text:
He received a 10/225 extension. Having hindsight and being able to see how the market unfolded, what would Votto's contract have been and who would he be playing for this year.
I'd say 8/200 donning Yankees' pinstripes.
He received a 10/225 extension. Having hindsight and being able to see how the market unfolded, what would Votto's contract have been and who would he be playing for this year.
I'd say 8/200 donning Yankees' pinstripes.
We found your stolen Prius, it was voting for Ralph Nader.
7 / 150
I do not think there is any way he would have gotten what he did on the open market.
As for where he might have ended up, I wonder if the Mariners would have decided to spend the money they gave Cano on Votto instead. Justin Smoak doesn't exactly have 1B locked down for the Ms.
If the knee injury happened before the extension he would have probably been extended for at least a decent amount less. Had the knee injury never happened I have to believe he would have been paid this year very similar to what his extension was for.
Always Red (02-07-2014)
Ellsbury also plays a premium defensive positon while Votto plays 1st base. I think after the terrible Pujols contract teams would have been a little less willing to give Votto, who recently had a knee injury and did not appear to completely recover the following year a deal north of $200 million.
He is obviously a much better hitter than Ellsbury though, and I do think he would get a bigger contract, so I will take my initial guess up to $170 mil. I would also like to point out that I think that Ellsbury contract is a freaking joke. He did not deserve close to 150.
I just do not think he would get near, at, or above $200 million.
He is an outstanding hitter, but he is a first basemen that had a knee injury, which we are still not sure if he has recovered from, played medicore to bad defense in 13, and is a terrible baserunner.
This is the time. The real Reds organization is back.
Is Votto a huge name? I think a lot of non-baseball fans do not know who he is. I have friends that follow the AL that know who he is , but they don't consider him a star or anything, they just consider him a good 1B, but not as good as Miguel Cabrera.
Votto is a sabr wet dream, but I think do not think he is a global star like Derek Jeter, Miguel Cabrera, Bryce Harper, Robinson Cano, etc.
Votto would be getting probably the same deal. His performance comes at a defensive position that allows a player to age. If he played SS or CF, the injuries would mount. First basemen, tend to stay relatively healthy.
Hugs, smiling, and interactive Twitter accounts, don't mean winning baseball. Until this community understands that we are cursed to relive the madness.
Red Raindog (02-04-2014)
He's a year younger than Cano and comparably productive. I could easily see 8/200 from somebody.
Games are won on run differential -- scoring more than your opponent. Runs are runs, scored or prevented they all count the same. Worry about scoring more and allowing fewer, not which positions contribute to which side of the equation or how "consistent" you are at your current level of performance.
Between Boston, NYY and Toronto, a bidding war would have driven Votto to $200 million easily. Picture Votto in Boston bouncing balls of the Monster all season. They may not have wanted to go long but it would have driven the ave salary up. Someone else would have then bought on.
Hugs, smiling, and interactive Twitter accounts, don't mean winning baseball. Until this community understands that we are cursed to relive the madness.
8/200 seems to be a reasonable estimate.
"Hey...Dad. Wanna Have A Catch?" Kevin Costner in "Field Of Dreams."
Board Moderators may, at their discretion and judgment, delete and/or edit any messages that violate any of the following guidelines: 1. Explicit references to alleged illegal or unlawful acts. 2. Graphic sexual descriptions. 3. Racial or ethnic slurs. 4. Use of edgy language (including masked profanity). 5. Direct personal attacks, flames, fights, trolling, baiting, name-calling, general nuisance, excessive player criticism or anything along those lines. 6. Posting spam. 7. Each person may have only one user account. It is fine to be critical here - that's what this board is for. But let's not beat a subject or a player to death, please.


text: Hi, when compiling a kernel version 2.2.14 my PS/2 mice won't work any more, having the same kernel options as with 2.2.12. The boot messages tell me that a PS/2 mouse port is found, but the cursor doesn't follow the mouse at all. Is there a trick, some other kernel options as in older kernels ...? Greetings, joachim

subset: commoncrawl


text:
Drawing Room Blue
No. 253
A clean blue hue
This rich blue is less purple than Pitch Blue and more lively than navy Stiffkey Blue. Inspired by the formal rooms in which ladies would traditionally retire after dinner, Drawing Room Blue has a clean, graphic feel that works particularly well alongside Pitch Black and Incarnadine. When contrasted with All White on woodwork, it becomes much deeper with a regal edge. Pair with our Dark Tones Primer & Undercoat.
Product Safety Information
Please Note
All Farrow & Ball finishes (except Limewash) contain isothiazolinones which may produce an allergic reaction.
Danger: Farrow & Ball Limewash contains calcium hydroxide which when in contact with skin causes severe skin burns and when in contact with eyes, eye damage.
For further information about our products including product advice and safety, click here to view our advice pages.


text:
India's increasing sales taxes on air tickets is negatively affecting the country's civil aviation industry, warn aviation experts.
"While taxes provide a tangible short-term revenue boost to the government coffers, increased taxes in the long term can be outweighed by the cost to the underlying economy," aviation finance expert Charles Tyler says.
Despite campaigns that stated the tax contravenes International Civil Aviation Organization (ICAO) policies, the Indian Finance Ministry extended airline sales taxes to all classes of domestic and international airline tickets.
Previously, the sales tax was only levied on international premium class tickets. These taxes were capped, but the Indian Finance Ministry is seeking to remove these upper limits, thus increasing the taxes further.
"Germany, India and Austria are not claiming their taxes are environmental. They are simply a financial grab on behalf of the respective governments. But aviation has long been regarded as a soft target for environmentalists and, in the past, some of these aviation taxes have been "greenwashed," Tyler quips.
He says that while business travelers may be able to write off additional or increased aviation taxes as costs associated with business, leisure travelers cannot. "It is this sector that is most likely to change its behavior based on increased taxes," Tyler points out.
Jeff Poole, IATA director of government and industry affairs, says the main problem is that in many cases finance ministries, which levy the taxes, do not look at the big picture.
"We are working closely with Oxford Economics to demonstrate the enormous benefits that aviation generates," he says. "The only way we can get the message through to finance ministries is if we provide hard numbers showing that taxes may raise revenues, but will also impact on other areas of the economy.
"Taxing aviation produces short-term cash benefits, but destroys one of the most beneficial economic catalysts that an economy can have," he continues. "It is slowly killing the goose that lays the golden egg."
IATA Chief Economist Brian Pearce also points out that there is a mistaken belief in some circles that because there is generally no Value Added Tax (VAT) or sales tax on international ticket sales, and no excise duty on aviation fuel for international flights, the aviation industry is under taxed. "But aviation pays for its infrastructure," counters Pearce.
"That must be compared to the huge government subsidies that are often handed out to road, rail and shipping. Aviation already pays its fair share."


text:
People fantasize about one another. I get that. And I know you can not control where you may encounter the hotties of your dreams.
I was surprised, though, to hear 88 percent of men admit to fantasizing about one of their co-workers.
That source of that stat was featured in the May issue of Cosmopolitan and comes from a 2009 Harlequin Romance Report.
Previously on OTE: romance between colleagues a bad idea.
But, if you are going to do it, here are some rules to follow.


text:
Wednesday brings yet another chance at a huge lottery winning, and it would instantly create a new empire owner. The current Powerball lottery from Pennsylvania is now up to $284 million. The Powerball jackpot starts at $40 million and grows until someone matches the winning Powerball lottery numbers.
What really stands out is that the $284 million annuity value actually has a cash value of about $162.7 million. Even after taxes, this still leaves people with empire-building money.
24/7 Wall St. wants to take this opportunity to warn and remind its readers that winning a lottery can come with many major pitfalls. For starters, many lottery winners end up bankrupt — some end up that way in just a few years.
We have developed our own 12-step program for lottery winners. This "to-do" list is presented in a different way than other lists you may find — it tells you exactly what NOT to do! The list also pertains to those who win unexpected judgments and those who come into large sums of money instantly.
If you win millions upon millions of dollars like this, it comes with great responsibility. There are just too many temptations, and perhaps too many new and existing people you know that make it too easy to separate your newly found empire from you.
We have suggestions based around what sort of financial advisors and what sort of tax planning you should consider. There are reasonable purchases, and unreasonable purchases to consider. Also, how to handle debt. Those are just some of the things to consider.
There is much more to do — and not do — for lotto winners. No one should end up in the poor house if they win an instant empire that this creates. Yet many do, and often in just a few years.


