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Atherosclerotic Ischemic Nephropathy as a Cause of Chronic Kidney Disease: What can be done to Prevent End-stage Renal Disease?
Lionel U Mailloux1, Abrar Husain2
1 Long Island Hypertension and Nephrology, Seaview Boulevard, Port Washington, NY, USA
2 Division of Nephrology and Hypertension, Department of Medicine, North Shore University Hospital, Manhasset, NY, USA
Mailloux LU, Husain A. Atherosclerotic Ischemic Nephropathy as a Cause of Chronic Kidney Disease: What can be done to Prevent End-stage Renal Disease?. Saudi J Kidney Dis Transpl 2002;13:311-9
Mailloux LU, Husain A. Atherosclerotic Ischemic Nephropathy as a Cause of Chronic Kidney Disease: What can be done to Prevent End-stage Renal Disease?. Saudi J Kidney Dis Transpl [serial online] 2002 [cited 2019 Jul 18];13:311-9. Available from: http://www.sjkdt.org/text.asp?2002/13/3/311/33798
Over the past decade, data have accumulated implicating atherosclerotic renal artery stenosis (ARAS) as an increasingly significant cause of end-stage renal disease (ESRD), ranging anywhere from 5 to 22% of incident ESRD patients. [1],[2],[3],[4],[5],[6],[7],[8] This apparently progressive vascular disease has also become the center of clinical controversy in view of the ease with which it can be diagnosed and radiologically corrected by interventional means i.e. balloon angioplasty with stenting either by interventional radiologists, interventional nephrologists or interventional cardiologists. [7],[8],[9],[10],[11] Most of the patients with ARAS also have a significant number of associated co-morbidities [1],[2],[5] [Figure - 1]. Also, patients with known unilateral atherosclerotic renal artery occlusion and renal insufficiency have been shown to have high mortality rates and some progression into renal failure, but not necessarily from occlusion of the remaining renal artery. [12] In addition, ARAS is being recognized with increasing frequency in patients with coronary artery disease and peripheral vascular disease, in as many as 20% of the patients undergoing coronary angiography. [13],[14],[15],[16] The presence of a significant stenosis identified by various imaging procedures, especially during another imaging procedure, has made it more difficult to ignore these lesions. Whether or not they are hemodynamically and physiologically significant is hard to evaluate.
Fibromuscular dysplasia, on the other hand, often leads to development of hypertension at a young age and responds particularly well to percutaneous intervention. However, this disorder does not usually cause significant renal insufficiency or progressive renal disease,
Clinical Dilemma
Atherosclerotic renal vascular disease is usually associated with a heavy burden of other vasculopathies, high mortality rate and poorer survival on dialysis. It can also be associated with hypertension, renal insufficiency and progressive renal failure leading to ESRD [Figure - 2]. The most difficult question to answer for nephrologists, cardiologists and other clinicians is: what proportion of patients with atherosclerotic renal vascular disease will develop progressive renal failure? How significant is the renal artery lesion? Should an intervention be considered?
The following four patients represent typical situations facing the clinicians.
Mr. RK came for a second opinion about the initiation of dialysis. He is a 62-year-old vasculopath, who has a long cigarette smoking history and known diffuse vascular disease. He underwent aorto-femoral bypass in the late 1980's, carotid endarterectomy in the late 1990's, has had resistant hypertension, proteinuria and intermittent claudication with renal insufficiency. A renal biopsy, performed in 1986 for the nephrotic syndrome, had revealed focal and segmental glomerulosclerosis. After the biopsy, he developed some deterioration of his chronic renal insufficiency and full evaluation revealed left renal artery stenosis, which was surgically bypassed in 1988 with apparently stable renal function. During the last 1.5 years, renal function continued to deteriorate slowly but the patient was clinically stable. In the fall of 2001, he underwent angiography, revealing significant aortoiliac disease, stenosis of both renal arteries right > left, with the kidneys measuring approximately 8.5 and 8.8 cm, left and right respectively. Balloon angioplasty and stent deployment into the right renal artery was undertaken. The patient developed acute renal failure despite acetylcysteine, had several atheroemboli to the feet and developed clinical uremia requiring initiation of dialysis. Soon thereafter, he had at least one cerebrovascular accident with some residual paresis. He now is on dialysis with ischemic hands and feet.
He was on anti-hypertensives, statins for hyperlipidemia, calcium carbonate and erythropoietin.
This patient is a 75-years-old lady, who has known ischemic heart disease, hypertension, hyperlipidemia, and in late 2000 underwent coronary angiography for angina. During that procedure, aortography revealed stenosis of the right renal artery. Renal size by sonography revealed both kidneys to be approximately 11.0 cm in length. There have been no symptoms of renal failure or recent congestive heart failure.
Her medications included antihypertensives/ and statins. She has not used any over-thecounter nonsteroidal anti-inflammatory drugs (NSAIDs) but does take Tylenol for her severe arthritis. She has an allergy to sulfur and aspirin.
Physical examination in early 2002 revealed blood pressure to be 150/70 mm Hg. There was no fluid overload. The patient is well and very active.
Comment: This patient presents the dilemma of the incidental discovery of what appears to be renal artery stenosis in the presence of atherosclerotic vascular disease and hypertension. Renal function is normal. Over the course of 1.5 years, the kidney has not decreased in size and the patient is tolerating her multiple drug therapy with no ill effect. It does not appear that she has suffered any ill effect from lack of intervention.
Mrs. EP is an 88-year-old lady, who was referred for hypertension and renal insufficiency. She was known to have hypertension for well over 40 years, coronary artery disease with angina pectoris, intermittent claudication and at least two transient ischemic attacks.
Medications: She was taking anti-hypertensives, statins and lorazepam. She had ingested some NSAIDs and Cox-2 inhibitors in the past. She also takes vitamins and calcium.
Initial physical examination revealed her to have blood pressures of 210/80-86 mm Hg on several occasions despite multiple anti-hypertensive drugs. There was no jugular venous distention, no gallop, negative hepato-jugular reflux, and no edema. There were bruits in the abdomen and over both femoral arteries with diminished tibial pulses and cool feet.
Data: Creatinine was 194 µmol/L with normal electrolytes (in the past she developed hyperkalemia on angiotensin converting enzyme (ACE) inhibitors). Renal duplex sonogram revealed a small left kidney. With treatment of her blood pressure, serum creatinine increased to 248 µmol/L. It was thought that she could have renal artery disease; duplex doppler assessment of her renal arteries revealed an atrophic left kidney and a high grade stenosis of the right renal artery. Renal angiography, balloon angioplasty and stent deployment were performed in October 2001. Her subsequent course revealed her serum creatinine to decrease to 194 µmol/L and blood pressure decreased to 160-170/74-76 mm Hg. Followup imaging revealed no duplex evidence of renal artery stenosis immediately postprocedure with good angiographic appearance of the stent. In January, the blood pressure increased again to the 190-210/90 mm Hg range with consequent increase in medications. Losartan was added. She then developed severe angina, requiring coronary angiography and stenting of two coronary arteries. Blood pressure was extremely difficult to control during that hospitalization and serum creatinine leveled off at 293 to 301 µmol/L. She also developed fluid retention and mild heart failure. Blood pressure remained markedly elevated and uncontrollable. Repeat duplex scanning revealed re-stenosis of the right renal artery proximal to the stent at the ostium of the renal artery. The patient was admitted and underwent C0 2 angiography with re-stenting of the right renal artery. In the spring of 2002, her serum creatinine has decreased to 212 µmol/L and blood pressure had minimally improved.
Comments: Clinically, it would appear that only a small portion of this patient's renal insufficiency and hypertension is due to ischemic nephropathy. This case, however, shows that re-stenosis can occur quite rapidly and that she can also tolerate angiotensin receptor blockers (ARBs) as one of the medications, without hyperkalemia.
Mrs. HL is an 82-year-old lady with an over 30 years history of hypertension, apparently easily controlled over that period of time. In December 2001, she experienced a large cerebrovascular accident with resulting hemiparesis and transient aphasia. Blood pressure at the time of admission to the emergency room and subsequently in the hospital, ranged from 180-210/90-104 mm Hg.
Medications: Her medications included anti-hyptensives, digoxin, vitamins and coumadin. Although, there was a previous cough and hyperkalemic reaction to ACE inhibitors, neither these agents nor ARBs were prescribed.
Physical examination revealed an alert elderly lady with obvious left sided weakness. There was no jugular venous distention, no gallop, negative hepato jugular reflux, and no edema. There were multiple bruits over the carotid artery, in the abdomen and in the femoral arteries. Blood pressure was 196/104 mm Hg.
Hospital Course: Labetalol, diuretics and calcium channel blockers were prescribed, with slight improvement in blood pressure control. The patient was eventually transferred to a rehabilitation facility where she experienced a seizure and was readmitted with blood pressure again uncontrolled. Valsartan was prescribed. Duplex Doppler renal sonogram revealed high-grade stenosis of the right renal artery with normal renal size and a small atrophic left kidney. The Valsartan was continued and the patient developed acute renal failure, with the creatinine increasing from 106 µmol/L to 380 µmol/L within seven days. The Valsartan was discontinued with prompt improvement in kidney function. Blood pressure was in normal range while on the ARB.
Comments: This elderly lady had clear-cut significant renal artery stenosis with blood pressure control and renal failure while on the angiotensin receptor blocking agent. This suggests that the renal artery lesion was functionally significant. Now, on four other classes of anti-hypertensive agents, including Clonidine, Labetolol, diuretic and Felodipine, her blood pressure is marginally controlled, in the 150-160/80 mm Hg range. She is recuperating in rehabilitation from her recent stroke and seizure activity. Renal angiography, balloon angioplasty and stent deployment will be scheduled after she recovers from her recent vascular events.
Diagnosis of ARAS
ARAS should be suspected in some particular settings: severe or refractory hypertension, an acute change in blood pressure course, asymmetry in renal size, recurrent episodes of flash pulmonary edema that can occur in patients with normal left ventricular systolic function, or an increase in the plasma creatinine concentration following the administration of an ACE inhibitor or an ARB agent [Table - 1]. However, some patients may have few, if any, of these processes except for diffuse and systemic atherosclerosis.
Based on retrospective arteriographic studies, rates of progression of renal artery stenosis [even to total occlusion] were estimated to range from 36 to 53% [17],[18] [Figure - 3]. In more recent studies using duplex doppler ultrasound in 170 patients followed for nearly three years, there was an overall progression in 31% of the patients. [19] The cumulative incidence of progression over three years was related to the original degree of stenosis, e.g. 18%, 28% and 49% progression for renal arteries initially classified as being normal, <60% stenosis and > 60% stenosis respectively, p<0.03 log rank test, with only nine renal artery occlusions. [19] Similarly, there was a 21% incidence of significant decrease in kidney size, which was associated with rising systolic blood pressure levels. [20] Renal atrophy correlated with changes in the serum creatinine. These data suggest that there is an inevitable, but slow, progression of ARAS in the susceptible patients. Although the absolute risk of developing ESRD is unknown, a recent editorial by Zierler stated a cumulative 5year incidence of 11.8%. [21]
