Commercial Crop Yields Reveal Strengths and Weaknesses for Organic Agriculture in the United States

Land area devoted to organic agriculture has increased steadily over the last 20 years in the United States, and elsewhere around the world. A primary criticism of organic agriculture is lower yield compared to non-organic systems. Previous analyses documenting the yield deficiency in organic production have relied mostly on data generated under experimental conditions, but these studies do not necessarily reflect the full range of innovation or practical limitations that are part of commercial agriculture. The analysis we present here offers a new perspective, based on organic yield data collected from over 10,000 organic farmers representing nearly 800,000 hectares of organic farmland. We used publicly available data from the United States Department of Agriculture to estimate yield differences between organic and conventional production methods for the 2014 production year. Similar to previous work, organic crop yields in our analysis were lower than conventional crop yields for most crops. Averaged across all crops, organic yield averaged 80% of conventional yield. However, several crops had no significant difference in yields between organic and conventional production, and organic yields surpassed conventional yields for some hay crops. The organic to conventional yield ratio varied widely among crops, and in some cases, among locations within a crop. For soybean (Glycine max) and potato (Solanum tuberosum), organic yield was more similar to conventional yield in states where conventional yield was greatest. The opposite trend was observed for barley (Hordeum vulgare), wheat (Triticum aestevum), and hay crops, however, suggesting the geographical yield potential has an inconsistent effect on the organic yield gap.     

Stimulation of electron transport from Photosystem II to Photosystem I in spinach chloroplasts

Electron transport from Photosystem II to Photosystem I of spinach chloroplasts can be stimulated by bicarbonate and various carbonyl or carboxyl compounds. Monovalent or divalent cations, which have hitherto been implicated in the energy distribution between the two photosystems, i.e., spillover phenomena at low light intensities, show a similar effect under high light conditions employed in this study. A mechanism for this stimulation of forward electron transport from Photosystem II to Photosystem I could involve inhibition of two types of Photosystem II partial reactions, which may involve cycling of electrons around Photosystem II. One of these is the DCMU-insensitive silicomolybdate reduction, and the other is ferricyanide reduction by Photosystem II at pH 8 in the presence of dibromothymoquinone. Greater stimulation of forward electron transport reactions is observed when both types of Photosystem II cyclic reactions are inhibited by bicarbonate, carbonyl and carboxyl-type compounds, or by certain mono- or divalent cations.Abbreviations used: DCMU, 3-(3,4-dichlorophenyl)-1, 1-dimethylurea; DCIP, 2,6-dichloroindophenol; DBMIB, 2,5-dibromo-3-methyl-6-isopropyl-p-benzoquinone; FeCN, potassium ferricyanide; MV, methylviologen; PS I, photosystem I; PS II, photosystem II; SM, silicomolybdic acid.     

Soil management effects on entomopathogenic fungi during the transition to organic agriculture in a feed grain rotation

The growing demand for organic products creates opportunities for farmers. Information on the consequences of management practices can help farmers transition to organic and take advantage of these prospects. We examined the interaction between soil disturbance and initial cover crop on naturally occurring entomopathogenic fungi (EPF) during the 3-year transition to organic production in a feed grain rotation in central Pennsylvania. Our experiment included four systems comprised of a factorial combination of two levels of primary tillage (full vs. reduced) and two types of initial cover crop (timothy/clover vs. rye/vetch). The cropping sequence consisted of an initial cover crop, followed by soybean, and finally, maize. The entire experiment was replicated in time, with the initiation lagged by 1 year. We detected four species of EPF (Metarhizium anisopliae, Beauveria bassiana, Isaria fumosorosea, and Isaria farinosa) by bioassay of soil samples collected four times during each field season. The latter three species were detected infrequently; therefore, we focused statistical analysis on M. anisopliae. Detection of M. anisopliae varied across sampling date, year in crop sequence, and experimental start, with no consistent trend across the 3-year transition period. M. anisopliae was isolated more frequently in the systems initiated with timothy/clover cover crops and utilizing full tillage; however, we only observed a tillage effect in one temporal replicate. M. anisopliae detection was negatively associated with soil moisture, organic matter, and zinc, sulfur, and copper concentrations in the soil. This study helps to inform farmers about management effects on soil function, specifically conservation biological control.     

Biotin attenuation of oxidative stress,mitochondrial dysfunction,lipid metabolism alteration and 7β-hydroxycholesterol-induced cell death in 158N murine oligodendrocytes

