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Mediators of Inflammation
Volume 2013 (2013), Article ID 641851, 10 pages
NAG-1/GDF15 Transgenic Mouse Has Less White Adipose Tissue and a Reduced Inflammatory Response
1Laboratory of Molecular Carcinogenesis, National Institutes of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
2Division of Structural and Functional Genomics, Korea National Institute of Health, Osong 363-951, Republic of Korea
3Biostatistics Branch, National Institutes of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
4National Toxicology Program, National Institutes of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
5Laboratory of Respiratory Biology, National Institutes of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA
6Department of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA
7Eicosanoid Biochemistry Section, Laboratory of Molecular Carcinogenesis, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, USA
Received 10 January 2013; Revised 18 March 2013; Accepted 3 April 2013
Academic Editor: Antonio Macciò
Copyright © 2013 J. M. Kim et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
NAG-1/GDF15 is a TGF-β superfamily member with poorly characterized biological activity proposed to inhibit inflammatory cytokine production. Transgenic mice expressing human NAG-1/GDF15 () are leaner with lower body weight and are resistant to chemically or genetically induced intestinal tumors. Because of the link between obesity, inflammation, and cancer, we examined whether these mice exhibit a reduced response to inflammatory stimuli. The mice had a reduced inflammatory response to LPS based on the serum levels of cytokines KC, IL-6, MCP-1, and TNFα. In contrast to literature reports and our in vivo results, NAG-1 did not inhibit LPS-induced cytokine expression in vitro in RAW264.7 cells, mouse peritoneal macrophages, or mouse liver Kupffer cells, suggesting that NAG-1/GDF15 does not directly inhibit LPS-induced inflammatory cytokine production. However, mice have less white adipose tissue, the major source of inflammatory adipokines including leptin. Basal and LPS-treated serum leptin and mRNA levels in the adipose tissue of mice were lower than those in WT mice. We propose that the reduced white adipose tissue and reduced leptin expression may be responsible, in part, for the reduced inflammatory response to LPS and the decrease in intestinal tumors observed in mice.
1. Introduction
Nonsteroidal anti-inflammatory drug-activated gene (NAG-1/GDF15) is a divergent member of the TGF-β superfamily and is also known as macrophage inhibitory cytokine (MIC-1) [1, 2]. NAG-1/GDF15 expression is induced by a number of anti-inflammatory drugs and chemicals known to have antitumorigenic activities, including cyclooxygenase inhibitors, dietary agents, PPAR agonist, and anticancer drugs [3]. The overexpression of NAG-1 in cancer cells stimulates apoptosis and inhibits tumor growth in mouse xenograft models [3]. A transgenic mouse was developed in this laboratory which ubiquitously expresses human NAG-1/GDF15 () under the control of the chicken β-actin promoter (CAG) [4]. In addition to expression in most tissues including skin, kidney, colon, brain, and lung, it is found at high levels in the serum (~50 ng/mL), as NAG-1 is a secreted protein. The mouse has no apparent phenotype except for being leaner with DEXA densitometry (PIXImus) analysis indicating less adipose tissue. Previously we reported that the transgenic mice are resistant to chemically and genetically induced intestinal tumors [4]. Treatment of the transgenic mice with the intestinal carcinogen azoxymethane (AOM) induced fewer intestinal tumors as compared to the wild-type (WT) mice. Crossing the NAG-1 transgenic mouse with the mouse that spontaneously develops polyps produced an mouse expressing NAG-1. This mouse developed fewer polyps than the WT mouse. These data support the notion that NAG-1 acts to suppress intestinal tumor formation during the early stages of tumorigenesis. Because overexpression of NAG-1 induces apoptosis in cultured cancer cells [5], we expected increased apoptosis to be one of the mechanisms for the inhibition of intestinal tumor growth in our mouse model. However, we did not observe spontaneous apoptosis in the mouse, suggesting other mechanisms are responsible for the tumor suppression.
Inflammation can be an important determinant in the development of cancer and is a driving force for the development of colorectal cancer [6, 7]. Many reports in the literature confirm the importance of inflammation in AOM-induced intestinal tumor formation. For example, genetic deletion of critical NFkB components reduces tumor formation [8] in mice treated with AOM. Inflammation also plays a critical role in the mouse model [9, 10]. Bootcov et al. [11] previously reported that NAG-1/GDF15 inhibits LPS-induced cytokine formation in macrophages, the experimental basis for naming the protein MIC-1 (macrophage inhibitory cytokine). Thus, we suspected one potential mechanism for the resistance of the to intestinal tumor formation was a lower inflammatory response.
In humans, the accumulation of white adipose tissue in obesity provides a source of chronic inflammation, which likely explains the fact that obese people are at increased risk for developing colorectal cancer [12]. Various mouse models have highlighted the pivotal role of white adipose-derived leptin as an inflammatory cytokine that plays a critical role in the development of intestinal cancer. Leptin is a secreted adipokine, whose levels are proportional to one's amount of white adipose tissue [13]. Obesity increases serum leptin levels, which acts as a growth and survival factor for colon epithelial cells and increases tumor growth in the AOM model [14]. Mice lacking the leptin gene () [14] have very high levels of white adipose tissue but are devoid of leptin expression and have a lower tumor burden after treatment with AOM. Furthermore, obese leptin receptor deficient () mice have decreased intestinal tumor formation after AOM treatment. Obese KK-Ay mice are highly susceptible to AOM-induced colorectal cancer [15], exhibit high serum leptin concentrations, and increased expression of inflammatory cytokines in their serum and visceral fat. These findings support the importance of leptin as an inflammatory link between white adipose tissue and intestinal tumorigenesis.
In this report, we test whether the mouse exhibits a reduced response to inflammatory stimuli, to help explain its protection against tumor formation in the AOM and models of intestinal tumorigenesis. The mice show a reduced systemic inflammatory response to lipopolysaccharide (LPS), exhibited by lower levels of inflammatory cytokines in their serum. Interestingly, this reduction was not due to direct inhibition of cytokine production by NAG-1 in macrophages. mice are leaner [4] and have significantly lower amounts of white adipose tissue (WAT) and thus lower levels of leptin. We propose that the smaller WAT and hence lower leptin expression may be responsible for the lower inflammatory response and lower intestinal polyp formation observed in the mouse. This study illustrates how white adipose tissue can alter inflammation.
2. Methods and Procedures
2.1. Animals
As described previously, we produced two independent transgenic mouse lines (1377 and 1398) that ubiquitously express human NAG-1 protein, , under the control of CAG, using traditional pronuclear microinjection on the C57/BL6 background [4]. Seven-to twelve-week-old male and female mice from lines 1377 and 1398 mice and NAG-1 wild-type (WT) littermates were used in these experiments. The mice were housed at NIEHS or ILS under guidelines for the ethical treatment of animals. All procedures conducted in this study were approved by the appropriate institutional animal care and use committees.
2.2. LPS Treatment and Cytokine Analysis
mice and nontransgenic WT littermates of both 1377 and 1398 lines were treated with LPS (25 mg/kg, Sigma) via intraperitoneal (i.p.) injection and then sacrificed by CO2 inhalation and the blood was collected at the times indicated in the figure legends. The serum was used for cytokine analysis using the Multiplex cytokine detection assay system according to the manufacturer's instructions (Bio-Plex mouse cytokine assay, Bio-Rad).
2.3. Real-Time Polymerase Chain Reaction and Primers
Total RNA was isolated using the RNeasy Mini Kit (Qiagen) according to the manufacturer's instructions. Following DNAse I treatment (Invitrogen), reverse transcription was carried out with 1 μg total RNA using the SuperScript II reverse transcription system (Invitrogen) according to the manufacturer's instructions. Real-time PCR was performed in duplicate with individual time-matched vehicle-treated controls using SYBR Green PCR Master Mix (BioRad), a BioRad iCycler Thermal Cycler and the following primers: hNAG-1, F: 5′-ctccagattccgagagttgc-3′, R: 5′-agagatacgcaggtgcaggt-3′ mGDF15, F: 5′-ttctgtggggacggtcag-3′, R: 5′-cgggtgaccaggctaattc-3′ mCOX-2, F: 5′-cccccacagtcaaagacact-3′, R: 5′-gagtccatgttccaggagga-3′ mMcp-1, F: 5′-aggtccctgtcatgcttctg-3′, R: 5′-tctggacccattccttcttg-3′ mKC, F: 5′-gcacccaaaccgaagtcata-3′, R: 5′-tggggacaccttttagcatc-3′ mIL-6, F: 5′-ccggagaggagacttcacag-3′, R: 5′-ggaaattggggtaggaagga-3′ mTNF-α, F: 5′-cgtcagccgatttgctatct-3′, R: 5′-cggactccgcaaagtctaag-3′ mLeptin, F: 5′-tgacaccaaaaccctcatca-3′, R: 5′-tgaagcccaggaatgaagtc-3′ mLeptin Receptor, F: 5′-gggaatgagcaaggtcaaaa-3′, R: 5′-tcaagtcccctttcatccag-3′ mIL-1β, F: 5′-caggcaggcagtatcactca-3′, R: 5′-tgtcctcatcctggaaggtc-3′ mGAPDH, F: 5′-caggagcgagaccccactaacat-3′, R: 5′-gtcagatccacgacggacacatt-3′ mβ-actin, F: 5′-tgacaggatgcagaaggaga-3′, R: 5′-cgctcaggaggagcaatg- 3′.
The following cycle parameters were used: 95°C for 10 minutes; 40 cycles of 95°C for 15 seconds, 60°C for 30 seconds; 95°C for 1 minute; 60°C for 1 minute; 81 cycles of 55°C for 10 seconds. BioRad iQ5 Version 2.0 software was used to calculate Ct values for all genes. Corrected Ct values were calculated by subtracting the average control gene (actin or GAPDH) Ct value from the average Ct value for a given gene. Fold differences were calculated using the corrected Ct values.
2.4. RAW Cell Culture and Transfections
RAW 264.7 (ATCC) cells were plated in 60 mm culture dishes and grown overnight in DMEM supplemented with 10% fetal bovine serum. The next day, the cells were transfected with either empty vector or an NAG-1 expression vector [16] using Lipofectamine 2000 according to the manufacturer's protocol (Invitrogen) for 24 hours. Cells were treated with LPS (1 µg/mL) or vehicle for 6 hours. The transfections were performed for three independent times. RNA isolation and RT-PCR were performed as described previously.
2.5. Isolation and Culture of Intraperitoneal Macrophages and Kupffer Cells
To obtain intraperitoneal macrophages, mice were injected i.p. with 3% thioglycollate solution to enhance macrophage recruitment and 3 days later peritoneal cells were isolated. Kupffer cell isolation was performed following Current Protocols in Toxicology [17]. Briefly, mouse livers were perfused by inserting and securing a catheter through the vena cava, severing the portal vein and perfused with prewarmed CMF-HBSS until clear, then pre-warmed 0.03% collagenase type IV in HBSS at a rate of 5 mL/min for 5 minutes. Perfused livers were kept on ice in a small volume of CMF-HBSS in sterile conical polypropylene tubes until all tissue collection was completed. To obtain adequate cell numbers, the livers of two mice per genotype were perfused and pooled prior to Kupffer cell isolation. After Percoll gradient centrifugation, pellets were resuspended in 1 ml HBSS and counted using an automated cell counter (Nexcelom Bioscience). Consistently, from both WT and mice, 1-2 million Kupffer cells were isolated per mouse liver. Equal numbers of either WT or Kupffer cells were plated in triplicate onto 6-well dishes containing RPMI 1640 with 10% FBS, cultured for 24 hours in a humidified incubator at 37°C containing 5% CO2, then treated with 10 ng/mL LPS or vehicle for 6 hours prior to harvest. Cell culture media were collected, spun briefly to remove cell debris, aliquoted, and frozen at –80°C until ELISA analysis was performed. In experiments using the recombinant protein, WT Kupffer cells were treated with either 50 ng/mL recombinant human GDF-15 (SBH Sciences, MA, USA) or vehicle for 2 hours prior to LPS treatment.
2.6. Recombinant NAG-1 Protein
Purified recombinant human NAG-1 was purchased from R&D Systems (Minneapolis, MN, USA) and from SBH Sciences (Natick, MA, USA). The R&D Systems protein contains an N-terminal 6-His tag, whereas the SBH Sciences protein does not. The lyophilized protein was reconstituted with 1% BSA in PBS and stored at 4°C.
2.7. Statistical Analysis
Student's test and standard deviation (SD) were calculated using Microsoft Excel (Microsoft, Redmond, WA, USA). Standard error was calculated with Stat View (Abacus Concept, Berkeley, CA, USA). Statistical analysis of cytokine levels in sera was done by analysis of variance (ANOVA).
3. Results
3.1. NAG-1 Transgenic Mice Have a Decreased Inflammatory Response to LPS
