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Alterations in the balance between ANG II/ACE and ANG 1–7/ACE2 in ANG II-dependent hypertension could reduce the generation of ANG 1–7 and contribute further to increased intrarenal ANG II. Upregulation of collecting duct (CD) renin may lead to increased ANG II formation during ANG II-dependent hypertension, thus contributing to this imbalance. We measured ANG I, ANG II, and ANG 1–7 contents, angiotensin-converting enzyme (ACE) and ACE2 gene expression, and renin activity in the renal cortex and medulla in the clipped kidneys (CK) and nonclipped kidneys (NCK) of 2K1C rats. After 3 wk of unilateral renal clipping, systolic blood pressure and plasma renin activity increased in 2K1C rats (n = 11) compared with sham rats (n = 9). Renal medullary angiotensin peptide levels were increased in 2K1C rats [ANG I: (CK = 171 ± 4; NCK = 251 ± 8 vs. sham = 55 ± 3 pg/g protein; P < 0.05); ANG II: (CK = 558 ± 79; NCK = 328 ± 18 vs. sham = 94 ± 7 pg/g protein; P < 0.001)]; and ANG 1–7 levels decreased (CK = 18 ± 2; NCK = 19 ± 2 pg/g vs. sham = 63 ± 10 pg/g; P < 0.001). In renal medullas of both kidneys of 2K1C rats, ACE mRNA levels and activity increased but ACE2 decreased. In further studies, we compared renal ACE and ACE2 mRNA levels and their activities from chronic ANG II-infused (n = 6) and sham-operated rats (n = 5). Although the ACE mRNA levels did not differ between ANG II rats and sham rats, the ANG II rats exhibited greater ACE activity and reduced ACE2 mRNA levels and activity. Renal medullary renin activity was similar in the CK and NCK of 2K1C rats but higher compared with sham. Thus, the differential regulation of ACE and ACE2 along with the upregulation of CD renin in both the CK and NCK in 2K1C hypertensive rats indicates that they are independent of perfusion pressure and contribute to the altered content of intrarenal ANG II and ANG 1–7.
- ANG II-dependent hypertension
- angiotensin peptides
- angiotensin-converting enzyme
- qRT-PCR
- immunohistochemistry
in angiotensin ii (ANG II)-dependent hypertension, increased circulating ANG II levels lead to progressive augmentation of intrarenal ANG II content (35, 57, 61). The increased intrarenal ANG II content results from AT1 receptor (AT1R)-mediated uptake of circulating ANG II, as well as de novo intrarenal ANG II generation (52). Increased local ANG II formation has been associated with augmentation of intrarenal angiotensinogen (AGT) synthesis and secretion by proximal tubule (PT) cells (27, 29, 59) leading to augmented urinary AGT excretion indicating that proximally secreted AGT traverses the distal nephron segments (27, 30).
Renin, primarily synthesized and released by juxtaglomerular (JG) cells, is also produced by principal cells of connecting tubules and collecting duct (CD) cells of rat, mouse, and human kidneys (22, 42, 48). Previous studies suggest that tubular renin is differentially regulated from renin in JG cells (20, 37, 42, 43, 47). In response to chronic ANG II infusions, renin mRNA and protein levels increase in principal cells from connecting tubules and CD, indicating stimulation of tubular renin during ANG II-dependent hypertension (42). This stimulatory effect of CD renin is prevented by treatment with AT1R blockers suggesting that it is mediated by an AT1R mechanism (43). Studies showing augmentation of CD renin in both clipped and unclipped kidneys of Goldblatt hypertensive rats indicate that the enhanced CD renin occurs independently of blood pressure (44). Thus, enhanced CD renin acting on AGT delivered from proximal nephron segments may contribute to increased ANG I generation that can then be converted to ANG II by the substantial angiotensin-converting enzyme (ACE) activity present in the CD (4, 5).
ACE2, the homolog of ACE, is abundantly expressed in the kidney and metabolizes ANG II to generate the heptapeptide ANG 1–7 (10, 51, 53). ANG 1–7 may antagonize the actions of ANG II especially in situations of an overactive renin-angiotensin system (RAS) (12, 13, 15, 51). Recent studies showed decreased ACE2 mRNA expression in spontaneous hypertensive rats and mRen2 hypertensive rats (7, 58). The decreased ACE2 expression is associated with the onset and severity of hypertension (53). ANG II has been shown to downregulate ACE2 expression in astrocytes, heart, and kidney, suggesting that during high-ANG II states, the generation of ANG 1–7 might be reduced (17–19). Alternatively, the reduced ACE2 expression might be due to the increased renal perfusion pressure observed in these models. Goldblatt hypertensive rats exhibit high intrarenal ANG II content in both kidneys, as well as upregulation of renin in distal nephron segments that may lead to regional differences in the content of intrarenal angiotensin peptides, as well as changes in the expression of ACE and ACE2 within the kidneys. Accordingly, the present study was performed to determine the regional changes in ANG II/ACE and ANG 1–7/ACE2 in ANG II-dependent hypertension by using Goldblatt hypertensive rats and examining the levels of ANG I, ANG II, and ANG 1–7, as well as ACE and ACE2 gene expression separately in renal cortical and medullary tissues from both kidneys of 2K1C hypertensive rats after 3 wk of unilateral renal artery clipping. Additional studies were performed in rats infused chronically with ANG II (80 ng/min) for 2 wk. We hypothesized that, in 2K1C hypertensive rats, the intrarenal contents of ANG 1–7 and ACE2 transcript levels are decreased in both clipped and unclipped kidneys. These results indicate that there is differential regulation of ACE/ACE2 in renal tissues of 2K1C rats, which may help to explain the reciprocal changes in ANG II and ANG 1–7 observed in the kidneys of Goldblatt hypertensive rats and ANG II-infused rats.
Experimental animals, sample collections, and tissue preparation.
All protocols were approved by the Tulane University Health Sciences Center Animal Care and Use Committee. Male Sprague-Dawley rats (150 to 175 g; Charles River Laboratories, Wilmington, MA) were anesthetized and a u-shaped silver clip (lumen diameter of 0.25 mm) was placed on the left renal artery (n = 11), or the rats were just subjected to a sham operation (n = 9). Following a training period, the systolic blood pressures (SBP) were measured by tail-cuff plethysmography (Visitech, BP-2000, Apex, NC) 1 day before placement of the silver clip (lumen diameter of 0.25 mm) on the left renal artery, and at the end of the first, second, and third weeks of the study. On day 25 after unilateral renal clipping, rats were euthanized by conscious decapitation and trunk blood samples and kidneys were harvested; the cortex and inner medulla were separated for measurements of tissue renin activity, ANG I, ANG II, and ANG 1–7 contents, and ACE and ACE2 gene expression studies, respectively. Additional kidney tissues from rats chronically infused with ANG II via SC minipumps (80 ng/min for 14 days; n = 6) and sham-operated (n = 5) were used to examine ACE and ACE2 gene expression and functional enzymatic activities.
Angiotensin peptides kidney content.
Renal cortical and medullary levels of ANG I, ANG II, and ANG 1–7 were extracted from kidney sample homogenates, purified in Sep-Pak-C18 columns (Waters, Milford, MA), and measured by HPLC as previously described (1). Peptides were identified according to retention time. The identity of eluted ANG I, ANG II, and ANG 1–7 was confirmed by direct sequencing (protein sequencer PPSQ-23; Shimadzu, Tokyo, Japan). For concentration determination, commercially available peptides were employed to develop a standard curve. Peptide levels were normalized according to total protein concentration and results were expressed as picograms per gram of protein.
ACE and ACE2 renal expression and functional activity.
Twenty nanograms per well of total RNA extracted from rat kidney cortex and inner medulla samples were quantified by real-time qRT-PCR for ACE and ACE2 mRNA levels, using protocols previously described (28, 42). Data of quantitative qRT-PCR were normalized by β-actin mRNA expression. The sequences of primers and probes of ACE, ACE2, and β-actin are provided in the methods expanded section (the online version of this article contains supplemental data). For ACE2 immunoexpression, affinity-purified primary antibody against ACE2 (Dr. C. M. Ferrario; Wake Forest University, NC) was assessed by the immunoperoxidase technique as previously described (44) at a dilution of 1:200 for ACE2. The ACE and ACE2 catalytic activities were determined fluorimetrically by two different laboratories using either the benzyloxycarbonyl-l-phenylalanyl-l-histidyl-l-leucine as a substrate (5) with values reported in nanomoles per milligram of protein; or the Fluorogenic Peptide Substrate VI [FPSVI, 7Mca-Y-V-A-D-A-P-K(Dnp)-OH; R&D Systems, Minneapolis, MN] as previously described (11) with values reported in reverse light units per milligram of protein. Details of these protocols are provided in the methods expanded section.
Total renin, renin, and (pro)renin activities in kidney cortical and medullary tissues.
Active renin was determined as previously described (56) by measuring the amount of ANG I generated per hour from the renal tissue homogenates incubated at 37°C over a period of 24 h with the renin substrate tetradecapeptide (Sigma, St. Louis, MO) and PMSF, as described in detail in the methods expanded section. Trypsinized tissue samples were also subjected to the above protocol to determine total renin activity. (Pro)renin activity levels were calculated as the difference between the total renin and the active renin. The results are corrected by intracellular protein and expressed as specific activity micrograms per microgram.
Statistical analyses.
Results are presented as means ± SE. Data were evaluated by Grubb's test (25) using GraphPad Software (San Diego, CA) and analyzed when appropriate by unpaired Student's t-test or by one-way ANOVA with Dunnett's Multiple Comparison tests using GraphPad Prism Software, Version 5.0 for Windows (GraphPad Software). A value of P < 0.05 was regarded as significant.
Table 1 shows the average body weights (BW), SBP, and plasma renin activities (PRA) of rats subjected to sham operation or clipping of the left renal artery during the 25 days. In 2K1C rats, the BW was slightly lower than in sham rats after 7 days of surgery (251 ± 5 vs. 236 ± 5 g) and this trend continued during the following 2 wk of the study (2K1C: 253 ± 6 g vs. sham: 280 ± 4 g, after 14 days; and 2K1C: 291 ± 8 g vs. sham: 320 ± 3 g, after 25 days; P < 0.05). SBP values were similar in both groups of rats at the beginning of the study (2K1C: 126 ± 2 vs. sham: 118 ± 3 mmHg); however, after 1 wk following placement of the clip, the SBP was increased in 2K1C rats relative to sham-operated rats (2K1C: 154 ± 5 vs. 129 ± 4 mmHg) and continued to increase during the second and third week following clipping (day 14 = 179 ± 6 vs. 126 ± 4 mmHg; day 25 = 183 ± 6 vs. 125 ± 4 mmHg; P < 0.001). At 25 days, PRA was elevated in 2K1C rats compared with sham-operated rats (13.0 ± 2 vs. 5.6 ± 1 ng ANG I·ml−1·h−1; P < 0.05).
The concentrations of ANG I, ANG II, and ANG 1–7 measured in renal cortical and medullary homogenates after 3 wk of unilateral renal clipping from two independent studies are shown in Fig. 1. Contents of all angiotensin peptides were higher in the renal medullary tissues than in the renal cortexes of 2K1C rats. In the cortex, only the CK showed higher ANG I and ANG II content than the sham kidney [ANG I (CK: 68 ± 10; NCK: 51 ± 8 vs. sham: 29 ± 2 pg/g; P < 0.05 CK vs. sham); ANG II (CK: 129 ± 17; NCK: 90 ± 11 vs. sham 91 ± 15 pg/g; P < 0.05 CK vs. sham)]. However, in the medulla, the levels of ANG I and ANG II of both the CK and NCK kidneys of 2K1C rats were significantly higher than in the sham kidneys [ANG I (CK = 171 ± 4; NCK = 251 ± 8 vs. sham = 55 ± 3 pg/g protein; P < 0.05 CK vs. sham, P < 0.01 NCK vs. sham); ANG II (CK = 558 ± 79; NCK = 328 ± 18 vs. sham = 94 ± 7 pg/g protein); P < 0.001 CK and NCK vs. sham]. In contrast, the content of ANG 1–7 was substantially lower in both the cortex and medulla of CK and NCK of 2K1C rats [cortex: (CK = 7 ± 1; NCK = 7 ± 2 pg/g); medulla: (CK = 18 ± 2; NCK = 19 ± 2 pg/g); P < 0.05 kidney cortex vs. kidney medulla] compared with sham rats [cortex: (36 ± 6 pg/g); medulla (63 ± 10 pg/g); P < 0.001 vs. sham].
In the renal cortex of 2K1C rats, ACE mRNA levels were increased in the CK but not in the NCK [ACE (CK: 1.6 ± 0.4; NCK: 1.0 ± 0 vs. 1.0 ± 0.0 AU; P < 0.05)]; however, ACE2 transcript levels were similar between the CK and the NCK [ACE2 (CK: 1.1 ± 0.2; NCK: 0.7 ± 0.2 vs. 1.0 ± 0.0 AU)]. In contrast, in the renal medulla, ACE mRNA levels were significantly increased in the CK and NCK of 2K1C rats compared with sham rats (CK: 1.9 ± 0.2; NCK: 1.6 ± 0.1 vs. 1.0 ± 0.1 AU; P < 0.001), while the levels of ACE2 mRNA levels were decreased (CK = 0.5 ± 0.1; NCK = 0.3 ± 0.1 vs. 1.0 ± 0.1 AU; P < 0.0001; Fig. 2). In addition, CK and NCK compared with sham kidneys showed activities significantly higher for ACE (CK: 7.5 ± 1.0; NCK: 6.8 ± 0.4 vs. 4.3 ± 0.2 nmol/mg protein; P < 0.05) but decreased for ACE2 (CK: 0.9 ± 0.2; NCK: 0.8 ± 0.1 vs. 1.5 ± 0.1 nmol/mg protein; P < 0.05).
To further validate the reciprocal changes in ACE and ACE2, we examined the mRNA abundance of ACE and ACE2, as well as their functional activities in kidney tissues from chronic ANG II-infused (n = 6) rats and sham-operated rats (n = 5). In these rats, although the ACE mRNA levels were not significantly different between the two groups, the ANG II rats exhibited substantially greater ACE activity in the kidneys than the control rats (ANG II = 2,712 ± 334 vs. sham = 487 ± 51 RLU/mg; P < 0.05). In addition, the ACE2 transcript levels were reduced in chronic ANG II-infused rats (ANG II = 0.6 ± 0.1 vs. sham = 1.0 ± 0.0 AU; P < 0.05) but we did find any difference in its activity (ANG II = 2,356 ± 786 vs. sham = 1,290 ± 225 RLU/mg) compared with sham rats.
Figure 3 depicts the specific immunoreactivity and semiquantitation for ACE2 immunostaining by using the immunoperoxidase technique on a kidney section from sham-operated (top panels); clipped and nonclipped kidneys of 2K1C rats (middle panels) and ANG II-infused rats (bottom panels). ACE2 immunoreactivity was predominantly observed in the cytoplasm of epithelial cells of PTs in the cortex and inner cortex (left panels) and to a lesser extent in the CD cells of the inner medulla.
Figure 4 reflects the specific renin activity measured as ANG I generated per hour over a period of 24 h from the time the tetradecapeptide was added and corrected by total protein in the tissue kidney lysates. Between 2 and 8 h of incubation with the tetradecapeptide, the specific activity of renin was significantly higher in the cortex of CK than in the cortex of NCK or sham kidneys. However, in the renal medullary tissues during the same period, the renin activities in both the CK and NCK were higher than in sham kidneys. By 12–14 h later, renin activities became comparable between the CK and the sham kidney. In addition, the incubation with the tetradecapeptide in the presence of trypsin showed that in the renal cortex, the maximum (pro)renin activity observed at 2 h was significantly higher in the CK, while in the renal medulla, the NCK exhibited greater (pro)renin activity.
The present study demonstrates that both kidneys of 2K1C hypertensive rats exhibit reciprocal changes in ANG II/ACE and ANG 1–7/ACE2 in association with an enhancement of CD renin activity. This observation provides the basis for an additional mechanism that may contribute to explain high intrarenal ANG II content in the kidneys during Goldblatt hypertension. In a previous study, we demonstrated that in 2K1C hypertensive rats evaluated after 25 days of unilateral renal artery clipping, there is an increased renin immunostaining in cortical and medullary CD cells accompanied by augmented renin mRNA and protein levels in the renal medullary tissues (44). The present study extends those observations by confirming that in the renal medullary regions of both kidneys of 2K1C rats, most of the renin present is active. In contrast, in the renal cortical region only the CK exhibits higher renin activity (Fig. 4). Thus, it is likely that the enhancement of renin activity in the renal medulla of 2K1C rats may contribute to increased intrarenal ANG I and ultimately ANG II content regardless of the suppression of JG renin such as occurs in the NCK of this experimental model of hypertension.
Compared with other organs, the kidney expresses relatively high levels of ACE2. In the rat kidney, mRNA for ACE2 has been detected in all nephron segments including PTs, CDs, and vasa recta (3, 33, 54). Although ACE2 was first shown to cleave ANG I to ANG 1–9 (10), subsequent studies revealed that this enzyme exhibits a greater catalytic activity for ANG II than ANG I (55). The consequences of intrarenal ACE2-mediated formation of ANG 1–7 from ANG II remain unclear. Evidence suggests that ANG 1–7 exerts a countering influence against ANG II, which could partially protect against the development of hypertension (2, 14, 16, 23, 34, 46). Recent studies demonstrated that ANG II downregulates ACE2 mRNA expression in the heart, kidney, and astrocytes (17–19). Furthermore, it has been suggested that ANG II downregulates ACE2 via the AT1R-ERK/p38 MAP kinase pathway (31). Chappell and Ferrario (7) reported pronounced increases in ACE2 transcript levels within the kidney of the normotensive Lewis and hypertensive mRen2.Lewis rats following ARB treatment with losartan. In the present study, we show that both the CK and the NCK medullary tissues exhibit decreased ACE2 immunoreactivity, activity, and transcript levels compared with kidneys from sham-operated rats. Reduced levels of ACE2 gene expression and activity are consistent also with our finding of decreased levels of ANG 1–7 content in the renal medulla of CK and NCK of 2K1C hypertensive rats. The observation of increased ANG I and ANG II contents in the renal medulla of both kidneys of 2K1C rats, along with the previous demonstration that levels of renin mRNA and protein as well as its activity are augmented in these tissues (44), suggests that the upregulation of CD renin may contribute to the increases in intrarenal ANG II content.
In the 2K1C Goldblatt hypertension model during the initial phase of hypertension, there are ANG II-dependent alterations in tubular reabsorption of the NCK due to the elevations in circulating and intrarenal ANG II levels (9, 21, 41). Accumulated evidence indicates that there is enough ACE activity in the CDs (4, 45) that may lead to intraluminal conversion of ANG I to ANG II in this part of the nephron (32) and contribute to the ANG II stimulation of epithelial sodium channel activity at the surface of the CD cells (40). In the present study, we found that in the renal cortical regions, ACE transcript levels are augmented only in the CK while in the renal medulla, ACE mRNA levels and its activity are augmented in both kidneys of 2K1C hypertensive rats. Guan et al. (21) suggested that the de novo formation of intrarenal ANG II in the NCK of 2K1C rats is partially due to augmented intrarenal ACE activity (21) and our current data support this notion. In the chronic ANG II-infused rat model, it has also been reported that augmentation of intrarenal ANG II content is likely related to an increase in intrarenal ACE protein since Harrison-Bernard et al. (24) observed an increase in ACE immunostaining in PTs; and Sadjadi et al. (50) reported increased renal ACE activity despite no changes in plasma ACE activity. Using the chronic ANG II hypertensive rat model, we found that, although renal ACE mRNA levels did not differ from those in sham rats, the ACE activity was also significantly augmented in the ANG II-infused rats. This is consistent with the report showing that changes in enzymatic activity may occur without transcriptional and/or posttranslational alterations; i.e., by changing the open structure of the specific protein conformation (26).
It has been suggested that ACE2 is the major enzyme involved in ANG 1–7 formation from ANG II in tissues; thus contributing to ANG II degradation (8, 60). Our data demonstrating reduced ACE2 mRNA levels and activity in both kidneys of Goldblatt hypertensive rats as well as decreased specific immunoreactivity of ACE2 in the kidneys of chronic ANG II-infused rats support a functional role for ACE2 to contribute to the increases of intrarenal ANG II content by reducing the ACE2-mediated degradation of ANG II. The collective effect of increased ACE leading to increased ANG II formation, coupled with decreased ACE2, diminishing ANG II degradation to ANG 1–7, would be to increase prevailing levels of ANG II, as well as reduce ANG 1–7 levels. These observations do not mean that this is the only mechanism responsible for the reciprocal changes in intrarenal ANG II/ANG 1–7 contents during ANG II-dependent hypertension. In this regard, it has been reported that augmentation of chymase activity in the ischemic kidney of 2K1C rats (49) and in diabetic renal vascular disease (39) is also a mechanism responsible for ACE-independent intrarenal ANG II production. The augmentation of renin activity in distal nephron segments along with increases in medullary ANG I content of both kidneys of 2K1C rats support the notion of increased intrarenal ANG II formation, which ultimately may stimulate sodium reabsorption in the CD and may explain the attenuation of the pressure natriuretic response to elevations in arterial blood pressure and the development and maintenance of hypertension in Goldblatt hypertensive rats. Therefore, the synergistic actions of distal nephron renin-mediated increases of ANG II, along with the diminished counteracting influence of ANG 1–7 associated with the direct effects of ANG II on distal nephron transport mechanisms could provide a powerful sodium-retaining stimulus in Goldblatt hypertension (2, 36, 38), thereby allowing for a greater influence in the progression of high blood pressure in the 2K1C hypertensive rats.
In summary, the present findings indicate that the upregulation of CD renin in the renal medulla of both CK and NCK of 2K1C rats is associated with reciprocal changes in the ANG II and ANG 1–7 contents in the medullary regions of the kidneys of these rats. During conditions of RAS activation, subsequent to clipping one of the renal arteries or during chronic ANG II infusion, there are increases in CD renin activity coupled with substantial decreases of ANG 1–7 content and ACE2 and increases in ANG II and ACE; which may contribute to the progression of high blood pressure during ANG II-dependent hypertension.
This work was supported by National Heart, Lung, and Blood Institute Grant HL-26731 and COBRE Grant P20-RR-017659 from National Center for Research Resources. M. C. Prieto is a Building Interdisciplinary Research Careers in Women's Health scholar supported by the Eunice Kennedy Shriver National Institute of Child Health & Human Development (K12HD043451) and the American Heart Association (09BGIA2280440). L. S. Lara is a recipient of a Coordinacion de Apoyo de Personas de Educacion Superior PostDoctoral Fellowship from Brazil.
No conflicts of interest, financial or otherwise, are declared by the author(s).
We thank Dr. C. M. Ferrario (Wake Forest Univ., NC) for generously providing the rat anti-ACE2 and anti-ANG 1–7 antibodies, Dr. E. Lazartigues (Louisiana Health Science Center, LA) for providing the facilities for the measurements of ACE and ACE2 activities in the chronic ANG II hypertensive rat model, and Dr. L. Bazzano for providing advice for the data statistical analyses. Digital images of histological specimens were obtained at the Imaging Core Facility of Hypertension and Renal Center of Excellence at Tulane University Health Sciences Center.
- Copyright © 2011 the American Physiological Society


