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In this article, the author relates how she integrated poetry and African-American history in her lessons. She also relates how she uses the story of Emitt Tills to impart to her students the reality of racism and injustice. Emitt Tills was a black 14-year-old boy from Chicago who lived during 1950s. He was killed with a bullet wound and was pulled from the Tallahatchie River after he allegedly flirted with a white store owner. Tills' killers, Roy Bryant, the owner of the store, and J. W. Milam, his brother-in-law, were found not guilty of the crime. The author, who believed that poetry is a soul's song to the world, relates how she made her students write reflection pieces expressing what they learned from the stories of hatred and abuse of African Americans. (Contains 1 table and 5 figures.)

The Ozarks Isoprene Experiment (OZIE) was conducted in July 1998 in Missouri, Illinois, Indiana, and Oklahoma. OZIE was designed to investigate the presumed strong isoprene emission rates from the Missouri Ozarks, where there is a high density of oak trees that are efficient isoprene emitters. Ground, balloon, and aircraft measurements were taken over a three-week study period; 0-D and 3-D chemical models were subsequently used to better understand the observed isoprene emissions from the Ozarks and to investigate their potential regional-scale impacts. Leaf-level measurements for two oak tree species yielded normalized average isoprene emission capacities of 66 mgC g-1 h-1, in good agreement with values used in current biogenic emissions models. However, the emission capacities exhibited a temperature dependence that is not captured by commonly used biogenic emission models. Isoprene mixing ratios measured aloft from tethered balloon systems were used to estimate isoprene fluxes. These measurement-derived fluxes agreed with BEIS3 estimates within the relatively large uncertainties in the estimates. Ground-level isoprene mixing ratios exhibited substantial spatial heterogeneity, ranging from

During the summer of 1992, isoprene emissions were measured in a mixed deciduous forest near Oak Ridge, Tennessee. Measurements were aimed at the experimental scale‐up of emissions from the leaf level to the forest canopy to the mixed layer. Results from the scale‐up study are compared to different canopy models for determining the leaf microclimate as input to isoprene emission algorithms. These include (1) no canopy effects, (2) a simple vertical scaling canopy model with a leaf energy balance, and (3) a numerical canopy model which accounts for leaf‐sun geometries, photosynthesis, respiration, transpiration, and gas transport in the canopy. Initial evaluation of the models was based upon a standard emission rate factor of 90 μgC g−1 hr−1 (0.42 nmol g−1 s−1) taken from leaf cuvette measurements and a biomass density factor of 203 g m−2 taken from biomass surveys and a flux footprint analysis. The results indicated that predicted fluxes were consistent among the models to within approximately ±20%, but that the models overestimated the mean flux by about a factor of 2 and overestimated the maximum observed flux by 30 to 50%. Adjusting the standard emission factor and biomass density each downward by 20% yielded predicted means approximately 20% greater than the observed means and predicted maxima approximately 25% less than the observed maxima. Accounting for changes in biomass density as a function of direction upwind of the tower improved the overall model performance.

Isoprene fluxes were estimated using eight different measurement techniques at a forested site near Oak Ridge, Tennessee, during July and August 1992. Fluxes from individual leaves and entire branches were estimated with four enclosure systems, including one system that controls leaf temperature and light. Variations in isoprene emission with changes in light, temperature, and canopy depth were investigated with leaf enclosure measurements. Representative emission rates for the dominant vegetation in the region were determined with branch enclosure measurements. Species from six tree genera had negligible isoprene emissions, while significant emissions were observed for Quercus, Liquidambar, and Nyssa species. Above‐canopy isoprene fluxes were estimated with surface layer gradients and relaxed eddy accumulation measurements from a 44‐m tower. Midday net emission fluxes from the canopy were typically 3 to 5 mg C m−2 h−1, although net isoprene deposition fluxes of −0.2 to −2 mg C m−2 h−1 were occasionally observed in early morning and late afternoon. Above‐canopy CO2 fluxes estimated by eddy correlation using either an open path sensor or a closed path sensor agreed within ±5%. Relaxed eddy accumulation estimates of CO2 fluxes were within 15% of the eddy correlation estimates. Daytime isoprene mixing ratios in the mixed layer were investigated with a tethered balloon sampling system and ranged from 0.2 to 5 ppbv, averaging 0.8 ppbv. The isoprene mixing ratios in the mixed layer above the forested landscape were used to estimate isoprene fluxes of 2 to 8 mg C m−2 h−1 with mixed layer gradient and mixed layer mass balance techniques. Total foliar density and dominant tree species composition for an approximately 8100 km2 region were estimated using high‐resolution (30 m) satellite data with classifications supervised by ground measurements. A biogenic isoprene emission model used to compare flux measurements, ranging from leaf scale (10 cm2) to landscape scale (102 km2), indicated agreement to within ±25%, the uncertainty associated with these measurement techniques. Existing biogenic emission models use isoprene emission rate capacities that range from 14.7 to 70 μg C g−1 h−1 (leaf temperature of 30°C and photosynthetically active radiation of 1000 μmol m−2 s−1) for oak foliage. An isoprene emission rate capacity of 100 μg C g−1 h−1 for oaks in this region is more realistic and is recommended, based on these measurements.