Treatment Modalities and Outcomes
The clinical approch to patients with suspected significant ARAS is difficult to follow because of the lack of clear-cut evidence supporting any given path. First the diagnosis must be suspected based on the patient's presentation [Table - 1]. In the older patient with multiple medical problems, one must rely heavily on imaging techniques and clinical acumen to make a decision about moving forward. Functional tests such as captopril renography and renal vein renins are of limited value in patients with renal dysfunction and in those with multiple medications that often include beta blockers, ARBs, ACE inhibitors, etc. Yet, lurking in the background (and subconsciously in the mind of most nephrologists and cardiologists) is the fear that missing the diagnosis of a significant renal artery lesion will eventually lead to uncontrolled refractory hypertension with its many vascular complications that are often disastrous clinically and eventually doom the patient to ESRD. A prudent approach is necessary so that an appropriate diagnosis is made and that the patient is dealt with in a clinically appropriate manner. Likewise, there are some clear-cut contra-indications to intervention, including advanced age with many co-morbid conditions, stable renal function, relatively easily controlled blood pressure, elevated resistive index of the non-stenotic kidney and apparent unilateral renal artery stenosis [Table - 2].
Appropriate data suggest that surgical techniques lead to longer lasting successful outcomes for control of blood pressure in the patient with ARAS. [22],[23],[24] Angioplasty with stent deployment is successful in dilating the stenotic blood vessel but does not appear to offer a long-lasting benefit to the patient. [19],[20],[25],[26] As a result, it is quite likely that when a physician moves forward it is often unclear whether the evaluation is logical and eventual outcome, of any benefit.
Intrarenal resistive indices along with hilar waveforms and the renal/aortic flow ratios are all helpful in detecting the presence of ARAS. In a recent study, a resistive index > 0.8 in the contralateral kidney predicts failure of intervention in patients with ARAS. [27] This would appear to be a valuable functional test, especially in patients with renal insufficiency. There are several tests of research interest; ultrafast spiral computerized tomogram angiography (but requires contrast), CO 2 /gadolinium angiography (pictures almost as good as the gold standard contrast angiogram), captopril dynamic magnetic resonance angiography (MRA), and high speed MRA with gadolinium [Table - 3].
The following clinical plan is suggested as logical and rational. [Figure - 4] presents a possible algorithm:
Clinical scenario 1:
The seriously ill arteriopath: Compile a comprehensive vascular disease inventory; if too many vascular beds are involved, then perhaps no intervention should be performed.
The patient with difficult to control hypertension: (i.e. at least four classes of agents at near to maximal dosing, unacceptable rise in serum creatinine with ACE inhibitors or ARBs) or with a combination of the two, stable cardiac condition. Perform appropriate imaging (duplex doppler, renal arterial study vs MRA with gadolinium depending on resource available in the community and body habitus). Other options include discontinuation of ACE inhibitors or ARBs to see if renal function improves, but blood pressure may increase and become difficult to control. [28] The major decision in this clinical scenario is to decide whether interventional radiology or cardiology is chosen first before vascular surgical expertise is called in.
Comment: This is the more typical clinical scenario where patients with atherosclerotic vascular disease also have ARAS with both hypertension and renal insufficiency. Imaging would most likely show renal artery stenosis, often significant unilaterally with atherosclerosis of the aorta and some other abnormalities on the contralateral kidney. The procedure is performed in an attempt to assist with blood pressure control and hopefully prevent further renal functional deterioration.
An elderly patient with many clinical features of atherosclerotic peripheral vascular disease and either ARAS diagnosed at the time of other imaging procedure or because of hypertension or other clinical indication. However, treatment with anti-hypertensives (ACE-inhibitors and/or ARBs) causes minimal increases in serum creatinine while controlling the blood pressure.
There is no change in kidney size by sonography during follow-up. No intervention is planned.
Renal vascular disease is more common than anticipated in elderly ESRD patients, especially in white patients with other vascular co-morbidities. Significant incidental ARAS may be detected in as many as 20% of patients undergoing coronary angiography or in the presence of peripheral vascular disease.
The usual screening tests work well in younger patients with normal renal function. Duplex doppler ultrasound has the highest specificity, but some technical failure rate. Normal ACE-inhibitor scintigraphy may obviate the need for renal angiography in patients with adequate renal function. However, digital intra-arterial angiography remains the 'gold standard' of diagnostic tests. Magnetic resonance angiography is a promising new technique due to stronger magnets, gadolinium and new software. Although the natural history of ARAS is not well established, progression and occlusion of the renal arteries ultimately is the outcome, with progression of stenosis occurring in up to 49% of patients. The diagnosis of ARAS should be suspected earlier when it is safe to perform invasive procedures and surgical therapeutic options. Medical or surgical therapy is dictated by the patient's co-existing vascular condition. Angioplasty has no significant role in therapy, but stents are helpful. Attention should be paid to all cardiovascular disease risk factors before the chronic kidney disease progresses to uremia. Small kidneys are contraindications to interventional therapy. It is quite clear that renal vascular disease is a significant cause of ESRD in the USA [Figure - 5]. Whether its incidence is really increasing or more nephrologists are looking for it, is unclear. It has also been reported that about 15 to 20% of patients undergoing cardiac catheterization have renal vascular disease. Based on these data, not all patients with anatomic renal artery stenosis progress to ESRD. In 2002, the clinician is still faced with the dilemma of deciding which patient will progress to ESRD and how to approach a patient with atherosclerotic renal vascular disease.
There is a need for a prospective randomized clinical trial comparing surgical therapies to interventional and aggressive medical therapy in these patients with diffuse atherosclerosis. In the absence of such trials, the clinician should treat the overall patient as aggressively as is possible, i.e. smoking cessation, cholesterol management, low goal blood pressure, ACE inhibition/ARB if tolerated, aspirin, folate administration, exercise and prudent diet, to deliver optimal medical care. If the patient is stable on this therapy then there is no need for intervention. It may be necessary to evaluate blood pressure control by 24hour monitoring. If renal function deteriorates and blood pressure cannot be controlled on such an aggressive routine, then the patient should be offered more invasive diagnoses and therapy.
1. Mailloux LU, Napolitano B, Bellucci AG, et al. Renal vascular disease causing endstage renal disease, incidence, clinical correlates, and outcomes: a 20-year clinical experience. Am J Kidney Dis 1994;24:622-9.
2. Fatica RA, Port FK, Young EW. Incidence trends and mortality in end-stage renal disease attributed to renovascular disease in the United States. Am J Kidney Dis 2001;37(6):1184-90.
3. Appel RG, Bleyer AJ, Reavis S, Hansen KJ. Renovascular disease in older patients beginning renal replacement therapy. Kidney Int 1995;48:171-6.
4. Greco BA, Breyer JA. Atherosclerotic ischemic renal disease. Am J Kidney Dis 1997;29:167-87.
5. United States Renal Data Systems. USRDS 2001 ADR. US Dep't of Health and Human Services. Bethesda, MD August 2001.
6. Safian RD, Textor SC. Renal-artery stenosis. N Engl J Med 2001;344:431-42.
7. Baboolal K, Evans C, Moore RH. Incidence of end-stage renal disease in medically treated patients with severe bilateral atherosclerotic renovascular disease. Am J Kidney Dis 1998;31:971-7.
8. Plouin PF, Rossignol P, Bobrie G. Atherosclerotic renal artery stenosis: to treat conservatively, to dilate, to stent, or to operate? J Am Soc Nephrol 2001;12:2190-6.
9. Isles CG, Robertson S, Hill D. Management of renovascular disease: a review of renal artery stenting in ten studies. QJM 1999; 92(3):159-67.
10. Burket MW, Cooper CJ, Kennedy DJ, et al. Renal artery angioplasty and stent placement: predictors of a favorable outcome. Am Heart J 2000;139:64-71.
11. Jaff MR, Olin JW. Atherosclerotic stenosis of the renal arteries. Indications for intervention. Tex Heart Inst J 1998;25:34-9.
12. Cheung CM, Wright JR, Shurrab AE, et al. Epidemiology of renal dysfunction and patient outcome in atherosclerotic renal artery occlusion. J Am Soc Nephrol 2002; 13:149-57.
13. Harding MB, Smith LR, Himmelstein SI, et al. Renal artery stenosis: prevalence and associated risk factors in patients undergoing routine cardiac catheterization. J Am Soc Nephrol 1992;2:1608-16.
14. Rihal CS, Textor SC, Breen JF, et al. Incidental renal artery stenosis among a prospective cohort of hypertensive patients undergoing coronary angiography. Mayo Clin Proc 2002;77:309-16.
15. Choudhri AH, Cleland JG, Rowlands PC, et al. Unsuspected renal artery stenosis in peripheral vascular disease. BMJ 1990; 301:1197-8.
16. Leertouwer TC, Pattynama PM, van den Berg-Husmans A. Incidental renal artery stenosis in peripheral vascular disease: a case for treatment? Kidney Int 2001;59: 1480-3.
17. Meaney TF, Dustan HP, McCormack LJ. Natural history of renal arterial disease. Radiology 1968;91:881-7.
18. Tollefson DF, Ernst CB. Natural history of atherosclerotic renal artery stenosis associated with aortic disease. J Vasc Surg 1991;14:327-31.
19. Caps MT, Perissinotto C, Zierler RE, et al. Prospective study of atherosclerotic disease progression in the renal artery. Circulation 1998;98(25):2866-72.
20. Caps MT, Zierler RE, Polissar NL, et al. Risk of atrophy in kidneys with atherosclerotic renal artery stenosis. Kidney Int 1998;53:735-42.
21. Zierler RE. Screening for renal artery stenosis: is it justified? Mayo Clin Proc 2002;77:307-8.
22. Novick AC. Long-term results of surgical revascularization for renal artery disease. Urol Clin North Am 2001;28:827-31.
23. Cherr GS, Hansen KJ, Craven TE, et al. Surgical management of atherosclerotic renovascular disease. J Vasc Surg 2002;35: 236-45.
24. Hansen KJ, Thomason RB, Craven TE, et al. Surgical management of dialysisdependent ischemic nephropathy. J Vasc Surg 1995;21:197-209.
25. Yutan E, Glickerman DJ, Caps MT, et al. Percutaneous transluminal revascularization for renal artery stenosis: Veterans Affairs Puget Sound Health Care System Experience. J Vasc Surg 2001;34:685-93.
26. Tullis MJ, Caps MT, Zierler RE, Dadal RE. Blood pressure, antihypertensive medication and atherosclerotic renal artery stenosis. Am J Kidney Dis 1999;33:675-81.
27. Radermacher J, Shavan A, Bleck J, et al. Use of doppler ultrasonography to predict outcome of therapy for renal artery stenosis. N Engl J Med 2001;344:410-7.
28. van de Ven PJ, Beutler JJ, Kaatee R, et al. Angiotensin converting enzyme inhibitorinduced renal dysfunction in atherosclerotic renovascular disease. Kidney Int 1998;53:986-93.
Lionel U Mailloux
Long Island Hypertension and Nephrology, 50 Seaview Boulevard, Port Washington, NY 11050
[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5]
[Table - 1], [Table - 2], [Table - 3]
Mailloux LU
Husain A
Treatment Modali...