text:
Diabetes mellitus is the most prevalent metabolic disorder in the United States, with costs for treatment and care of diagnosed patients running over $174 billion. The pathological pathway of the disease revolves around inappropriate glucose metabolism, which occurs as a result of absolute deficiency of insulin secretion, reduction in the biological effectiveness of insulin, or a combination of the two. Dysfunctional insulin, in turn, leads to hyperglycemic conditions. 80-90% of cases presented in the United States are diagnosed with Type II diabetes mellitus, which is an increased risk factor for a number of deadly conditions: Read More>>
Diabetes mellitus is the most prevalent metabolic disorder in the United States, with costs for treatment and care of diagnosed patients running over $174 billion. The pathological pathway of the disease revolves around inappropriate glucose metabolism, which occurs as a result of absolute deficiency of insulin secretion, reduction in the biological effectiveness of insulin, or a combination of the two. Dysfunctional insulin, in turn, leads to hyperglycemic conditions. 80-90% of cases presented in the United States are diagnosed with Type II diabetes mellitus, which is an increased risk factor for a number of deadly conditions: heart disease and stroke, high blood pressure, blindness, kidney disease, nervous system disease, complications leading to amputation, and complications of pregnancy and surgery, to name a few. Arguably not coincidental, all of the conditions mentioned above also are associated with insufficient nitric oxide (NO) production [1]. Furthermore, endothelial dysfunction, which leads to reduced NO levels and bioavailability, plays a major role in the pathogenesis of diabetic vascular disease, and thus could provide the link between metabolic disorders (diabetes) and cardiovascular disease. Current anti-diabetic drugs are effective in managing blood glucose levels, but have highly adverse side effects that result in the increased incidence of CV complications, including heart attack and stroke. A NO based therapeutic regime, administered in conjunction with anti-diabetic rugs, could result in an improved prognosis; managed glucose levels and amelioration of the cardiovascular complications.
The Diabetes Burden:
About 7.8 percent of the United States population suffers from diabetes, which, according to the 2007 National Diabetes Statistics of the National Institutes of Health (NIH), is about 23.6 million people. These 23.6 million people have a risk of death twice that of their age match counterparts, which can be primarily attributed to their diabetes acting as a major independent risk factor for coronary artery disease [4,5]. In 2004, heart disease was the cause of death on 68% of diabetes-related death certificates in people 65 years of age or older. Adults with diabetes are 2-4 times more prone to heart-disease related deaths than their non-diabetic counterparts.
Diabetes also results in a 2-4 fold increase in the risk of stroke, a marked increase in blood pressure, and contributes to about 60% of non-traumatic lower limb amputations. All these pathologies mount to around $116 billion in direct medical costs and an additional $58 billion in indirect costs (disability, work loss, premature mortality). After a numerical adjustment for age and sex differences, it is estimated that average medical expenditures amongst people with diabetes is around 2.3 times higher than those without. As aforementioned, the link between endothelial dysfunction and vascular disease in the diabetic provides a salient strategy, via nitric oxide, in managing the patient's quality of life. Eventually, this management could even lead to a reduction in the overall cost of diabetes on the entire health care system.
The nitric oxide metabolism and implications on pathogenesis of diabetes mellitus:
A healthy, functional endothelium synthesizes and secretes a number of factors and signaling molecules that are crucial in CV maintenance. NO, generated by the constitutive enzyme, Nitric Oxide Synthase (NOS), is one such factor that is essential for normal physiological regulation of blood flow and nutrient delivery to tissues; NO also doubles as an anti-leukocyte and anti-platelet factor 7]. NO is such an important signaling molecule that the absence of it, or a deficiency in the production of it, is considered to be one of the earliest indicators of disease. A loss of function of NOS is shown to have a direct correlation with major CV risk factors, such as hyperlipidemia, diabetes, hypertension, smoking and severity of atherosclerosis. NOS activity might also provide a degree of predictive potential for atherosclerotic disease progression [8-11]. Interestingly enough, in vitro animal models of diabetes mellitus have shown a tendency towards endothelial dysfunction [12-15, 79]. Furthermore, isolated rat aorta from diabetic rats show a deficiency in endothelial NO release that can only be partially rescued by supplementation by the NO precursor, L-Arginine [12-14, 16]. Most commercial supplements target NO restoration through this L-Arginine supplementation channel, and thus aren't very effective in restoring NO levels. This also suggests that decreased NO levels aren't primarily based on reduced L-Arginine levels, but rather, are rooted at another source. Such a source might be the onset of endothelial dysfunction, which is extremely common in patients of diabetes mellitus [17,18]. These patients normally test low for NO, and also exhibit cardiovascular complications, which aren't necessarily mutually exclusive. There are a variety of mechanisms which are affected by diabetes mellitus that might lead to reduced eNOS function, and in turn, reduced NO levels.
Type II diabetes mellitus, by definition, causes a spike in blood glucose, insulin and cytokine levels. In vitro, every single one of these factors has been shown to hinder eNOS activity [14,15]. Additionally, diabetes also causes an increase in advanced glycosylation products in the blood serum; these products act as quenching agents for NO, further exacerbating endothelium dependent functionality [19-21, 80]. In vitro, isolated femoral, renal and renal vessels also show decreased vasodilation when exposed to glycosylated hemoglobin [20]. One more mechanism that could provide the link between diabetes and endothelial dysfunction is mediated by vessel wall oxidant production. Under diabetic conditions, smooth muscle cells and the endothelium tend to produce reactive oxygen species, which have been shown to attenuate eNOS and endothelial functionality [22]. Furthermore, recent studies have shown that high glucose serum levels and increased glycosylation products, such as methylglyoxal (MG), increase protein expression of arginase [81].
The additive effect of these factors on the eNOS system in the diabetic population leads to a significant decrease in vascular NO production, which in turn reduces circulation to a variety of organs. Reduced circulation to organs can present a number of complications, especially in the cardiovascular system. This reduced blood flow to the heart could result in the high prevalence of CVD in diabetics. Therefore, replenishing NO could greatly reduce the burden of CVD in the diabetes realm, and in turn improve disease prognosis and reduce the financial burden of CVD in diabetic and non-diabetic populations.
To date, trials revolving around L-Arginine supplementation and antioxidants have consistently failed, with the only exception being the success of a D-Arginine based trial whose results were specific to limiting arginase activity [81]. Organic nitrate, inhalative NO therapy and downstream phosphodiasterase inhibitors constitute a majority of the therapeutics on the market today, but supplements that employ L-Citrulline (a feedback activator of L-Arginine) and ingredients proven to bolster eNOS activity have shown to be most effective in treating endothelial dysfunction. Such therapies, if normalized in the diabetic population, could greatly reduce the CVD implications of diabetes and improve vascular health.
Insulin and NO signaling:
Insulin, in conjunction with endothelial NO, acts as a vasodialator [23]. In fact, the major role of insulin as a cardio-protective agent results from the phosphatidylinositol 3′-kinase-protein kinase B-endothelial NOS (PI3K-AkteNOS)-dependent signalling mechanism; this along with its metabolic regulation renders insulin as an important organ protector. Furthermore, the aforementioned PI3K kinase pathway acts to phosphorylate eNOS and increase NO production [24]. This pathway is crucial, in fact, as impariment in PI3K signaling can be dually interpreted as insulin resistance at the molecular level [25].
The apparent parallelism between metabolic insulin signaling in glucose uptake and vasodilation provides important insight into the link between diabetes and endothelial dysfunciton. In fact, it has been proven that GLUT4 receptor translocation impairment in adipocytes and muscle cells conincides with eNOS impairment in the endothelium, when the PI3K pathway is impaired due to insulin resistance [27, 82]. As expected by the argument presented above, both point mutations in human subjects and homozygous null mice tests of the insulin receptor substrate 1 gene (IRS-1) have been shown to cause impaired endothilium derived vasodialation and insulin resistance; alternatively, these case studies have also cast light on the genetic link for endothelial dysfunction [27,28].
In more recent studies, another pathway has been linked into the PI3KAKT mechanism. Mammalian target of rapamyacin (mTOR), traditionally thought of as a gene prevalent in human cancers, has emerged in modern molecular medicine as an important contributing agent in angiogenesis and an important regulatory factor of angiogenic factors, such as NO. Acting mainly downstream of insulin signaling on the PI3 kinase, mTOR acts to further phosphorylate AKT and thus is a postitive effector of eNOS activation via phosphorylation [83]. Furthermore, inhibition of any kinase in this system, PI3K, mTOR, or AKT, has been shown to significantly reduce production of angiogenic actors, such as nitric oxide [83]. There is substantial evidence of impairment of this pathway in diabetes, either through disruption of Akt phosphorylation and expression [30] which then disrupts insulin secretion [31], and/or eNOS phosphorylation and activation [24]. Additionally, eNOS knockout mice reguarly show symptoms consistent with diabetes, including hyperlipidimia, hypertension and, perhaphs most importantly, insulin resistance [32]. This established association between type II diabetes and endothelial dysfunction through the PI3K/mTOR/AKT pathway provides insight into future supplementary treatments of diabetic patients that could be instrumental in lowering the CVD risk assocaited with the metabolic disorder.
AMP Kinase, nitric oxide and diabetes:
AMP kinase, long standing as the energy gauge of the body (activated during times of high energy phosphate depletion), has emerged in recent years as a therapeutic agent for diabetic vascular disease. In fact, studies centered on AMPK activation have shown improved endothelial and smooth function [84]. The two leading diabetic drugs, namely metformin and rosiglitazone, show their metabolic effects partially through AMPK. These data, along with evidence from studies showing that chemical activation of AMPK in vivo with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) improves blood glucose concentrations and lipid profiles, make this enzyme an attractive pharmacological target for the treatment of Type II diabetes and other metabolic disorders. AMPK, addtionally, has been shown to increase eNOS phosphorylation, not unlike the PI3K/mTOR/AKT pathway [37,84]. eNOS activation conversly aides in AMPK modulation of glucose uptake via GLUT4 receptor translocation [38]. Restoring NO production through this pathway will likely provide benefit to diabetic patients and may even increase efficacy of existing drugs and prevent the unwanted cardiovascular side effects.
Nitrite restores nitric oxide homeostasis:
Several studies now demonstrate that exogenous nitrite contributes to whole body NO production and homeostasis and is an alternate source of NO in vivo. Coadministration of nitrite with a NOS inhibitor for 3 weeks significantly attenuates hypertension [39]. Considerable published support for this theory derives from the following facts: NO produced from nitrite in the upper intestine is up to 10,000 times the concentrations that occur in tissues from enzymatic synthesis [40], nitrite can act as a circulating NO donor [41], can activate soluble guanylyl cyclase (sGC), change gene expression profiles [42], and nitrite can itself perform many actions previously attributable to NO [43] without the intermediacy of NO [42]. In fact, it has been shown that nitrite may be the endocrine mediator of NO based signaling [44]. Enhancing nitrite availability through therapeutic intervention by administering bolus nitrite prior to cardiovascular insult has shown remarkable effects in reducing the injury from myocardial infarction, ischemic liver and kidney injury, stroke and cerebral vasospasm [45-50] in animal models. It was recently revealed that nitrite, when given orally, is absorbed with greater than 95% bioavailability and is rapidly absorbed [51].
Nitrite seems to have residual effects long after it has been metabolized and cleared from the body by preconditioning the myocardium when given 24 hours prior to ischemic insult [52]. Nitrite has also been shown to augment ischemia induced angiogenesis and arteriogenesis [53]. Inhaled nebulized nitrite is a selective pulmonary vasodilator [54] and inhibits hypoxic and inflammatory pulmonary arterial hypertension [55]. Nitrite therapy has recently been shown to improve cardiac and neurological function and enhance survival after cardiac arrest [56]. Nitrite is also showing remarkable efficacy at promoting regional blood flow in sickle cell patients [57]. We now know that nitrite is just as efficacious when given orally at restoring NO biochemistry [58], reversing hypertension from NOS inhibition [39], protecting from myocardial ischemia-reperfusion injury [59] and even protecting from vascular inflammation, reversing endothelial dysfunction and reducing levels of C-reactive protein as a result of a high fat diet [60]. Most recently inorganic nitrate was shown to reverse features of metabolic syndrome in eNOS knockout mice through repletion of nitrite and NO homeostasis [3]. In humans, dietary nitrate and nitrite sources have been demonstrated to lower blood pressure [61-63] and decrease oxygen consumption during sub-maximal and maximal aerobic exercise [64, 65]. Collectively, these studies clearly reveal the benefits of nitrite as a means to restore or enhance NO bioavailability and/or homeostasis in an endothelium independent manner, offering a chance to correct NO homeostasis when endothelium derived NO is insufficient or dysfunctional as in diabetes. Mice homozygous for the diabetes spontaneous mutation Leprdb become obese at 3-4 weeks of age. The mutant db/db mice are polyphagic, polydipsic, and polyuric. Thus, this mouse model recapitulates Type II diabetes well. Our preliminary data indicated that NO production was perturbed in db/db mice, and that provided justification for the use of nitrite as an alternate source of NO independent of endothelium derived NO. Providing exogenous nitrite likely improved insulin sensitivity and insulin signaling since less insulin was needed to maintain euglycemia and there was less weight gain in the diabetic mice.