LPS is a commonly used and well-studied systemic inflammatory agent that signals through the Toll-like Receptor 4 (TLR4) leading to NFκB pathway activation and the subsequent expression of inflammatory cytokines. Treatment of mice with LPS increases the circulating levels of inflammatory cytokines, offering a convenient and suitable assay to determine how alterations in the expression of specific genes modulate the inflammatory response. The concentrations of several inflammatory cytokines were measured in serum from WT and mice 4 hours after treatment with LPS (Figure 1(a)). Serum concentrations of the cytokines IL-6, KC, and MCP-1 were significantly lower in the mice, as compared to WT littermates following LPS treatment. To evaluate the kinetics of cytokine production in the mice, serum was collected at 2, 4, and 6 hours after LPS treatment. At all time points examined, we observed lower levels of IL-6, KC, and MCP-1 in the mice as compared to their WT littermates, with the most dramatic reduction observed for TNF-α at 2 hours (Figure 1(b)). No significant differences were observed between the responses of 1377 and 1398 lines to LPS, and only the results from 1398 are reported. No statistically significant difference between male and female (data not shown) was found. These results suggest that mice have a reduced response to inflammatory stimuli and that NAG-1 may have anti-inflammatory activity.
3.2. Macrophages, NAG-1, and NFκB Pathway
Activation of the NFκB pathway and the subsequent increase in the production of inflammatory cytokines are important components of the systemic response to LPS. The NFκB pathway also plays an important role in intestinal inflammation and tumor formation [3]. Thus, we examined whether NAG-1 could directly inhibit this pathway. Macrophages were chosen for these experiments, as they are one of the major sources of inflammatory cytokines in response to LPS and are a suitable model system to study the NFκB pathway [8] and previous studies have demonstrated that NAG-1/GDF15 inhibits cytokine production from macrophages [11]. RAW 264.7 cells, a mouse macrophage cell line responsive to LPS, were treated with 10 to 100 ng/mL recombinant mature human NAG-1 protein (rhNAG-1) for 2 hours prior to LPS treatment (5 ng/mL) and incubated for the indicated times. Two different preparations of purified recombinant human NAG-1 protein were used. One preparation, which is reported to have activity in a number of biological systems, contains an N-terminal 6-His tag and the second is tagless [18, 19]. RNA isolated from the cells was used for real-time PCR analysis for several inflammatory mouse cytokines (TNF-α, IL-1β, and IL-6). As shown in Figure 2(a), while LPS stimulated inflammatory cytokine gene expression in RAW 264.7 cells, pretreatment with rhNAG-1 did not reproducibly inhibit TNF-α, IL-1β, and IL-6 mRNA levels. We also measured mouse GDF15 mRNA levels using real-time PCR to rule out the possibility that the endogenous protein was contributing towards our phenotype. While mGDF15 mRNA levels increased in response to rhNAG-1, treatment of RAW cells with LPS alone led to an equivalent fold induction of mGDF15. Next, a human NAG-1 expression vector was transfected into RAW 264.7 cells, and cytokine expression was measured using real-time PCR, after 6 hours of treatment with LPS or vehicle. Using primers specific to the human NAG-1 mRNA, we confirmed that human NAG-1 is highly expressed only in the NAG-1 transfected cells. However, as shown in Figure 2(b), there was no difference in cytokine production between empty vector transfected and NAG-1 transfected cells after LPS treatment, despite lower MCP-1 and IL-6 levels in vehicle-treated NAG-1 transfected cells. We also measured mGDF15 using primers specific to the mouse GDF15 mRNA. LPS treatment led to similar induction of mGDF15 in both empty vector and NAG-1 transfected cells (data not shown). Together, these data suggest that NAG-1 does not directly inhibit the TLR4/NFκB pathway.
To test the hypothesis that expression of the transgene in the developing mouse could alter inflammatory signaling components and explain the reduced response to LPS, peritoneal macrophages were isolated from WT and mice, cultured and treated with 5 ng/mL LPS. The levels of secreted TNF-α and IL-6 after LPS treatment were measured in the culture supernatants at the times indicated using cytokine-specific ELISAs. As shown in Figure 3, the production of TNF-α and IL-6 in response to LPS was similar in WT and macrophages, indicating that macrophages ex vivo do not have impaired TLR4/ NFκB signaling. Furthermore, preincubation of peritoneal macrophages isolated from WT mice with rhNAG-1 did not alter their response to LPS (data not shown). Thus, NAG-1 does not directly inhibit or alter the LPS-activated TLR4/ NFκB pathway in macrophages. The reduction in the inflammatory response to LPS observed in the mouse does not appear to be a consequence of direct inhibition of macrophage-derived cytokine production.
3.3. NAG-1 and Kupffer Cells
Because Kupffer cells, the resident liver macrophages, are an important source of LPS-induced inflammatory cytokines, we chose to examine their response to LPS ex vivo, taking two different approaches. First, we isolated Kupffer cells from WT mice and cultured them in the presence of rhNAG-1 or vehicle prior to LPS treatment. While LPS treatment led to an increase in the media concentrations of IL-6 and TNF-α as measured by ELISA, pretreatment with rhNAG-1 had no effect on cytokine production (Figure 4(a)). Taking a second approach, we isolated and cultured Kupffer cells from and WT mice, treated them with LPS, and measured IL-6 and TNF-α production. Again, the Kupffer cells responded to the inflammatory stimulus, but there was no difference in the responses between the and WT control cells (Figure 4(b)).
3.4. Leptin and LPS-Induced Inflammation
Leptin is a proinflammatory cytokine and appears to be a pivotal mediator of inflammation in mice [20]. mice lacking the leptin gene have a reduced inflammatory response to LPS [21]. Leptin expression is increased by LPS treatment and plays a role in LPS-induced increases in inflammatory cytokine formation [22, 23]. Interestingly, mice have reduced fat content as measured by DEXA densitometry (PIXImus) [4]. Based on these findings, we suspected that mice would have less white adipose tissue and lower basal leptin levels. To test this hypothesis, the body weights, abdominal fat, and serum leptin concentrations of WT and mice were measured. The body weights of the were significantly lower than their WT littermates with significantly less abdominal white fat (Figure 5). Likewise, basal serum leptin levels were significantly lower in the mice than their WT littermates (Figure 6). Treatment with LPS increased serum leptin levels in both WT and mice; however, like basal levels, the final leptin level was significantly higher in WT mice than in the mice. The basal expression of leptin as measured by RT-PCR in the abdominal white fat was approximately 2-fold higher in the WT mice than in the mice (Figure 6). We also measured the expression of leptin and various inflammatory cytokines in the abdominal fat collected 4 hours after LPS treatment (Figure 6). While there were no significant differences in any of the inflammatory cytokines measured, relative WT leptin levels were approximately 3-fold higher than in mice. Thus the mice, having less abdominal fat, express lower levels of leptin and have lower serum concentrations of leptin than WT mice, both before and after LPS treatment.
4. Discussion
In this study, we demonstrate that the transgenic mice expressing hNAG-1 ubiquitously, mice, have less white adipose tissue and a lower serum level of the inflammatory cytokine leptin. These mice have a reduced response to the systemic inflammatory agent LPS. Although NAG-1 is reported to directly inhibit inflammatory cytokine production in macrophages following LPS treatment [20], we could not confirm this inhibition. Kupffer cells and peritoneal macrophages isolated from WT and mice responded similarly to LPS treatment, despite pretreatment with purified recombinant NAG-1 protein from two different commercial sources. In addition, overexpression of NAG-1 in RAW cells did not alter the cytokine production in the presence of LPS. Thus NAG-1 does not directly inhibit the TLR4/NFkB pathway activated by LPS and may not be a direct inhibitor of macrophage cytokine formation, as reported by others [20].
If NAG-1 does not inhibit cytokine formation, why do mice have a lower inflammatory response and why are these mice resistant to inflammatory driven intestinal tumors? When DEXA densitometry indicated the only apparent phenotype of mice to be less white adipose tissue, we realized that this difference could be indirectly responsible for the LPS phenotype. We propose NAG-1 to have an indirect effect on suppressing the LPS response, based on the finding that mice have significantly lower levels of white adipose tissue, lower leptin expression in their white adipose tissue, and lower serum leptin levels. While we have no direct experimental evidence that leptin is altering the LPS response in the mice and cannot exclude other factors contributing towards the phenotype, we point to the significant body of the literature showing the importance of leptin signaling in the LPS response. For example, pretreatment of peritoneal macrophages with recombinant leptin leads to a significant increase in LPS-induced cytokine production [15]. Furthermore, leptin deficient mice and fa/fa mice which have reduced leptin receptor expression show a significantly decreased response to LPS [21], and mice are more sensitive to LPS-induced lethality [24]. We were able to detect high levels of leptin receptor in both RAW cells and peritoneal macrophages isolated from WT and mice using RT-PCR (data not shown). Leptin expression is reported to be proportional to total adipose mass, yet the levels per gram of white adipose tissue in our mice are lower than those in WT mice, suggesting an additional level of regulation by NAG-1. NAG-1's ability to lower white adipose and circulating leptin levels is not unique to our transgenic mouse model, as it has also been observed in an xenograft model using DU145 cells expressing NAG-1 [25].
Leptin is the critical regulator of intestinal inflammation [26] and a number of studies demonstrate that increases or decreases in the serum levels of leptin can, respectively, increase or decrease the AOM-induced and models of intestinal tumorigenesis [27, 28]. Based on the literature, we propose that the lower white adipose tissue and lower circulating leptin levels may be responsible, in part, for the resistance to intestinal polyps formation observed in the two mouse models of intestinal cancer we previously tested.
Interestingly, the deletion of NAG-1/GDF15 in mice negates the chemoprevention afforded by sulindac treatment [29], suggesting the human and mouse proteins share some common function. However, untreated GDF15−/− mice on the background do not show an increase in polyp number. GDF15 knockout mice and their WT littermates have similar body, adipose tissue weights, and serum leptin levels (data not shown). Likewise, we found that the GDF15 knockout and WT mice have similar responses to LPS as measured by cytokine levels in the serum (data not shown). Two key points can help explain why the GDF15 knockout mouse does not show the opposite phenotype of the mouse. First, mouse NAG-1/GDF15 is expressed mainly in the liver whereas the mice express human GDF15 constitutively and ubiquitously. Second, the mouse and human proteins share only 57% amino acid identity, making it possible that the proteins have unique functions. Future discovery of the structures and receptors of both mouse and human GDF15 will allow for better understanding of their differences. The findings with the GDF15 knockout mice are consistent with the hypothesis that the difference in the amount of adipose tissue and circulating leptin between the and WT mice is an important determinant of the inflammatory response to LPS.
5. Conclusions
In conclusion, we propose that the lower adipose and hence the lower leptin expression may attenuate the response to LPS treatment and may also be responsible for reduced intestinal tumor formation in mice. This hypothesis is in agreement with the critical role of the leptin in mediating intestinal inflammation and tumor growth. The lower expression of leptin as a result of a reduction in white adipose tissue and the reduced leptin expression within the adipose tissue in the mouse provide one mechanism by which NAG-1 may act to alter inflammation and tumor growth. These results also highlight the link between white adipose tissue mass and inflammation.
|Growth differentiation factor-15
|NSAID-activated gene
|C57Bl6 mice expressing human NAG-1
|Keratinocyte-derived cytokine
|Monocyte chemotactic protein-1
|Tumor necrosis factor-alpha
|Enzyme-linked immunosorbent assay
|Mice, leptin deleted obese mice
|Wild-type, db/db, leptin receptor deleted mice.
Conflict of Interests
There is no conflict of interests with any author on this paper.
Authors' Contribution
J. M. Kim and J. P. Kosak contributed equally to this paper.
The authors thank Colleen Anna, NIEHS, and Kyung-Won Min for their excellent technical assistance, the staff of ILS for their support, and Nichelle Whitlock (University of Tennessee) for mouse genotyping. They also thank James Clark, NIEHS for his expertise performing the mouse liver perfusions. This research was supported, in part, by NIH, NIEHS Intramural Research Program: Projects (Zeldin) Z01 ES025043 and (Eling) Z01- ES010016-14. The current address of J. M. Kim is the Division of Structural and Functional Genomics at Korea National Institute of Health, Osong, Republic of Korea.
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subset: commoncrawl