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Google India conducted a multi-city road show to help Bloggers and online content creators leverage video as an alternative means of expression to complement text/graphics. The session also highlighted the YouTube Partner Program and revenue sharing model.
I attended the session in Bangalore on June 16, 2012. This post is a summary of key points and some of the related thoughts that my mind pondered over.
Google is of course, the undisputed leader among search-engines. It is relatively, lesser known that YouTube happens to be the second largest (not Bing or Yahoo). These are some of the India specific numbers that the G-Team shared (as of June 2012).
Value proposition: What really stands out from these data points is that YouTube reaches out to wealthy young Indians. It has been able to engage the audience more effectively (25 mins) than any other contemporary channel and an overwhelming majority (86%) connect to YouTube when they are relaxed (at home). Furthermore, every time you visit YouTube to watch a video of your choice, statistics say that you will almost certainly watch 6-10 more videos that Google suggests you.
Now that's a terrific proposition. Both for entertainment and business; there is enough money to be made.
Who owns the content? Who makes the money?
Suppose, you come up with a cute-cat-video or the next best thing to Kolaveri-Di and upload on YouTube. If your video can get a million views, can you encash that creativity of yours into some hard cash? Can you host advertisements on your video and make some cash? Do you need Google's permission?
Also, it is interesting to note that Google too cannot place random advertisements on all videos on YouTube. Because, user-uploaded videos are Intellectual Property (IP) of the user and Google cant make money out of its popularity without the user's consent.
Here's the common ground. This is the deal that Google offers.
"You post interesting videos; we will place relevant advertisements on them. Let's split the revenue in 55:45. Users get the larger share. Oh yes, you'll have to sign up for the partner program"
Well, the Google team took additional efforts to emphasize that revenue sharing model is standard across the globe and the company does not negotiate on this.
Here's a video on the partner program.
One can sign up for the partner program through the link below.
When it comes to Social media, to be or not to be; that is no longer the question. The relevant question is, Can you afford to be yourself?
My 19 year old cousin was telling me the other day why he likes Facebook. He said that he could call 'spade a spade' and his bunch of friends on Facebook would understand. He added that FB and Blog were his personal space and mature people would respect it.
I wish, I could tell him it were true. Or better, I wish it were true.
But we know better. Don't we..
Once upon a time in a distant land, there used to be a king. To break the monotony of observing protocols and living a life that conformed to the public scrutiny, he used to make occasional private trips to the nearby jungle. In the jungle for that brief time, he had his personal space. He yelled the unacceptable; sang the forbidden tune; behaved irresponsible and cared for no one. In the unknown and unexplored jungle he relieved his thoughts and feelings that would otherwise remain oppressed. After a brief while he would promptly return to his noble lifestyle. In a way, his brief jungle stints complemented his nobility and helped him have a balanced and satisfied life.
Fast forward to Zuckerberg era. The world has come a long way from Hotmail Ids and Yahoo chatrooms. The jungle of WWW and Social Media is significantly explored and manipulated. The jungle is replete with artificial flora and fauna and creatures pursuing personal agenda. The landscape is full of invisible eyes and ears that is forever trying to identify patterns and make sense out of your random behaviors.
It will be quite a sight when my cousin grows up to realize that the SPADE was monitoring his conversations all the while he called it Spade and his FB friend list will inevitably include his managers, customers and clients.
The irrefutable law of the digital age states that, 'google empowers everyone equally'. Think about it. If you can know a thing or two about the company before you walk into that job interview, be assured the company knows just as much or even more about you.
With all the information that is available online, how would one understand and and interpret people and organizations?
It stands to logic that one gets judged based on your actions. The most consistent online actions are considered behavior; over which opinions are formed and judgment passed.
A good anomaly that I can draw is between the credit rankings as applicable to the banking system and the reputation of a person/organization in the digital world. Just as banks decide ones credibility based on verifiable credit history so do people form an opinion based on your presence/actions on digital space. The set of your actions and coherence in your expressions are vital ingredients to forming an opinion.
So, the bigger question is, will you protect your opinions on the online space; choose to hide or do you seize the opportunity to build yourself a formidable reputation?
Life reminds us of it's invaluable lessons in mysterious ways. I refreshed my lessons at this addictive game of Angry Birds. If you don't know what it is, it may help to read one of my earlier posts 'Angry Birds - The addiction'.
Pretending that the problems don't exist and procrastinating has never helped. The first step is to acknowledge the problem and understand it. As Robert Frost has said, "The best way out of a difficulty is through it". The obstacles come in different forms; just as wood, steel and glass in the game. Also, they could confront us as one big challenge made up of all the individual obstacles.
The key to success is playing by one's strength. To do that one has to know his cards well. Invest time in understanding your key strengths. Just like a piano; once tuned cannot be played forever. It requires tuning often to be in the best of shape. Hone your strengths frequently.
There is a bird for every obstacle just as there is a work around for every problem in life. However complex the obstacles look, there is always a way to overcome them. The trick is to breakdown the challenges into its constituent obstacles and address each one with the appropriate means. It is not hard to understand that the different obstacle takes different approach to beat. Play to your strengths. Break the wood, splatter the glass or blow up the concrete - use the appropriate means for each problem.
Somewhere hidden among all the rubble and chaos are opportunities in our lives. Just the kind that can make your life far more exciting and easier. Keep an eye out for them. Make that extra effort to get them. Nailing these opportunities will help in achieving more than what is seems possible.
One hammer has never fit all the needs; however big it may be. In a team game one has to play with their strength and towards the common goal. Use your birds judiciously. Every bird has a purpose and the key to winning the game lies in approaching the obstacles in strategic moves.
Have you had a feeling that you've been trying hard but the results aren't coming. Are you struck in that elusive rounds wherein, you've felt that there ought to have been one more bird at hand. What will you do in life if you were in one such situation. Will you push it or simply quit? What we persevere at becomes easy. Not that the task becomes easier; our ability to do so gets increased.
If one thing that Angry Birds teach us is that there is more than one way to do things. It is perhaps the best take away from the game. The feeling of learning an easier way to accomplishing things is invaluable; more so after persevering hard at something. In a way, perseverance leads to innovation.
All said and done; its just a game. Lie too, in the end, is not worth taking too seriously. Try not to control everything in life. Let go; explore things and enjoy the ride. Play safe and enjoy your game .. er.. your life.
Of all the flightless birds that there are in this world, two have found extraordinary recognition. Dodo for getting extinct; Angry Birds for seeming to live on forever.
The game was launched in December 2009 on Apple's iOS platform at an initial cost of 100,000 Euros. The game went on to become Apple's top selling paid application by mid 2010. It gets downloaded more than 1 million times within 24 hours of its release on Android Market. The makers of the game generate over USD 1 Million in revenues every month from the advertisements in the free version for Android.
The success of the game is unquestionable. What makes it so popular?
The first and foremost reasons for the widespread adoption is the availability of the game itself on all possible platforms. Rovio ensured that there is a version available for every possible platform that there could be - Windows, MAC, iOS, Andriod, PSP etc. The enthusiasts could easily identify a version appropriate for their device easily. A valuable lesson for marketing folks - The goods ought to hit the stores before you spread the word across. The good ought to be on the shelf, before you tell me so on the television.
Remember the time when you had bought a new game but realized that processor had to be upgraded, the RAM capacity had to be increased or an advanced graphics card to be inserted ? Well, Angry Birds isn't gonna throw up one such scenario. The game does not require heavy processing or display infrastructure.
The game is very easy to understand and play. 5 minutes of fiddling and you'll know all there there is to know about it. 15 mins into the game and you get addicted. As simple as that. There are not too many input parameters to control or master. There is just one sling and a handful of birds. The best part is that the entire game lays before you in one viewing frame unlike many other strategy games that require you to understand a large landscape to play efficiently.
The game does not impress you through its visual extravagance or adrenaline boosting. It gets you hooked through witty challenges bundled in a simple layout. The more the one plays the game, he will understand that Angry Birds is more than just hurling birds at pigs. The little challenges to slingshot the appropriate bird against the right obstacle (Wood, Glass, Metal) keeps one interested.
Now, you read about what I like the most about this game. Do let me know what aspect of it has got you hooked to it.
Soon after the ape man built himself a house and took to farming he craved to be heard and understood by his neighbor. Since then human beings have yearned too much become social beings. To be known, heard, understood and accepted has always been a top priority from then on.
Socialization can be defined in the traditional sense as the "process of accumulating skills and habits necessary for participating within their own society; one that is formed through a plurality of shared norms, customs, values, traditions, social roles, symbols and languages".
For long, the social networking was only possible through personal interactions. Any form of communication demanded the people to be physically present. The concept of reaching out to masses with an idea/information was inconceivable and hence non-existent. It can easily be understood why it took ages for civilizations to evolve. In 1943, Abraham Maslow published his research 'A theory of Human Motivation', wherein he explained that the 'Sense of Belonging' and 'Being Accepted' by fellow men is actually a human need that forms the basis for holding a good self-esteem.
With the advent of mass communication system and in particular the TV challenged the accepted model of social networking. For the first time an idea/opinion could be shared with people at low cost and instantaneously. The culture, values and traditions started to be packaged into interactive programs and beamed to masses. Soon, the multimedia platforms of mass communication became effective tools to reach out to the people and influence their way of thinking, behaviour and opinions.
There was still something missing in the overall picture. A platform was still desired that could actually engage the masses among themselves. It was this need that the internet and the plethora of social networking platforms that followed catered to.
Internet followed the popularity and the availability of the desktops and laptops. The rapid growth and the deep penetration of internet were ideal for the social networking sites to emerge and flourish. In a short span of time platforms like Wikipedia, Youtube, Orkut, Facebook, Twitter took over the bulk of traffic on the internet. Today one can use facebook to be in touch with one's friends. One can share not only his thoughts there but also pictures, videos and just about anything that can be digitally archived. Blogging is in vogue and people air their opinions, ideas, thoughts and reach out to the masses with utmost ease.
For the first time in the history of mankind, the physical and geographical barriers for personal interaction and social networking at large were convincingly shattered. These 'Social Networking Tools' have literally transformed the world from an age of information deficiency to that in which ideas are to be copyrighted as it has become impossible to hide anything from anyone anymore.
These social networks have created a whole world within themselves. They in collaboration with each other are today's most comprehensive database of knowledge and most reliable source of news. They host the most preferred entertainment avenues and are proven tools to influence the likes and dislikes of the people. It is also widely accepted that they decide the fate of a community and a nation at large as demonstrated in the recently held presidential elections in USA.
There are instances of HR/Administrative agencies employing SNA to determine whether or not a particular individual has criminal tendencies. Brand Managers/PR's are another set of people who closely monitor the networks to understand how their brand/product is perceived by the masses. Not to forget the digital marketers to whom the Social Network is THE new marketplace to sell their products.


