Valorization of cow manure via hydrothermal carbonization for phosphorus recovery and adsorbents for water treatment.

The increased quantities of manure being generated by livestock and their extensive agronomic use have raised concerns around run-off impacting soil and groundwater quality. Manure contains valuable nutrients (especially phosphorus) that are critical to agriculture, but when directly land-applied the run-off of such nutrients contributes to eutrophication of waterways. This study investigates the hydrothermal carbonization of cow manure at two industrially feasible process extremes: 190 °C, 1 h and 230 °C, 3 h, to concentrate and then recover phosphorus from the solid hydrochar via acid leaching and precipitation. Up to 98 wt% of phosphorus initially present in the hydrochar (88% in the raw manure) can be recovered, with the dominant crystalline species being hydroxyapatite. Acid leached hydrochars were subsequently pyrolyzed at 600 °C for 30 min, and then evaluated as adsorbent materials for water remediation by using methylene blue as a model adsorbate. Although pyrolyzed hydrochars have surface areas an order of magnitude higher (160-236 m2/g) than the non-pyrolyzed acid leached hydrochars (11-23 m2/g), their adsorption capacity is three times lower. Furthermore, while the higher carbonization temperature leads to greater recovery of phosphorus, it likewise leads to higher heavy metal concentrations in the precipitate (ranging from 0.1 to 100 mgmetal/gppt). As such, lower temperature carbonization followed by acid-extraction - without further solid processing - is a potential pathway to recover phosphorus and adsorbent materials.

Expansion of cytotoxic tissue-resident CD8+ T cells and CCR6+CD161+ CD4+ T cells in the nasal mucosa following mRNA COVID-19 vaccination.

Vaccines against SARS-CoV-2 have shown high efficacy in clinical trials, yet a full immunologic characterization of these vaccines, particularly within the human upper respiratory tract, is less well known. Here, we enumerate and phenotype T cells in nasal mucosa and blood using flow cytometry before and after vaccination with the Pfizer-BioNTech COVID-19 vaccine (n = 21). Tissue-resident memory (Trm) CD8+ T cells expressing CD69+CD103+ increase in number ~12 days following the first and second doses, by 0.31 and 0.43 log10 cells per swab respectively (p = 0.058 and p = 0.009 in adjusted linear mixed models). CD69+CD103+CD8+ T cells in the blood decrease post-vaccination. Similar increases in nasal CD8+CD69+CD103- T cells are observed, particularly following the second dose. CD4+ cells co-expressing CCR6 and CD161 are also increased in abundance following both doses. Stimulation of nasal CD8+ T cells with SARS-CoV-2 spike peptides elevates expression of CD107a at 2- and 6-months (p = 0.0096) post second vaccine dose, with a subset of donors also expressing increased cytokines. These data suggest that nasal T cells may be induced and contribute to the protective immunity afforded by this vaccine.

Comparative proteomic analyses demonstrate enhanced interferon and STAT-1 activation in reovirus T3D-infected HeLa cells.

As obligate intracellular parasites, viruses are exclusively and intimately dependent upon their host cells for replication. During replication viruses induce profound changes within cells, including: induction of signaling pathways, morphological changes, and cell death. Many such cellular perturbations have been analyzed at the transcriptomic level by gene arrays and recent efforts have begun to analyze cellular proteomic responses. We recently described comparative stable isotopic (SILAC) analyses of reovirus, strain type 3 Dearing (T3D)-infected HeLa cells. For the present study we employed the complementary labeling strategy of iTRAQ (isobaric tags for relative and absolute quantitation) to examine HeLa cell changes induced by T3D, another reovirus strain, type 1 Lang, and UV-inactivated T3D (UV-T3D). Triplicate replicates of cytosolic and nuclear fractions identified a total of 2375 proteins, of which 50, 57, and 46 were significantly up-regulated, and 37, 26, and 44 were significantly down-regulated by T1L, T3D, and UV-T3D, respectively. Several pathways, most notably the Interferon signaling pathway and the EIF2 and ILK signaling pathways, were induced by virus infection. Western blots confirmed that cells were more strongly activated by live T3D as demonstrated by elevated levels of key proteins like STAT-1, ISG-15, IFIT-1, IFIT-3, and Mx1. This study expands our understanding of reovirus-induced host responses.