Conclusion and future research considerations:
This article has been dedicated to providing insight into the potential linking mechanisms between diabetes mellitus and cardiovascular disease. Endothelial dysfunction emerges as the major underlying link between the two, particularly through pathways affecting the activation of eNOS and further downstream, the bioavailabiity of NO.
Therapautic efforts centered around restoring the eNOS system, either through the PI3K/AKT pathway, though regualtion of the mTOR gene, activation of the AMP kinase, or though dietary nitrite supplementation, provide a novel approach in reducing the burden of CVD in diabetic populations. Rescue of the system though L-Arginine supplementation, on the other hand, has not shown promising results, and thus negates a majority of the supplements avalabile through the retail channel today.
Reference List:
1. Potenza, M.A., et al., Endothelial dysfunction in diabetes: from mechanisms to
therapeutic targets. Curr Med Chem, 2009. 16(1): p. 94-112.
2. Huang, P.L., eNOS, metabolic syndrome and cardiovascular disease. Trends
Endocrinol Metab, 2009. 20(6): p. 295-302.
3. Carlstrom, M., et al., Dietary inorganic nitrate reverses features of metabolic
syndrome in endothelial nitric oxide synthase-deficient mice. Proc Natl Acad Sci
4. Root, H., Bland EF, Gordon, WH and PW White, Coronary arteriosclerosis in
diabetes mellitus. JAMA, 1939(118): p. 27-30.
5. Goldenberg, S., Alex, M and HT Blumenthal, Sequelae of arteriosclerosis of the
aorta and coronary arteries. Diabetes, 1958(7): p. 98-108.
6. Sheetz, M.J. and G.L. King, Molecular understanding of hyperglycemia's adverse
effects for diabetic complications. Jama, 2002. 288(20): p. 2579-88.
7. Loscalzo, J. and G. Welch, Nitric oxide and its role in the cardiovascular system.
Prog Cardiovasc Dis, 1995. 38(2): p. 87-104.
8. Schachinger, V., M.B. Britten, and A.M. Zeiher, Prognostic impact of coronary
vasodilator dysfunction on adverse long-term outcome of coronary heart disease.
Circulation, 2000. 101(16): p. 1899-906.
9. Halcox, J.P., et al., Prognostic value of coronary vascular endothelial
dysfunction. Circulation, 2002. 106(6): p. 653-8.
10. Bugiardini, R., et al., Endothelial function predicts future development of
coronary artery disease: a study of women with chest pain and normal coronary
angiograms. Circulation, 2004. 109(21): p. 2518-23.
11. Lerman, A. and A.M. Zeiher, Endothelial function: cardiac events. Circulation,
2005. 111(3): p. 363-8.
12. Pieper, G.M., P. Langenstroer, and W. Siebeneich, Diabetic-induced endothelial
dysfunction in rat aorta: role of hydroxyl radicals. Cardiovasc Res, 1997. 34(1):
p. 145-56.
13. Pieper, G.M. and G.J. Gross, Oxygen free radicals abolish endotheliumdependent
relaxation in diabetic rat aorta. Am J Physiol, 1988. 255(4 Pt 2): p.
14. Pieper, G.M., D.A. Meier, and S.R. Hager, Endothelial dysfunction in a model of
hyperglycemia and hyperinsulinemia. Am J Physiol, 1995. 269(3 Pt 2): p. H845-
15. Tesfamariam, B. and R.A. Cohen, Free radicals mediate endothelial cell
dysfunction caused by elevated glucose. Am J Physiol, 1992. 263(2 Pt 2): p.
16. Pieper, G.M., Review of alterations in endothelial nitric oxide production in
diabetes: protective role of arginine on endothelial dysfunction. Hypertension,
1998. 31(5): p. 1047-60.
17. Williams, S.B., et al., Impaired nitric oxide-mediated vasodilation in patients with
non-insulin-dependent diabetes mellitus. J Am Coll Cardiol, 1996. 27(3): p. 567-
18. Saenz de Tejada, I., et al., Impaired neurogenic and endothelium-mediated
relaxation of penile smooth muscle from diabetic men with impotence. N Engl J
Med, 1989. 320(16): p. 1025-30.
19. Bucala, R., K.J. Tracey, and A. Cerami, Advanced glycosylation products quench
nitric oxide and mediate defective endothelium-dependent vasodilatation in
experimental diabetes. J Clin Invest, 1991. 87(2): p. 432-8.
20. Rodriguez-Manas, L., et al., Interference of glycosylated human hemoglobin with
endothelium-dependent responses. Circulation, 1993. 88(5 Pt 1): p. 2111-6.
21. Oltman, C.L., et al., Effects of glycosylated hemoglobin on vascular responses in
vitro. Cardiovasc Res, 1997. 34(1): p. 179-84.
22. Kojda, G. and D. Harrison, Interactions between NO and reactive oxygen species:
pathophysiological importance in atherosclerosis, hypertension, diabetes and
heart failure. Cardiovasc Res, 1999. 43(3): p. 562-71.
23. Steinberg, H.O., et al., Insulin-mediated skeletal muscle vasodilation is nitric
oxide dependent. A novel action of insulin to increase nitric oxide release. J Clin
Invest, 1994. 94(3): p. 1172-9.
24. Dimmeler, S., et al., Activation of nitric oxide synthase in endothelial cells by Aktdependent
phosphorylation. Nature, 1999. 399(6736): p. 601-5.
25. Nystrom, F.H. and M.J. Quon, Insulin signalling: metabolic pathways and
mechanisms for specificity. Cell Signal, 1999. 11(8): p. 563-74.
26. Kim, J.A., K.K. Koh, and M.J. Quon, The union of vascular and metabolic
actions of insulin in sickness and in health. Arterioscler Thromb Vasc Biol, 2005.
25(5): p. 889-91.
27. Federici, M., et al., G972R IRS-1 variant impairs insulin regulation of endothelial
nitric oxide synthase in cultured human endothelial cells. Circulation, 2004.
109(3): p. 399-405.
28. Abe, H., et al., Hypertension, hypertriglyceridemia, and impaired endotheliumdependent
vascular relaxation in mice lacking insulin receptor substrate-1. J Clin
Invest, 1998. 101(8): p. 1784-8.
29. Zeng, G., et al., Roles for insulin receptor, PI3-kinase, and Akt in insulinsignaling
pathways related to production of nitric oxide in human vascular
endothelial cells. Circulation, 2000. 101(13): p. 1539-45.
30. Kobayashi, T., et al., Impairment of PI3-K/Akt pathway underlies attenuated
endothelial function in aorta of type 2 diabetic mouse model. Hypertension, 2004.
44(6): p. 956-62.
31. Bernal-Mizrachi, E., et al., Defective insulin secretion and increased susceptibility
to experimental diabetes are induced by reduced Akt activity in pancreatic islet
beta cells. J Clin Invest, 2004. 114(7): p. 928-36.
32. Duplain, H., et al., Insulin resistance, hyperlipidemia, and hypertension in mice
lacking endothelial nitric oxide synthase. Circulation, 2001. 104(3): p. 342-5.
33. Musi, N., et al., AMP-activated protein kinase (AMPK) is activated in muscle of
subjects with type 2 diabetes during exercise. Diabetes, 2001. 50(5): p. 921-7.
34. Kudo, N., et al., High rates of fatty acid oxidation during reperfusion of ischemic
hearts are associated with a decrease in malonyl-CoA levels due to an increase in
5′-AMP-activated protein kinase inhibition of acetyl-CoA carboxylase. J Biol
Chem, 1995. 270(29): p. 17513-20.
35. Marsin, A.S., et al., Phosphorylation and activation of heart PFK-2 by AMPK has
a role in the stimulation of glycolysis during ischaemia. Curr Biol, 2000. 10(20):
p. 1247-55.
36. Winder, W.W. and D.G. Hardie, AMP-activated protein kinase, a metabolic
master switch: possible roles in type 2 diabetes. Am J Physiol, 1999. 277(1 Pt 1):
p. E1-10.
37. Chen, Z.P., et al., AMP-activated protein kinase phosphorylation of endothelial
NO synthase. FEBS Lett, 1999. 443(3): p. 285-9.
38. Li, J., et al., Role of the nitric oxide pathway in AMPK-mediated glucose uptake
and GLUT4 translocation in heart muscle. Am J Physiol Endocrinol Metab, 2004.
287(5): p. E834-41.
39. Tsuchiya, K., et al., Nitrite is an alternative source of NO in vivo. Am J Physiol
Heart Circ Physiol, 2005. 288(5): p. H2163-70.
40. McKnight, G.M., et al., Chemical synthesis of nitric oxide in the stomach from
dietary nitrate in humans. Gut, 1997. 40(2): p. 211-214.
41. Dejam, A., et al., Emerging role of nitrite in human biology. Blood Cells Mol Dis,
2004. 32(3): p. 423-429.
42. Bryan, N.S., et al., Nitrite is a signaling molecule and regulator of gene
expression in mammalian tissues. Nat Chem Biol, 2005. 1(5): p. 290-7.
43. Gladwin, M.T., et al., The emerging biology of the nitrite anion. Nature Chemical
Biology, 2005. 1(6): p. 308-314.
44. Elrod, J.W., et al., Nitric oxide promotes distant organ protection: Evidence for
an endocrine role of nitric oxide. Proc Natl Acad Sci U S A, 2008. 105(32): p.
45. Lu, P., et al., Nitrite-derived nitric oxide by xanthine oxidoreductase protects the
liver against ischemia-reperfusion injury. Hepatobiliary Pancreat Dis Int, 2005.
4(3): p. 350-5.
46. Duranski, M.R., et al., Cytoprotective effects of nitrite during in vivo ischemiareperfusion
of the heart and liver. J Clin Invest, 2005. 115(5): p. 1232-40.
47. Webb, A., et al., Reduction of nitrite to nitric oxide during ischemia protects
against myocardial ischemia-reperfusion damage. Proc Natl Acad Sci USA,
2004. 101(13683-13688).
48. Pluta, R.M., et al., Nitrite infusions to prevent delayed cerebral vasospasm in a
primate model of subarachnoid hemorrhage. Jama, 2005. 293(12): p. 1477-84.
49. Jung, K.H., et al., Early intravenous infusion of sodium nitrite protects brain
against in vivo ischemia-reperfusion injury. Stroke, 2006. 37(11): p. 2744-50.
50. Tripatara, P., et al., Nitrite-derived nitric oxide protects the rat kidney against
ischemia/reperfusion injury in vivo: role for xanthine oxidoreductase. J Am Soc
Nephrol, 2007. 18(2): p. 570-80.
51. Hunault, C.C., et al., Bioavailability of sodium nitrite from an aqueous solution in
healthy adults. Toxicol Lett, 2009. 190(1): p. 48-53.
52. Shiva, S., et al., Nitrite augments tolerance to ischemia/reperfusion injury via the
modulation of mitochondrial electron transfer. Journal of Experimental Medicine,
2007. 204(9): p. 2089-2102.
53. Kumar, D., et al., Chronic sodium nitrite therapy augments ischemia-induced
angiogenesis and arteriogenesis. Proc Natl Acad Sci U S A, 2008. 105(21): p.
54. Hunter, C.J., et al., Inhaled nebulized nitrite is a hypoxia-sensitive NO-dependent
selective pulmonary vasodilator. Nat Med, 2004. 10: p. 1122-1127.
55. Zuckerbraun, B.S., et al., Nitrite potently inhibits hypoxic and inflammatory
pulmonary arterial hypertension and smooth muscle proliferation via xanthine
oxidoreductase-dependent nitric oxide generation. Circulation, 2010. 121(1): p.
56. Dezfulian, C., et al., Nitrite therapy after cardiac arrest reduces reactive oxygen
species generation, improves cardiac and neurological function, and enhances
survival via reversible inhibition of mitochondrial complex I. Circulation, 2009.
120(10): p. 897-905.
57. Mack, A.K., et al., Sodium nitrite promotes regional blood flow in patients with
sickle cell disease: a phase I/II study. Br J Haematol, 2008. 142(6): p. 971-8.
58. Bryan, N.S., et al., Dietary nitrite restores NO homeostasis and is
cardioprotective in endothelial nitric oxide synthase-deficient mice. Free Radic
Biol Med, 2008. 45(4): p. 468-74.
59. Bryan, N.S., et al., Dietary nitrite supplementation protects against myocardial
ischemia-reperfusion injury. Proc Natl Acad Sci U S A, 2007. 104(48): p. 19144-
60. Stokes, K.Y., et al., Dietary nitrite prevents hypercholesterolemic microvascular
inflammation and reverses endothelial dysfunction. Am J Physiol Heart Circ
Physiol, 2009. 296(5): p. H1281-8.
61. Kapil, V., et al., Inorganic Nitrate Supplementation Lowers Blood Pressure in
Humans. Role for Nitrite-Derived NO. Hypertension, 2010.
62. Webb, A.J., et al., Acute blood pressure lowering, vasoprotective, and antiplatelet
properties of dietary nitrate via bioconversion to nitrite. Hypertension, 2008.
51(3): p. 784-90.
63. Larsen, F.J., et al., Effects of dietary nitrate on blood pressure in healthy
volunteers. N Engl J Med, 2006. 355(26): p. 2792-3.
64. Larsen, F.J., et al., Effects of dietary nitrate on oxygen cost during exercise. Acta
Physiol (Oxf), 2007. 191(1): p. 59-66.
65. Larsen, F.J., et al., Dietary nitrate reduces maximal oxygen consumption while
maintaining work performance in maximal exercise. Free Radic Biol Med, 2010.
48(2): p. 342-7.
66. Schmidt, H.H., et al., Insulin secretion from pancreatic B cells caused by Larginine-
derived nitrogen oxides. Science, 1992. 255(5045): p. 721-3.
67. Salehi, A., et al., Islet constitutive nitric oxide synthase: biochemical
determination and regulatory function. Am J Physiol, 1996. 270(6 Pt 1): p.
68. Lajoix, A.D., et al., A neuronal isoform of nitric oxide synthase expressed in
pancreatic beta-cells controls insulin secretion. Diabetes, 2001. 50(6): p. 1311-
69. Nakata, M., et al., Citrulline-argininosuccinate-arginine cycle coupled to Ca2+-
signaling in rat pancreatic beta-cells. Biochem Biophys Res Commun, 1997.
235(3): p. 619-24.
70. Floyd, J.C., Jr., et al., Stimulation of insulin secretion by amino acids. J Clin
Invest, 1966. 45(9): p. 1487-502.
71. Qian, Q., et al., Nitric oxide stimulates insulin release in liver cells expressing
human insulin. Biochem Biophys Res Commun, 2005. 329(4): p. 1329-33.
72. Smukler, S.R., et al., Exogenous nitric oxide and endogenous glucose-stimulated
beta-cell nitric oxide augment insulin release. Diabetes, 2002. 51(12): p. 3450-60.
73. Muniyappa, R., et al., Cardiovascular actions of insulin. Endocr Rev, 2007.
28(5): p. 463-91.
74. Baron, A.D., et al., Insulin-mediated skeletal muscle vasodilation contributes to
both insulin sensitivity and responsiveness in lean humans. J Clin Invest, 1995.
96(2): p. 786-92.
75. Montagnani, M., et al., Insulin-stimulated activation of eNOS is independent of
Ca2+ but requires phosphorylation by Akt at Ser(1179). J Biol Chem, 2001.
276(32): p. 30392-8.
76. Potashnik, R., et al., IRS1 degradation and increased serine phosphorylation
cannot predict the degree of metabolic insulin resistance induced by oxidative
stress. Diabetologia, 2003. 46(5): p. 639-48.
77. Cosby, K., et al., Nitrite reduction to nitric oxide by deoxyhemoglobin vasodilates
the human circulation. Nature Medicine, 2003. 9: p. 1498-1505.
78. Combet, S., et al., A specific method for measurement of nitric oxide synthase
enzymatic activity in peritoneal biopsies. Kidney Int, 2000. 57(1): p. 332-8.
79. Wang, JS, et al., Influence of high blood glucose fluctutaiton on endothelial
function of type 2 diabetes mellitus rats and effects of Panax Quinquefolius
saponin of stem and leaf. Chinese Journal of Integrated Medicine, 2012. Epub
ahead of print.
80. Mohar, DS, et al., Atherosclerosis in chronic kidney disease: lessons learned from
glycation in diabetes. Medical Clinics of North America, 2012. 96(1): p. 57-65
81. Dhar, I., et al., D-arginine attenuates methyglyoxal- and high glucose-induced
endothelial dysfunction and oxidative stress by an eNOS-independent mechanism.
The Journal of Pharmocology and experimental therapeutics, 2012. Epub ahead of
82. Tousková, V., Haluzik, M., Insulin resistance and nitric oxide: molecular
mechanisms and pathophysiological associations. Ceskoslovenská fysiologie /
Ústrední ústav biologický, 2011. 60(2): p. 40-7.
83. Karar, J., Maity, A., PI3K/AKT/mTOR Pathway in Angiogenesis. Frontiers in
Molecular Neuroscience, 2011. 4 (51). Epub.
84. Ewart, MA., Kennedy, S., Diabetic cardiovascular disease AMP-activated
protein kinase (AMPK) as a therapeuctic target. Cardiovascular and
Hematological Agents in Medicinal Chemistry, 2012. Epub ahead of print.


