Daily Archives: May 28, 2013

Carbon dioxide increases soybean productivity

Tracy E. Twine, Jarod J. Bryant, Katherine Richter, Carl J. Bernacchi, Kelly D. McConnaughay, Sherri J. Morris, Andrew D. B. Leakey. Impacts of elevated CO2 concentration on the productivity and surface energy budget of the soybean and maize agroecosystem in the Midwest U.S. Global Change Biology. doi: 10.1111/gcb.12270

The physiological response of vegetation to increasing atmospheric carbon dioxide concentration ([CO2]) modifies productivity and surface energy and water fluxes. Quantifying this response is required for assessments of future climate change. Many global climate models account for this response; however, significant uncertainty remains in model simulations of this vegetation response and its impacts. Data from in situ field experiments provide evidence that previous modeling studies may have overestimated the increase in productivity at elevated [CO2], and the impact on large-scale water cycling is largely unknown. We parameterized the Agro-IBIS dynamic global vegetation model with observations from the SoyFACE experiment to simulate the response of soybean and maize to an increase in [CO2] from 375 ppm to 550 ppm. The two key model parameters that were found to vary with [CO2] were the maximum carboxylation rate of photosynthesis and specific leaf area. Tests of the model that used SoyFACE parameter values showed a good fit to site-level data for all variables except latent heat flux over soybean and sensible heat flux over both crops. Simulations driven with historic climate data over the central U.S. showed that increased [CO2] resulted in decreased latent heat flux and increased sensible heat flux from both crops when averaged over 30 years. Thirty-year average soybean yield increased everywhere (~10%); however, there was no increase in maize yield except during dry years. Without accounting for CO2 effects on the maximum carboxylation rate of photosynthesis and specific leaf area, soybean simulations at 550 ppm overestimated leaf area and yield. Our results highlight important model parameter values that, if not modified in other models, could result in biases when projecting future crop-climate-water relationships.

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China Medieval Warming Period temperatures comparable to today.

Reconstruction of temperature changes over the past 2000 years in China and found the Medieval Warming Period temperatures during AD 981–AD 1100 and AD 1201–AD 1270 comparable to the Present Warm Period.

Q. Ge, Z. Hao, J. Zheng, and X. Shao. Temperature changes over the past 2000 yr in China and comparison with the Northern Hemisphere. Clim. Past, 9, 1153-1160, 2013. http://www.clim-past.net/9/1153/2013/

We use principal component regression and partial least squares regression to separately reconstruct a composite series of temperature variations in China, and associated uncertainties, at a decadal resolution over the past 2000 yr. The reconstruction is developed using proxy temperature data with relatively high confidence levels from five regions across China, and using a temperature series from observations by the Chinese Meteorological Administration, covering the period from 1871 to 2000. Relative to the 1851–1950 climatology, our two reconstructions show four warm intervals during AD 1–AD 200, AD 551–AD 760, AD 951–AD 1320, and after AD 1921, and four cold intervals during AD 201–AD 350, AD 441–AD 530, AD 781–AD 950, and AD 1321–AD 1920. The temperatures during AD 981–AD 1100 and AD 1201–AD 1270 are comparable to those of the Present Warm Period, but have an uncertainty of ±0.28 °C to ±0.42 °C at the 95% confidence interval. Temperature variations over China are typically in phase with those of the Northern Hemisphere (NH) after 1000, a period which covers the Medieval Climate Anomaly, the Little Ice Age, and the Present Warm Period. In contrast, a warm period in China during AD 541–AD 740 is not obviously seen in the NH.

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Fluoride-elicited developmental testicular toxicity in rats

Zhang S, Jiang C, Liu H, Guan Z, Zeng Q, Zhang C, Lei R, Xia T, Gao H, Yang L, Chen Y, Wu X, Zhang X, Cui Y, Yu L, Wang A. Fluoride-Elicited Developmental Testicular Toxicity in Rats: Roles of Endoplasmic Reticulum Stress and Inflammatory Response. Toxicol Appl Pharmacol. 2013 May 22. pii: S0041-008X(13)00217-2. doi: 10.1016/j.taap.2013.04.033.

Long-term excessive fluoride intake is known to be toxic and can damage a variety of organs and tissues in the human body. However, the molecular mechanisms underlying fluoride-induced male reproductive toxicity are not well understood. In this study, we used a rat model to simulate the situations of human exposure and aimed to evaluate the roles of endoplasmic reticulum (ER) stress and inflammatory response in fluoride-induced testicular injury. Sprague-Dawley rats were administered with sodium fluoride (NaF) at 25, 50 and 100 mg/L via drinking water from pre-pregnancy to gestation, birth and finally to post-puberty. And then the testes of male offspring were studied at 8 weeks of age. Our results demonstrated that fluoride treatment increased MDA accumulation, decreased SOD activity, and enhanced germ cell apoptosis. In addition, fluoride elevated mRNA and protein levels of Glucose-regulated protein 78 (GRP78), inositol requiring ER-to-nucleus signal kinase 1 (IRE1), C/EBP homologous protein (CHOP), indicating activation of ER stress signaling. Furthermore, fluoride also induced testicular inflammation, as manifested by genes up-regulation of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in a nuclear factor-κB (NF-κB)-dependent manner. These were associated with marked histopathological lesions including injury of spermatogonia, decrease of spermatocytes and absence of elongated spermatids, as well as severe ultrastructural abnormalities in testes. Taken together, our results provide compelling evidence that ER stress and inflammation would be novel and significant mechanisms responsible for fluoride-induced disturbance of spermatogenesis and germ cell loss in addition to oxidative stress.

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