Low Internal Air Space In Plants With Crassulacean Acid Metabolism May Be An Anatomical Spandrel

Crassulacean Acid Metabolism (CAM) is a photosynthetic adaptation found in at least 38 plant families. Typically, the anatomy of CAM plants is characterised by large photosynthetic cells and a low percentage of leaf volume comprised of internal air space (% IAS). It has been suggested that reduced mesophyll conductance (gm) arising from low % IAS benefits CAM plants by preventing the movement of CO2 out of cells and ultimately minimising leakage of CO2 from leaves into the atmosphere during day-time decarboxylation. Here, we propose that low % IAS does not provide any adaptive benefit to CAM plants, because stomatal closure during phase III of CAM will result in internal concentrations of CO2 becoming saturated, meaning low gm will not have any meaningful impact on the flux of gasses within leaves. We suggest that low % IAS is more likely an indirect consequence of maximising the cellular volume within a leaf, to provide space for the overnight storage of malic acid during the CAM cycle

Pennsylvania Folklife Vol. 38, No. 4

• Celebrating Twenty-Five Years of Quintessential Quilts • The Folk Art of Fraktur • Molding & Spinning Pewter • Kaleidoscopes & Unique Stained Glass • Dolls are Not Just for Children Anymore • Paint Decorated Chests of the Pennsylvania Dutch • Festival Focus • Festival Programs • Tiffany-Style Stained Glass Lamps • Be Aware of What Might be Hiding in Grandma\u27s Attic • The Medicine Show • Pennsylvania Dutch Music & More • A Poor Damsel\u27s Fate • Silk Screening • Long Time Favorite Festival Foodshttps://digitalcommons.ursinus.edu/pafolklifemag/1124/thumbnail.jp

Dysregulated RasGRP1 Responds to Cytokine Receptor Input in T Cell Leukemogenesis

Enhanced signaling by the small guanosine triphosphatase Ras is common in T cell acute lymphoblastic leukemia/lymphoma (T-ALL), but the underlying mechanisms are unclear. We identified the guanine nucleotide exchange factor RasGRP1 (Rasgrp1 in mice) as a Ras activator that contributes to leukemogenesis. We found increased RasGRP1 expression in many pediatric T-ALL patients, which is not observed in rare early T cell precursor T-ALL patients with KRAS and NRAS mutations, such as K-Ras[superscript G12D]. Leukemia screens in wild-type mice, but not in mice expressing the mutant K-Ras[superscript G12D] that encodes a constitutively active Ras, yielded frequent retroviral insertions that led to increased Rasgrp1 expression. Rasgrp1 and oncogenic K-Ras[superscript G12D] promoted T-ALL through distinct mechanisms. In K-Ras[superscript G12D] T-ALLs, enhanced Ras activation had to be uncoupled from cell cycle arrest to promote cell proliferation. In mouse T-ALL cells with increased Rasgrp1 expression, we found that Rasgrp1 contributed to a previously uncharacterized cytokine receptor–activated Ras pathway that stimulated the proliferation of T-ALL cells in vivo, which was accompanied by dynamic patterns of activation of effector kinases downstream of Ras in individual T-ALLs. Reduction of Rasgrp1 abundance reduced cytokine-stimulated Ras signaling and decreased the proliferation of T-ALL in vivo. The position of RasGRP1 downstream of cytokine receptors as well as the different clinical outcomes that we observed as a function of RasGRP1 abundance make RasGRP1 an attractive future stratification marker for T-ALL.National Institutes of Health (U.S.). Pioneer AwardNational Cancer Institute (U.S.). Physical Sciences-Oncology Center (U54CA143874)National Institutes of Health (U.S.). (P01 AI091580

Sustainable Alternative Wastewater Treatment for Beneficial Reuse of Industrial Wastewater

EMD Millipore is considering approaches for recycling wastewater from its manufacturing processes for re-use as process water. They currently own and operate a wastewater treatment plant (WWTP) at their Jaffrey, NH facility in order to treat organic contaminants. Wastewater chemistries from EMD Millipore’s operations were analyzed and assessed for reclamation potential. Ozone oxidation and activated carbon adsorption technologies were identified for constituent removal. Bench-scale experimental results suggested that ozone and ozone-hydrogen peroxide oxidation are feasible treatment options for EMD Millipore’s wastewater, however further research should be conducted. A pilot-scale ozone system for wastewater reclamation was designed for implementation at the facility