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Home » News » 100 Years of Adventist Education at Stanborough School
100 Years of Adventist Education at Stanborough School
The weekend of 6-7 July saw crowds of over 1500 people coming together in recognition of something very special within the British Union Conference (BUC). This year 2019 marked the centenary y ear (1919-2019) of Stanborough Primary and Secondary School. To mark this special occasion two events were planned, a Sabbath service held on the Stanborough Park grounds under a marquee, followed by a family fun and recreation day held on the Sunday. Both well-planned events proved to be well supported not only by the Adventist membership but visitors from within the local community.
The Sabbath service saw higher than expected attendance with all 700 seats within the marquee taken and the welcomed task of having to create more seating on the ou tside. The morning's proceedings began with opening remarks and welcome from Judy Clements (Chair of Governors for Stanborough Secondary School) acknowledging the unique and significant moment of Adventist Education in the British Isles. After a 'walk through history' highlighting the past 100 years in picture form, Acting Head for Stanborough Secondary School, Eileen Hussey in her mission report, shared the important values that underpinned the ethos of the School and how its missional outlook has sought to make a positive impact in the life of each pupil.
The morning service planned in a creative way saw intermittent praise and w orship, with greetings from the General Conference Education director, Dr Lisa Beardsley-Hardy and Peter Taylor, Mayor of Watford. Angelika Horwood, Co-Headteacher for Stanborough Primary School led out in the children's story with Heather Hanna whose father, Ivor Margerison, played an instrumental role in the development of Stanborough Secondary School when serving as headteacher.
A representative of SEC Pathfinders led in a procession during the dedication ceremony, which saw the cutting of the ribbon by Peter Taylor and the dedicatory prayer given by South England Conf erence President Dr Emmanuel Osei.
Musical items were p rovided by the Stanborough Secondary School Orchestra and Stanborough Primary School Junior Choir. The main speaker for the day was Dr Daniel Duda, (Trans-European Division Education Director) who spoke on the people of 'The Book', that provides a story to help us see the complexities of life and allows us to understand the principles behind it to allow us to think outside of the box, to reflect, serve better and help change the community.
With the day being bright and sunny the Park provided the perfect setting for lunch which was prepared for all by the BUC Treasurer Earl Ramharacksingh and his committed team of volunteers.
The afternoon segment of the day saw various items taken by the children of Stanborough Secondary and Primary School which included, songs, poems, dram a and instrumental music. Incoming BUC Education director Gina Abbequaye shared a vision for Adventist Education. She spoke of the endless possibilities that can be achieved when home, school and church work together, "we produce children who would, accept God as their Creator… true Adventist Education is not limited to the four walls of the school building… now mor e than ever there is a need for Adventist education," she exclaimed.
The closing vote of thanks was presented by Eileen Hussey and Angelika Horwood, where amongst many who were acknowledged, Kerrine Guthrie, who led the overall planning and coordin ation of the event.
The next day, despite the morning rain the weather turned out to be quite pleasant for the fun day which attracted several hundred people throughout the afternoon.
The weekend proved to be hugely successful considering the many challenges that Adventist Education within the British Isles has faced within the past 100 years. The Adventist schools have prevailed and continues to be a major contributor within the Union in helping prepare children for the kingdom and effective citizens in the community.
However, like most other faith schools today, there are real challenges that lie ahead and if our Adventist schools are to continue in providing an education based on high levels of intellectual and spiritual standards they will need the support of the membership at large and within the entire structure of the Church to ensure it will thrive both now and well into the future under the motto 'Dominus Magister Ludi Nostri' – God is the Master of our School.
[Richard Daly - Photos Costa Vaggas and Theo Guthrie]