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Where's your hat?<quoted text>Dear Brian, for some reason I feel you are full O crap. I remember you as well as Chief posting page after page on a thread that asked if Homosexuality was a sin. If I remember you thought it was and sick. Yet now its AOK.
Judge overturns California's ban on same-sex marriage
There are 201885 comments on the www.cnn.com story from Aug 4, 2010, titled Judge overturns California's ban on same-sex marriage. In it, www.cnn.com reports that:
A federal judge in California has knocked down the state's voter-approved ban on same-sex marriage, ruling Wednesday that the state's controversial Proposition 8 violates the U.S. Constitution.
Join the discussion below, or Read more at www.cnn.com.
#178528 Feb 6, 2013
#178529 Feb 6, 2013
With the times moving so fast what's a person to do?
Has there been a vote taken?
"CO2 is Gaseous Love"
Since: Dec 08
Home, sweet home.
#178530 Feb 6, 2013
The statement above is untrue; I've always written there is nothing wrong with homosexuals or homosexuality. I've never discussed sin or written homosexuality is sick, those are Jazybird58'S words, not mine.
Many homosexuals believe in protecting male/female marriage too. Conservatism doesn't have a sexual orientation.
#178531 Feb 6, 2013
Even though I disagree with your position on same sex marriage I will back you up on that.
Your posts often state you have nothing against homosexuals, only same sex marriage.
#178532 Feb 6, 2013
Former California Highway Patrol lieutenant is looking at seriuos prison time for molested two underage relatives.
El Centro, California a jury on Feburary 05, 2013 Tuesday convicted 46-year-old John Swaim on four counts of lewd acts on a child under 14.
The female victims, who are related to Swaim, are now 17 and 20 years old.
Just activate the firing squad to save the California tax payers money.
#178533 Feb 6, 2013
Protecting? I dont understand, homosexual marriage does not attack heterosexual marriage in any way at all. There are over 18,0000 legal homosexual marriages in California now, It certainly did not hurt my marriage, how did it hurt yours?
#178534 Feb 6, 2013
A detective with the San Luis Obispo Police Department was arrested by the FBI.
Small time police departments hate it when they are found out and arrested for playing fast and lose.
#178539 Feb 6, 2013
The argument is that once we make marriage mean everything, it will mean nothing.
It is a valid argument until you consider that who marries who is self limiting. There just won't be that many gay, poly or incestuous marriages to cause that problem.
Poly and incest marriages won't hurt your marriage either.
#178545 Feb 6, 2013
The argument is moot, Homosexuals already can marry, in many states, hundreds of thousands are legally married now
I dont care about poly marriage that is Frankies obsession not mine. Poly marriage is not about to be made legal in the next couple of decades, religious fanatics following that path have made certain of that.
but for same sex marriage, it is already a reality, and it has not hurt heterosexual marriages one tiny little bit.
It is a moot argument
#178546 Feb 6, 2013
I was there just last year, you didn't see me? It's such a tiny little country you should have seen me. Maybe you just don't remember.
Even if I was never there, I've seen enough of you guys fly out of there to know you're a very gay country! What with that sissy accent too!
#178547 Feb 6, 2013
What did I just say jackass? What a dope!
You consider poly my "obsession", and "off topic", and not reality only because you fear discussing it.
What do you have against three atheist men marrying? How will it hurt you or your marriage?
"Busting Kimare's"
Since: Feb 13
#178551 Feb 6, 2013
Kimare, you have yet to back up a previous statement, so I'll ask again:
In which culture/s was SSM legally recognized previously? Still waiting for your answer.
Just pull down your drawers and talk to the mangina. Don't keep you internal lesbian waiting.
#178556 Feb 6, 2013
Learn to read, poly is your obsession not mine, I could give a flip about it, and nothing is about to change with regard to law for the next couple of decades
I dont have anything against you, but am informing you that nothing is going to come of it in the foreseeable future, religious fanatics have already made certain of that.
Not true with same sex marriage, that is a reality today, more and more states and nations are recognizing same sex marriage, and it has not hurt anyones heterosexual marriage at all. That argument has already been made in court, no harm was shown to heterosexual marriage whatsoever.
#178558 Feb 6, 2013
Did I say poly was your obsession dummy? Learn to read.
So what if you don't give a flip about poly? Most people don't give a flip about SSM. What do I care what you give a flip about? So what if it might not be decades? Are these your real reasons to deny equal rights?
By what logic do you insist on the traditional, arbitrary, religious and discriminatory number of two?
#178559 Feb 6, 2013
As I said, you obsession, I am not interested, and nothing whatsoever is going to come of it, as there are groups of people that have put a stain on that concept that will linger for some time.
You should be ranting at them, not me.
"Reality bites"
Since: Dec 11
Location hidden
#178560 Feb 6, 2013
So I will not find any post by you on this thread, correct?
#178562 Feb 6, 2013
If someone mentions Mars in conversations about the solar system do you whine to them that they have an "obsession" with Mars?
And so what if they do? They're not allowed to? You go out of your way to complain and censor them or filibuster religion? You'll call them liars?
What a jerk.
Since: Mar 09
Location hidden
#178563 Feb 6, 2013
Police don't put in any regulations, numpty. It ain't their job. They're not even working in prisons. That would be the prison guards jobs. To date what we've got from Brian_G on prisons and same sex marriage is some rather odd claim that it will cause FORCED marriages to occur in prisons. When aske for evidence of these FORCED marriages all he's come up with are 3, yup, three, marriages in Canadian federal prisons since 2005! Not one shred of evidence that any one of them was FORCED! Yup, smart and creative.
#178564 Feb 6, 2013
That's ignorance and bigotry.
Some homosexuals are bad too. Does that mean we should not allow SSM? Of course not.
Since: Mar 09
Location hidden
#178565 Feb 6, 2013
Jen Ewe Wine LOL!
Point out to me where Brian_G has proven, with valid evidence and argument, that same sex marriage will create FORCED marriages in prison. His evidence to date consists of 3 same sex marriages performed in Canadian federal prisons since 2005. Bubbas are just lining up to force their weak little cell mates to marry 'em aren't they?
I call people stupid when they've made it painfully clear that they are. Got it, stupid?
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text: Road Guy 7,002 Report post Posted February 21, 2012 Our first of what will hopefully be many to come.. The first vendor giveaway comes to us from a vendor who wishes to remain anonymous, free 6 minute solution book of your choice.To be eligible you need to be a eb.com supporting member and simply post in this thread. Winner will be chosen randomly and contacted on February 29,2012.Definition of random, is all names will be put in a box and a winner be selected.Winner will be announced February 29th and winning user will have 24 hours to private message road guy with your shipping info and desired book.Do not post more than once in this thread or you will be disqualified.THANKS AND GOOD LUCK! Share this post Link to post Share on other sites


