DG Level Research Articles

CPW-Fed UWB-MIMO Antenna with Triple-band Notched and High Isolation using Double Y-shaped Decoupling Structure

A ultra-wideband (UWB) multiple-input-multiple-output (MIMO) antenna using double Y-shaped decoupling structure with high isolation and triple notched-band is presented. The designed antenna composed of two orthogonally placed monopole elements, coplanar ground and double Y-shaped branch. The defected substrate structure is used to achieve miniaturization. By slotting successively C-shaped slot, semi-circular slot and rectangular slot on the radiation patch and the ground, achieved three notched bands at 3.5 GHz WiMAX, 5.25 GHz WLAN, and 7.5 GHz X-band. The proposed antenna can operate in range of 2.56-12 GHz with triple notched bands of 3.31-3.96 GHz, 4.58-5.67 GHz and 6.57-8.16 GHz. Considering all the results, it can be concluded that the antenna presented has a great performance in terms of good radiation, high isolation (>24 dB), a low level ECC (<0.01) and a high DG level (>9.99), which proves the presented antenna has good prospect in UWB-MIMO systems.

Effect of feeding condensed tannins in high protein finishing diets containing corn distillers grains on ruminal fermentation, nutrient digestibility, and route of nitrogen excretion in beef cattle.

Eight ruminally cannulated crossbred beef heifers (427 ± 41.2 kg, body weight) were used in a replicated 4 × 4 Latin square to determine the effects of feeding a condensed tannin (CT) extract with high protein diets containing corn dried distillers grains and solubles (DG) on ruminal fermentation, nutrient digestibility, and route of nitrogen (N) excretion. Dietary treatments included [dry matter (DM) basis]: 0 (0DG), 20 (20DG), and 40% DG (40DG), and 40% DG with 2.5% CT extract (1.33% CT) from Acacia mearnsii (40DGCT). The DG and CT extract were substituted for grain in a barley-based diet that contained 91% concentrate and 9% silage (DM basis) and was fed as a total mixed ration once daily. The crude protein concentrations of the diets were 12.9, 16.8, 20.4, and 20.5% for 0DG, 20DG, 40DG, and 40DGCT, respectively. Periods were 5 wk with 2 wk for transition to the DG level of the diets, 1 wk for adaptation to CT, and 2 wk for measurements. Feed offered and refused were measured daily. Total urine and fecal output were collected daily for 4 d consecutively. Data were analyzed using a mixed linear model with diet and period as fixed effects and square and animal within square as random effects. There was no effect (P ≥ 0.22) of CT on DM intake, but 40% DG in the diet (40DG and 40DGCT) decreased (P ≤ 0.015) DM intake compared with 20DG. As a result, nitrogen (N) intake was not different (P > 0.15) among heifers fed 20DG, 40DG, and 40DGCT (313 g N/d) and was less (P ≤ 0.001) for heifers fed 0DG (220 ± 18 g N/d). Apparent total tract N digestibility was less (P ≤ 0.001) in heifers fed 40DGCT (70.6 ± 1.07%) compared with to 0DG, 20DG, and 40DG (78.4%). There was no effect (P = 0.84) of CT (40DGCT vs. 40DG) on the total N output, however, feeding 40DGCT decreased (P ≤ 0.001) the excretion of total urinary N and urea N in urine by 17 and 21%, respectively, compared with heifers fed 40DG and was equivalent (P ≥ 0.12) to the amount excreted by heifers fed 20DG. The reduction of N digestibility reflected the protein binding effects of CT within the gastrointestinal tract and the shift in excess N excretion from labile urea N in urine to bound NDIN and ADIN in feces (P ≤ 0.001) in heifers fed 40DGCT compared with 40DG. Supplementation of CT in high protein diets fed to feedlot cattle reduced urinary N and increased the capture of N in manure to potentially lesson the loss of N as ammonia and provide opportunities for improved nutrient management of beef production.

Fluctuating plasma phosphorus level by changes in dietary phosphorus intake induces endothelial dysfunction.

High serum phosphorus (P) impairs endothelial function by increasing oxidative stress and decreasing nitric oxide production. Serum P levels fluctuate due to circadian rhythms or dietary P intake in healthy people and due to dialysis in end-stage chronic kidney disease patients. Here we examined whether fluctuating plasma P caused by changes in dietary P intake may be involved in endothelial dysfunction, resulting in increased cardiovascular risk. Rats were fed a diet containing 0.6% P for 16 days (control group), or a diet alternating between 0.02% P and 1.2% P (LH group) or between 1.2% P and 0.02% P (HL group) every 2 days; the total amount of P intake among the groups during the feeding period was similar. In the LH and HL groups, endothelial-dependent vasodilation significantly decreased plasma 8-(OH)dG level significantly increased, and the expression of inflammatory factors such as MCP-1 increased in the endothelium as compared with the control group. These data indicate that repetitive fluctuations of plasma P caused by varying dietary P intake can impair endothelial function via increased oxidative stress and inflammatory response. Taken together, these results suggest that habitual fluctuation of dietary P intake might be a cause of cardiovascular disease through endothelial dysfunction, especially in chronic kidney disease patients.