redpajama_set_name: RedPajamaCommonCrawl


All 400 E Randolph condos for sale and rent. Extensive building, neighborhood and unit information. We work for you, not the sellers. Request a showing.
400 E Randolph apartments with a condo form of ownership range from studios to 3 bedrooms. Studios have 500 to 650 SF. One bedroom apartments have 525 to 1300 SF. Two bedroom apartments have 1145 to 1400 SF. Penthouses are on the 37th floor.
Most of the condos have balconies. Cooking appliances are gas. All of the units recently got new doors which was determined to be more cost effective than maintaining the nearly 50 year old doors.
Some of the condos have a washer and dryer. Most do not. New laundry hookups can no longer be installed.
400 E Randolph prices range from under $200K to over $1.2M. See the listings below for current list prices.
400 E Randolph was built in 1963 and named Outer Drive East since it was east of Lake Shore Drive at the time. Lake Shore Drive was later moved to the east to remove its s-curve.
Back then it was the world's largest apartment building. The high-rise houses 955 condos in its 40 stories. The building has a domed indoor pool, bike room, sauna, sundeck, exercise room, common laundry, party room, racquetball and basketball court. It also has a dry cleaner, hair salon, restaurant and bar, and a food mart. Parking is leased. Pets are ok.
The T-shaped building provides 3 types of views. Those units on the south side of the building (top of the T) have outstanding views of Lake Michigan, Millennium Park and the city. Those on the north and west side of the building have excellent city views and some have small views of Millennium Park to the south. Those on the east and north side of the building have partial lake views which are interrupted by other high-rises.
400 E Randolph condos are self managed. They do not utilize an outside property management company. You can reach the property management office at (312) 321-0613. The phone number for the front desk is (312) 321-0600. For more information on the condo association see 400 E Randolph Condominium.
400 East Randolph is located between Field Blvd and Harbor Drive just north of Millennium Park. Chicago's lakefront is 2 blocks east. Michigan Avenue is 3 blocks west.
There's a 2-story Marino's grocery store just a block away. A CVS Pharmacy is 3 blocks away. To learn more about the neighborhood visit NewEastside.org.
The building currently has a Walk Score of 86, a Transit Score of 100 and a Bike Score of 82. The #60 Blue Island/26th bus stops in front of 400 E Randolph. The building also has its own shuttle. The stop for almost every L line is half a mile away at State and Lake. There are multiple car sharing services nearby.


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.no je vrhovna internetska domena (country code top-level domain - ccTLD) za Norvešku. Domenom upravlja UNINETT Norid.

Vanjske poveznice
 IANA .no whois informacija

Vrhovne internetske domene država
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sv:Toppdomän#N

redpajama_set_name: RedPajamaWikipedia


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Al Amin reigns supreme in long jump
Myanmar urged to restore full citizenship rights to Rohingyas
Rohingya Crisis
From Russia, no love
Multi-purpose Bangabandhu National Stadium now hosts agriculture
Tribune Report
Published at 09:05 pm January 16th, 2018
Bangabandhu National Stadium, a venue that serves as a multipurpose sports arena has now seen a new use for the outer field as a vegetable cultivation spot. A video on social media recently came to light which showed vegetables being grown at the Paltan end of the stadium. The vegetation stretches from the end of the athletics track till the fences of the spectator gallery. Considering the strangeness of the situation, the commentator expressed his amusement and questions the lack of action taken by the stadium's authority. This might not be the first stadium to host a garden of vegetables, but it is certainly the first in our agrarian country and the soil in the stadium seems well suited to grow the crops.
Five coaching staff members opt out of Pakistan tour
Rabada slammed by Holding, Pietersen after celebration ban
No prize money in BBPL
Khulna, Rajshahi brace for ultimate battle
Bangabandhu National Stadium
Dhaka Stadium


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Aldridge, Texas is a ghost town in Jasper County. Formerly located on the Burr's Ferry, Browndell, and Chester Railroad, the town's economy was based on the lumber industry. However, in the 1910s, the city's sawmill burned down multiple times, and in 1927 the railroad line running through the city was abandoned due to exhaustion of the local wood resources.