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I'm typing this not even knowing if I am going to hit "save" so that you'll read this. It's kinda touchy, and I like my job.
You may have heard that Dan Cathy, president of Chick Fil A (please PLEASE expand to Las Vegas!!) has been taking heat for his stance on gay marriage. (Here's the transcript.)
Why does it seem like 90% of the time an "outspoken Christian" is in the news, it's for something deemed "unpopular," or "out of touch" or racist/homophobic/etc.?
The easy answer...the low hanging fruit...is to blame media bias. It's Christians vs. the world. They bait us with their jaded questions. They seize on words or phrases, maybe even out of context, to paint us with a broad brush.
But let's be honest. Occasionally (maybe more than occasionally), somebody who shares our faith feeds them a perfectly insensitive, poorly thought out sound bite. Or we simply take the bait, with the best of intentions.
I have decided that any time I ever get the opportunity to talk about some terribly sensitive, polarizing topic, I am going to run it through this filter. It's a quote shared by the wise (and really tall) Carlos Whittaker:
Want proof? I just did a quick count of His major commands. There were about 51 of them. Nine of them were of the "don't" nature. (Like "don't lie, don't murder," etc.) The rest of them....a whopping 82% of them told me to DO GOOD THINGS. Love others. Forgive. Be merciful. Help those in need. Love my enemies. Pray and fast in private.
It's time for Christians to decide THOSE are the things we want to be known for.
I promise you this: very few people will be surprised about your beliefs on today's "hot button" issues. (So what if you're "for this" and "against that." Who isn't??)
Yet can you imagine how shocked those in your world would be when they saw you repeatedly loving your enemies? Being the first to graciously forgive? Choosing NOT to throw stones? Turning the other cheek?
That's the stuff we should be known for. I believe that satan himself uses our good intentions...our desire to take moral stands...to distract us from our Ultimate Calling. In fact, I contend that IF we could truly emulate Christ the way we were commanded, the things that so vex us would disappear. Because love wins. Always.
I am best known for my generousity. Main example is that I put others before myself. Not only do I lend my ear to a friend, I also lend my shoulder. I have also helped others with food and clothing by giving a portion of what I have (even though I also have limited food and clothes, and was diagnosed with hypoglycemia a year ago where I must snack every two hours). I also volunter at my church every Wednesday, Saturday, and Sunday; I go to Central Christian Church in Henderson (13 miles away from my apartment). I also tithe weekly (Sunday) even though I have not had any source of income (except food stamps)since June 21, 2011. God has blessed me this last year, and I know he will ever forsaken me because I trust him with my life through the life of his son: Jesus Christ.
For my love of God's creations. Even snakes. Snakes are beautiful and symbolic of God to me. Their beauty, ability to swallow prey whole, and climbing ability have amazed me for the longest time. I don't know a day when I hated animals. I am also on the autism spectrum.
All the hoopalala in the media over Chic-Fil-A tells me we're not living in a Christ-friendly time. I hope people I come in contact with remember me as a "follower of Christ and doer of Gods Word" and not somebody that was shallow and lacking in substance.
Lord help me to flesh out your words!!!