text:
Designer(s): Yves Behar
Dan Semo
Gabrielle DeGama
Kei Koyama
George De'Ath, United States
Category: Print, Professional
User's Profile : -
Entry Description:
Cobalt is an indoor security robot, utilizing 60+ sensors
to detect and report anomalies in the workplace. A fabric
skirt hides technology equivalent to an autonomous
vehicle, making the robot a friendly presence in the
office. A human co-pilot, located offsite, is able to video
in for human interactions and support when needed.
The central motif of the Cobalt brand identity is around
the balance of approachability and discretion, carried
across from the design of the product. The logo
highlights the CO of Cobalt, as the collaboration
between human and robot (co-robot) is core to the
business. Fluid, continuous motion guided the design of
the letterform in the logo. The delicate custom font is
used in contrast to the traditional heaviness of robot
companies. Cobalt stone and cobalt deep blue are the
core brand colors, with the possibility to customize
fabric colors to match interior décor and furniture.
About the Designer/Company
No information has been provided


text:
( Originally Published 1879 )
SICKNESS brings a share of blessings with it. What stores of human love and sympathy it reveals. What constant affectionate care is ours. What kindly greetings from friends and associates. This very loosening of our hold upon life calls out such wealth of human sympathy that life seems richer than before. Then it teaches humility. Our absence is scarcely felt or noticed. From the noisy, wrestling world without we are separated completely, as if the moss was on our tombstones; yet our place is filled and all moves on without us. So we learn that when at last we shall sink forever beneath the waves of the sea of life, there will be but one ripple and the current will move steadily on. On the sick-bed the sober truth comes home with startling. emphasis:
"The gay will laugh
We cannot too soon convince ourselves how easily we may be dispensed with in the world. What in portant personages we imagine ourselves to be! We think that we alone are the life of the circle in which we move; in our absence we fancy that life, existence and breath will come to a general pause; and alas! the gap which we leave is scarcely perceptible, so quickly is it filled again; nay, it is often but the place, if not for something better, at least for something more agreeable.
When sickness has drawn a vail over the gayety of our hearts, or adversity eclipsed the splendor of our outward circumstances; when some intervening cloud has darkened the pleasing scenes of life, or disappointments opened our eyes; then vice loses her fallacious allurements and the world appears as an empty, delusive cheat; then Jesus and the Gospel beam forth with inimitable luster, and Christian virtue gains loveliness from such lowering providences, and treads the shades with more than mortal charms. May this reconcile me, and all the sons of sorrow, to our appointed share of sufferings. If tribulations tend to refine the soul and prepare it for glory, welcome distress, or whatever our peevish passions may miscall calamities. These are not judgments or marks of displeasure to God's children, but necessary and salutary chastisements, as well as tokens of his parental concern for our spiritual and eternal welfare. Afflictions should, therefore, sit easy upon us, since they increase our knowledge and humility, pro-mote our faith and love, and work out for us a far more exceeding and eternal weight of glory.
Sickness scours us of our rust, and however the wicked, like trees in the wilderness, grow without culture, yet the saints, like trees in the garden, must be pruned to be made fruitful, and sickness does this. God will prune his people, but not hew them down; the right hand of his mercy knows what the left hand of his severity is doing. There is as much difference between the sufferings of the saints and those of the ungodly, as between the cords with which an executioner pinions a condemned malefactor, and the band-ages wherewith a tender surgeon binds his patient.
Sickness and disease are, in weak minds, the sources of melancholy; but that which is painful to the body may be profitable to the soul. Sickness, the mother of modesty, puts us in mind of our mortality, and while we drive on heedlessly in the full career of worldly pomp and jollity, kindly pulls us by the ear, and brings us to a proper sense of our duty.
A minister was recovering of a dangerous illness, when one of his friends addressed him thus: "Sir, though God seems to be bringing you up from the gates of death, yet it will be a long time before you will sufficiently retrieve your 'strength and regain vigor enough of mind to preach as usual." The good man answered: "You are mistaken, my friend; for this six weeks' illness has taught me more divinity than all my past studies and all my ten years' ministry put together."
Dr. Payson being ill, a friend coming into his room remarked, in a familiar way: "Well, I am sorry to see you lying here on your back." "Do you know what God puts us on our backs for ?" asked Dr. Payson, smiling "No," was the answer. "In order that we may look upward." His friend said to him, "I am not come to condole but to rejoice with you, for it seems to me that this is no time for mourning." "Well, I am glad to hear that," was the reply, "it is not often that I am addressed in such a way. The fact is I never had less need of condolence, and yet everybody persists in offering it; whereas, when I was prosperous and well, and a successful preacher, and really needed condolence, they flattered and congratulated me." Whom the Lord loveth he chasteneth, and if we endure chastening, God dealeth with us as with sons and daughters.