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This is what is asked of you: to act justly, to love tenderly, and to walk humbly with your God. ~Micah 6:8
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FOR STARTING A LOCAL GROUP: The Pax Christi Local Group Organizing Toolkit, "Creating a More Peaceful, Just and Sustainable World"
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The Biggest Climate Rally in U.S. History
Editor's Note: Australia's Prime Minister, Julia Gillard, has just said that the entire country of Australia is being "challenged by nature". I think it's a sad way of looking at what we're facing — it's as if we're the innocent victims. Rather, I think nature is being challenged by us. Nature is having a hard time 'keeping it together' in the face of all we're throwing at it. We are entering an age of potential runaway feedback loops that can render all our good work redundant, and yet at the just-ended World Economic Forum in Davos, Switzerland, the key focus was still, predictably, about stimulating more economic growth. I don't for a minute expect corporate-bought political systems to react appropriately, but I think a massive turn-out for a rally like the one below can at least give some hope for discussion on the issues that matter — an opportunity for systemic solutions to get their day in the sun.
On Monday during the inauguration, President Obama opened his term with a clarion call for action on climate change. Our response?
Time to organize.
President Obama said, "We will respond to the threat of climate change, knowing that the failure to do so would betray our children and future generations."
These are great words, in a big speech. But pardon us if we're not sitting on our hands basking in the glow of a job well done. We've seen good talk before, and the President's talk – while very good in this case – is not the same as action.
So it's time to hold his feet to the fire. Luckily, we've got a great opportunity to do just that.
Oil Change International is proud to partner with 350.org, the Sierra Club and many other organizations on the upcoming Forward on Climate rally in Washington, DC, a rally that, with your help, will be the largest climate-focused event in U.S. history.
The proposed Keystone XL pipeline – that zombie project that keeps coming back from the dead – will be on the President's desk sometime in the next few months. And we need to show him, without a doubt, that if he's serious about tackling climate change he must reject this pipeline.*
Will you join us in DC on February 17th to ensure we move Forward on Climate? (Don't live in DC? Not to worry – organizers are in the midst of arranging buses and other transportation options to bring folks in. The best way to keep up to date on these options is to sign up!)
This is an event you won't want to miss. You'll be hearing from us again soon with more details…but for now, be sure to sign up to join us in DC.
* Last week Oil Change International made headlines when we released our latest report: "Petroleum Coke, the Coal Hiding in the Tar Sands" exposing the fact that the greenhouse gas estimates of the pipeline have been significantly underestimated.
One thought on "The Biggest Climate Rally in U.S. History"
id be there if I wasnt here… lets show them we are serious on climate change