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SEOUL, Feb. 21 (UPI) -- The annual South Korean-U.S. military drill will be next month to improve the forces' capabilities against North Korean threats, it was announced Thursday.
The Combined Forces Command's announcement comes as North Korea continues with provocations, the latest being its long-range rocket launch Dec. 12 and its third nuclear test Feb. 12.
The CFC said in a release that the Key Resolve drill will be March 11-25 and involve about 10,000 South Korean and 3,500 U.S. troops.
The drill, using computer simulation, will test various scenarios with the South Korean Joint Chiefs of Staff taking a lead role in conducting operations as the country prepares to regain its wartime operational control from Washington at the end of 2015.
"This is the first year that the Key Resolve exercise is being led by the Republic of Korea JCS, not the Combined Forces Command," the CFC said. "This will help improve the ROK (South Korean) military's operational command capabilities and establish a basis for the wartime operations control transition."
The two sides also plan the Foal Eagle land, sea and air maneuvers from March 1-April 30. It will involve mobilizing about 200,000 Korean and 10,000 U.S. troops, mostly from overseas, the release said.
The CFC said the North Korean military has been informed of the exercises.


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To no one's surprise, former Massachusetts governor and candidate for the Republican Presidential candidate nomination, Mitt Romney, won the New Hampshire primary yesterday. He won with an amount (39%) beyond what pundits claimed would otherwise show trouble, and he easily cleared Texas Congressman Ron Paul, who earned 23%. Former Utah Governor Jon Huntsman claimed third place (with an enthusiasm almost more appropriate for a Saturday Night Live skit -- watch Huntsman's primary speech here) by garnering 17% of the vote. Check out a good look at all the numbers from WMUR, including former Speaker of the House Newt Gingrich and former U.S. Senator Rick Santorum each with 9%. Texas Governor Rick Perry mustered 1% (and gets some love from Smart Girl Politics).
So what happened? More like, what didn't happen.
What didn't happen was a collapse of Romney's stature in what is practically his home state, regardless of his "I like to fire" statement that's been played up by Gingrich. What also didn't happen is Huntsman getting up to or past Ron Paul. And even his improvement from the Iowa showing, where he didn't campaign, gets knocked down a couple of notches because Iowa and New Hampshire voters don't have much in common. And for those rooting for Huntsman, you won't really need popcorn -- South Carolina is a lot more like Iowa (more about that in a minute).
Jan. 7, 2012 - Derry, New Hampshire, U.S. - Republican presidential frontrunner MITT ROMNEY greets supporters at a rally at Pinkerton Academy where he cautioned supporters against over confidence before Tuesday's primary. 'Don't get too confident with those polls,' he said at a breakfast rally in a gym at Pinkerton Academy. 'I've watched polls come and go. Things change. it's very fluid.' (Credit Image: © Mary F. Calvert/ZUMAPRESS.com)
Although turnout appears to have been turned down from high hopes, it was not as depressed as originally thought. But, as the exit polls show, Gingrich and Santorum simply don't have as much of a natural constituency in New Hampshire as Romney did, and, once people got to know him, Huntsman seemed to find. Paul's strength appeared to come from the youth in the state as well as voters who live in regions that are rarely visited. In a word, he and Huntsman were tireless in their efforts in the state and that paid off in conjunction with voters sentiments.
For those of us who are comfy online and off, coverage for the platform agnostic political junkie was resplendent! Just look at BlogHer Executive Editor Julie Ross Godar's post, Mashable's review of the candidates' use of social media in the primary and this set of infographics about Facebook and the wannabees -- sounds like a band name.
Of course what is absent now from that coverage is women, except for those we see who are either spouses, daughters or voters. I don't know about you, but I really miss seeing a woman on the stage or in the screen shots and speeches. Michele Bachmann was never going to get a vote from me, but I cheered for her, publicly, on a regular basis for sticking in there.
As for NH's voters, the exit poll says that New Hampshire's women went for Romney by a big margin (40%), then Ron Paul at 20% and then Huntsman with 18%. I'm not sure what that's about other than familiarity. If you need to get a female politician's fix, Sarah Palin appeared on Fox twice, first with Megyn Kelly and Bret Baier and then with Eric Bolling.
As yet, I've not seen any article analyze the female conservative voters' sentiments now, but as a plain ole female voter, I was sorry to see Bachmann go buh-bye.
What about South Carolina, with its primary on Saturday, January 21? A few things: they have serious unemployment and budget issues, while Iowa, comparatively speaking, is not suffering from those as heavily. It's expected that this difference is going to make SC voters focus more heavily on electability as in beating Obama, and Romney has owned that moniker from the start. In addition, he has SC Governor Nikki Haley's endorsement. How much that will matter is up for debate given her somewhat rocky first year, and the reality that South Carolina is home to U.S. Senator Jim DeMint, arguably the most well-known and powerful Tea Party personality -- not a Romney supporter.
Ultimately, though, this situation is just like when a friend of mine was looking to move up from a Mercury to a Camry but really wanted the Lexus. He test drove the Camry, liked it and felt it was a great deal he could afford but couldn't give in to not having the Lexus. So he tortured himself for six weeks, test driving the Lexus and trying to find a deal he could afford. Finally, he went with the Camry -- which I knew he'd end up getting all along.
Republican voters and Mitt Romney are like my friend and that Camry: they know that if they want Obama out, they cannot afford any other candidate to beat Romney, no matter how much Romney isn't the conservative voter's dream car.
In The Arena: Jill Miller Zimon, Pepper Pike City Council Member
More analysis:
PJMedia: Newt Gingrich, Mitt Romney and the Mystery of the Female Vote
Hillary Clinton's New Hampshire Primary Victory Speech (2008)
More from entertainment


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It's Christmas Day - and what better way to celebrate than by combining Christmas with reality TV?
They're Back! The Cast of 'Teen Mom 2' Is Back With An All-New Trailer for Next Season
Cracked.com created this very funny spoof of MTV's 16 and Pregnant starring the Virgin Mary herself as the pregnant teenager. Clearly, someone has been watching a lot of old episodes of the show, because all of the details are there, from Mary's monologue about herself that ends with "...because I'm pregnant" to the written-on-notepaper graphics and the "I'm going to step up and be a dad" speech from Joseph.
Hmm... what do you think Teen Moms like Amber Portwood and Farrah Abraham would think of this sketch?


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Pianist Chris Engbretson of Bothell, Wash., will perform Saturday, May 19, at 8 p.m. in the Richard and Lucille Ice Auditorium, located in Melrose Hall at Linfield. A piano performance major, Engbretson recently received the Piano Award at the Oregon Music Teachers Association Scholarship Competition and was chosen as a winner in the Portland Monday Musical Club. He is an assistant conductor with the Concert Choir and a guest conductor with the Linfield Wind Symphony. Following graduation from Linfield, he plans to pursue a graduate degree in choral conducting.
Works by composer Casey Frantum of Baker City will be performed Sunday, May 20, at 4 p.m. also in Ice Auditorium. Frantum will be accompanied by a number of Linfield student musicians including the Linfield Jazz Band as he performs his own compositions.
The evenings are free and open to the public. Receptions will follow the performances in Jonasson Hall, lower level of Melrose Hall. For more information, call the Linfield Music Department at 503-883-2275.


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Ukraine has failed to pay its bill for natural gas delivered in April, despite receiving an initial bailout payment from the International Monetary Fund (IMF) on Tuesday, bringing state-owned oil and gas incumbent Naftogaz's debt to Russian Gazprom to $3.5bn (€2.51bn), Gazprom has confirmed.
Naftogaz had until 7 May to pay for gas supplied during April. Missing this payment will mean Gazprom will start demanding advance payment and will only supply gas to Ukraine in pre-paid volumes ( see ESGM 25 April 2014 ). In April, Gazprom Export's CEO Alexander Medvedev said Ukraine would have until 31 May to pre-pay the volumes it wants to receive in June. Until 31 May Ukraine would continue to receive gas in line with the current contractual conditions.
The National Bank of Ukraine confirmed to ICIS on Thursday it received the first $3.19bn loan from the IMF under a $17.01bn aid package for the embattled country. A spokesman said over $1bn of this first tranche of loans would be used to replenish the gold and foreign exchange reserves of the bank, with the remaining funds to be channelled into the budget. The bank could not confirm that any funds from the first tranche would be used to pay off Ukraine's gas bill.
The IMF's two-year stand-by arrangement targets 2018 for the elimination of Ukraine's deficit, which would be achieved through reforms to improve efficiency and transparency ( see ESGM 1 May 2014 ).
In the worst case scenario, if no advance payment is made for June, gas deliveries to Ukraine would stop but Gazprom will continue to supply to the Ukrainian border all volumes nominated by its European customers and use an early warning mechanism. The mechanism is a tool set up after the 2009 supply crisis, which Gazprom uses to let the EU know if supplies through Ukraine to Europe are disrupted. Gazprom and EU representatives would also establish joint groups to monitor transit of this gas via the Ukrainian system on to Europe.
Ukraine's supply contract with Gazprom from 2009 stipulates a 52 billion cubic metre/year supply volume to Ukraine on a 80% take-or-pay basis. Miriam Siers


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As a horror movie by an Australian director topped the American box office charts on the weekend, there was an impressive debut for a Saudi Arabian film by a director who trained in Sydney.
James Wan's Insidious Chapter 2 took $US41 million ($44.3 million) – the second hit in two months for the Melbourne-raised director after The Conjuring took $US135 million in North America and another $US135 million elsewhere in the world.
According to the website Box Office Mojo, it is only the second time a director has had two movies open with more than $US40 million at the US box office in the same year — the Wachowski siblings did it with The Matrix Reloaded and Revolutions in 2003. Just as impressively, the Insidious sequel had one of the best debuts for a supernatural horror film despite costing just $US5 million to produce.
In a fast-rising Hollywood career since creating the first Saw movie with Leigh Whannell – the writer of Insidious Chapter 2 and friend since they studied media arts at Royal Melbourne Institute of Technology together – Wan is currently directing Fast & Furious 7.
In arthouse cinemas, Haifaa Al Mansour's Wadjda took more than $US40,000 in three cinemas, which The Hollywood Reporter called "arguably the best showing of the weekend among new limited releases".
The drama, Saudi Arabia's first ever entry in the Oscar race for best foreign language film, is about a 12-year-old girl who dreams of having a bicycle in a segregated country where that was discouraged until recently as not being virtuous for women.
When Wadjda was selected in competition at this year's Sydney Film Festival, Al Mansour told Fairfax Media that she often had to sit inside a van and speak to her actors via walkie-talkie lest she be visible on the streets of Saudi Arabia.
Conservative relatives were so concerned about her directing films that they wrote letters to her father suggesting she was being corrupted.
To became the country's first female filmmaker, she spent a year studying for a masters degree in film at the University of Sydney.
"I had a great time," she said. "I had my first son. I went to school when I was pregnant and my professors were very supportive."
As one of 12 children growing up in a liberal family in a small town, Al Mansour's film education started with movies on video and she later made corporate videos for an oil company.
"To be a woman in Saudi is very hard," she said. "You don't feel like your voice matters.
"I wanted to do something just for me as therapy, just to find my voice. So I decided to make a short."