Oxidative Stress Parameters in Blood and Urine of Metal Shelf Production Factory Workers

Objectives: We have investigated the level of antioxidants (glutathione (GSH), GSH-reductase, GSH-peroxidase, GSHtransferase, catalase (CAT) and superoxide dismutase (SOD)), lipid peroxidation products (plasma, erythrocyte and urinary malondialdehyde (MDA)) and urinary DNA damage product 8-hydroxydeoxyguanosine (8-OH-2’-dG) in metal-shelf factory workers and compared the levels to those of a control group working in a different work area.Methods: Twenty four workers working in a metal shelf production factory and sixteen apparently healthy male volunteers without environmental and work place exposure were included in the study. Blood and urine samples were examined for oxidative stress parameters. Measurement of 8-OH-2’-dG was by high performance liquid chromatography (HPLC), while other parameters were measured by colorimetric methods.Results: GSH-transferase, CAT, SOD activities and plasma, erythrocyte and urinary MDA levels of metal shelf production factory workers were higher than for the control group, whereas, GSH-peroxidase and GSH in workers were lower than for controls. Moreover, while GSH-reductase activity was lower, 8-OH-2’-dG level was higher than the control group but the difference was not statistically significant.Conclusion: As a result of increased industrialization, air pollution and hazardous working conditions there is a deterioration of the balance between oxidant and antioxidant levels which affects the structure of macromolecules such as DNA, lipids and proteins

DNA methylation by dimethyl sulfoxide and methionine sulfoxide triggered by hydroxyl radical and implications for epigenetic modifications

In this Letter, we demonstrate the formation of m(5)dC from dC or in DNA by dimethylsulfoxide (DMSO) and methionine sulfoxide (MetO), under physiological conditions in the presence of the Fenton reagent in vitro. DMSO reportedly affects the cellular epigenetic profile, and enhances the metastatic potential of cultured epithelial cells. The methionine sulfoxide reductase (Msr) gene was suggested to be a metastatis suppressor gene, and the accumulation of MetO in proteins may induce metastatic cancer. Our findings are compatible with these biological data and support the hypothesis that chemical cytosine methylation via methyl radicals is one of the mechanisms of DNA hypermethylation during carcinogenesis. In addition to m(5)dC, the formation of 8-methyldeoxyguanosine (m(8)dG) was also detected in DNA under the same reaction conditions. The m(8)dG level in human DNA may be a useful indicator of DNA methylation by radical mechanisms.

Preparation of monoclonal antibodies against oh(8)dG and their biological characteristics

To prepare monoclonal antibodies against oh(8)dG and to evaluate the relationship between Hp infection and oxidative DNA damage by detecting oh8dG in gastric mucosa. BALB/C mice were immunized with BSA-oh(8)dG conjugate, monoclonal antibodies were prepared by hybridoma technique, the biological characteristics of antibodies were analysed by competitive ELISA, Western blot and immunohistochemistry. Two strains of hybridoma cell were obtained. ELISA and Western blot indicated that the antibodies were fairly specific for oh(8)dG. In immunohistochemistry,the positive rate of oh(8)dG expression in Hp positive tissues and Hp negative tissues was 55% and 5%, respectively(P<0.01). The prepared antibodies can specially recognize oh(8)dG and immunohistochemistry with the monoclonal antibodies showed Hp infection can increase oh(8)dG level in gastric mucosa.

Melatonin protects against ischemia and reperfusion-induced oxidative lipid and DNA damage in fetal rat brain.

To investigate whether melatonin reduces the susceptibility of the fetal rat brain to oxidative damage of lipids and DNA, we created a model of fetal ischemia/reperfusion using rats at day 19 of pregnancy. Fetal ischemia was induced by bilateral occlusion of the utero-ovarian artery for 20 min. Reperfusion was achieved by releasing the occlusion and restoring the circulation for 30 min. A sham operation was performed in control rats. Melatonin (10 mg/kg) or vehicle was injected intraperitoneally 60 min prior to the occlusion. We measured the concentration of thiobarbituric acid reactive substances (TBARS) in fetal brain homogenates, as well as levels of deoxyguanosine (dG) and 8-hydroxydeoxyguanosine (8-OHdG) in DNA extracted from those homogenates. Ischemia for 20 min did not significantly alter the levels of dG, 8-OHdG, and TBARS. Subsequent reperfusion, however, led to a significant reduction in the dG level (P < 0.05) and to significant increases in the levels of 8-OHdG (P < 0.05) and TBARS (P < 0.05), and in the 8-OHdG/dG ratio (P < 0.005). Melatonin administration prior to ischemia significantly reduced the ischemia/reperfusion-induced increases in the levels of 8-OHdG (14.33 +/- 6.52-5.15 +/- 3.28 pmol/mg of DNA, P < 0.001) and TBARS (11.61 +/- 3.85-4.73 +/- 3.80 nmol/mg of protein, P < 0.001) as well as in the 8-OHdG/dG ratio (7.19 +/- 2.49-1.61 +/- 0.98, P < 0.001). Furthermore, melatonin significantly increased the dG level (210.19 +/- 49.02-299.33 +/- 65.08 nmol/mg of DNA, P < 0.05). Results indicate that melatonin administration to the pregnant rat may prevent the ischemia/reperfusion-induced oxidative lipid and DNA damage in fetal rat brain.