Adipose Depletion and Apoptosis Induced by Trans-10, Cis-12 Conjugated Linoleic Acid in Mice

Objective: To compare the effectiveness of a conjugated linoleic acid (CLA) isomer mixture (mCLA) with each main isomer [trans-10,cis-12 CLA (CLA10,12) and cis-9,trans-11 CLA (CLA9,11)] in causing body lipid loss and adipose tissue apoptosis. Research Methods and Procedures: Mice selected over 16 generations for high (MH) or low (ML) energy expenditure and a control group (MC) were fed diets containing either soy oil or soy oil plus mCLA, CLA10,12, or CLA9,11 for 5 days in one study and 14 days in a second study. Results: Mice fed mCLA or CLA10,12 had less body lipid (p _ 0.05), smaller retroperitoneal fat pads (p \u3c 0.05), and ate less (p \u3c 0.01) than mice fed no CLA or CLA9,11 for 5 days. Mice consuming 1% mCLA or 0.5% CLA10,12 gained less weight (p \u3c 0.01) and had less body lipid (p \u3c 0.05) and smaller epididymal (p \u3c 0.05) and retroperitoneal fat pads (p \u3c 0.01) than mice consuming either control or 0.5% CLA9,11-containing diets for 14 days. Only mCLA and CLA10,12 increased apoptosis in retroperitoneal fat pads (p \u3c 0.01). The effects of mCLA and CLA10,12 were independent of genetic line except for the effect on adipocyte apoptosis. Mice of the MH line were slightly less sensitive than MC or ML mice to CLA-induced adipose tissue apoptosis. Discussion: CLA10,12, but not CLA9,11, can induce both body fat loss and adipose apoptosis. Although mice of a genotype with less body fat and greater metabolic rate and feed intake appear less sensitive, these CLA effects are robust for mice of varying metabolic background

Enhanced inhibition of adipogenesis and induction of apoptosis in 3T3-L1 adipocytes with combinations of resveratrol and quercetin

Certain flavonoids have been shown to have specific effects on biochemical and metabolic functions of adipocytes. In this study, we investigated the effects of combinations of resveratrol and quercetin on adipogenesis and apoptosis in 3T3-L1 cells. In maturing preadipocytes resveratrol and quercetin at 25 μM individually suppressed intracellular lipid accumulation by 9.4 ± 3.9% (p \u3c 0.01) and 15.9 ± 2.5%, respectively, (p \u3c 0.001). The combination of resveratrol and quercetin at the same dose, however, decreased lipid accumulation by 68.6 ± 0.7% (p \u3c 0.001). In addition, combinations of resveratrol and quercetin at 25 μM significantly decreased the expression of peroxisome proliferators-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein (C/EBP)α, both of which act as key transcription factors. In mature adipocytes resveratrol and quercetin at 100 μM individually decreased viability by 18.1 ± 0.6% (p \u3c 0.001) and 15.8 ± 1% (p \u3c 0.001) and increased apoptosis (100 μM) by 120.5 ± 8.3% (p \u3c 0.001) and 85.3 ± 10% (p \u3c 0.001) at 48 h, respectively. Combinations of resveratrol and quercetin further decreased viability (73.5 ± 0.9%, p \u3c 0.001) and increased apoptosis (310.3 ± 9.6%, p \u3c 0.001) more than single compounds alone. The combination of resveratrol and quercetin at 100 μM increased release of cytochrome c from mitochondria to cytosol and decreased ERK 1/2 phosphorylation. Taken together, our data indicate that combinations of resveratrol and quercetin can exert potential anti-obesity effects by inhibiting differentiation of preadipocytes and inducing apoptosis of mature adipocytes. © 2008 Elsevier Inc. All rights reserved