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Rev. Al Sharpton Says Judge Paul Deen 'Fairly'
Paula Deen recently thanked Rev. Al Sharpton for his support when the civil rights activist seemed to come to her defense recently.
Deen, the 66-year-old restaurateur and cooking show host, made headlines last week when one of her former restaurant employees alleged that she made racial jokes at the establishment. In a testimony from a Deen's deposition on May 17, the Food Network host admitted to using the N-word in the past.
Sharpton, a Baptist minister, recently commented on Deen's situation.
"I think that it was just not about her using racial language," Sharpton told TMZ recently. "A lot of us have said things in the past that we regretted saying years ago."
Deen caught wind of Sharpton's comments and took to Twitter to thank the civil rights activist.
"I want to thank Reverend Sharpton for his kind, kind words," Deen tweeted
However, the reverend made it clear that he was not necessarily defending Deen. Instead, Sharpton told TMZ that he is defending treating Deen fairly.
"I mean she deserves what's fair…I think you cannot deal with what is fair and not fair till we seek out in the present the circumstances she's accused of, not something from 20 years ago," Sharpton told TMZ.
Although some are questioning Deen admitting that she previously used the N-word, representatives for Sharpton said he is focused on the present accusations brought against her by her former employees.
"There is more current information that is being divulged that we might need to be concerned about," Sharpton's spokeswoman told The Huffington Post.
While the fate of Deen's lawsuit has yet to be determined, Food Network is reportedly ready to part ways with the cooking host, according to a press release that network released last week. Deen has been on the network since 2002 when she appeared on "Paula's Home Cooking" and later added "Paula's Best Dishes" to the channel in 2008.


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Brantley breaking out after slow start
Brantley breaking out after slow start
But Brantley's slow start seems to be a thing of the past.
Entering Thursday, the Indians center fielder was hitting .326 (29 of 89) with nine doubles and 10 RBIs in his last 22 games, dating back to April 25. Brantley improved his batting average from .196 to .276 during that span, and he has sparked the Indians from numerous spots in the lineup.
"Michael just gives you quality at-bats," Acta said. "He got in a deep hole at the beginning of the season, but he doesn't panic."
Brantley has hit fifth, sixth and seventh, in addition to the leadoff spot this season. He's hitting only .237 in the top spot, but is a sizzling .346 anywhere else in the order.
"When he gets guys on base, he can pick up those cheap RBIs and then give you quality at-bats when guys are in scoring position with two outs," Acta said. "He can start a rally if he's leading off the inning. He's very versatile for us, and I value his at-bats."


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Read the full story here Web Link posted Thursday, April 16, 2009, 7:00 AM
Town Square
Presentation on schools budget and Measure C
Original post made on Apr 15, 2009
Read the full story here Web Link posted Thursday, April 16, 2009, 7:00 AM
Comments (4)
a resident of Walnut Creek
on Apr 15, 2009 at 7:04 am
The Walnut Creek Chamber Civic Affairs Committee voted unanimously, on 4/14, to recommend to the Chamber Board it endorse Measure C in this mail-only ballot, received last Saturday, by most registered voters of the SRVUSD. Some voters have already sent in their ballots. A previous parcel tax election in SRVUSD failed by only one vote to get a super-majority of 2/3. It was pointed out that property owners over 65 years old may apply for exemption from taxation in a parcel tax election in CA.
a resident of San Ramon
on Apr 15, 2009 at 3:25 pm
I am voting "No" on Measure C. Our District is sitting on 6.9 million dolars for times of "economic uncertainty," plus it is sitting on another 5.6 million dollars in "unencumbered reserves," and it has another 1 million dollars to aid with school needed purchases (replacement desks, etc.).
The Measure C campaign wants you to believe that class-size reduction would "go away." Why the scare tactics? Are you voters putting two and two together when reading one of the ballot arguments, which supposes that a "yes" vote will help retain qualified teachers? The last time we had a parcel tax vote, the teachers received a series of permanent raises. While I believe that no parcel tax funds will be used for teacher's salaries, I know that class size reduction has, in years past, been paid for out of the general fund. If we don't pay class-size reduction from the general fund, then it frees up money in the general fund to pay for teacher's raises. It's moving money from one pot to the next (strategies they have used before) so they aren't "technically" breaking their promises. This type of behavior/strategy is exactly what makes the voters mistrust the District. Also, in years past, almost all pink slips issued were rescinded prior to the start of the new school year and very few jobs were lost.
Vote NO on Measure C. Have the courage to find out just how resourceful our District can be when it HAS TO BE.
Danville Weekly reporter
on Apr 15, 2009 at 5:00 pm
Geoff Gillette is a registered user.
The school district has asked us to let folks know that the meeting tomorrow night is actually at 7 p.m. at Stone Valley Middle School. Superintendent Enoch will be on hand to discuss Measure C and the district's financial situation.
Geoff Gillette
a resident of San Ramon Valley High School
on Apr 16, 2009 at 5:19 pm
Dear Dolores and Geoff,
THANK YOU for announcing a fair opportunity for all positions on Measure C to challenge SRVUSD Board and Superintendent. This is inclusive government at its best and media support focused to readership.
It is what you do best as a function of your exceptional journalism!
I hope all positions come tonight with all UNANSWERED concerns and respect those that have already done their in-depth study and choice. Of all the services we provide ourselves, education is the greatest source of future for our region, county, state and country. We must afford the legitimate costs of education and ALWAYS challenge the uses of such funding.
It is critically important to those that have no voice, our students. So, let's reach out to students and understand the issues at the classroom level and then act on their behalf in insuring education at legitimate costs is a priority.
A tale of two creeks
By Tim Hunt | 3 comments | 407 views


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68 - 83 Final
Providence knocks off No. 8 VillanovaJan 27, 2011 - 3:11 AM Providence, RI (Sports Network) - Vincent Council led a balanced attack with 16 points, eight rebounds and eight assists, as the Providence Friars upset the eighth-ranked Villanova Wildcats, 83-68, in a Big East Conference clash.
Marshon Brooks had a game-high 20 points with eight boards for the Friars (13-8, 2-6 Big East), who have won two in a row since a six-game skid.
Gerard Coleman chipped in with 16 points for Providence, which improved to 12-2 at home this season. Kadeem Batts donated 11 points and nine rebounds.
Antonio Pena had 17 points and 15 boards to pace the Wildcats (17-3, 5-2), who have lost two of three. Maalik Wayns tallied 18 points in the setback.
The Friars jumped out to an early 6-0 lead and never looked back.
Holding a 16-14 lead, Providence ripped off eight straight points. Council's jumper made it a 24-14 game with under 6 1/2 minutes left in the first half. It was 34-25 at the break.
The Friars scored the first four points of the second half to build a 38-25 margin.
Pena's jumper with over 10 minutes to play cut the gap to seven, 50-43. But Providence responded with an 8-3 spurt to essentially put the game away.
Villanova never got closer than eight the rest of the way.
Game Notes
Villanova still owns a 51-35 series advantage versus Providence. The Wildcats had won eight in a row against the Friars...Providence made 31-of-38 shots from the foul line, while the Wildcats went 14-of-18 from the charity stripe.
Jan 26 9:08 PM
Jan 26 7:48 PM
- 119
rootsRUWTbot Added 119 roots (Upset)
Villanova(8) 25, Providence 34 HalfJan 26 7:48 PM
1st Half - 20:00
Jan 26 7:05 PM
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- NCAA title game top scorer Booth returns healthy for Nova Sep 14
- Coaching legend Massimino dies at 82 Aug 30
- Villanova's buzzer-beater Jenkins to stay for senior season May 3
- Villanova receives $22.6 million gift for arena renovation Apr 20
- National champion Wildcats bask in celebratory perks Apr 12
- Philadelphia cheers NCAA champs Villanova with parade Apr 8
- Classes off, party on: a Philly bash for champion Villanova Apr 6
- Oklahoma and Villanova face the shooting woes of NRG Stadium Apr 2
- 'Nova looks to show growth since 1st game against Oklahoma Mar 31
- Cooley hopes to be at Providence 'for life' with extension Mar 30


text: I just transferred ANG units to take an ATC slot. Found out after signing on the dotted line that I have been put into a radar slot. Considering I will not be able to obtain a CTO while in a radar slot, how screwed am I? What can I do with radar rating? I'm not exactly happy right now, so I'd love to hear what my options are.