text: Hi there. >> I just "stumbled" across linux-2.3.0.tar.bz2. So what's in it?? :) > Same as in 2.2.8.In that case, why does 2.2.8 and 2.3.0 have different sizes, anddifferent times for the most recently modified file therein?Courtesy my Linux Kernel Versions list: Q> 11,212,277 Tue 11 May 1999 18:37 linux-2.2.8.tar.bz2 Q> 11,208,792 Tue 11 May 1999 21:05 linux-2.3.0.tar.bz2Note that the 2.3.0 archive is some 3.5k smaller than the 2.2.8 one,and also has at least one file that was updated over 2 hours laterthan any file in the 2.2.8 archive...Best wishes from Riley.+----------------------------------------------------------------------+| There is something frustrating about the quality and speed of Linux || development, ie., the quality is too high and the speed is too high, || in other words, I can implement this XXXX feature, but I bet someone || else has already done so and is just about to release their patch. |+----------------------------------------------------------------------+ * ftp://ftp.MemAlpha.cx/pub/rhw/Linux * http://www.MemAlpha.cx/kernel.versions.html-To unsubscribe from this list: send the line "unsubscribe linux-kernel" inthe body of a message to firstname.lastname@example.com read the FAQ at http://www.tux.org/lkml/


text:
|Perl: the Markov chain saw
Find a file with same name but different extensionby Jalcock501 (Sexton)
|on Sep 24, 2013 at 13:10 UTC ( #1055485=perlquestion: print w/replies, xml )
|Need Help??
Jalcock501 has asked for the
wisdom of the Perl Monks concerning the following question:
Hey Guys
Another glorious day in scripting heaven, when all of a sudden a wild request appears. I need to create a script that checks two files together that have the same name but a different extension. i.e. (*.in) and (*.out)So far I have managed to get the information I need from the *.in file but I have no idea how to check it against the information in the .out file.
Also I need to check that the file names(without the extension match)This is my code so far:
At the moment it only prints the unique identifier from the *.in the file to a seperate file to check that this is correct. The identifier is A00000 (one alpha 5 numeric) and is the 72nd bit offset from the 4th line, in the *.in file. However is 2nd line in and the 28th bit across in the *.out file. Please help!
Back to Seekers of Perl Wisdom


text:
The Giants have made an early-season change on their practice squad, signing wide receiver
Collins was signed as a rookie free agent on May 14 from Southeastern Louisiana and was with the team until he was waived on Aug. 27. He played in the Giants' first three preseason games, but did not have a reception.
Goodin was a rookie free agent from Nebraska-Kearney. He was waived in the final cutdown on Friday and signed to the practice squad on Saturday.


