the fluorescent labelled dopamine D1-receptor antagonist Bodipy-SCH 23390 for the cellular localization of D1-ligand binding sites in the retinae of different vertebrates (teleosts, Xenopus, turtle, rat and rabbit). Competition experiments with unfixed cryosections of fish retina were performed to characterize the binding conditions of Bodipy-labelled SCH 23390. Tissue bound [3H]SCH 23390 was displaceable with increased amounts of bodipy-SCH 23390. The pharmacological specificity of the D1 fluorescent antagonist was determined by competition experiments with an excess of unlabelled SCH 23390. This treatment significantly reduced the level of fluorescence of the retina confirming the specificity of the binding. We observed a homogeneously distributed fluorescence signal in both plexiform layers in unfixed cryosections of fish, frog, turtle, rat and rabbit. Similar staining intensities of both plexiform layers were found in frog, turtle, rat and rabbit retina. In teleosts, the label of the outer plexiform layer was markedly more intense. Non-specific label was associated with photoreceptor outer and inner segments. The specific labelling of both plexiform layers indicates a mismatch of dopamine releasing and D1-binding sites, and suggests a possible extrasynaptic localization of the D1-receptor. The physiological significance of the observed distribution of D1-ligand binding sites is discussed with respect to the role of dopamine in controlling adaptational processes in the retina.     

In vitro triggering of somatic mutation in human naive B cells

During T cell-dependent immune response, germinal center B cells accumulate somatic mutations in their Ig V(D)J genes and give rise to affinity-selected B cells. We tested several culture conditions for triggering somatic mutation in human tonsillar naive slgD+CD23+ cells after cross-linking their membrane Igs. CD40 activation, in the presence of exogenous cytokines (IL-2, IL-4, and IL-10), induced proliferation and isotype switch without somatic mutation. In contrast, after coculture with anti-CD3-activated cloned T cells, somatic mutation accumulated in a fraction of naive B cells. Mutations included shared as well as independent events in clonally related sequences, allowing reconstitution of genealogic trees generated in vitro. Naive tonsillar B cells sorted for slgD expression can be induced to mutate their Ig V(H) gene upon coculture with activated T cells, thereby providing a model to study somatic hypermutation in vitro.