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Random Q.
Does anyone know where I can legally download Sweet Female Attitude - Flowers?
I'm doing a retro party next friday and that was one of the songs to be requested...
I've tried everywhere and even Itunes doesn't have it...
Also, can anyone give me some more names of classic Uk Garage songs to play in a UK Garage 30 minute mix next week!?
All the Best


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"Northern Stars: Twentieth Century Finnish Design"
Where: Mingei International Museum, Balboa Park
When: Through April 22
Admission: $8
Phone: (619) 239-0003
Online: mingei.org
Organized by the Design Museum in Helsinki, and on a world tour that has already included Europe and South America, "Northern Stars" promises to put those pieces of Finnish or Scandinavian furniture you might have at home into context. The show promises dozens of objects spanning the entire century, with examples of textiles, ceramics, glass and furniture that demonstrate the designers' seamless integration of form and function, the sculptural and the practical. The big names in Finnish design — Alvar Aalto and Timo Sarpaneva — will be represented, as will brands like Marimekko and Fiskars.Copyright © 2017, The San Diego Union-Tribune


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« Researchers characterize algae parasite that impacts on algae biofuel | Main | Volkswagen to produce XL1 diesel plug-in hybrid at Osnabrück; 261 mpg US »
Audi to show the A3 e-tron plug-in hybrid at Geneva
21 February 2013
|A3 e-tron. Click to enlarge.
Audi will showcase the A3 e-tron plug-in hybrid at the 2013 Geneva Motor Show. The Audi A3 e-tron delivers 150 kW (204 hp) of system power and 350 nm (258 lb-ft) of system torque; projected fuel consumption is 1.5 liters per 100 km (157 mpg US), according to the ECE standard for plug-in hybrid automobiles. This corresponds to CO2 emissions of 35 grams per km (56 g/mile).
The A3 e-tron accelerates from 0 to 100 km/h (62 mph) in 7.6 seconds, and has a top speed of 222 km/h (138 mph). In electric mode, the Audi A3 e-tron reaches a top speed of 130 km/h (81 mph) and has a maximum range of 50 km (31 miles).
The combustion engine is a modified 1.4 TFSI producing 110 kW (150 hp). A clutch links the TFSI to an electric motor with an output of 75 kW. The disc-shaped electric motor is integrated into a newly designed six-speed e-S tronic, which transfers the power to the front wheels.
The two powerplants complement one another. The electric motor delivers its peak torque from start to around 2000 rpm, and the TFSI's maximum pulling power is available in a range from 1,750 to 4,000 rpm.
The Audi A3 e-tron can be driven with just the combustion engine, just the electric drive or in hybrid mode. The driver can choose to have both powerplants active at the same time ("boosting"). When the driver lets up on the accelerator, they both deactivate temporarily ("gliding"). In this way motor braking torque is eliminated and efficiency increases.
February 21, 2013 in Hybrids, Plug-ins | Permalink | Comments (3) | TrackBack (0)
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Appears to be a VOLT chaser. With both power plants active the regen function only engages when brake is applied? - how is this effective downhill? Without this braking toque it is a different feel from EVs I've driven.
Don't see specs on the battery, though is appears to be somewhat less than the 16kW Volt. Good luck Audi. You have a lot of catching up to do.
Folk don't actually realise the breadth and depth of what the VW group including Audi are doing in electrification.
They have a completely new platform, which was designed from the start to take a host of alternative engines and drives trains with minimal alteration so that short production runs are viable.
The MQB platform covers everything above the tiny Up, as far as their SUVs.
On it they can put a natural gas drivetrain, fuel cells, BEVs or plug in hybrids.
Their main effort though is going to plug ins, with Volt like EV range:
'A PowerPoint slide displayed to the five journalists in attendance showed a plug-in hybrid version of the Porsche 918 Spyder going into production in 2013—followed by no fewer than six plug-in hybrids beginning in 2014. That list included plug-in hybrid versions of the Audi A3, Audi A6, Audi A8, Audi Q7, as well as PHEV variants of the VW Golf and Passat. This lineup would be added to—rather than replacing—the VW e-up! and e-Golf that will be introduced in Europe in later this year. He did not specify how many of the future PHEVs would be sold in the United States—but gave the impression that VW was seeking a leadership role in plug-in cars in all global markets, in order to achieve the 3-percent target in five years.'
Although what they are up to is being almost ignored by the US media, they are aiming to own the plug in hybrid drive space, and have invested billions to do this, although some have released earlier than them they are, IMO, the toughest competitor of the lot.
GM, Ford, and everyone else had better watch out.
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text:
Counting down the top 50 players in the American League:
No. 20 Josh Donaldson
Position: 3B
Age: 28
Team: Oakland Athletics
Lowdown: A's GM Billy Beane can claim one of the biggest bargains in 2013. For a little less than $500K, the A's got themselves an MVP candidate in Donaldson's first full year in the majors. He slashed .301/.384/.499 with 24 homers and 93 RBIs as the A's won their second straight AL West title. A good glove also helped Donaldson (7.7) top the likes of Miguel Cabrera (7.6), Evan Longoria (6.8), Manny Machado (6.2) and Adrian Beltre (5.2) in WAR, according to fangraphs.com. The question is this: Can Donaldson replicate a 2013 campaign that seem to come out of nowhere?


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CARLSBAD ---- Mary Ahlstrom has been named director of sales at Hilton Carlsbad Oceanfront Resort and Spa. Under construction, the resort is at 1 Ponto Road, across from Carlsbad State Beach. The hotel is scheduled to open in summer 2012. Ahlstrom most recently served as director of sales at the Inn at Rancho Santa Fe. Visit hiltoncarlsbad.com or call 760-602-0800.
Hilton names Ahlstrom as director
Copyright © 2017, The San Diego Union-Tribune


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Better than stock
Reviewed By Joe B (CLAYTON, NC) Reviewed for a 2004 Chevy Suburban —7/4/2016 9:39 AM
I have an '04 Suburban 2500 and tow an 8500 lb camper. After another after market set of pads failed to last me more than 1 year, I switched to the EBC Green Supreme Pads. I am happy with the stopping power they provide up front. Well worth the purchase!


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Guitarist Dave Wright comes from a famous jazz lineage. His father, Rayburn Wright, was head of the Jazz and Contemporary Music Department at the Eastman School of Music, following a successful career as a composer, arranger, conductor, and former arranger and co-director of music at Radio City Music Hall. He was also a film composer whose scores were nominated twice for Emmy awards.
Son Dave's schooling came, in part, from lessons with guitarist Gene Bertoncini and Tom Rizzo, and he studied at the Studio Jazz Program at the University of Miami, Coral Gables. As a performer Dave has worked in the Radio City Music Hall Orchestra, done New York studio work, performed with the Rochester Philharmonic Pops Orchestra and performed on the largest cruise ship in the world.
9 Dreams finds Wright working in a straight-ahead, yet modern oriented, organ trio - with organist Scott Bradley and drummer Jared Schonig - augmented by guest saxophonists Matt Pivec and Bill Tiberio. Overall the CD is full of pleasant and attractive music solidly locked in the tradition except for some interesting metric and rhythmic diversions. "Tracey's Revenge," for example, has a rock-ish veneer that allows both Schonig and Wright room to let it rip. Together the two build the piece straight on to the end within a series of cyclic vamps. The melody's quirky offbeat accents are a perfect preamble for the tune's closing solos.
A diversion from the CDs ensemble format is Wright's nice unaccompanied electric guitar take on the Thelonious Monk standard "Crepescule With Nellie." Wright makes the tune his own by imbuing it with a taut rhythmic structure similar to the manner Monk would use when he played it without his band.
Other highlights include the title track. Opening with delicate phrases the piece morphs into a hot double-time ride before the solos take over. Wright's solo is slightly constrained before Tiberio comes in to lay down some searing lines in his all-too-brief solo. The piece just seems to get going when a reflective ending section stops the wonderful mayhem; here Wright solos the tune to its end. He truly nails the emotion in his solo with beautifully constructed lines based on this section's new ensemble sonic characteristics. One wishes this part of the piece had had some real length; not only is it truly scenic music played exceptionally well but it would also have been nice to hear where Wright would have taken his solo had he allowed himself to further develop his ideas.
While most of the music is wonderful some tunes seem a bit flat. Wayne Shorter's "Elegant People" lacks the spark Shorter's bandmates always bring to his own performances of this piece and the standard "Knocks Me Off My Feet" doesn't move. These letdowns, however, don't ruin the disc's many fine qualities.