text:
Our Pontypridd Taxi service is Committed to providing you excellent service, so you always choose us for your travel needs. We are a Taxi service in Rhydyfelin and we offer 4 to 8 seater Taxis forGroup Bookings, Airport Transfers, Hospitals, Nights Out, Local and Long Trips. All the vehicles are Wheelchair Accessible for disabled customers.
A & l Taxis provide licensed taxis in pontypridd south wales. We are a local affordable and reliable taxi company with a & l taxis you will be travelling in brand new and clean luxury vehicles. 1 to 8seater taxis,airport transfers,nights out,contract work accounts welcome, friendly & reliable service!!!
We are a professional taxi company who specialise in 4, 6 and 8 seater taxis that are less than 6 months old for your comfort and safety. Treforest Taxis has been running for 4 years as a familybusiness and we pride ourselves on our quality of service. As well as a great service we also offer specialise student and business travel and card payments both online and in car. We also offer all our business customers a 14 day account subject to a credit check by Experian Credit Reference Agency.
Our Treforest taxis are reliable, and specially chosen to cater for any of your special requirements. Our taxi drivers are friendly, experienced, and have a good knowledge of the Pontypridd &Treforest areas as well as other areas of the UK. All of our Treforest taxi drivers carry photographic identification - Your safety is our priority.
We understand the importance of keeping a driver rolling, and our fleet of quality, fully maintained, safe and presentable vehicles fulfill all the requirements of the job. Our flexible terms and easyweekly payments make renting a breeze. As there is no credit involved, this 'pay-as-you-go' all inclusive approach couldn't be more simple. For example - Our Cardiff location ONLY supplies vehicles that are licenced for Cardiff. Dublin for Dublin and so on.
City Taxis Cardiff established as taxi firm in Cardiff, City Taxis Cardiff is a family run business offering various services including taxi, private hire, mini buses and wedding services. City TaxisCardiff staff and drivers have vast amounts of experience, our reliable team offer taxi services, along with private hire cars, 4 - 8 seat mini buses, local transportation. We also cover all areas of Cardiff and all UK airports.
Welcome to AirportTravelWales - We are based in vibrant Capital city of Wales - Cardiff. AirportTravelWales offers a range of specialised service for discerning clients, including airport transfer orseaport, sports and social events, private tour, business trips or wait&return service. Whether you require our service for business or pleasure, we will be on hand to ensure your itinerary is completed in timely, discreet and comfortable manners.
Dragon Taxis is the largest and most professional Taxi company in Cardiff with over 500 vehicles. Dragon Taxis are a company that you can trust. Vehicles and drivers are licensed by Cardiff CountyCouncil. Drivers have also undergone criminal record checks, driver licence checks and knowledge school training.
Cardiff cabs are the no.1 taxi service in Cardiff. We've been trading for the last 5 years based in Cardiff Bay and offers larger than average cabs to suit one to 8 people plus our 17-seater minibus -all with professional drivers. Cardiff Cabs offer a professional meet and greet service and low fixed prices quotes online. Our fleet of vehicles provide safety and comfort. For business travellers or special occasions we also provide executive vehicles.
At Cardiff Airport Taxis we provide a first class airport transfer service and have been doing this for over 50 years at Cardiff Airport. We pride ourselves on having a fleet of clean and wellmaintained taxis, along with uniformed professional and experienced drivers. We always deliver a comfortable, safe and efficient taxi service.


text: Steven Klauber is a senior security analyst at John Jay College. In that capacity, he has been training graduate students to conduct vulnerability assessments for nonprofit organizations in the New York City area, as well as conducting research for the present study. Previously, he served for many years at William Grant & Sons USA in a variety of senior positions, including senior vice president for strategic and operational projects, vice president of finance and administration, treasurer, and corporate secretary.


text:
Submitted by chrisws on
The site has been update to use HTTPS. This has required a slight change to the URL. The new address is:
HTTPS provides a level of security for your password when logging in.
Please let me know if you have any access issues.
- Log in to post comments
chrisws replied on Permalink
Oops, this broke the [Online]
Oops, this broke the [Online] examples. so I've reverted the change for now.
- Log in to post comments
chrisws replied on Permalink
Moving online samples to github
To allow the switch to HTTPS to proceed, I'm planning to move the online examples to github pages.
I made a program to extract all the 'Code library' files to individual files:
The resulting files have been uploaded here:
These appear in github page here:
^ (note: http, not https)
You can download the entire set as a zip file:
The change won't happen until the next SmallBASIC update. It would be great to keep getting help maintaining the online samples (hope you're okay with the change MGA!)
- Log in to post comments
MGA replied on Permalink
I'm OK as long as I can access everything from this site as usual.
All this is for secure access to run the samples while On-line over the Internet, I am assuming.
I confess, I have lost interest when my Android device failed to run the samples properly from some Android update (I am assuming).
I haven't checked recently, but they did run fine as always on my laptop.
I thought I was seeing the samples at their worst over my Android device, so it was an interesting challenge to get them working both on my laptop with landscape screen and on Android device with touch screen (no mouse and crappy keypad) and portrait or landscape screen but with extremely different xmax, ymax and pixels per whatever...
I should explain something. I think On-line samples are particularly suited for Android devices because those who have laptops would prefer to try stuff out from code library. I have sort of had that in mind when picking out code samples. "What would be great for Android device or like with a cell phone?" Probably stuff that minimizes use of keypad and time, is my guess.
- Log in to post comments


text:
January 15, 2014
Hungarian Team Taking Big Steps For Google Lunar XPRIZE
Lee Rannals for redOrbit.com - Your Universe Online
A Hungarian team competing for the Google Lunar XPRIZE has completed a successful simulation of its rover mission.The Google Lunar XPRIZE is offering $40 million to the first private company that is able to land safely on the surface of the Moon. The competition also requires the rover to travel 1,600 feet above, below or on the Lunar surface, as well as send two videos or photos back to Earth.
Team Puli said that during its rover's field test, it drove 1,900 feet across soft, lose soil similar to that found on the lunar surface and broadcast high-resolution images and video from its starting and end points. The team used the new PISCES facility located on the slopes of Mauna Kea. This facility is acknowledged as being among the closest analogs to lunar soil found on Earth due to the volcanic soil.
The team members verified several core aspects of their upcoming Google Lunar XPRIZE mission during its December testing, including the planning processes for the rover's route, testing the rover's mobility across the lunar analog terrains, and trialing the Mission Control software.
Mission Control for the Puli simulation was located in Budapest Town Hall, Hungary, which is where the team would be controlling its actual Google Lunar XPRIZE attempt.
"The Puli rover has a unique wheel-leg (wheg) construction, designed explicitly for rough terrain," Puli team leader Dr. Tibor Pacher said in a statement. "This is not the first time that Puli has been tested in analog sites – we took part in a field test in Morocco in early 2013 – but the PISCES facility offers the most challenging and realistic scenario that our rover has faced to date. To simulate the Mooncast that we will need to transmit back from the Moon, we have completed a 'Maunacast' with panoramic shots of our start and finish sites, waypoint identifications and distant verifications. We are delighted with how the Puli rover has performed."
The Team Puli members had already visited the PISCES facility before the simulation while mentoring students for the 2012 MoonBots LEGO Mindstorms Challenge. Team Puli mentored the Hungarobot students during this competition, who won a VIP trip to test their LEGO lunar robots at the PISCES facility.
"Because of Hungary's strong traditions in engineering and science I saw huge opportunities in a Hungarian Google Lunar XPRIZE project to create sustainable values – in education and society as well as engineering," said Pacher. "Team Puli was extremely happy and proud last year when the junior version of the Google Lunar XPRIZE competition, MoonBots, was won for the first time by a European – Hungarian – team. Through initial contacts made during the Hungarobots trip to PISCES, we have developed further links with PISCES and are now testing the hardware for our actual lunar mission here. Our participation in a STEM project has not only provided an inspirational opportunity for the students, but has actually helped us in reaching our goal to send a spacecraft to the Moon."


text: In the Republic of Georgia in Eastern Europe for the first time ever (starting October 1, 2010), defendants have the option of being tried by a jury of their peers. This staple of the American court system was made part of the Georgia constitution six years ago. It's only just now being offered on a limited basis. But as Mary Stucky reports, the United States has been part of a rather unconventional effort to get the country ready.


text:
TO: Joint Procedure Committee
FROM: Mike Hagburg
DATE: Jan. 31, 2011
RE: Rule 26, N.D.R.Civ.P., General Provisions Governing Discovery
Rule 26 came before the Committee at the September 2010 meeting. The Committee considered whether amendment of the rule to clarify protections for communications between attorneys and expert witnesses would be appropriate.
Committee member Larry Boschee proposed that Rule 26(B)(4) be amended to clarify that a party through interrogatories is entitled to request all the information that a party in federal court would obtain in a required expert disclosure. The attached Rule 26 proposal contains amendments adding the federal items.
One point to consider regarding these proposed amendments is that the federal rule's disclosure laundry list applies "if the witness is one retained or specially employed to provide expert testimony in the case or one whose duties as the party's employee regularly involve giving expert testimony." Many frequently called expert witnesses, such as treating physicians or highway patrol accident analysts, do not fit this definition and it might be difficult for them to provide all the information that can be sought from a retained expert.
The Chair brought the December 2010 amendments to Fed.R.Civ.P. 26 to the Committee's attention. These amendments have now been approved and provide specific details on which attorney/expert communications are subject to discovery.
The report of the judicial conference explained why the amendments to Fed.R.Civ.P. 26 were considered necessary:
The proposed amendments to Rule 26 recognize that discovery into the bases of an
expert's opinion is critical. The amendments make clear that while discovery into draft reports and many communications between an expert and retaining lawyer is subject to work-product protection, discovery is not limited for the areas important to learning the strengths and weaknesses of an expert's opinion. The amended rule specifically provides that communications between lawyer and expert about the following are open to discovery: (1) compensation for the expert's study or testimony; (2) facts or data provided by the lawyer that the expert considered in forming opinions; and (3) assumptions provided to the expert by the lawyer that the expert relied upon in forming an opinion.
Amendments based on the federal changes are included in the attached Rule 26 proposal. A copy of Fed.R.Civ.P. 26 and explanatory material on the 2010 amendments is also attached.