Mitochondrial dysfunction and oxidative stress are involved in neurodegenerative diseases associated with an enhancement of lipid peroxidation products such as 7β-hydroxycholesterol (7β-OHC). It is, therefore, important to study the ability of 7β-OHC to trigger mitochondrial defects, oxidative stress, metabolic dysfunctions and cell death, which are hallmarks of neurodegeneration, and to identify cytoprotective molecules. The effects of biotin were evaluated on 158N murine oligodendrocytes, which are myelin synthesizing cells, exposed to 7β-OHC (50?µM) with or without biotin (10 and 100?nM) or α-tocopherol (positive control of cytoprotection). The effects of biotin on 7β-OHC activities were determined using different criteria: cell adhesion; plasma membrane integrity; redox status. The impact on mitochondria was characterized by the measurement of transmembrane mitochondrial potential (ΔΨm), reactive oxygen species (ROS) overproduction, mitochondrial mass, quantification of cardiolipins and organic acids. Sterols and fatty acids were also quantified. Cell death (apoptosis, autophagy) was characterized by the enumeration of apoptotic cells, caspase-3 activation, identification of autophagic vesicles, and activation of LC3-I into LC3-II. Biotin attenuates 7β-OHC-induced cytotoxicity: loss of cell adhesion was reduced; antioxidant activities were normalized. ROS overproduction, protein and lipid oxidation products were decreased. Biotin partially restores mitochondrial functions: attenuation of the loss of ΔΨm; reduced levels of mitochondrial O₂^?? overproduction; normalization of cardiolipins and organic acid levels. Biotin also normalizes cholesterol and fatty acid synthesis, and prevents apoptosis and autophagy (oxiapoptophagy). Our data support that biotin, which prevents oligodendrocytes damages, could be useful in the treatment of neurodegeneration and demyelination.     

Sirt3-mediated deacetylation of evolutionarily conserved lysine 122 regulates MnSOD activity in response to stress

Genetic deletion of the mitochondrial deacetylase sirtuin-3 (Sirt3) results in increased mitochondrial superoxide, a tumor-permissive environment, and mammary tumor development. MnSOD contains a nutrient- and ionizing radiation (IR)-dependent reversible acetyl-lysine that is hyperacetylated in Sirt3?/? livers at 3 months of age. Livers of Sirt3?/? mice exhibit decreased MnSOD activity, but not immunoreactive protein, relative to wild-type livers. Reintroduction of wild-type but not deacetylation null Sirt3 into Sirt3?/? MEFs deacetylated lysine and restored MnSOD activity. Site-directed mutagenesis of MnSOD lysine 122 to an arginine, mimicking deacetylation (lenti-MnSOD(K122-R)), increased MnSOD activity when expressed in MnSOD?/? MEFs, suggesting acetylation directly regulates function. Furthermore, infection of Sirt3?/? MEFs with lenti-MnSOD(K122-R) inhibited in vitro immortalization by an oncogene (Ras), inhibited IR-induced genomic instability, and decreased mitochondrial superoxide. Finally, IR was unable to induce MnSOD deacetylation or activity in Sirt3?/? livers, and these irradiated livers displayed significant IR-induced cell damage and microvacuolization in their hepatocytes.     

MyD88 is pivotal for the early inflammatory response and subsequent bacterial clearance and survival in a mouse model of Chlamydia pneumoniae pneumonia

Chlamydia pneumoniae is the causative agent of respiratory tract infections and a number of chronic diseases. Here we investigated the involvement of the common TLR adaptor molecule MyD88 in host responses to C. pneumoniae-induced pneumonia in mice. MyD88-deficient mice were severely impaired in their ability to mount an acute early inflammatory response toward C. pneumoniae. Although the bacterial burden in the lungs was comparable 5 days after infection, MyD88-deficient mice exhibited only minor signs of pneumonia and reduced expression of inflammatory mediators. MyD88-deficient mice were unable to up-regulate proinflammatory cytokines and chemokines, demonstrated delayed recruitment of CD8+ and CD4+ T cells to the lungs, and were unable to clear the pathogen from their lungs at day 14. At day 14 the MyD88-deficent mice developed a severe, chronic lung inflammation with elevated IL-1beta and IFN-gamma leading to increased mortality, whereas wild-type mice as well as TLR2- or TLR4-deficient mice recovered from acute pneumonia and did not show delayed bacterial clearance. Thus, MyD88 is essential to recognize C. pneumoniae infection and initiate a prompt and effective immune host response against this organism leading to clearance of bacteria from infected lungs.     

Genetic polymorphism of lysyl oxidase,glutathione S-transferase M1, glutathione-S-transferase T1, and glutathione S-transferase P1 genes as risk factors for lung cancer in Egyptian patients

Lung cancer is a lethal malignancy and is affected by genetic polymorphisms that contribute to an individual’s susceptibility to developing the disease. Several studies on lung cancer showed conflicting results. The aim of this study is to investigate whether individual or combined modifying effects of LOX G/A, GSTM1 active/null, GSTT1 active/null and GSTP1 Ile/Val polymorphisms are related to the risk of lung cancer in relation to smoking in the Egyptian population. This study is a hospital-based case control study that included 200 patients and 200 control subjects. Genotyping of the 4 studied genes was determined by Multiplex PCR for GSTM1 and GSTT1 and Taq man SNP assay for GSTP1 and LOX genes. The LOX G/A and GSTP1 Ile/Val in both homozygous and heterozygous variants, and the GSTM1 and GSTT1 null genotype showed significant association with lung cancer. Combination between gene polymorphism and smoking increased the risk of developing cancer by 2.7 fold in the LOX GA+AA variant, 1.9 fold in the GSTM1 null variant, 4.8 fold in the GSTT1 null variant and 4.3 fold in the GSTP1 Ile/Val+Val/Val variant. The genetic combination (LOX GA+AA/GSTT1 active, LOX GG/GSTT1 null, LOX GA+AA/GSTT1 null, LOX GA+AA/GSTP1 Ile/Ile, LOX GG/GSTP1 Ile/Val+Val/Val and LOX GA+AA/GSTP1 Ile/Val+Val/Val) led to a higher lung cancer risk, compared to the reference group. The LOX GA/AA, GSTM1 null, GSTT1 null and GSTP1 Ile/Val, Val/Val genotypes contributed to increased lung cancer susceptibility. To the best of our knowledge, this is the first study of LOX genotyping in the Egyptian population. The combination of genotypes increased the risk of cancer, indicating the importance of gene–gene interaction and giving a targeted preventive approach.