Prolonged activation of phospholipase D in Chinese hamster ovary cells expressing platelet-activating-factor receptor lacking cytoplasmic C-terminal tail.

The mechanism and role of phospholipase D (PLD) activation by platelet-activating factor (PAF) were examined with Chinese hamster ovary cells stably expressing wild-type PAF receptor (WT-H cells) and truncated PAF receptor lacking the C-terminal cytoplasmic tail (D-H cells). Treatment of D-H cells with PAF resulted in the rapid formation of Ins(1,4,5)P3, which was followed by a sustained phase for more than 10 min. In these cells, PAF-induced PLD activation lasted for more than 20 min. In contrast, PLD activation in WT-H cells was transient. PAF stimulation caused the biphasic formation of 1,2-diacylglycerol (DG) in both types of cell. The first phase was rapid and transient, coinciding with the Ins(1,4,5)P3 peak. The second sustained phase of DG formation was attenuated by butanol, which produces phosphatidylbutanol at the expense of phosphatidic acid (PA) by transphosphatidylation activity of PLD, and by propranolol, a selective inhibitor for PA phosphohydrolase catalysing the conversion of PA into DG. The DG level returned nearly to basal at 20 min after PAF stimulation in WT-H cells, whereas in D-H cells the elevated DG level was sustained for more than 20 min. The profile of translocation of protein kinase Calpha (PKCalpha) to membrane was similar to that of DG formation. In WT-H cells, PKCalpha was transiently associated with membranes and then returned to the cytosol. However, in D-H cells PKCalpha was rapidly translocated to and remained in membranes for more than 20 min. Butanol suppressed this sustained translocation of PKCalpha. Furthermore the mRNA levels of c-fos and c-jun by PAF in WT-H cells were much lower than those in D-H cells. Propranolol and butanol at concentrations that inhibited the formation of DG suppressed the PAF-induced mRNA expression of c-fos and c-jun. Taken together, the prolonged PLD activation in D-H cells confirmed a primary role for phospholipase C/PKC in PLD activation by PAF. Furthermore the results obtained here suggest that sustained PLD activation in turn leads to chronic activation and membrane translocation of PKCalpha, which might play an important role in the expression of c-fos and c-jun.

Inhibition of the proliferation of cultured immortalized Schwann cells by forskolin with a decreased basal level of diacylglycerol.

The repetitive passages of a Schwann cell culture results in the appearance of immortalized cells. In order to investigate the direct effects of cyclic AMP (cAMP) on Schwann cell proliferation, we used the immortalized Schwann cells because the responses of a short-term Schwann cell culture to agents increasing the intracellular cAMP are more complicated and it does not seem that all of them are due to the direct effects of cAMP. By adding up to 200 microM of forskolin, an adenylate cyclase activator, to the culture medium, Schwann cell proliferation was inhibited and the intracellular 1,2-diacylglycerol (DG) level was decreased in a dose-dependent manner to 44 and 53% of the control values, respectively. The protein phosphorylation activity in the cytosol from the cell treated with 100 microM forskolin, assayed with myelin basic protein as the acceptor, decreased to 78% and this inhibition was then reversed by the addition of 1-oleoyl-2-acetyl-sn-glycerol (OAG), a membrane-permeable DG, to the assay mixture. The cell proliferation inhibited by forskolin was also restored by the addition of OAG. These data suggest that cAMP inhibits both the activity of protein kinase C (PKC) and consequently cell proliferation through suppression of intracellular DG level, an activator of PKC. Since the inositol 1,4,5-triphosphate level and the hydrolysis of phosphatidylcholine to DG and phosphorylcholine were not affected, forskolin therefore appears to suppress the de novo synthesis of DG.

A rise and fall in 1,2-diacylglycerol content signal hexamethylene bisacetamide-induced erythropoiesis.