References

Geography of Jasper County, Texas


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CATEGORIES green bay packers Chicago Bears Ha Ha Clinton-Dix Josh Josh Blake Martinez Kevin King Josh Hawkins Kentrell Brice Kenny Clark Dean Lowry Clay Matthews Nick Perry Ahmad Brooks Morgan Burnett Featured Chicago Bears Green Bay Packers
Packers Defense in Middle of Youth Movement
The Packers defense is getting younger and it's also getting better.
By ChrisPeterson
The Green Bay Packers dominated the Chicago Bears Thursday night and as well as Aaron Rodgers played, the defense was a huge part of it.
After forcing just two turnovers in the first three games, the Green Bay defense notched four against the Bears Thursday. The Packers also held the Bears to just 14 points, with one touchdown coming in gargabe time.
Through four games, the Packers defense ranks 11th in points allowed with 20.3. The defense also ranks eighth in yards allowed and seventh in pass defense. There is a ways to go, but if Green Bay can consistently hold teams under 20, it will win a lot of games.
Obviously, the Packers haven't had to face a ton of great quarterbacks, but Matt Ryan, Russell Wilson and Andy Dalton, all have impressive resumes. Mike Glennon, not so much, but Green Bay has also faced some of the better receivers in the NFL in A.J. Green, Julio Jones and Doug Baldwin.
So far the defense has held up well and one of the reasons why is the youth movement that is now taking place.
When I was watching the Packers and Bears the other night, it hit me -- a majority of key contributors for the defense are first or second-year players. Think about it.
Kenny Clark, Dean Lowry, Blake Martinez, Marwin Evans and Josh Hawkins are all in their second season with the Packers, while Josh Jones and Kevin King are in their first.
Of course, guys like Mike Daniels, Clay Matthews, Morgan Burnett, Ha Ha Clinton-Dix and Nick Perry have been around, and they are probably still the five best and most important players on that side of the ball. However, youngsters are starting to make an impact at all three levels of the defense and suddenly, a defense that felt slow, seems a lot more athletic.
Martinez has often been the lone true linebacker in the Nitro package and so far in 2017, he has done an exceptional job. He has a team-high 19 tackles, in addition to a sack and a fumble recovery. He's tough, physical, holds up decently in coverage and always seems to be around the ball.
Jones, who is playing alongside him at inside linebacker, even though he's naturally a safety, has also been playing well. He has 16 tackles and two sacks in two weeks and can run sideline-to-sideline. Hawkins also looked good in extended action against Chicago, while Clark and Lowry have both been effective inside in the absence of Daniels.
The defense is also benefiting from veteran additions such as Ahmad Brooks, Quinton Dial and Ricky-Jean Francois (for the second time). It seems Ted Thompson finally learned, that veterans, even if they have aged, can still contribute. Brooks, who has a sack already, has been evidence of that.
But the key to the defensive turnaround, has been the play of the young defensive backs. Kevin King seems to be getting better and better. Brice also had an interception last week.
King, Jones, Brice and Hawkins are going to make mistakes and in fact, they already have. But they are long, they are athletic, and they are getting better.
Green Bay is winning with them now and as the season goes along, logic would dictate that they would only get better. Certainly, anything can happen and nothing is guaranteed, but the Packers have a good history of developing young players and right now, with the defense, that development is paying off.
Chris is a sports journalist from Montana and has been blogging about the Packers since 2011. Chris has been a staff writer for CheeseheadTV since 2017 and looks forward to the day when Aaron Rodgers wins his second Super Bowl. Follow him @thepackersguru
NFL Categories:
Several people pointed out over the last off-season that TT has been in the process of a roster makeover, even though it hasn't necessarily been viewed that way. The only positions that haven't really been touched by it are QB and K...maybe WR.
Still, the example of Atlanta's young defense last season coming together to support the offense on its SB run is a good one to keep in mind.
1 replies + - | show all | hide all
flackcatcher
Packers started their defensive 'makeover' in 2013 concentrating on the LB position. In 2015 they pretty much scrapped their LB group and in 2016 redefined the position by moving Burnett inside and Hyde to the slot. After their successful run to the championship game using what amounted to a proto nitro package the team went all in this year. Picking up in free agency Brice and Evans last year and drafting Jones this year along with Brooks and later Dial on mass cut day, added quality players with the added bonus of Dial's youth. With so many new players on the D side on the ball, it will take time for Capers to get the defensive parts in sync. But even with the injuries, the speed and raw physical ability on this unit shines though. If, IF this unit does not suffer any serious season ending injuries, they could be an excellent defense come playoff time.
ChrisPeterson
I think the biggest thing for me is that the defense has the talent now. I didn't feel that way last year. They might have bad games but there is enough there to be really good. As good as it was a couple years ago when the offense really struggled.
I'd love to see another front-7 guy emerge as a pass-rusher. It would be nice to have another player to divert focus from the other guys. Maybe it will be Vince Biegel or Montravius Adams or Dean Lowry...
croatpackfan
If TT read this site, must have stomach pain - from laughing...
KenEllis
Defense in the middle of ridding itself of some recent God awful premium round TT draft picks.
Datone Jones. Gone.
Quinton Rollins. Deep on the bench.
Damarious Randall. Benched.
Kyler Fackrell. Hopefully relegated to special teams once Odom comes around and Biegel gets activated.
Hard to be a decent D when a two 1sts, a 2nd, and a 3rd all bomb out.
Don't care where the players come from...just find them.
stockholder
Fackrell slow, Rollins slow, Jones slow, Randall swelled head. Defense should be the 1st pick again. Wr 2nd pick.
The TKstinator
Or O-line.
So Josh Jones and Fackrell are slow huh?
Why don't YOU go give us their combine 40 times.
I mean you are the guy who called them slow
Handsback
Right now I'm happy if House comes back next week. If not.....that D is always going to have trouble stopping those passing attacks.
Rossonero
It's partially a youth movement. As noted in the article, the free agents are also providing crucial contributions. Ted must've seen what New England has done and finally realized if he's ever going to compete, he can't do it with 21 and 22 year old projects. Good on him for that.
Seems like a good mix.
On a different note: Dalvin Cook looks like he just blew out a knee...noncontact injury. Maybe that game in two weeks looks a little less daunting.
Yep. Lions won and that defense looks good. Even if their getting away with Holding.
They've got a road win against a good divisional opponent. That was a big win for them.
HankScorpio
The pre-MRI diagnosis is a near complete tear for Cook, according to Ian Rapoport. I hate to see that.
However, the Vikes offense surely did not do much without him today.
The Case Keenum who showed up to play against the Lions was not the Case Keenum who blasted Tampa last week.
The Packers have been fortunate in the sense that, yes, they're beat up. But there are no starters on IR, yet, and they should get most of their starters back for Sunday. It's like playing chess: you can lose pawns all day, but when you start losing back-row pieces is when it starts getting tough. The Vikes losing Cook was like losing a rook or maybe even your queen.
BPEARSON21
Yeah we were good against the Falcons.... lol who cares if our defense is good enough to beat the bears? Seriously who cares..? Our defense has to be good enough to beat the Falcons, Cowboys, Patriots or Chiefs. Are we...? I'll remind you of the last 3 times we played ATL before you answer. The goal is championships right? Then who cares how we play against the cellar dwelling Bears.
That defense with what amounted to 5 SS playing pretty much shut down every teams passing game during the run to NFL championship last year. Yeah, a very damaged secondary got the Packers to the NFL championship last year. Think about that, then ask your question again.
Flackcatcher you think our secondary got us to the NFC championship game...? You think our bottom 5 passing defense last year got us there...? Really..? It was Aaron's rodgers perfection. Remember when Dallas almost came back to win? Or when ATL put up 40+ points in the championship game? If you think the Packers secondary "got us to the championship game" you clearly weren't watching.
Fans see the game differently depending at what they are looking at. With Randall and Rollins playing injured, Gunter became the packers shutdown corner. More often than not Hyde took on the other teams no 2 WR. Burnett played the slot and had their no 3 WR or TE. That's a serious deficit of quickness and speed in the secondary last year. On top of that Capers gambled on going to man up during the 6 game run last year. That secondary with rookie Brice and Clinton-Dix shut down Washington, Lions in the second half, and denied Dallas the end zone twice in the final minutes at Dallas. A: Don't be so snotty. B: Bears still suck. Ha Ha Ha.....
Who cares how they play in a week 2 regular season game either? If the goal is to win championships, all that matters is that they make the playoffs and win each game once there. Through 4 games, they are well on track to accomplishing the goal of making the playoffs. They are showing the possibility of having a team that can accomplish the 2nd part as well.
The Patriots are 1 Tom Brady miracle away from having 3 home losses in 2017. The Falcons just lost to the Bills in Atlanta (aided by a Micah Hyde int) and got all they could handle from those same cellar-dwelling Bears. The Cowboys lost to the Rams at home. The Chiefs have Alex Smith as their QB
The point is that Packer fans watch their team and see every weakness and flaw. And we worry about them. But other teams have flaws, too. The Packers are good enough to beat anyone. We just have to wait for the games to be played to see if they do.
That's fine, I'll wait. I waited all offseason too when I predicted we'd get lit up by ATL again.... don't have to wait on that game it already happened.
I'll wait for us to get torched in the play offs again.
Lemme guess, you think Randall and Rollins are really good players too?
I do agree with you though, I think because of Aaron Rodgers we can beat any team, but I also know our defense isn't close to being elite and will rely on Rodgers to drag us to the finish line.
Wrong guess on Randall and Rollins.
Well we agree on that at least haha
NickPerry
"The Chiefs have Alex Smith as their QB".
I don't think Smith is a bad QB, I actually think he's a pretty good QB. IMO Smith will always be compared to Aaron Rodgers since he was picked 1st overall and 23 picks in front of Rodgers (Or whatever is was).
BUT I agree with your whole comment Hank. Everything you said is right on the money, especially the part about how the Packers played in week 2. The Packers haven't even come close to hitting their stride yet.
"Then who cares how we play against the cellar dwelling Bears."
All I care about is whether the offense and defense are good enough to make them 1-0 on a given week.
Look at Atlanta...they got humbled at home by Buffalo today. Just have to be good enough THIS week...and they weren't.
Buffalo got two weeks of video of Atlanta at home, and it showed. Atlanta's turf advantage went away and their under sized defense exposed. There are no secrets in the NFL.
You are right that the Falcons ate our lunch the last 3 times we played them.
BUT.... lets play them healthy, on grass, in the cold and lets see how they do.....
Since'61
Chris to be fair and accurate, the Packers defense has allowed 67 points in 4 games so far this season for an average of 16.75 points per game. Our opponents have scored 2 defensive TDs against the Packers so far this season and hopefully no more.
So I would revise your article to state that if the Packers defense holds opponents to 17 points or less then the Packers will win most of their games. Shows how well the Packers defense is playing so far this season.
The youth movement is having an impact and it's good to see MM and Capers giving the young and better players the chance to make some plays. Thanks, Since '61
Packer_Fan
I like the youth movement. King, Jones and Hawkins are being given a chance to develop during the year. We need athleticism and speed in the defense. Randall and Rollins just aren't performing well enough to earn their playing time. Yes the Bears are not the offensive juggernaut that can stretch the defense. But we need King, Jones and Hawkins to show if they can get better and be something different than Randall/Rollins.
There seems to be something wrong with Randall. MM is giving us a hint with the phrase "grow up". Until he does, good teams will exploit him. So no reason to play him.
I see the best seven DB are House, King, Hawkins, Jones, Barnett, Dix and Bryce. Keep playing them until they can't perform.
The play of Hawkins really stood out to me. The difference between him and Randall was stark. Unlike Randall, he seemed stride for stride right there with the receiver and used his long arms quite effectively. Hope Hawkins earned himself a start and see if he can become "little Sam Shields" like I read they were calling him in training camp. In with the best and out with the rest. Next man up.
Thegreatreynoldo
" a majority of key contributors for the defense are first or second-year players. Think about it. Kenny Clark, Dean Lowry, Blake Martinez, Marwin Evans and Josh Hawkins are all in their second season with the Packers, while Josh Jones and Kevin King are in their first."
Yeah, that's a pretty reasonable statement. GB has its normal number of bigger money guys on the team: 11 by my count. On D, they'd be CM3, Perry, Daniels, and Burnett. Looks like TT hit a home run with Josh Jones, who is providing an immediate impact. We're getting real solid contributions from Clark (hope for more) and Martinez, and contributions from Lowry, Brice/Evans, and Fackrell. We've gotten some flashes from King and Hawkins.
Brian Lee
I really like Hawkins. I think he once he gains a little more experience Hawkins will be a big upgrade from Randall/Rollins. Donatello Brown will also end up being another big upgrade at CB, possibly later this year but more probably not until next year.
It would not surprise me if Randall and Rollins are both gone by the beginning of next season. Both have poor football instincts leading to getting caught flat-footed and taking extremely poor angles to the ball. Both have absolutely zero ability to follow receivers across the field on crossing patters. When a receiver makes there cut they accelerate away from Randall/Rollins like they are stuck in quicksand.
Almost forgot about Pipkins too.
MarkLee22
I hate to be Negative Nancy again, but we are hearing the same thing every year for about 6 years now.... if the defense comes together, or if the defense matures, or if the defense stays healthy, etc, etc.
Once again we need to count on the arm and even legs (now that Ty and Jamaal are down) of Aaron Rodgers to get us to the promised land.