text:
Every year, lots of students graduate from colleges and enter the corporate world. This is a new phase of their life and is drastically different from their carefree college days. All freshers face the dilemma of crossing the Great Divide of college and the corporate world and take time to get used to the new role. But in today's competitive environment, it is important to be on your toes all the time. One needs to adapt as quickly as possible and avoid anything that may portray him as an underperforming employee. Maintaining the code of conduct at workplace is as important as proving your mettle at work.
It is important to know the basics of the corporate conducting in order to fit into it efficiently. Although the workplace rules are different form one organization to the other, the core corporate values are more or less the same. Observance of these minute details can help a college fresher to achieve greater corporate success.
Business protocol
College freshers must keep in mind that business or corporate manners matters significantly. They must remember that it is vital to acknowledge everyone with respect. College freshers should take the work and break timings very seriously and avoid arriving late.
Dress the corporate way
It is time for college freshers to discard their old denims and casual t-shirts. How you dress reflects your personality and to some extent helps in being successful at work. If you want to be taken seriously, dress accordingly. Stick to the basic corporate dressing of trousers and full sleeved crisp shirts to make a positive impression. Follow the dress code of the organization.
Workplace conduct
Limit personal calls to zero during your first few weeks at work. Keep the ringer volume low, so that it is audible only to you. College freshers may find it difficult, but it is important to maintain a quiet profile in your initial days at work.
Sustain individual space
Freshers should learn to interact and network with their colleagues and people from other departments. However, refrain from giving out too much personal information and gossiping. Maintain the individual space and restrain your interaction to the corporate level.
Lunchtime Lessons
Lunchtime is the best time for a college fresher to interact and know other colleagues. Have lunch with everybody at the cafeteria or lunchroom so that you get a chance to know them. Avoid going out with your college friends for every meal and use this opportunity to build your corporate network.
Workplace resources and other working habits
College freshers should never exploit workplace assets, such as using office e-mail or surfing the internet for personal reasons. Avoid using the desk phone to make long personal calls. Freshers should be willing to take on extra work and show interest in helping other colleagues. Try and address the colleagues with their names (add Mr, Miss, Sir… according to the organization's conduct) to add a warm touch. Keep these tips in mind and make your mark in the corporate world!
We have many more Career Help Articles Now Available.


text:
China Mobile, Posco, Reliance, Toshiba: Asian Stocks Preview
The following companies may have unusual price changes in Asian trading on April 23. Stock symbols are in parentheses and share prices are as of the latest close. The information in each item was released after markets shut unless stated otherwise.
Hong Kong developers: Hong Kong's secondary private residential property prices rose 0.7 percent in the week ended April 15 from a week earlier, Centaline Property Agency said on its website.
Sun Hung Kai Properties Ltd. (16) (16 HK), Hong Kong's biggest developer, rose less than 0.1 percent to HK$93.90. Cheung Kong (Holdings) Ltd. (1 HK), controlled by billionaire Li Ka-shing, advanced 0.1 percent to HK$101.90.
China Mobile Ltd. (941) (941 HK): The world's biggest phone company by subscribers said net income rose 3.5 percent to 27.8 billion yuan ($4.4 billion) for the three months ended March 31 from a year earlier. That missed the 28.2 billion yuan median estimate of four analysts in a Bloomberg News survey. The stock rose 1.5 percent to HK$87.45.
Cairn India Ltd. (CAIR) : The explorer's fourth-quarter group profit declined 11 percent from a year earlier to 21.9 billion rupees, according to a filing. That missed the 23.7 billion-rupee median estimate in a Bloomberg News survey of 33 analysts. Shares slid 0.9 percent to 347.55 rupees
JFE Holdings Inc. (5411) (5411 JT), Megachips Corp. (6875) (6875 JT): JFE, Japan's second-biggest steelmaker, will sell its Kawasaki Microelectronics subsidiary to Megachips for 8.5 billion yen ($104 million), according to a statement. JFE retreated 3.3 percent to 1,557 yen. Megachips, a maker of digital monitoring systems, rose 2.7 percent to 1,731 yen.
Kentucky Fried Chicken Japan Ltd. (9873) (9873 JT): The restaurant operator's net income amounted to 1.1 billion yen in the year ended March 31, missing its forecast by 21 percent on higher tax costs, according to a preliminary earnings statement. The stock added 0.1 percent to 2,090 yen.
Koa Corp. (6999) (6999 JT): The electronic-parts maker said profit fell 38 percent to 1.65 billion yen in the year ended March 31 on falling sales, citing the stronger yen and higher raw materials costs. The stock slumped 2.6 percent to 849 yen.
Mitsubishi Motors Corp. (7211) (7211 JT): The automaker's profit was 23.9 billion yen in the year ended March 31, 20 percent more than its forecast,on lower costs and foreign exchange gains, according to a preliminary earnings statement. The stock was unchanged at 90 yen.
Nippon Koei Co. (1954 JT): Marubeni Corp., Sumitomo Corp., and Sojitz Corp. will support the consulting company's feasibility study on building industrial parks and infrastructure in Myanmar as the nation opens up to investment, according to an official at the trade ministry who declined to be identified due to policy. Nippon Koei rose 0.7 percent to 281 yen.
Nippon Yusen K.K. (9101) (9101 JT): Japan's top shipping line by sales posted a 73 billion yen less in the year ended March 31, wider than its forecast of 26 billion yen, due to the reversal of deferred tax assets, according to a preliminary earnings statement. The stock climbed 1.7 percent to 241 yen.
Posco (005490) (005490 KS): The world's third-biggest steelmaker by output said first-quarter profit fell 42 percent because of rising raw-material costs and waning demand for the metal used in cars, ships and buildings. The shares lost 0.4 percent to 378,500 won.
Reliance Industries Ltd. (RIL) : The Indian company, owner of the world's biggest oil-refining complex, reported a 21 percent drop in fourth-quarter profit to 42.4 billion rupees. That compared with a median estimate of 42.8 billion rupees in a Bloomberg News survey of 30 analysts. Shares retreated 1.5 percent to 730.85 rupees.
Rakuten Inc. (4755) (4755 JQ): Rakuten and Baidu Inc. will end an online e-commerce service Lekutian in China next month because of increasing competition, according to statement on Rakuten's website. Rakuten fell 1.1 percent to 89,300 yen.
Sanki Engineering Co. (1961) (1961 JT): The engineering company's profit was 170 million yen in the year ended March 31, missing its forecast by 88 percent, due to losses at affiliates, according to a preliminary earnings statement. The stock added 0.2 percent to 433 yen.
Taihei Dengyo Kaisha Ltd. (1968) (1968 JT): The plant engineering company said it will retire 4.68 percent of its outstanding shares on May 15. The stock was unchanged at 668 yen.
Tokyo Steel Manufacturing Co. (5423) (5423 JT): The company's loss widened to 14.3 billion yen in the year ended March 31 from 10.4 billion yen a year earlier on higher production costs. The stock rose 0.7 percent to 695 yen.
Toshiba Corp. (6502) (6502 JT): The electronics maker signed a 14- year take-off agreement with Canada's GoviEx Uranium Inc. (2965898Z NL) for a "significant portion" of the annual uranium output from GoviEx's Niger project, Toshiba said on its website. Toshiba slid 2.4 percent to 330 yen.
To contact the reporter on this story: Norie Kuboyama in Tokyo at email@example.com
To contact the editor responsible for this story: Nick Gentle at email@example.com


text:
I'm having a difficult time understanding why the wife of the governor adjusting to her new home (TNT, 3-4) is more important (half of the first page) than U.S. Secretary of State Kerry giving Egypt $190 million with the promise of more while America is financially in ruins (TNT, 3-4).
Whether you are a Democrat, Republican or independent, everyone must be as stunned as I am.
I just consider the continual bankrupting of our country by politicians a lot more important than Trudi Inslee relaxing at the Governor's Mansion.
Why not just bury the entire article? It's obvious you didn't want to print it. You even revamped the article about police dogs to fill the page. Oh, and thank God tanning beds will be spared (TNT, 3-4). Really? That's what you consider "front-page news"?
Who cares about news? At least we still have the comic section; print that on the front page.


text:
FELLOWSHIP: Allergy/Immunology, University of Tennessee, Knoxville, Tennessee, 1975
RESIDENCY: Internal Medicine, University of Tennessee, City of Memphis Hospital, Memphis, Tennessee, 1971
INTERNSHIP: University of Tennessee, City of Memphis Hospital, Memphis, Tennessee, 1969
MD: University of Louisville School of Medicine, Louisville, Kentucky, 1968
UNDERGRADUATE: University of Louisville, Louisville, Kentucky, 1964
LEXINGTON CLINIC AFFILIATION: October 1975
Dr. Lamkin is board-certified in Allergy/Immunology and Internal Medicine. He provides services in adult and pediatric allergy and immunology, allergy diagnostic testing, allergy injections, allergic rhinitis and nasal disorders, anaphylaxis, asthma, drug allergy evaluation, food allergy and insect allergy. Dr. Lamkin's professional interests include the entire spectrum of allergic disorders, asthma, rhinitis, urticaria and allergic dermatoses, insect allergy, anaphylaxis, food allergy and drug hypersensitivity.
Dr. Lamkin can be reached at (859) 258-5244.