Prior infection can generate protective immunity against subsequent infection, although the efficacy of such immunity can vary considerably. Live-attenuated vaccines (LAVs) are one of the most effective methods for mimicking this natural process, and analysis of their efficacy has proven instrumental in the identification of protective immune mechanisms. Here, we address the question of what makes a LAV efficacious by characterising immune responses to a LAV, termed TAS2010, which is highly protective (80–90%) against lethal murine salmonellosis, in comparison with a moderately protective (40–50%) LAV, BRD509. Mice vaccinated with TAS2010 developed immunity systemically and were protected against gut-associated virulent infection in a CD4+ T cell-dependent manner. TAS2010-vaccinated mice showed increased activation of Th1 responses compared with their BRD509-vaccinated counterparts, leading to increased Th1 memory populations in both lymphoid and non-lymphoid organs. The optimal development of Th1-driven immunity was closely correlated with the activation of CD11b+Ly6GnegLy6Chi inflammatory monocytes (IMs), the activation of which can be modulated proportionally by bacterial load in vivo. Upon vaccination with the LAV, IMs expressed T cell chemoattractant CXCL9 that attracted CD4+ T cells to the foci of infection, where IMs also served as a potent source of antigen presentation and Th1-promoting cytokine IL-12. The expression of MHC-II in IMs was rapidly upregulated following vaccination and then maintained at an elevated level in immune mice, suggesting IMs may have a role in sustained antigen stimulation. Our findings present a longitudinal analysis of CD4+ T cell development post-vaccination with an intracellular bacterial LAV, and highlight the benefit of inflammation in the development of Th1 immunity. Future studies focusing on the induction of IMs may reveal key strategies for improving vaccine-induced T cell immunity. Author summary: Salmonella enterica infections exemplify the immunological challenges posed by intracellular bacterial pathogens, for which there are often limited or no effective vaccines and antimicrobial resistance is rapidly on the rise. A common signature among these infections is a strong dependence on CD4+ T cell responses for host immunity, although how such responses can be effectively induced in a vaccine setting remains a key challenge. Using two live-attenuated vaccines that offer distinct levels of protection against lethal salmonellosis in a murine model, we investigated what properties of vaccine-induced immune responses can be targeted for improving vaccine efficacy. Our data show that the longevity of activated CD4+ T cells in lymphoid and non-lymphoid organs is closely linked with vaccine efficacy. At the cellular level, we have shown that CD11b+Ly6GnegLy6Chi inflammatory monocytes play an important role in stimulating antigen-specific CD4+ T cells through antigen presentation mechanisms, as well as the production of CXCL9 and IL-12. Since our data suggest that acute inflammation is beneficial for optimising vaccine-induced T cell immunity, considerations should be given to preserving the targets of inflammatory signalling pathways as a means for improving vaccine efficacy in future development. [ABSTRACT FROM AUTHOR]

Localized estimates of biogenic volatile organic compound (BVOC) emissions are important inputs for photochemical oxidant simulation models. Since forest tree species are the primary emitters of BVOCs, it is important to develop reliable estimates of their areal coverage and BVOC emission rates. A new system is used to estimate these emissions in the Atlanta area for specific tree genera at hourly and county levels. The U.S. Department of Agriculture, Forest Service Forest Inventory and Analysis data and an associated urban vegetation survey are used to estimate canopy occupancy by genus in the Atlanta area. A simple canopy model is used to adjust photosynthetically active solar radiation at five vertical levels in the canopy. Lraf temperature and photosynthetically active radiation derived from ambient conditions above the forest canopy are then used to drive empirical equations to estimate genus level emission rates of BVOCs vertically through forest canopies. These genera-level estimates are then aggregated to county and regional levels for input into air quality models and for comparison with (1) the regulatory model currently used and (2) previous estimates for the Atlanta area by local researchers. Estimated hourly emissions from the three approaches during a documented ozone event day are compared. The proposed model yields peak diurnal isoprene emission rates that are over a factor of three times higher than previous estimates. This results in total BVOC emission rates that are roughly a factor of two times higher than previous estimates. These emissions are compared with observed emissions from forests of similar composition. Possible implications for oxidant events are discussed. © 1995.

Gastrointestinal cancers are frequently associated with chronic inflammation and excessive secretion of IL-6 family cytokines, which promote tumorigenesis through persistent activation of the GP130/JAK/STAT3 pathway. Although tumor progression can be prevented by genetic ablation of Stat3 in mice, this transcription factor remains a challenging therapeutic target with a paucity of clinically approved inhibitors. Here, we uncovered parallel and excessive activation of mTOR complex 1 (mTORC1) alongside STAT3 in human intestinal-type gastric cancers (IGCs). Furthermore, in a preclinical mouse model of IGC, GP130 ligand administration simultaneously activated mTORC1/S6 kinase and STAT3 signaling. We therefore investigated whether mTORC1 activation was required for inflammation-associated gastrointestinal tumorigenesis. Strikingly, the mTORC1-specific inhibitor RAD001 potently suppressed initiation and progression of both murine IGC and colitis-associated colon cancer. The therapeutic effect of RAD001 was associated with reduced tumor vascularization and cell proliferation but occurred independently of STAT3 activity. We analyzed the mechanism of GP130-mediated mTORC1 activation in cells and mice and revealed a requirement for JAK and PI3K activity but not for GP130 tyrosine phosphorylation or STAT3. Our results suggest that GP130-dependent activation of the druggable PI3K/mTORC1 pathway is required for inflammation-associated gastrointestinal tumorigenesis. These findings advocate clinical application of PI3K/mTORC1 inhibitors for the treatment of corresponding human malignancies., Introduction During the multistep process of tumor formation conditions within the tissue microenvironment can influence the fate of premalignant cells. In inflammation-associated cancers, tumor promotion is thought to be facilitated [...]