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May Bartens
Kate Dunning Capen
Just submitted some changes. Thank you
This is taken from Pennsylvania, Death Certificates, 1906-1963
Name Kate Capen
Gender Female
Race White
Age 63
Birth Date 16 Feb 1860
Birth Place Maryland
Death Date 24 Aug 1943
Death Place Middletown, Delaware, Pennsylvania, USA
Father Name Robert Dunning
Father Birth Place Maryland
Mother Name Elizabeth Cox
Mother Birth Place Maryland
Spouse Name Erastus Capen
Certificate Number 72017
Added by
May Bartens
on Nov 11, 2015 1:42 PM
Robert "Scott" Patrick
RE: William and Mary Wilson memorials
Thanks Rich, I'm glad I could help. If you find out what became of Mrs Wilson and her children please pass the info on to me.
Added by
Robert "Scott" Patrick
on Dec 21, 2013 6:49 PM
RE: Mary Anna Capen Thacher
I'd be glad to manage the memorial for Mary Anna Capen Thacher.
I am John Thacher (Muletrain) Find A Grave #47206526
Added by
on Oct 03, 2013 2:12 PM
sheila hartsel
Frederick Hartsel
Hi my name is Sheila Hartsel. I am now considered our family historian, and have been searching out the family tree and documenting all as I go to secure this information for generations to come. I am working very hard to find where all realtives are buried and link them all thru Find A Grave. Frederick is the grt grand uncle of my husband Terry Hartsel. Frederick and my husband's Great Grandfather Frank Hartsel were brothers. Just about all of the Hartsel's grew up in or around Polk Ohio. I am documenting and linking all Hartsels in the Polk cemetery now and there are 31 of Frederick's relatives buried there.
My goal is to maintain and provide detailed information etc on the memorials so anyone in the future has free access and can easily follow the family lines through the links.
Thank you so much for considering transfering Frederick to me.
Sheila Hartsel
Added by
sheila hartsel
on Jan 30, 2013 10:25 AM
Kenneth L. Gailey
Jesse N. Nicholas
Has anyone taken a tombstone photo or found it yet?
Jesse N. was born in 1869 and the father died in 1866.
Added by
Kenneth L. Gailey
on Dec 03, 2012 9:42 AM
Shirley Reeve
Irma Spore
I made the changes as requested. If you'd like me to transfer the memorial to you, I'd be glad to do so. Let me know.
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Shirley Reeve
on Nov 08, 2012 10:11 PM
John McNally
I just posted a photo of the gravestone for both Elizabeth Capen & William Spargo. JMC
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John McNally
on Jun 21, 2012 8:37 AM
Linda Jenkins Werts
RE: George B. Capen #88475217
Look at the photo for #56619313. It's not good quality - but I've seen the stone and it's definitely "Capen". The Metro records for Lone Fir show:
Last name Capen
First name Infant
Death or burial date 8/18/1904
Cemetery Lone Fir Pioneer Cemetery
Southeast 21st Avenue and Morrison Street
Portland, Oregon
Grave number 2N
Lot 26
Section 21
This is the same lot for George, Eva, and Lucy Anna, and the only stone showing.
Added by
Linda Jenkins Werts
on Apr 25, 2012 9:55 AM
Linda Jenkins Werts
RE: George B. Capen #88475217
Baby Capen "born and died 1904" FG #56619313. Metro has her buried on August 18, 1904, but, of course, being Metro, there is no birth date. Her stone is the only one found in the lot where the other Capens are buried - and it doesn't look to me to be original. I've added Lucy Anna's information and linked her to her parents.
Added by
Linda Jenkins Werts
on Apr 22, 2012 10:48 PM
Linda Jenkins Werts
George B. Capen #88475217
I've added some information from Ancestry.com on George and Mrs. George (who I find is Eva Waddell). If they didn't marry until 1889, do you know who the Baby Capen d. 1883 is? And the Baby Capen b. and d. 1904 is not theirs, but they are all buried in Block 21 Lot 26 and only the 1904 baby has a marker. Nothing for George and Eva and the 1883 baby - not even the temporary cemetery ones.
Added by
Linda Jenkins Werts
on Apr 22, 2012 12:07 AM
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> Mike McDonough (mpm(at)goldwiretech(dot)com) reports a bug with a severity of 2 > Solaris ODBC - linker flag needs to be set when building shared objects > Long Description > Linker flag which needs to be set when building shared objects to > prevent a symbol in the executable overriding one in the shared > object: '-Bsymbolic' needs to be set in Makefile.shlib. This flag is > set for linux builds, but not for solaris. > #+++rwhit, 12/12/00 added -Bsymbolic to fix SQLPrimaryKeys() - it's calls > # to other SQL*() functions were being resolved by > # the driver manager versions rather than the pgsql > # versions Can you explain why this flag is needed? What call is getting resolved how and how should it have been resolved? Since this flag is only portable to ELF systems the problem should really be fixed some other way. -- Peter Eisentraut peter_e(at)gmx(dot)net http://yi.org/peter-e/
Next: From: Andriy Rozeluk Date: 2000-12-14 00:02:44 Subject: setQueryTimeout in JDBC driver seems unimplemented Previous: From: Hiroshi Inoue Date: 2000-12-13 00:21:06 Subject: Re: plpgsql function error after alter table add