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Is Android development getting easier?
The biggest problem with Google's open-source software, has always been that it's open-source.
Fantastic for customisability, adding new features, but ends up on hundreds of variations of hardware devices. Different screen sizes, different processors... It's exhausting enough to write about, let alone develop!
However, considering Android has a 70% worldwide smartphone shipment rate (according to IDC in Q4 2012) it's important that...
By Ryan Daws, 08 May 2013, 0 comments. Categories: Android, App Stores, Development Tools, Industry, Platforms, Testing.
Linux kernel 3.4 gets you Android developing
A new Linux kernel 3.4 has been released, according to a post from Linux fellow Linus Torvalds.
Often a huge barrier for aficionados of both Tux and Android; they now play nicely as Linux kernel brings support for development on Google's OS along with SSD caching and other Jelly Bean-sweet improvements.
For Android development, the Goldfish VDE has been the choice inclusion allowing developers to start an instance of Google's software on a kernel...
By Ryan Daws, 03 May 2013, 0 comments. Categories: Android, Development Tools, Industry, Languages, Platforms, Testing.
Apple's iOS 7 to arrive on time
Don't worry Apple fans; you won't have to wait too long for iOS 7.
iOS 7 delay rumors have been shut down, and according to recent reports iOS 7 is on its way. It will be available for a preview release in June and will...
By Mike Brown, 03 May 2013, 0 comments. Categories: Apple, App Stores, Development Tools, iOS, Platforms, Testing.
The Pros & Cons of the major mobile operating systems
Smartphone operating systems often inspire dire loyalty in their users. Once someone owns an iPhone/Android/Windows Phone they rarely switch. But sometimes it's...
By Mike Brown, 02 May 2013, 0 comments. Categories: Android, App Stores, BlackBerry, Design, Development Tools, iOS, Microsoft, Platforms.
Codassium offers real-time "brogramming" with WebRTC
Codassium, an online code platform by Wreally Studios, allows for two parties to conduct a coding session using Mozilla's "Ace" editor alongside live video chat for increased collaboration.
The platform uses the WebRTC standard currently being proposed by W3C who is hoping to use it to provide a web-based suite of tools to share data, audio, and video all in real-time across multiple devices.
Moving beyond collaborative work, this platform could potentially be used to conduct live interviews...
By Ryan Daws, 02 May 2013, 1 comment. Categories: Android, Development Tools, HTML5, Industry, iOS, Platforms, Social media, Testing.
5 steps to becoming an Appreneur
I have been asked on many occasions if making apps really does make you money. Well, I would like to answer that in simple terms. To make money in any industry you need to invest time and effort into your product, from the first...
By Leah Goodman, 02 May 2013, 1 comment. Categories: Android, App Stores, Development Tools, iOS, Monetisation, Platforms.
Windows 8 devs bemoaning lack of ad money
Many developers rely on in-app advertising to fund development; from initial release through to expansion. Windows 8 developers have been wondering, where has their ad revenue has gone?
The advertisements provided in both Windows 8 and mobile OS equivalent Windows Phone 8 is provided by pubCenter.
Since March 31 however, these ads are just not being displayed. Potentially apps which should be getting millions of impressions aren't converting into cash.
So what's happening? Despite many posts on...
By Ryan Daws, 01 May 2013, 0 comments. Categories: Advertising, Analytics, Development Tools, Marketing, Microsoft, Monetisation, Platforms.
Eyes are on WWDC as Apple's stock drops
One of the most highly covered companies in news, rumours, and spectacular leaks, Apple is currently in a lull of new products amidst disappointment in latest software updates.
Stocks in the company relate this by shares heading...
By Ryan Daws, 30 April 2013, 0 comments. Categories: Apple, Development Tools, Industry, iOS, iPad, Platforms.
Do 7-day retention rates matter in mobile apps?
Jason Wu will be a speaker at Kontagent Konnect 2013 in San Francisco on May 20-21. Register now–space is limited.
When it comes to mobile, getting customers to try your application is a challenge, but...
By Kontagent Kaleidoscope, 30 April 2013, 0 comments. Categories: Analytics, Android, App Stores, Industry, iOS, Marketing, Platforms.
iPad remains the number one tablet according to J.D. Power
Many take J.D. Power's satisfaction surveys as the "de facto" source of approval from consumers, taking into account; Performance, Ease of Operation, Styling and Design, Features, and Cost.
Almost consistently dominated by a certain Californian-based company, will Volume 1 of the "2013 U.S. Tablet Satisfaction Study" prove any different?
Nope, Apple's iPad is still up there at the top. The iOS-based device scoring a fantastic 836 on a 1000-point scale; customers are clearly very...
By Ryan Daws, 29 April 2013, 0 comments. Categories: Android, Apple, Devices, Industry, iOS, iPad, Platforms.