text:
I know why you're here. You are looking for content. Isn't that what we all seek? Honest and informative content that turns search into serendipity. I'm Steve Guzman and I can help.
Meet Steve
Meet Steve
Content Marketing Matters
However, in our world of Attention Economics, resources are scarce. The content is the yummy banana and marketing is the peel. Your readers don't want the peel.
Get the Banana
Get the Banana
Visual Content Captures
A researcher's quest for content moves at the speed of light. Do you want their attention? Nothing catches the eye like an image with a story to tell.
See the Picture
See the Picture


text:
Heating Oil Mar '13 (HOH13)
Price PerformanceSee More
|Period Low
|Period High
2.9639 +0.27%
on 02/28/13
3.2575 -8.77%
on 02/08/13
-0.0824 (-2.70%)since 01/28/13
2.9013 +2.43%
on 12/10/12
3.2575 -8.77%
on 02/08/13
-0.0402 (-1.33%)since 11/28/12
More Heating Oil QuotesAll Futures
Most Recent StoriesMore News
Todays calls and the results
We've discussed the record-setting imbalance between the speculative and commercial trader positions in the crude oil market both here and in our Commitment of Traders column for Modern Trader ...
Crude oil is seen now in wave four, so be aware of another break to the upside, into a fifth wave that can run into 66.00-66.50 zone where energy may slow down.
Oil has been holding above 60$ critical support early March despite the selling pressure. Price recovered and pushed above 64.20$ and is now back above 65$ close to the 66.70$ January highs.
D.R. Futures Trading Daily Report on Support and Resistance Levels based on our algorithm for the eminis (ES,NQ, and YM), Gold and Crude Oil, outlook, and possible targets. Find out how we use our proprietary...
These were calls sent out at 7:30 pm yesterday to our subscribers
Oil sold off on tariff fears but rallied back as Saudi Arabia is signaling that they are just crazy about production cuts and want an extension. Its tariff fears versus ring demand and falling supply for...
Let's not kid ourselves!
Stocks are lower, but do they stay down? Where to buy Crude? Resistance in Gold?
You can talk all you want about rising U.S. oil production, but the fact is that U.S. oil supply is below average. The Energy Information Agency, in its weekly report, said that U.S. commercial crude oil...


text:
Musicians Chris Brown (R) and Rihanna perform during the Z100 Jingle Ball in New York, in this December 13, 2008 file photo. Grammy organizers said on February 7, 2012 that Brown will perform at this Sunday's Grammy Awards. Rumors have flown among fans and celebrity watchers in recent weeks that the pair may be secretly dating again - speculation Brown's representatives have dismissed. (REUTERS/Lucas Jackson/Files)
Test your knowledge of the past week's news and current events.
View Survey


text:
The Work Of The Holy Spirit
The Work Of The Holy Spirit
Much confusion exists about the person and work of the Holy Spirit because of careless exegesis and flippant use of Bible terms. For instance, the baptism of the Spirit is referred to directly only seven times in the New Testament. The first five references are prophetic (Matthew 3:11; Mark 1:8; Luke 3:16; John 1:26-33; Acts 1:5) and refer to John's preaching. One is historical (Acts 11:16) and only one is doctrinal (1 Corinthians 12:13). It is this last reference that gives us the spiritual significance of the baptism. It has nothing to do with tongues or super-holiness. It has to do with placing people as members into the mystical body of Christ.
a. I am now in Christ: the baptism (1 Corinthians 12:13)
b. Christ is now in me:
(1) The gift (Acts 2:38)
(2) The indwelling (1 Corinthians 3:16, 6:19)
a. The present: the seal (Ephesians 1:13)
"You are eternally mine"
b. The prospect: the earnest (Ephesians 1:14)
"I am eternally yours"
a. To make me spiritual: the filling (Ephesians 5:18)
b. To make me successful: the anointing (1 John 2:20)


text:
07-26-2012 #1Bigbones87 Guest
No video or sound on Backwords compatible PS3 help?
I bought this chechA01 on ebay for cheap, because it wouldnt turn on. I opened it up (had already been opened before) and fixed the mangled ribbon cable for the on/off button. After that it turned on just fine. Worked like a champ. Then I decided i would take it apart and replace the thermal paste on it.
Once i got it opened it appeared that the thermal compound had already been replaced before, because it was still tacky and grey, not white. I went ahead and cleaned it and applied new paste anyway, then reassembled it. Turned it on and it wouldn't give me a picture. I reset input by holding down the power button and got it to show up. Then i walked away for a few minutes.
When i returned it was shut off blinking red light. I turned it off then back on. Now it gives me a green light, but wont give video or sound. If I just leave it on, after a few minutes it will shut off. When i try to hold down the power button on start up, it doesn't reset input, it just turns it off. Never shows ylod. Any idea? Possible that this had been heat gunned before and taking it apart brought back some bad juju? Thanks in advance for any input.
Oh yeah, i did try it on a different hdmi cable, and also tried using the rca cord it came with on another tv. No luck.
07-26-2012 #2windrider42 Guest
What type of Thermal paste did you use. I always use Arctic Silver 5. You only need enough like a dime spread on it.
Are you able to go into recovery mode. Try Options 3, then 4
Or you could just do Option 5.
07-26-2012 #3Bigbones87 Guest
Thanks for the post, but I actually know a decent amount about the ps3. I have tried everything that i can think of. The thermal paste isnt the issue, as i have applied thermal paste to about 6 ps3s and all are working fine. I cant actually access recover mode. When i turn it on. I press and hold the power button, but it never beeps to reset the video.
It just shuts off after like 15 or 20 seconds. Then i turn it back on and hold it again, same thing. No matter how long or how many times i hold the power button, the only thing it accomplishes is turning off. I think it might be the rsx chip lost connection. Just wondering if anyone else had any thoughts. Thanks again
i used mx-4 thermal paste, and applied about a dime size on each chip. It is thin and maybe a little bigger than a dime after being compressed. Is that ok? I like mx-4 because there is no cure time. Don't take my response wrong. I am in no way an expert, or think i know more than anyone. I am only stating that i have tried the obvious fixes. Thanks
07-26-2012 #4smokyyuwe Guest
If it worked before, I would say just open it up again and double check everything. If it's not outputting video, opening it back up one more time can't hurt.
07-26-2012 #5Bigbones87 Guest
Just got through with that. Great minds think alike. heh. I took it apart and just double checked everything. It appeared i put just a little too much thermal paste, because it covered the whole chip with a thin layer. Some say cover the whole thing. Others say just the middle.
Anyway, dont think that is the problem. I wiped a little off anyway. Everything else seemed to be correct. I read online somewhere that if is is the gpu not getting good contact, that would cause it. They were saying that if you put some washers on the screws when putting it back together to apply more pressure, it may give you picture back.
If it does then you will know it is the gpu connection. I cant help but get this naggin suspicion that this unit has been doctored before and maybe not too good of a job. I did get it working, but i never got to use it extensively. I only ever powered it on for about 20 min to see if i fixed it. May have been destined for failure. Sure would like to bring it back tho. Thanks to everyone who took time to respond.
07-29-2012 #6B4rtj4h Guest
I think you are playing on luck here my friend. Seems to me that your soldering might be screwing with you. Assembling and de-assembling might just knock things in to the right place. I know you get some picture in the beginning... but it's cold then. When it heats up things get bigger... I think heat gunning your PS3 might fix the thing once and for all... Case closed.
07-29-2012 #7Bigbones87 Guest
Thank you for the response. I am afraid you may have misunderstood me. I HAD a picture before I took it apart to repaste it. The unit stayed on fine for 20 minutes before that. Once I took it apart, repasted it, then put it back together, it came up with no picture. I was able to reset the input with power button, and then it came up to a picture.
When I came back a few minutes later, it was shut off blinking red light. Now when I turn it on I get no picture, and holding the power button doesn't reset the input. All it does is turns on with green light. It will stay on as long as I want, but holding the power button down doesn't beep or respond. If you hold it long enough it will turn it off, but that is all. No recovery, no input reset. Thanks
Close thread. I am gonna have it reballed so maybe that will help with it. Thanks for all the input.


text:
I think I've circulated this before, but to put it back on the record with a findable Subject: line, here is a page that partially documents a worked example I hope we'll study in more depth in WP6 http://www.w3.org/2001/sw/Europe/plan/workpackages/live/esw-wp-6.html for the Month 21 deliverable, (6.2: xml_sw_prototype_math_logic). The writeup and test data is at http://www.w3.org/2002/04/corpinfo/semweb-scenario ...and includes files (http://www.w3.org/2002/04/corpinfo/) that give basic 'company reports' markup for several companies, in RDF. There is also an N3 representation of some mathematical rules relating the various things that appear in these reports. Very much work in progress (except that nobody is actively working on it) but interesting I think as a testbed for exploring when MathML makes sense, when RDF rules are more appropriate, and how it all fits together. DanReceived on Tuesday, 21 January 2003 16:24:10 UTC
This archive was generated by hypermail 2.3.1 : Tuesday, 6 January 2015 19:56:37 UTC