text:
Yesterday I asked about the availability of any public domain FORTRAN
compiler. I received several responses. Most of the people suggested
"f2c" available from 'research.att.com' (login netlib). Thanks to
every one for a quick response. (I have NOT yet received my own email
which I sent yesterday.)
I have FTPed "f2c" but yet to install and test it. I received different
opinions about the performance of "f2c". Mark Maimone (firstname.lastname@example.com)
cautioned, "f2c + sunCC is typically significantly slower than f77
processed code". But according to email@example.com, "Rumor has it it's
pretty good".
Malcolm Strickland also mentioned --
There is a PD compiler in the works from free software foundation but
it wont available for some time.
Following people suggested "f2c". Thanks !!
Bill Bogstad (email@example.com)
email@example.com (Mark Maimone)
email@example.com (Mike Halderman)
David Fetrow <email@example.com>
email@example.com (Barry Shein)
Peter Kaldis <email@example.com>
email@example.com (Marcel Bernards)
Malcolm Strickland (email@example.com)
firstname.lastname@example.com (Bruce Oneel )
============ My original question ===============
Hi Sun Managers,
Subject line says it all. I am looking for a public domain FORTRAN
compiler (something like 'gcc') to run on a SPARCstation 2 (OS 4.1.2).
We have a comercial software (LINDO - a software to solve linear
programs) which is written and compiled in FORTRAN. With the executable
code of LINDO, we received a "routine library" too. There is a way to
link the C routines with the LINDO routines (in the library). But, it
needs some FORTRAN routines (during linking) to create the new
executable. We don't have a FORTRAN compilers on any of our
SPARCstations and we don't want to buy one (can't afford!!) just for
this purpose. Is there any other way to create the executable ? Will a
public domain FORTRAN compiler, if exists, will work ?
Thanks. I will summarize.
============== Details about f2c ===============
From: email@example.com (Mark Maimone)
Newsgroups: comp.lang.fortran,comp.lang.c
Subject: Re: Fortran to C translator
Keywords: fortran, C, translator, f2c
Date: 13 Sep 90 01:43:30 GMT
Organization: Carnegie-Mellon University, CS/RI
Since there have been several requests for a Fortran to C translator
in the past week, I'm reposting the announcement about f2c. The short
answer is you can get f2c by anonymous-ftp from research.att.com in
directory dist/f2c.
Source for f2c, a Fortran 77 to C translator jointly developed by
folks from Bell Labs, Bellcore, and Carnegie Mellon, is now freely
F2c was derived from the original UNIX operating system's f77(1),
and the generated C follows f77's calling conventions; on some machines, the
resulting object files are interchangeable with (and behave
indistinguishably from) objects compiled by f77. The main "advantage" of
f2c is that it converts ANSI standard Fortran 77 into C without manual
intervention, at least when invoked by a suitable script or makefile (that
may need to exercise an f2c option to ensure that COMMON blocks are defined
just once). The main "problems" are that f2c does no code restructuring
(e.g., gotos are preserved) and that Fortran I/O gets converted into a bunch
of calls; thus the translated C code doesn't look too pretty, and in general
one would need to maintain the Fortran rather than its translation into C.
[F2c is not meant to displace the services of commercial vendors whose
business is to convert Fortran into maintainable C.]
There is a plethora of options, many of which exist to support
different compilation environments for the translated C (e.g., ANSI C or C++
compatability, different type sizes, separate files for COMMON blocks to
appease "smart" linkers). So far f2c (and f2c-generated source) has
compiled successfully on many machines: Sun, Vax, IBMRT, Apollo, SGI, MIPS,
and Cray to name a few.
F2c has been under test by the net community for over a year
and has been verified on the NBS tests, several large math libraries,
floating point tests, even code for laying cable on the ocean floor!
To find out about f2c, send the following E-mail message to netlib
(firstname.lastname@example.com or research!netlib):
send index from f2c
Your message will be answered automatically (by a program -- see CACM vol.
30 #5 (May, 1987), pp. 403-407). You will receive a reply explaining how to
automatically acquire f2c source (about 600K), f2c library source (130K),
and supporting info (man page, etc). Or you can anonymous-FTP to
research.att.com and look in directory dist/f2c at these files:
all.Z -- 250K compressed shar file for f2c
f2c.ps.Z -- 24 page tech report describing f2c
index -- general info about files
libf77.Z, libi77.Z -- compressed shar files for libraries
Careful! Anything free comes with no guarantee.
Mark Maimone phone: (412) 268 - 7698
Carnegie Mellon Computer Science email: email@example.com
f2c + sunCC is typically significantly slower than f77 processed code.
This archive was generated by hypermail 2.1.2 : Fri Sep 28 2001 - 23:06:39 CDT


text:
Future Hall Of Famer Jim Thome chairs a charity fundraiser event Saturday, January 14th 2012. Charity event entertainment ideas like dueling pianos will help you rake in the funds. Seriously! Everyone LOVES dueling pianos and when you bring us to your fundraising party or your company event, you'll be pleasantly surprised by the turn out.
Central Illinois Dueling Pianos produces the entertainment for events like this with dignity and grace. Over 850 people will be in attendance. Live music and comedy makes your fundraising job all that much easier. Call us NOW! Thanks.


