Spinal cord injury (SCI) is a devastating condition affecting 270,000 people in the United States. A potential treatment for decreasing the secondary inflammation, excitotoxic damage, and neuronal apoptosis associated with SCI, is the anti-inflammatory cytokine interleukin-10. The best characterized effects of IL-10 are anti-inflammatory-it downregulates pro-inflammatory species interleukin-1β (IL-1β), interleukin-2 (IL-2), interleukin-6 (IL-6), tumor necrosis factor-α, interferon-γ, matrix metalloproteinase-9, nitric oxide synthase, myeloperoxidase, and reactive oxygen species. Pro-apoptotic factors cytochrome c, caspase 3, and Bax are downregulated by IL-10, whereas anti-apoptotic factors B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X, B-cell lymphoma-extra large (Bcl-xl) are upregulated by IL-10. IL-10 also provides trophic support to neurons through the IL-10 receptor. Increased tissue sparing, functional recovery, and neuroprotection are seen with an immediate post-SCI systemic administration of IL-10. Treatment of SCI with IL-10 has been used successfully in combination with Schwann cell and olfactory glial cell grafts, as well as methylprednisolone. Minocycline, tetramethylpyrazine, and hyperbaric oxygen treatment all increase IL-10 levels in a SCI models and result in increased tissue sparing and functional recovery. A chronic systemic administration of IL-10 does not appear to be beneficial to SCI recovery and causes increased susceptibility to septicemia, pneumonia, and peripheral neuropathy. However, a localized upregulation of IL-10 has been shown to be beneficial and can be achieved by herpes simplex virus gene therapy, injection of poliovirus replicons, or surgical placement of a slow-release compound. IL-10 shows promise as a treatment for SCI, although research on local IL-10 delivery timeline and dosage needs to be expanded.

In this study, we set out to identify regulators of intact amyloid-β40/42 (Aβ) levels in A549 (p53 wild-type) and H1299 (p53-null) lung cancer cell media. Higher Aβ levels were detected in the media of A549 than H1299 cells without or with treatment with 4-methylumbelliferone (4-MU) and/or the anti-CD44 antibody (5F12). Using inhibitors, we found that PI3K, AKT, and NFκB are likely involved in regulating Aβ levels in the media. However, increased Aβ levels that more closely resembled those found upon 4-MU co-treatment resulted from MMP2/9 inhibition, suggesting that MMP2/9 maybe the main contributors to regulation of Aβ levels in the media. Differences in Aβ levels might be accounted for, in part, by p53 since blocking p53 function in A549 cells resulted in decreased Aβ levels, increased MMP2/9 levels, increased PI3K/AKT activities and the phospho/total NFκB ratio. Using siRNA targeted against MMP2 or MMP9, we found increased Aβ levels in the media, however, MMP2 knockdown led to Aβ levels closely mimicking those detected by co-treatment with 4-MU. Cell viability or apoptosis upon treatment with either MMP2 or MMP9 siRNA along with Aβ immunodepletion, showed that MMP2 is the predominant regulator of the cytotoxic effects induced by Aβ in lung cancer cells.

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A review of the literature indicates that the stomates of leaves must be open for smog damage to occur (3,7,8,9,11). However, there is no direct relationship between degree of opening and extent of injury, nor has it been proven that injury is prevented when the stomates are closed. Moreover, most of the earlier work dealt with the reaction product of ozone and gasoline or ozone and an olefin (8,10,16 Because subsequent assays of plant leaf damage from the oxidant were desired, the rate of apparent photosynthesis was expressed on a nine-plant basis rather than on the leaf area or dry weight basis.

Open‐top field chambers are the most widely used technology for evaluating the impacts of air pollutants on vegetation. This study was conducted to evaluate the long‐term effects of chambers on Valencia orange trees (Citrus sinensis [L.] Osbeck). The trees were exposed to ambient ozone (O3) for 51 months in large (4.3‐m diam. by 2.9‐m high) nonfiltered open‐top chambers (NF) and in ambient air without chambers (AA). During this period, the 12‐h daytime (M12) average O3 concentration was approximately 8% lower, and the cumulative O3 exposure for hourly average concentrations >0.1 µL L−1 (SUM10) was 29% lower than for NF than for AA trees. By December 1984 (after eight months in chambers), canopy volume for NF trees was 67% greater than for AA trees; and by March 1988 canopy volume for NF trees was 104% greater than for AA trees (P < 0.001). Specific leaf areas (cm2 g−1) were larger for NF than AA trees (P < 0.05). Total harvestable fruit weight combined for years 1986, 1987 and 1988 was 98% higher for NF than for AA trees (P < 0.01). The higher yield for NF trees was associated with lower immature fruit drop, especially during the growing seasons prior to the 1986 and 1987 harvests (P < 0.01). Warm season (April–October) rates of stomatal conductance and transpiration were 14 and 12% lower, respectively, for NF than AA trees; which coincided with 29% more negative leaf water potentials for NF than AA trees (P < 0.05) . In contrast, cool season net photosynthetic rates were 18% lower for NF than for AA trees, and starch concentrations were 31% higher in leaves from NF compared to AA trees in February 1988 (P < 0.05). Overall, the yield increases for NF compared to AA trees could, in part, be accounted for by decreased flux of O3 into leaves (based on decreased O3 exposure and leaf conductance). However, other factors, i.e., increased tree growth, altered leaf C allocation, and lack of wind stress occurring only in chambers, likely contributed to higher NF tree yields.

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