     

Effects of a 6-week periodized squat training with or without whole-body vibration upon short-term adaptations in squat strength and body composition

The purpose of this study was to examine the effects of a 6-week, periodized squat training program, with or without whole-body low-frequency vibration (WBLFV), applied before and between sets to 1RM squat strength and body composition. Thirty men aged between 20 and 30 years with at least 6 months of recreational weight training experience completed the study. Subjects were randomly assigned to either 1 of 2 training groups or to an active control group (CON). Group 1 (CON; n = 6) did not participate in the training protocol but participated only in testing sessions. Group 2 (SQTV, n = 13) performed 6 weeks of squat training while receiving WBLFV (50 Hz), before, and in-between sets. The third group (SQT, n = 11) performed 6 weeks of squat training only. Subjects completed 12 workouts with variable loads (55-90% one repetition maximum [1RM]) and sets (), performing squats twice weekly separated by 72 hours. The RM measures were recorded on weeks (W) 1, 3, and 7. During the second workout of a week, the load was reduced by 10-15%, with "speed squats" performed during the final 3 weeks. Rest periods in between sets were set at 240 seconds. The WBLFV was applied while subjects stood on a WBLFV platform holding an isometric quarter squat position (knee angle 135 ± 5°). Initially, WBLFV was applied at 50 Hz for 30 seconds at low amplitude (peak-peak 2-4 mm). A rest period of 180 seconds followed WBLFV exposure before the first set of squats. The WBLFV was then applied intermittently (3 × 10 seconds) at 50 Hz, high amplitude (peak-peak, 4-6 mm) at time points, 60, 120, and 180 seconds into the 240-second rest period. Total body dual x-ray absorptiometry scans were performed at W0 (week before training) and W7 (week after training). Measures recorded included total body mass (kg), total body lean mass (TLBM, kg), trunk lean mass (kg), leg lean mass (kg), total body fat percentage, trunk fat percentage, and leg fat percentage (LF%). Repeated-measures analysis of variance and analysis of covariance revealed 1RM increased significantly between W1-W3, W3-W7, and W1-W7 for both experimental groups but not for control (p = 0.001, effect size [ES] = 0.237, 1 - β = 0.947). No significant differences were seen for %Δ (p > 0.05). Significant group by trial and group effects were seen for TLBM, SQTV > CON at W7 (p = 0.044). A significant main effect for time was seen for LF%, W0 vs. W7 (p = 0.047). No other significant differences were seen (p > 0.05). "Practical trends" were seen favoring "short-term" neuromuscular adaptations for the SQTV group during the first 3 weeks (p = 0.10, ES = 0.157, 1 - β = 0.443, mean diff; SQTV week 3 4.72 kg > CON and 2.53 kg > SQT). Differences in motor unit activation patterns, hypertrophic responses, and dietary intake during the training period could account for the trends seen.     

Chlamydia pneumoniae infection induced allergic airway sensitization is controlled by regulatory T-cells and plasmacytoid dendritic cells

Chlamydia pneumoniae (CP) is associated with induction and exacerbation of asthma. CP infection can induce allergic airway sensitization in mice in a dose- and time-dependent manner. Allergen exposure 5 days after a low dose (mild-moderate), but not a high dose (severe) CP infection induces antigen sensitization in mice. Innate immune signals play a critical role in controlling CP infection induced allergic airway sensitization, however these mechanisms have not been fully elucidated. Wild-type, TLR2-/-, and TLR4-/- mice were infected intranasally (i.n.) with a low dose of CP, followed by i.n. exposure to human serum albumin (HSA) and challenged with HSA 2 weeks later. Airway inflammation, immunoglobulins, eosinophils, and goblet cells were measured. Low dose CP infection induced allergic sensitization in TLR2-/- mice, but not in TLR4-/- mice, due to differential Treg responses in these genotypes. TLR2-/- mice had reduced numbers of Tregs in the lung during CP infection while TLR4-/- mice had increased numbers. High dose CP infection resulted in an increase in Tregs and pDCs in lungs, which prevented antigen sensitization in WT mice. Depletion of Tregs or pDCs resulted in allergic airway sensitization. We conclude that Tregs and pDCs are critical determinants regulating CP infection-induced allergic sensitization. Furthermore, TLR2 and TLR4 signaling during CP infection may play a regulatory role through the modulation of Tregs.