text:
Local Dish Customers Upset Over Loss of Channels
Amherst Co., VA - Some Dish Network customers in our area are fuming because they are not getting to see some of their favorite shows on the CW and Fox channels. Dish did not re-sign a contract with Grant Group who owns Fox 21-27 because they say Grant wanted them to pay three times the amount they had already been paying.
The channels were cut Saturday. People were affected in certain pockets of four states, and Central Virginia is one of those areas.
"We're very upset with Dish. They expect their pay, yet we don't get the channels," said Bonnie Hicks, a Dish customer.
Hicks wants to make one thing clear:
"Don't mess with my family and Mascara," said Hicks.
Hicks and her family cannot get enough of the sport.
"Whether it be a movie, whether it be mints, or whether it be a car," said Hicks as she showed off some memorabilia.
So you can probably guess what happened Saturday, when her husband turned on the TV and Nascar was not on.
"You can only imagine what he might have said!" Exclaimed Hicks. "Of all the times to cut it out, it is Nascar time."
This past Sunday, Fox 21-27 posted the following on their Facebook page: "We are still in the midst of negotiations with Dish to get our channels back on the air as quickly as possible."
As of Wednesday, Dish says they have not reached an agreement.
"We have no legal right to broadcast their signal," said a Dish Network representative.
They say until they come to an agreement, do not expect to see anything on the local CW or FOX affiliates.
"We don't want the customers to go without their channels, but at the same time, we're not going to settle for an increase of three times of what we were paying them," said a Dish Network representative. "We do understand that the Daytona 500 is important and we are working around the clock to come to an agreement with Grant Group."
But customers like Hicks call it, bologna.
"We are one upset family! With Dish. Thank you!" said Hicks.
According to Debbie Reardon, Corporate Director of Marketing for the Grant Group, the company says they are shocked and confused over why service was canceled in the first place. They say they had an agreement with Dish for an extension until Friday of this week and were surprised when service was shut off. They say they probably would have agreed to the offer.
As for them asking Dish to pay three times the amount, Grant Group says it is literally the difference of cents.


text:
The Other Sides Of Seuss
SoHo has recently become the habitat for some extraordinarily rare species, including the Tufted Gustard, the Two-Horned Drouberhannis, the Blue Green Abelard and the Andulovian Grackler. These odd animals, some liberated from a chicken coop in upstate New York, have hardly ever been glimpsed in Manhattan or, for that matter, anywhere else. And to think that I saw them on Broome Street.
Such wild creatures originated not in some far-flung continent but in the imagination of Theodor Seuss Geisel, better known as Dr. Seuss. Carved in wood, these 1930's sculptures are in ''The Art of Dr. Seuss,'' a show at the Animazing Gallery.
Dr. Seuss the sculptor? This display also features Dr. Seuss the advertising genius, Dr. Seuss the magazine illustrator, Dr. Seuss the political cartoonist and Dr. Seuss the Surrealist, as well as sketches from his beloved children's books. (The Cat in the Hat will greet children at the show tomorrow through Monday, from 11 a.m. to 6 p.m.) Much of the art has never been exhibited before.
''He was a private person and not a very confident man,'' said Heidi Leigh, the gallery's director. ''He knew that with his children's books and in the advertising arena he was successful. I think he didn't dare to expose himself as a fine artist.''
An example of his self-effacement is ''Man Who Made an Unwise Purchase,'' a colorful painting of a Chaplinesque fellow carrying on his shoulder a huge, yellow, unmistakably Seussian bird. ''What the painting is about is the 18th publisher, who bought his first book,'' Ms. Leigh said. That tale, ''And to Think That I Saw It on Mulberry Street,'' had been rejected by 17 others.Continue reading the main story
But Dr. Seuss was self-assured in his political views. Complementing his ad campaign for bug repellent is a 1942 illustration of Uncle Sam administering ''mental insecticide'' to a startled man, blasting a ''racial prejudice bug'' out of the man's ear.
The show even includes a bit of bawdy doggerel and a few nudes. But don't worry: Dr. Seuss's illustrations for his book ''The Seven Lady Godivas'' are no more anatomically correct than Barbie dolls. But they are much more Rubenesque and have something Mattel's creations don't: a sense of humor.
''The Art of Dr. Seuss,'' through June at Animazing Gallery, 461 Broome Street, near Greene Street, SoHo, (212) 226-7374. Free.
Want Pickles With That?
The world offers many ways to make a living. But few people have résumés listing Rob Williams's skill: he makes a bologna sandwich, including mustard and garnish, in less than three minutes. With his feet.
Mr. Williams is paid for this, but you'll probably be relieved to hear that he is not employed by a New York deli. He is, however, performing the feat on a New York stage as part of ''Idiots Adios: The Flaming Idiots' Very, Very, Very, Very, Very Last Show'' at the New Victory Theater. There Mr. Williams, known in his idiot persona as Gyro, and his fiery fellows Pyro (Jon O'Connor) and Walter (Kevin Hunt) are ending a 20-year-career as jugglers, contortionists, gymnasts, magicians and all-around comedians.
''With 'Friends' and 'Frasier' ending, we figured it was time for another comedy giant to go,'' Mr. Williams said. Quickly adding that he was kidding, he explained that the trio was, well, burned out. He invoked another famous comedy: ''We wanted to go out like 'Seinfeld,' at the height of our success.''
This show, which Mr. Williams described as a kind of greatest hits, includes the Swami Walter routine, in which Mr. Hunt eats three-foot balloons, and the Spanky Carmichael routine, in which Mr. O'Connor does coin tricks. They also do strange things with leaf blowers, ladders, straitjackets and, of course, flames.
He said the Idiots, whose name derives from a Monty Python bit, were of the same school as Penn and Teller, though with more sketch comedy. They also involve the audience in their show. ''It reminds me a little of 'Fear Factor,' '' Mr. Williams said. ''You're getting people to do things they'd never thought they'd do. Although it's not as gross and scary.''
Just be prepared to eat that bologna sandwich.
''Idiots Adios,'' at the New Victory Theater, 209 West 42nd Street, Manhattan, (212) 239-6200. Tonight at 7; tomorrow at 2 and 7 p.m.; Sunday at noon and 5 p.m.; Monday at 3 and 8 p.m. Tickets: $10, $25 and $40.
Dabbling in the Deep
During most cruises, sea animals are in the waves or below the surface. But in the one offered tomorrow by the South Street Seaport Museum, they will be honored guests on deck.
In a new family adventure, ''Program Afloat: Explore Marine Ecology Aboard the Schooner Pioneer,'' a marine educator will explain the ecosystem as visitors enjoy a two-hour sail. Because the harbor is an estuary -- where fresh and saltwater meet -- it offers a rich variety of species. Children will be able to examine and hold creatures like sea stars and horseshoe and spider crabs.
''It's an 1885 schooner, so it's really fun for kids,'' said Debra Wexler, the museum's director of public programs. ''Whoever goes is invited to help raise the sail.''
And if you miss the boat tomorrow, the seaport plans to repeat the program each month through August.
''Program Afloat,'' tomorrow, June 26, July 31 and Aug. 28, from 4 to 6 p.m. on the Schooner Pioneer. Meet at the Visitors Center at Pier 16, Fulton and South Streets, South Street Seaport. Fee: $30; students and 65+, $20; 12 and under, $15. Reservations advised: (212) 748-8735.Continue reading the main story


text:
Christmas has come early with the release of Saucony's Irish Coffee pack. Consisting of three shoes in Saucony's iconic Shadow 6000 silhouette, the colourways are inspired by the key elements required to brew Irish blend: coffee, whiskey and cream.
This model is inspired by the black coffee and comes in this beautiful minimal colourway. The theme continues through to the creamily soft suede uppers which sit atop a crisp white mid-sole with durable gum outsole. The understated clean aesthetic is only broken up by textural overlays and perforated details at the side panels and toe box.
These beautiful shoes are available in store and online now, get them before they're gone.
UK Delivery (click here for full details)
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We ship all over Europe and Worldwide from £9, this rate depends on the weight of the parcel and your location, for an exact quote add items to your basket and select your country.
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text: LINK Houston Texans Football Toss Game AKA Ladder Golf AKA Backyard Golf AKA Redneck Golf AKA Bolo Toss Its kinda expensive @ $79.99 but with a 30% coupon or something its not so bad. Im going to make my own and try to save some money and have a little fun with it. Should be a great addition to any tailgate party, or party in general.


text:
University Health Network Whiplash Intervention Trial (WIT)
This study has been completed.
University Health Network, Toronto
AVIVA Canada
Canadian Institutes of Health Research (CIHR)
Information provided by (Responsible Party):
University Health Network, Toronto
ClinicalTrials.gov Identifier:
First received: October 18, 2007
Last updated: May 23, 2012
Last verified: May 2012
- Full Text View
- Tabular View
- No Study Results Posted
- Disclaimer
- How to Read a Study Record
No Study Results Posted on ClinicalTrials.gov for this Study
|Study Status:
|This study has been completed.
|Study Completion Date:
|May 2012
|Primary Completion Date:
|May 2012 (Final data collection date for primary outcome measure)