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PRINCE Charles braved the rain but stopped short of hugging a baby in Bondi today.
During a freak storm, the future of King of England shook hands with hundreds of onlookers who braved the foul weather to greet him.
A young girl gave Prince Charles a teddy bear, but when a mother offered him her young baby he stopped short and told he had to "rush''.
He then turned, remarking "cuddling babies'' and laughed before walking away.
"I grew up with God Save the Queen,'' Bondi resident Michelle Mekler-Peled said,
"We came down at 12 and watched the black clouds roll in closer and closer and saw the lightning bolts come down. But he shook my hand so it was worth it,'' she said.
"It was so exciting. He's the future king''.
The royal couple were probably expecting snags and sunshine as Sydney heads towards a sweltering summer but Prince Charles and Camilla have been dogged by bad weather during their Australian trip.
The royal pair were forced to take refuge from a snap storm that bedraggled Bondi beach as Hobart - the couple's most recent destination - was hit by wet weather and a tornado.
The Prince of Wales pulled up in a car at the back of the Bondi Pavilion in the midst of the storm shortly before 2pm, having just enjoyed a meal nearby at trendy lunch spot Icebergs.
Much of the media pack were caught out by the storm, with drenched reporters and camera crews searching the boardwalk for a spot of shelter.
Some members of the public braved the inclement weather to catch a glimpse of the royal couple, huddling under umbrellas alongside scantily-clad beachgoers and ignoring the severe weather warning.
Charles was to watch a demonstration of an NRL program for indigenous kids, and the storm clouds cleared on cue as Charles walked down to the beach to watch a footy match on the sand.
On the concrete wall above him hung the sign "say G'day to Betty for me", along with a string of British flags.
Behind the prince, surfers kept catching waves, unfazed by the fuss onshore as hundreds of people cheered and clapped.
"Charlie, Charlie," locals screamed, as the crowd swelled to more than a thousand.
The prince, flushed from all the fuss, stopped to talk to them, shaking hands and getting his photo taken.
'I didn't realise you were real'
But they haven't let it cramp their style - visiting Sydney Harbor and Prince Charles enjoying an unreal moment with a fashion model at the Museum of Contemporary Art today.
There to support The Campaign For Wool, the prince couldn't help but be distracted by live models displaying garnets by some of Australia's top fashion designers.
Model Bec Bisset - wearing an Akira Isogawa design and holding a toy sheep - caught the Prince's eye and he even took a detour to speak with her.
"He said, 'I didn't realise you were real' - he thought I was a mannequin," she said.
"But I said, 'The sheep isn't real'.
"He asked me about my clothes, whether they were warm and comfortable and he also asked who designed them."
Prince Charles himself was dressed in a navy suit made of Australian merino wool from Tasmania and designed by tailors Anderson and Sheppard in the UK.
The Campaign For Wool was launched globally on Australia Day 2010 in an effort to support struggling farmers.
Today, Prince Charles was greeted with an enthusiastic crowd and a cheeky message from the P&O cruise ship moored in Circular Quay right outside the MCA.
The large banner declared "Royal Suite Available".
As part of his visit, the prince met with designers Josh Goot, Dion Lee, Kym Ellery, Camilla Freeman-Topper and Isogawa.
Southern Highlands Christian School student Brooke Pearce won a meet and greet with Prince Charles thanks to her own fashion design using Australian wool.
"He was pretty casual so it made it a lot easier on me - I was so scared," she said.
"When he came up he was quite calm so that made me calm."
Their trip came after a group of Sydneysiders met the pair on the Harbor.
Victoria Crabtree, 19, from Potts Point was waiting from 8.30am for this "once in a lifetime" experience.
"I'm from England and I thought his would be a on e in a lifetime opportunity to see the royals," she said.
"My grandmother was a bit of a royalist so I grew up with it. I'm not but because my family can't be here I'm going to take a few snaps for my mum."
Camilla walked off the barge in an elegant cream dress and wide brimmed straw hat and when asked about her trip she said she was "loving it."
"It's a very beautiful country, very warm people. We've had a beautiful welcome,"she said "Apart from losing my voice - too much talking," she joked.
Emilia Grzeskiewicz was thrilled that Camilla stopped for a photo.
"I was surprised she stopped, we saw them walking down the middle of the path and assumed we wouldn't get to talk to them, but she met people at the barrier," she said.
"It was very exciting, you don't get to meet a royal every day."
Charles wore a navy pinstriped suit and was also happy to chat to well wishers Erin Clarke, seaman, talked to the prince about her job.
"He asked if I was based at Cuttle and do you go to sea much and I told him I'd been to sea and he said do you see your family, she said. "I was happy that he stopped and chatted to me."
After greeting the crowd, the royal couple were then welcomed by the Chief of the Defence Force General David Hurley.
His Royal highness received a royal salute with musical honours before he inspected he Guard of Honour and the navy band.
The royal couple touched down at Sydney Airport last night and the rain stopped just in time for them to have a quick chat with Governor Marie Bashir and Premier Barry O'Farrell before dashing off to their awaiting car.
Prince Charles was dressed in a smart grey pin-striped suit with a poppy in his lapel.
Camilla, wearing a camel trench coat, looked a little tired after the couple's busy day in Tasmania. After watching sheep run about in Hobart yesterday morning, the royal couple will spend today taking in the beauty of the Harbour and beaches.
The couple will then split up to make the most of their only day in Sydney.
Prince Charles will head to the Museum of Contemporary Art to show his support for the The Campaign for Wool and introduce himself to some of Australia's best fashion designers in Dion Lee, Josh Goot and Akira Isogawa. The prince is the international patron for wool and a dapper dresser, so he will no doubt be keen to exchange style notes.
He will then move on to Bondi Icebergs for a chat with lifeguards, emergency workers and Mr O'Farrell.
The public will have a chance to see Charles in action when he hits the sand for a touch football match with NRL stars and indigenous students.
Meanwhile, Camilla will be appointed as the colonel-in-chief of the Royal Australian Corps of Military Police in a ceremony at Victoria Barracks in Paddington.
She will also host the Women of the World reception at Government House in the afternoon.
The couple's itinerary gives them time for a quick nap and a costume change before they visit the Sydney Opera House for the Diamond Jubilee Reception, hosted by Ms Bashir. And finally, Governor-General Quentin Bryce will host a dinner for the royals at Admiralty House in Kirribilli where the couple will spend the night before flying to Canberra tomorrow.
Originally published as 'Cuddling babies? I've no time for that'


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Yesterday the information literacy video I made almost a year ago reached 10,000 views on YouTube. Thank you to everyone who has watched and/or shared it.
It seems as though I ought to do something more to mark the occasion. Is it time for another educational musical parody? What about a song about footnotes and references, called "Cited Work" – to the tune of Katy Perry's "Firework"?


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Insulated Wire and Cable: A Global Strategic Business Report
San Jose, California (PRWEB) June 10, 2014
Demand for insulated wires and cables is strongly influenced by economic growth. GDP growth, and health of major end-use industries such as, construction, automotive, electronics, energy generation, and telecom, therefore play key roles in influencing market prospects. Resurgence of the construction industry from the recessionary slump is benefitting demand for insulated wires and cables. Major factors driving growth in developed economies include residential repair, remodelling and repair activity, introduction of stricter building codes, and increasing need for improved energy efficiency, while in developing countries, increased investments in infrastructure in China, India, Brazil, and Russia is spearheading market growth. Stringent government regulation calling for mandatory renovations of ageing buildings and electrical works, both residential and commercial, represents another major factor driving demand. Positive outlook for the automotive industry also bodes well for automotive wires and cables.
As stated by the new market research report on Insulated Wire and Cable, Asia-Pacific represents the largest and the fastest growing market with a CAGR of 7.9% over the analysis period. Growth in the region is led by robust construction activity, significant infrastructure improvement in power and telecom industries, and strong automobile production. Telecommunication data wire & cable represents the largest and the fastest growing market worldwide. Insulated cable deployment in the telecom sector is gaining strength with telecom operators making active efforts to expand capacity in line with escalating demand for Internet video and data traffic amidst increasing use of mobile devices, such as smartphones and tablets.
The shift towards broadband networks and the on-going transition to 4G networks is having a significant impact on demand for fiber optic cables. Fiber optic networks are also being deployed at newer and remote locations, and for addressing newer applications, such as those required for high-frequency trading. Growing demand for energy, especially in emerging countries such as India and China, is compelling governments to step up production levels. Most nations are looking beyond traditional power sources, and are focusing on alternative energy. Investments in power infrastructure development is therefore expected to create enormous opportunity for growth of insulated wires and cables, as all the integrated components in power grids require insulation for eliminating transmission losses, short circuits, and other electrical related ambiguities.
Global commitment to effect a reduction in greenhouse gas emission and focus on conformance to Kyoto protocol agreement is also expected to force countries to legislate norms to ensure effective building insulation, since insulation is considered as the most viable as well as the cost-effective way to reduce energy consumption and fight climate change. Proper insulation can bring down heat flow, reducing cooling needs by more than 70%.
Key players covered in the report include ABL Electronic Supplies Inc., AFC Cable Systems Inc., Amphenol Corp., Asia-Pacific Wire & Cable Corporation Limited, Belden Inc., Brand-Rex Ltd., Cable USA Inc., Carlisle Interconnect Technologies, Cerro Wire LLC, Coleman Cable Inc., CommScope Inc., Corning Incorporated, Delphi Corporation, Ducommun LaBarge Technologies, Electrical Components International, Encore Wire Corporation, Finolex Cables Ltd., Fujikura Ltd., AFL, Furukawa Electric Company Limited, General Cable Corporation, Hitachi Cable Ltd., LS Cable & System Limited, Superior Essex Incorporated, MOLEX Inc., NEXANS SA, Olex Cables Limited , NKT Cables Group GmbH, Permanoid Ltd., Prysmian Group S.p.A. , Rea Magnet Wire Company Inc., Southwire Company, Sumitomo Electric Industries Ltd., TE Connectivity, Tele-Fonika Kable Handel S.A., The Okonite Company, among others.
The research report titled "Insulated Wire and Cable: A Global Strategic Business Report" announced by Global Industry Analysts Inc., provides a comprehensive review of market trends, growth drivers, issues, mergers and acquisitions and other strategic corporate initiatives of major and niche global and regional players. The report provides market estimates and projections in US$ Million for all major geographic markets, including the United States, Canada, Japan, Europe (France, Germany, Italy, UK, Spain, Russia and Rest of Europe), Asia-Pacific (China, India and Rest of Asia Pacific), and Latin America (Brazil and Rest of Latin America). Key product segments analyzed at the global level include Building Wire & Cable; Electronic Wire & Cable; Power Wire & Cable; Telecommunications, Data Wire & Cable; and Others.
For more details about this comprehensive market research report, please visit http://www.strategyr.com/Insulated_Wire_And_Cable_Market_Report.asp.
About Global Industry Analysts, Inc.
Global Industry Analysts, Inc., (GIA) is a leading publisher of off-the-shelf market research. Founded in 1987, the company currently employs over 800 people worldwide. Annually, GIA publishes 1500+ full-scale research reports and analyzes 40,000+ market and technology trends while monitoring more than 126,000 Companies worldwide. Serving over 9500 clients in 27 countries, GIA is recognized today, as one of the world's largest and reputed market research firms.
Global Industry Analysts, Inc.
Telephone: 408-528-9966
Fax: 408-528-9977
Email: press(at)StrategyR(dot)com
Web Site: http://www.StrategyR.com/