Previous studies have suggested a role for protein kinase C (PKC) during induction of murine erythroleukemia cell (MELC) differentiation by hexamethylene bisacetamide (HMBA) (Melloni, E., Pontremoli, S., Viotti, P. L., Patrone, M., Marks, P. A., and Rifkind, R. A. (1989) J. Biol. Chem. 264, 18414-18418). The present studies assess the effect of HMBA on the content of 1,2-diacylglycerol (DG), the physiologic activator of PKC, in MELC variants. Exposure of parental Sc9 cells to HMBA induced a rapid rise and fall in DG content. The DG level increased within seconds from 225 pmol.10(6) cells-1 to a maximum of 305 pmol.10(6) cells-1 at 5 min. Thereafter, DG content fell reaching control levels at 30 min and 46% of control at 4 h. Similar DG elevations were detected in HMBA-resistant, phorbol ester-resistant, and vincristine-resistant MELC lines. Early DG elevation was followed by the characteristic rapid fall in both the phorbol ester-resistant and vincristine-resistant lines, both of which differentiate rapidly in response to HMBA. In contrast, in an HMBA-resistant MELC the DG level failed to fall for at least 10 h. Selection of HMBA-resistant cells for vincristine resistance restores both HMBA sensitivity and the rapid fall in DG content. Addition of a synthetic DG, 1-oleyl-2-acetyl glycerol (OAG), along with HMBA and every 2 h for the next 48 h blocked differentiation, as measured by accumulation of benzidine-reactive cells or by the commitment assay in methyl-cellulose. However, if addition of OAG was delayed for just a few minutes, until endogenous DG levels began to fall, differentiation was no longer inhibited. Rapid elevation of DG content is the earliest reported event during HMBA action and a subsequent fall in the DG content appears to be a critical step in the process of commitment to terminal differentiation.

Effect of staurosporine on fMet-Leu-Phe-stimulated human neutrophils: dissociated release of inositol 1,4,5-triphosphate, diacylglycerol and intracellular calcium

Staurosporine, a microbial alkaloid, enhances inositol 1,4,5-triphosphate (IP 3) and 1,2-diacylglycerol (DG) production rapidly and dose-dependently in fMet-Leu-Phe (FMLP)-stimulated human neutrophils showing maximal effects at 1 μM concentration. The IP 3 increase was specific for staurosporine as three other putative protein kinase C (PKC) inhibitors, H7, sphingosine and palmitoylcarnitine were unable to enhance the IP 3 generation in FMLP-stimulated human neutrophils. Staurosporine, at concentrations 0.3–1.0 μM, did not affect the initial mobilization of FMLP-induced intracellular Ca 2+ (Ca 2+ i), although a sustained elevation of cytosolic Ca 2+ level was observed within 5 min. This effect could not be suppressed, even by 1 μM phorbolmyristate 12,13-acetate (PMA). Whereas lower concentrations of staurosporine (≤ 100 nM) were unable to affect FMLP-induced IP 3 production, DG accumulation and Ca 2+ i, the PMA-inhibited initial Ca 2+ i signal and IP 3 formation triggered by FMLP were almost completely restored. At higher concentrations (≥ 300 nM) staurosporine reversed the inhibitory effect of other protein kinases, distinct from the PMA-inducible one, which may be responsible for the phosphatidyl inositol 4,5-biphospinate (PIP i) breakdown, thus causing accumulation of IP 3 and DG and an elevation of Ca 2+ i level. Whereas IP 3 declined to basal level within 5 min, the DG level remained elevated during the same period. This phenomenon is attributed to phospholipase D (PLD) stimulation by staurosporine, which augments the DG synthesis, in part through PA degradation via phosphatidic acid (PA) phosphohydrolase.

Angiogenin activates phospholipase C and elicits a rapid incorporation of fatty acid into cholesterol esters in vascular smooth muscle cells

Angiogenin activates the phosphoinositide-specific phospholipase C (PLC) in cultured rat aortic smooth muscle cells to yield a transient (30 s) peak of 1,2-diacylglycerol (DG) and inositol trisphosphate. Within 1 min, the DG level falls below that of the control and remains so for at least 20 min. A transient increase in monoacylglycerol indicates that depletion of DG may be the consequence of hydrolysis by DG lipase. In addition to these changes in second messengers, a rapid increase in incorporation of radiolabeled tracer into cellular cholesterol esters is observed. Stimulated cholesterol ester labeling is inhibited by preincubation with either the DG lipase inhibitor RHC 80267 or the acyl coenzyme A:cholesterol acyltransferase inhibitor Sandoz 58035. Cells prelabeled with [3H]arachidonate show a sustained increase in labeling of cholesterol esters following exposure to angiogenin. In contrast, cells prelabeled with [3H]oleate show only a transient elevation that returns to the basal level by 5 min. This suggests initial cholesterol esterification by oleate followed by arachidonate that is released by stimulation of the PLC/DG lipase pathway.