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October 15, 2010 - 1:34am —
If you read writing blogs, watch podcasts, attend workshops,
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often a skill learned through study, hard work, and practice, rather
than simply a natural-born talent possessed by all authors.
AuthorsRising.com is a place for up-and-coming authors
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Witches and Super Heroes and Bunnies and Zombies will soon be at your door. You've purchased the Halloween candy. You've eaten the Halloween candy. You've purchased it again… Well, that's the routine around here. To help wrap up the season of Haunting we're offering a magical file download this month. Your download includes AI, SVG, EPS, […]


text:
Anabolic Steroids: Abuse & Addiction
What are anabolic steroids?
Synthetically derived variants of testosterone – the male sex hormone, are known as anabolic steroids. They are technically known as androgenic anabolic steroids or AAS [1], where 'androgenic' refers to the promotion of masculine characteristics, while 'anabolic' refers to the growth process involved. These steroids help in the growth of skeletal muscle tissue in the body and therefore, lead to an increase in lean body mass. These are prescribed in conditions that result from hormone deficiency – such as delayed onset of puberty and for treatment of diseases such as cancer and AIDS which are accompanied by muscle atrophy or loss of muscle tissue. They are also used in the treatment of some forms of anaemia, osteoporosis and primary biliary obstruction, which is an autoimmune disease pertaining to the liver.
In recent times though, anabolic steroids are being used as performance enhancement drugs by athletes competing in various sports. Since, anabolic steroids increase the rate at which protein synthesis happens in cells, they promote growth of muscle tissue and consequently enhance size of the muscle; hence, they are frequently consumed by bodybuilders to improve physical appearance. In addition to their anabolic characteristics, these steroids promote competitiveness and aggressiveness, which may be attributed to their androgenic effects. These traits are certainly desirable for intense competitive sporting activities.
How are anabolic steroids consumed?
Anabolic steroids can be taken orally or can be injected into the bloodstream. Topical applications in the form of gels, creams and patches are also commonly available. The type and dosage depends on the age of the patient, along with the type of medical condition and its severity.
When these steroids are consumed for performance enhancement, the dosage varies significantly, and at times may even be more than 100 times the upper limit of the recommended dosage. Users of anabolic steroids believe that by arranging and manipulating the dosage and combination of drugs, effectiveness can be increased significantly; at the same time, the body is given time to adjust in a manner that harmful side effects are avoided. The two most common methods used are 'stacking' and 'pyramiding'. Stacking involves the consumption of two or more anabolic steroids under the belief that these interacting steroids will have increased effectiveness in comparison to when they are consumed individually. Pyramiding refers to the process of gradually increasing the dosage of the steroids and then tapering it back to zero, over a period of 8 to 12 weeks. This is subsequently followed by a period of no usage, when the body returns to normal production of hormones. However, such theories have not been scientifically proven and are based on personal experiments conducted by steroid users.
How do anabolic steroids work?
Anabolic steroids work in two primary ways – firstly, by stimulating protein synthesis in the cells of muscle tissue, thereby promoting cellular growth; secondly, by blocking the hormone cortisol, which is released during bouts of intense exercise and leads to muscle tissue breakdown. In such a manner, not only does muscle wastage get prevented, consumers believe that steroid usage leads to muscle growth thereby enhancing performance exponentially.
What is the prevalence of anabolic steroid usage?
According to the study 'Monitoring the future' conducted by National Institute on Drug Abuse (NIDA) in 2002, 46.1% of 12th graders surveyed, 33.2% of 10th graders and 22% of 8th graders surveyed, said that it was easy to obtain anabolic steroids [2]. Centre for Disease Control and Prevention (CDC) data reveals that more than 0.6 million students have used steroids in the year 2005 [3]. In the National Household Survey on Drug Abuse conducted by Substance Abuse & Mental Health Services Administration in 1994, the number of Americans using anabolic steroids was pegged at 1.08 million [4]. It was also revealed that the usage was more prevalent among men, but this trend has been changing in recent times. A number of women, especially teenage girls, are turning to anabolic steroids for reducing body fat. By 1997, the number of teenage girls admitting to steroid usage had jumped to 175,000 [5]; a 100% increase from 1991 figures. All these figures, covering the past two decades, indicate that not only are anabolic steroids easily available, they are also being consumed in large quantities by the population, irrespective of age and sex.
What are the side effects of anabolic steroid usage?
The myriad side effects of anabolic steroid usage are commonly observed. Some side effects are reversible, while long term and unguided usage may lead to permanent damage to the body. The major side effects include liver damage, liver tumours, jaundice, renal failure, high blood pressure, fluid retention, an increase in LDL and decrease in HDL that may lead to cardiovascular and coronary artery diseases. Side effects also include decrease in natural production of testosterone in the body, alteration in thyroid functioning, headaches, nosebleeds, cramps and insulin insensitivity. In men, testicular atrophy or shrinking of testicles along with a reduction in sperm count, infertility, erectile dysfunction and impotency have been observed. Loss of hair leading to baldness and development of breasts, also called gynecomastia are also common. In women, enlargement of the clitoris, facial hair growth, baldness and menstrual cycle issues are common side effects. In adolescents, changes due to puberty get accelerated, and skeletal development may be stunted in case consumption of anabolic steroids is done prior to growth spurt that is generally experienced. In addition to these side effects, anabolic steroids are commonly injected, which increases the risk of contracting hepatitis and HIV that eventually leads to AIDS.
Apart from the physiological side effects associated with consumption of anabolic steroids, significant psychological effects have also been observed. Symptoms include over aggression, mania and violence. Although cases are less frequent, long term side effects such as psychosis and suicide have also been seen.
Are anabolic steroids addictive in nature?
Unlike other drugs of abuse, anabolic steroids do not have similar acute effects on the brain. Specifically, consumption of these steroids does not lead to an increase in the neurotransmitter Dopamine, which is responsible for providing the 'kick' or 'high' that eventually leads to addiction. However, long term usage has shown to impact chemical pathways of the brain that are also affected by other drugs. This leads to impacting the mood and behaviour of the individual consuming the steroid. It is because of the reinforcing effects that anabolic steroids are addictive in nature.
When consumption of anabolic steroids is stopped, withdrawal symptoms are experienced. These include fatigue, restlessness, mood swings, anxiety, insomnia, loss of appetite and reduced libido. The biggest danger is from clinical depression which enhances suicidal as well as homicidal tendencies. Quite often, people in these situations, turn to other forms of substance abuse, in order to control the withdrawal symptoms.
Considering the immediate benefits that are provided by anabolic steroids, it is no surprise that these performance enhancers attract sportsmen and body builders and increase psychological dependence. Consumption of steroids, coupled with good exercise and nutrition leads to increase in lean muscle tissue and enhanced performance. Consequently, when consumption is stopped at the end of the cycle, reduction in performance growth rate is experienced. This, along with decreased level of testosterone leads to a low mood and a state of depression. As can be expected, once a person starts consuming anabolic steroids, it becomes extremely difficult to get off them. Avoiding them completely is therefore the only fool proof way of avoiding all the side effects that can damage lives completely.


text:
POLICE are hunting a cyclist in connection with a meat theft.
Steaks and lamb chops were stolen from Sainsbury's in Hamlet Court Road, Westcliff at about 12.30pm on May 15. Police have now released a CCTV image of a woman they want to speak to in connection with the theft.
The woman police want to speak to is described as white, with black hair and aged between 30 and 40-years-old. On the day of the theft she wore pink or red coloured trousers, white trainers, a black t-shirt and sunglasses.
They are also wanting to speak to her after a meat theft from the same store on April 23 at about 11.45am.
Anyone with information should call Pc Amber Sawyer at Southend Police Station on 101, or Crimestoppers anonymously on 0800 555 111.


text:
Magnetic Wall Mount Letter Board, 24 x 18, Black, Gray Aluminum FrameItem#: YYAZ-QRT901M | Model#: 901M
Currently Out Of Stock!
Quartet® Magnetic Wall Mount Letter Boar Product Details
SpecificationsBOARD,MSG,OPN FACE2'X1.5'
Global Product Type: Boards-Magnetic Letter
Board Type: Magnetic Letterboard
Board Width: 24"
Board Height: 18"
Surface Material: Painted Steel
Surface Color: Black
Frame Material: Aluminum
Frame Color: Gray Aluminum
Mounting Details: Hardware Included
Pre-Consumer Recycled Content Percent: 0%
Post-Consumer Recycled Content Percent: 0%
Total Recycled Content Percent: 0%
Manufactured by: Acco
Warranty provided by: Acco
UPC No: 034138901908
Mfg Part No: 901M
Box Size:
( Length:0, Width:0, Depth:0)
Shipping Weight: 10.0000 pound(s)
Click here for full warranty and support information
- Acco logos are registered trademarks of Acco. All others trademarks and copyrights mentioned herein are the property of their respective owners.