Effect of resveratrol on fat mobilization

Higher levels of body fat are associated with increased risk for development of numerous adverse health conditions. Phytochemicals are potential agents to inhibit differentiation of preadipocytes, stimulate lipolysis, and induce apoptosis of existing adipocytes, thereby reducing adipose tissue mass. Resveratrol decreased adipogenesis and viability in maturing preadipocytes; these effects were mediated not only through down-regulating adipocyte specific transcription factors and enzymes but also by genes that modulate mitochondrial function. Additionally, resveratrol increased lipolysis and reduced lipogenesis in mature adipocytes. In addition, combining resveratrol with other natural products produced synergistic activities from actions on multiple molecular targets in the adipocyte life cycle. Treatment of mice with resveratrol alone was shown to improve resistance to weight gain caused by a high-fat diet. Moreover, dietary supplementation of aged ovariectomized rats with a combination of resveratrol and vitamin D, quercetin, and genistein not only decreased weight gain but also inhibited bone loss. Combining several phytochemicals, including resveratrol, or using them as templates for synthesizing new drugs, provides a large potential for using phytochemicals to target adipocyte adipogenesis, apoptosis, and lipolysis. © 2011 New York Academy of Sciences

Central leptin versus ghrelin: Effects on bone marrow adiposity and gene expression

This study compared the central effects of ghrelin and leptin on body and bone marrow adiposity and gene expression in adipose tissue and bone marrow. Male Sprague-Dawley rats were injected intracerebroventricular (ICV) twice daily with control, 66 ng ghrelin (G66), 330 ng ghrelin (G330), or 5 μg leptin (L5) for 5 days. Food intake (FI) and body weight (BW) were measured daily. Gene expression in adipose tissue and bone marrow was assessed using RT-PCR. Leptin reduced FI (P \u3c 0.05) and BW (P \u3c 0.05), whereas ghrelin increased BW (P \u3c 0.05) without affecting FI. Leptin decreased fat pad weights, whereas ghrelin (G330) increased fat pad weights (P \u3c 0.05). In epididymal adipose tissue, leptin increased expression of lipolysis marker ADRB2 and thermogenesis marker MFN2 and decreased expression of adipogenic markers, FASN, SLC2A4, and SCD1, whereas ghrelin increased expression of FASN and SCD1. Leptin decreased bone marrow adipocyte size and number; however, ghrelin had no effect on these parameters. In whole bone marrow, leptin decreased expression of FASN and SCD1 and increased expression of DLK1, whereas ghrelin (G330) decreased expression of COL1A1. Thus, leptin induces similar changes in bone marrow and adipose tissue gene expression, reflecting the decreased adiposity in both compartments

Regulation of adipogenesis by medium-chain fatty acids in the absence of hormonal cocktail

We report here that octanoate and decanoate, 8-carbon and 10-carbon medium-chain fatty acids (MCFA), decreased adipogenesis in 3T3-L1 preadipocytes when treated with standard hormonal cocktail, but increased adipogenesis in a dose-dependent manner (with decanoate being more effective) when treated with basal media. Addition of dexamethasone to basal medium with either octanoate or decanoate further increased adipogenesis. In order to understand the adipogenic effects of MCFA in the absence of standard hormonal cocktail, postconfluent 3T3-L1 preadipocytes were treated with octanoate or decanoate, and the change in the expression of several adipogenic transcription factors and enzymes was investigated using real-time RT-PCR. Octanoate and decanoate up-regulated the mRNA expression of peroxisome-proliferator-activated receptor (PPAR) γ, CCAAT/enhancer-binding protein (C/EBP) α, fatty-acid-binding protein, sterol-regulatory element binding protein 1c, lipoprotein lipase and hormone-sensitive lipase, and the protein expression of PPARγ and C/EBPα, with decanoate being more effective. Moreover, the PPARγ antagonist GW9662 inhibited MCFA-induced lipid accumulation by about 50%. Decanoate and octanoate, to a lesser degree, increased lipid accumulation, which was associated with an increase in glycerol-3-phosphate dehydrogenase activity. These results show that octanoate and decanoate may stimulate differentiation of preadipocytes, at least in part, by their influence on the expression of PPARγ and other adipocyte-specific factors. © 2009 Elsevier Inc. All rights reserved