text:
The next evolution in Yoga, Fitness and Dance: Underground Yoga™ Lifestyle System coming to the Tampa Bay Area March
Tampa Bay Area, Florida March 16th & 17th, 2013
Back to the future! Tampa Native and movement trendsetter, Michelle LeMay, returns from Los Angeles to launch Underground Yoga™ Lifestyle Workshops at Shapes Total Fitness in Palm Harbor. Filled with tools to promote happier, healthier, stress free and creative living, Underground Yoga™ Lifestyle System weaves yoga, dancing, fitness, stretching, breath-work, live music and meditation together into a system that positively affects your mind body and soul. Workshops are for people interested in Personal Empowerment and also for Instructors interested in certification.
Underground Yoga™ is the Dance Inspired Yoga technique that
puts rhythm in your Asanas and Pranayama in your Groove!!! It's edgy and creative with a live DJ to motivate the groovy movement within the Yoga Asana sequences. Most yoga is linear compared to the multidirectional movement of Underground Yoga™. It prepares you for Underground Yoga Dance as it makes you feel alive in your body!!!
Underground Yoga™ Dance is a freestyle dance technique that ignites your most powerful Dancer to shine! Instead of learning choreography, you are guided to movement that is indigenous to your own being. Underground Yoga Dance teaches you how to use Dance as therapy, increases your confidence and library of movement, and celebrates your unique magnificence! No Dance experience necessary … this will Ignite your passion for movement!!!
A Live DJ using specific music with layers of sound that wakes up dormant areas of your brain makes this workout extra FUN and mentally beneficial as well. The Underground Yoga™ Music is also created in specific keys to stimulate different chakras, the body's energy centers.
Michelle LeMay began her career in the Tampa Bay area as a Fitness and Health Reporter for WTVT, channel 13 and as the director of 13 Health clubs, then known as Mademoiselle Spas and the American Fitness Centers- now Shapes Total Womens Fitness. She went on to having a National TV career on shows like ESPN's "Gotta Sweat" and Fox Sports "Body Waves", as well as, to touring worldwide with NIKE pioneering the Cardio Hip Hop Movement and then with RYKA pioneering the Softer Forms of Exercise Movement. This trendsetter is not slowing down. At 50, Michelle can dance circles around most 20 year olds, and is launching what she believes to be her most important contribution to the world: Underground Yoga™ Lifestyle, a healthy lifestyle system that promotes well being not only physically, but also mentally, emotionally and spiritually.


text:
More information about "Zimbabwe"
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Stanley Goreraza
tag:blogger.com,1999:blog-1360613821135121274 2012-04-13T00:47:35.827+02:00 "VISION FOR ZIMBABWE!" Here we invite Zimbabweans and all concerned friends of Zimbabwe …
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Zimbabwe - Simbarashe mumbengegwi News topix from Zimbabwe focusing on newspaper articles on subjects from Foreign Affairs Minister Simbarashe ...
Lionel Dyke
In 1980, the newly independent and democratic Zimbabwe was a beacon of hope in a troubled region. Three decades later, Zimbabwe became the focus of...
Benjamin Mwaruwaru
Knowledge is the key for Zimbabwe. Posted on December 8, 2010 | Category: Politics; Business, Sport www.fifa.com. When Zimbabwe talisman Benjamin Mwaruwaru, …
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London, Aug 3 (ANI): Liverpool hero Steven Gerrard has urged his Liverpool team-mate and friend Luis Suarez to chase his Champions League dream wisely and follow his own example of being an ultimate one-club man.
According to the Mirror, the latest offer to tempt Gerrard away from Anfield was made less than a year ago and was met with the same response as the other attempts and it is this example that he has offered as evidence to Arsenal target Suarez, to persuade his teammate to stay.
Gerrard said that he had a chance to move to a Champions League club last year, but there was no temptation because he had been through enough of it before, and that was the message for Luis.
The Reds player said that Suarez will get many more chances to move on if that was what he wanted to do further down the line, but a player of his level and quality deserved to play in one of the best teams in world football in Barcelona or Madrid. (ANI)


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- February 25, 2014, 6:20 PM
Deliveries of the Airbus Helicopters EC135 T3/P3, an upgraded variant of the EC135 light twin, will begin in the fourth quarter of this year, instead of early 2014 asannounced last year,according to an Airbus Helicopters spokesperson.
The new helicopter offers several improvements over the current EC135 T2i/P2i, yielding a 66-pound increase in mtow and improved hot/high performance–an additional 440 pounds of payload at about 5,000 feet, ISA+20.
The "P" versions are powered by a pair of Pratt & Whitney Canada PW206B2 turboshafts, while the "T" versions have two Turbomeca Arrius 2B2 engines.


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Autopsy Shows Parkinson's Drug's Progress[ ... Read the full article ... ]
By RANDOLPH E. SCHMID
The Associated Press
Friday, July 1, 2005; 3:57 PM
WASHINGTON -- A drug withdrawn from clinical trials because of safety concerns was helping regrow nerve fibers in the brain of a man with Parkinson's disease, scientists report.
The finding probably will renew debate over the drug, GDNF. It had offered encouragement to people with Parkinson's who reported improvement when using it in trials. But the drug was withdrawn by the manufacturer, Amgen, this year.
Some of those patients in the trial sued Amgen to get continued supplies of the drug. They were turned down by a federal judge in New York in June. A second suit is pending.
Seth Love, Steven S. Gill and colleagues at Frenchay Hospital in Bristol, England, report in Monday's issue of the journal Nature Medicine that an autopsy of the brain of one of the patients who received the drug in an early trial shows that nerve fibers that are lost in the disease were growing back.
Anthony H. Risser
neuroscience | neuropsychology | brain | parkinson disease


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A GANG of thieves posing as police officers have struck at least 10 times, stealing thousands of pounds from their victims.
The group have been targeting tourists in Edinburgh over the last three weeks, convincing their victims with fake identification. Dressed in dark clothing and often wearing a police-style earpiece they then carry out a swift sting to search visitors' bags.
Police Scotland officers in the capital are appealing for help from the public in order to catch the group.
Loading article content
The latest victims were targeted on Wednesday when a mother and daughter on holiday from Chile had over £1000 stolen from a bag.
The pair were approached by a man on Magdala Crescent who handed them a camera and asked them to take a photograph of him.
Another two men soon approached, stating they were plain-clothes police officers. They produced a photo card with the word "police" on it and then demanded to check identities.
They initially searched the bag of the man with the camera, who immediately complied, and then looked through a bag belonging to the Chilean tourists, managing to steal a large sum of dollars and sterling.
Detective Chief Inspector Stuart Houston said: "There is clearly a group of thieves operating in Edinburgh who are falsely presenting themselves as police officers in order to search the bags of unsuspecting tourists.
"These crimes are being carried out in streets across the city centre. And unfortunately the so-called 'officers' act so quickly that the victims are being duped into thinking the cash is still in their wallets or bags.
"We would urge members of the public to look out for men who are acting suspiciously, especially around tourists, and contact police immediately the minute they see something untoward."
The first incidents were reported at the start of the month. In one case, a woman had cash stolen from her purse after she was approached by a man pretending to be a tourist in St Andrews Square before two men, who told her they were police officers, appeared and spoke to her.
They asked to see her wallet to check for counterfeit currency and identification. They then took notes out, sniffed them and handed the wallet back, only for the woman to discover later that there was £140 missing from her wallet. Other crimes have taken place in Princes Street and Johnston Terrace.
Police Scotland have issued a description of the three suspects linked to the various crimes that have taken place this month.
The first is an Asian man in his late 30s or early 40s, 5ft 10ins and of medium build. The second man is also Asian, in his mid 40s, 5ft 7ins and of slim build.
A third suspect is of Mediterranean appearance, aged 30 to 35, 6ft 2in and of medium build.


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Helping vulnerable families to a brighter future for over 25 years
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31 Spa Road
Registered Charity No. 1088622.
We are a day centre for disadvantaged and vulnerable families with children under 5 in Gloucestershire.
We were established in 1988 to help families living in B&B or unsuitable accommodation, those with mental health issues, victims of domestic abuse and pre-school children with additional needs by providing a warm, caring and supportive day centre where assistance and encouragement is available to help them to improve the quality of their lives.
The Family Haven takes an holistic approach to helping the whole family.


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About the Program
Distress Line 416-408-HELP (4357) -Distress Centres' trained volunteers provide telephone support for individuals experiencing emotional distress, marginalization, social isolation and those who may require crisis intervention and suicide/family violence intervention services. Universal access means that both volunteers and callers reflect the diversity of the community.
For 24 hours a day, 7 days a week, trained volunteers, with the support of professional staff, respond to a wide variety of callers with an equally diverse range of emotional needs. Multiple support services are delivered through our central access number, 416-408-HELP, including:
- An emotional support service for those with chronic mental health problems
- Support and crisis intervention services for those currently experiencing situational distress or crisis
- Family violence response
- Suicide prevention services
- Emergency intervention and response
Distress Centres enables callers to continue functioning independently in the community when possible, refers them to other appropriate community or professional resources if needed, intervenes in life-threatening situations, and provides direct help in suicidal and other emergency situations. In particular, Distress Line volunteers provide invaluable support to individuals with chronic mental health problems living in the community, or those individuals experiencing a period of life transition or who are suicidal or in crisis. Distress Line volunteers respond to the immediate and changing needs of the callers, taking into account their diverse cultures, perspectives and problem-solving abilities.
In 1999, a 175-language interpreter service was made available for callers with limited English capabilities. In addition, Bell Relay services are being used to respond to the needs of the hearing impaired. The goal of universal access is now a reality as barriers to usage have been eliminated.
Distress Centres works collaboratively with medical and mental health professionals to ensure that those at risk are made aware of our 24-hour service. Various agencies, psychiatrists and counsellors leave the Distress Centres phone number on their voicemail for after-hours support.
The 408-HELP Line is open 24 hours a day, 7 days a week, 365 days a year.
Our long-term goal is to decrease the risk of suicide by improving the emotional well-being and personal resiliency of those who call.


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I wish it would just sink in already.
Following pretty much every athletic achievement I've ever covered, a reporter – and I'm guilty of this, too – will ask the same, horrific question: "Has ______ sunk in yet?"
No, he or she will answer.
Said person doesn't know if it ever will.
One day the Earth is going to be upside out, inside down, and we're going to realize it's all of these athletic achievements finally sinking in.
That would be strange.
So, too, is the rest of my list of head-scratchers that you come across while covering high school sports.
The others:
Can I see some ID?
After explaining to those working the gate at various high school sporting events that I'm a reporter with the Observer-Reporter, a claim usually supported by the computer I'm lugging or the recorder and clipboard I'm carrying, I'm often asked for identification.
As if using this equipment to skirt the gate fees at high school sporting events – five bucks! – was some sort of grand scheme.
Yes, I know it'd be easier if we issued press passes. We don't. At least not lanyards.
I carry a card inside my wallet, which I'm forced to show more times than I would expect.
"Let me talk to my team"
Hey coach. Good to see you. Congrats. Talk to you for a minute?
Then the bomb drops.
"Let me talk to my team."
Are teams going to come apart at the seams, players running in circles, screaming and squirting each other with Super Soakers, if coaches handle media obligations before the postgame talk?
Coaches, nightly deadlines.
Nightly deadlines, coaches.
And what in the name of Vince Lombardi do we think high school kids who just won a game in front of their friends and family are really retaining from this conversation?
No score please
Note to high school public-address announcers: Pretty much 99 percent of the free world has what's called DVR, including those of us who like to watch sports AND work at night.
Oh, and don't forget about those nifty things called smart phones.
There might be, believe it or not, a few of us who taped the Penguins game and do not want the score announced.
Those who do – just a guess here – might be able to find it using that Internet thing.
Press boxes
Please change the name of these things.
They are not for press, which last I checked is a term used to describe for those who write things that eventually get printed on a press.
Kids, that's where your newspapers come from; has nothing to do with an iPad. Or baking.
Maybe call them Parent Boxes?
Or Radio Broadcaster Boxes?
Or the School Administrator Hangout Center.
Rare are the press boxes that allocate space to press.
You're better than that
Winning teams celebrate – wondering, of course, when everything will sink in.
Before that? They have to "come together as a team," the most hideous cliché any athlete can offer.
It's also the most popular among high school kids, hands down.
How has this 12-game winning streak been possible, you might ask? Well, we've really come together as a team.
Yes, better than as an individual. And clearly better than a circus, a labor union or a small business.
Please stop this.
You take insanely hard classes and polish them off with AP exams. You make speeches, win awards and get into great schools.
I know there's more going on in your heads than this.
Ring, ring … ring
Last one. And this one seems popular, though I honestly can't figure out why.
Call a coach, call a player, no answer, leave a message.
If I can't answer the return call, it seems the culture today dictates not a message left in return but instead back-to-back return calls.
Why is this? Is this done with the assumption that this is an office phone? I'm curious.
Apparently, old age has finally started to sink in.
Jason Mackey can be reached at firstname.lastname@example.com.
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Spectacular Citrus Salad Recipe
A delightfully different salad is what I was looking for when I came across the original version of this recipe. I altered it a bit to fit my taste. Each time I serve this salad, it gets raves for being so colorful and refreshing.
- 1/2 cup vegetable oil
- 1/4 cup orange juice
- 2 tablespoons honey
- 2 tablespoons lime juice
- 2 teaspoons poppy seeds
- 1 teaspoon grated orange peel
- 1/2 teaspoon grated lime peel
- 12 cups torn red and green leaf lettuce
- 3 medium oranges, peeled and sectioned
- 3/4 cup thinly sliced red onion
- 2/3 cup pecan halves, toasted
- 1. In a jar with tight-fitting lid, combine the first seven ingredients; shake well. In a large salad bowl, combine lettuce, oranges, onion and pecans. Add dressing and toss to coat; serve immediately. Yield: 10-12 servings.
Nutritional Facts
1 cup: 168 calories, 14g fat (2g saturated fat), 0 cholesterol, 6mg sodium, 12g carbohydrate (8g sugars, 3g fiber), 2g protein.
Reviews for Spectacular Citrus Salad
Average Rating
© 2017 RDA Enthusiast Brands, LLC


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Hudson Golf Club to close down
HUDSON, Wis. -- A representative of the Hudson Golf Club's owners came to the city Plan Commission last week looking for support to redevelop the 18-hole course.
He didn't get any.
"I'm not inclined to do much," said Mary Yacoub, the City Council's representative on the commission. The comment appeared to sum up the general feeling of the commission.
Hudson attorney Jeff Redmon spoke on behalf of Hanson Brothers Golf Holdings LLC, the family corporation that purchased the 141-acre golf course and clubhouse in April 2010 for a reported $3.6 million.
At the time, the golf club's board of directors said the cash purchase would eliminate the club's debt.
"Hanson Bros. has committed to the club being private, at least for 2010, and maintaining the golf facility for a minimum of 10 years," the board said in a letter to shareholders prior to the sale.
But in July of this year, Chris Hanson and Redmon announced that this season would be the last for the golf club.
"After serving the Hudson community since the 1950s, the financial viability of the golf course is simply unsustainable," Hanson, the father and head of the family company, said in a news release.
On Oct. 24, Redmon told the Plan Commission that the decision to close the golf club was final.
"This isn't going to be a golf course," he said.
Redmon indicated that he suggested a working session with the Plan Commission to discuss options for the property, but after talking to city officials, decided that would be premature.
He said Hanson Brothers signed a covenant agreeing not to do anything that would prevent the operation of the golf course for the next 10 years, but didn't promise to keep it open that long.
When Yacoub challenged the statement, saying club shareholders were given the impression that the course would continue in operation for at least 10 years, Redmon said he negotiated and drafted the agreement, and knows what's in it.
He said that when the former golf club dissolved, the power to release Hanson Brothers from the agreement passed to the City Council.
There are six years remaining on the agreement.
Redmon noted that the current zoning of the course, except for the clubhouse and two development lots, is one-family residential (R-1).
He said Hanson Brothers has talked to a number of residential and commercial developers about the golf club, and that there is strong interest in it from a couple of both types of developers.
Redmon said the Hansons won't ask the city for a waiver from the covenant barring development of the property until they have selected a developer and have a specific proposal.
'A huge loss for the community'
Yacoub told Redmon that she felt misled by Hanson Brothers when they came to city a year ago asking for permission to subdivide the course, creating a separate commercial lot for the clubhouse and two development lots along Carmichael Road.
She said the Plan Commission had a lengthy discussion about preserving the integrity of the golf course so it could continue to operate, and the Hansons gave no indication at that time that they were going to shut down the course.
Yacoub said she may have voted against the subdivision if she knew then that the Hansons would close the golf course a year later.
A year ago, Redmon told the City Council that the Hansons intended to continue operating the course, and to use the cart storage building as a clubhouse if the present clubhouse was sold.
Plan Commission members Fred Yoerg and Mary Claire Potter agreed with Yacoub.
"We were painted a picture that was untrue," Yoerg said.
"Maybe they don't know how to run a golf club. That's not our problem," he added.
Addressing Redmon's claim that there are just too many courses in the area for the Hudson Golf Club to be profitable, Potter said, "There are profitable golf courses out there.
"I think it is a huge loss for the community," she said.
The final round
Meanwhile, Joe Merchak of the town of Troy, his son Tommy of Hudson and Don Nitzkowski of Woodbury are believed to be the final golfers to play a round on the course.
Merchak said two golf club employees met them in the parking lot to take their carts when they finished play shortly after 6 p.m. Sunday.
"They told us it was the last day of the season and we were the last ones there," Merchak said. "They were anxious to close up.
"It was a great day," he said. "When we got to the 17th green, we looked at each other and said, this is really kind of an emotional time."
Nitzkowski took a photo of the father and son on the 18th fairway, with the iconic hedge logo containing the initials HGC in the background.
Merchak remembered playing the course (then known as the Hudson Country Club) with his father in the 1960s. He took up the game only recently, following the lead of Tommy and another son, J.P.
"The course is a fun one to play. I have always found the course and its greens exceptionally well-maintained," Merchak said. "I'll be sorry to see it go if it does close this year."


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