Everyone choosing watch is all according to their identity, styles and hobbies. Some are mature, some are energetic, and some are personal. So what kind of watch is suitable for you? Only you can know by your own.
In the following we bring you two kinds of best replica watches. Do they fit for you?
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Designers of the IWC watches are constantly innovating in materials. The titanium cases watches are also inspired by typical F1 racing materials. All details strengthen the usual precision instrument temperament of this wristwatch.
Which Fake Watch Is Suitable For Men In 30 Years Old?


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Q: Why does Python/Django create duplicate files I am new to Django and have gone through the tutorial. The example directory looks like this
polls/
    __init__.py
    models.py
    tests.py
    views.py

mine is slightly different (still works)
polls/
    __init__.py
    __init__.pyc
    models.py
    models.py~
    models.pyc
    tests.py
    views.py

What do the extra file extensions mean? why are there multiple duplicate files?
The extensions added are .pyc and .py~
Thanks

A: pyc files are python compilation files - It contains byte code that the Python interpreter compiles from the source file.
So, once you run the application, pyc files are created automatically.
py~ are temporary/backup files - It is created by the editor to save the previous versions of the file.


Painting a room can be a quick, transformative update for new homeowners to accomplish. Offer these tips to help them get started.
Find out the most searched-for home furniture items based on Google shopping data and broken down by state.
Asbestos is only considered dangerous when contaminated materials have been worn down or damaged, which is a standard part of most renovation or remodeling work.
What's your home improvement persona: The Sensible Improver, the Project Planner, the Reliable Renovator, the Visionary, or the Extrovert? View this infographic.


The rpart package. It's crantastic!
rpart_4.1-13. Released about 1 year ago.
rpart_4.1-12. Released over 1 year ago.
rpart_4.1-11. Released about 2 years ago.
rpart_4.1-10. Released almost 4 years ago.
rpart_4.1-9. Released about 4 years ago.
rpart_4.1-8. Released about 5 years ago.
rpart_4.1-7. Released about 5 years ago.
rpart_4.1-6. Released about 5 years ago.
rpart_4.1-5. Released about 5 years ago.
rpart_4.1-4. Released over 5 years ago.
rpart_4.1-3. Released over 5 years ago.
rpart_4.1-2. Released over 5 years ago.
rpart_4.1-1. Released about 6 years ago.
rpart_4.1-0. Released over 6 years ago.
rpart_4.0-3. Released over 6 years ago.
rpart_4.0-2. Released over 6 years ago.
rpart_4.0-1. Released over 6 years ago.
rpart_3.1-55. Released over 6 years ago.
rpart_3.1-54. Released almost 7 years ago.
rpart_3.1-53. Released almost 7 years ago.
rpart_3.1-52. Released about 7 years ago.
rpart_3.1-51. Released over 7 years ago.
rpart_3.1-50. Released about 8 years ago.
rpart_3.1-48. Released over 8 years ago.
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rpart_3.1-45. Released over 9 years ago.
rpart_3.1-44. Released almost 10 years ago.
rpart_3.1-41. Released about 11 years ago.
rpart_3.1-38. Released over 2018 years ago.
No one has written a review of rpart yet. Want to be the first? Write one now.
Search for rpart on google, google scholar, r-help, r-devel.
Visit rpart on R Graphical Manual.


text:
Q: Android Studio gives error can't run the app When I open Android Studio after closing suddenly Android Studio reports an error Could not reserve enough space for 1572864KB object heap and the RUN button is disabled. How can I recover?
To see error click here
This Image describe the problem.

A: After some time i find the solution. The gradle.properties file contains the error. The HeapSize for configure gradle is not correct i replace the -Xmx1572m with -Xmx1024m and close the android project and open it again and sync it, rebuild it.


text:
Royal Enfield bicycle with motor still a neat idea
The history of Royal Enfield is simple: build a bike, then add a motor.
Mankind's urge to travel farther, faster has taken the Royal Enfield brand name on a curious, circular journey.
Founded in England to make bicycles, it added motors to the bicycles and went on to earn its greatest reputation making motorcycles, first in England and, now, in India.
Along the way, an almost unrelated line of Royal Enfield bicycles, manufactured in Asia, were sold in the U.S.
Inevitably, some of these Asian bicycles have been motorized, creating vehicles that might have been recognized by the early factory workers in Redditch.
Reader Jeffrey Baker pointed out this ad, on CraigsList, for one of these U.S. market bicycles, which date from the 1980s, equipped with a tidy looking motor.
This English style motorized bicycle is for sale for $450 in Uxbridge, Mass. The seller writes that he would be willing to trade for a motorized helicopter!
The motor appears to be a SkyHawk two-stroke, which comes as a complete kit, from China. According to the company that markets it, Spooky Tooth Cycles, the little motor is surprisingly sophisticated:
"To meet the strict 2008 US EPA/CARB importation restrictions, all SkyHawk motors are now equipped with a catalytic converter exhaust muffler which incorporates a Palladium Cartridge filter imported from Germany."
The tank is black powder coated, with internal chrome plating. The fuel valve is brass instead of the more common aluminum, the company boasts.
Just as comforting is the promise that assembly instructions come "in clear English."
In a burst of transparency, the company identifies its motor as a true 66cc, although it is in the category of Asian motor normally sold as 80cc.
The difference, it explains, is that "in the East, the displacement of an engine includes the area of the cylinder head's combustion chamber as well as the volume of the cylinder. In the U.S. however, the volume of the cylinder is only considered when identifying engine displacement."
Cost of the bicycle engine kit is $225. Spooky Tooth says it will deliver 150 miles per gallon, and speeds of 19 to 45 mph depending on gear ratio.
Labels: bicycle


text:
#ifndef ALIESDCALOCELLS_H
#define ALIESDCALOCELLS_H

//-------------------------------------------------------------------------
/// \class AliESDCaloCells
/// \brief Class for calorimeter cell ESD data handling
///
/// ESD class to store calorimeter cell data
/// Clone of AliAODCaloCells made by Markus Oldenburg, CERN.
///
/// Data is stored in different arrays, each entry of the array corresponding to a cell.
/// The data stored is the cell energy, time, high gain bool, absolute id number,
/// MC label that deposited most energy, and a container for the MC embedded energy.
///
///  \author Gustavo Conesa Balbastre, <Gustavo.Conesa.Balbastre@cern.ch>, LPSC-Grenoble
///
//-------------------------------------------------------------------------

#include <AliVCaloCells.h>
#include <TMath.h>

class AliESDCaloCells : public AliVCaloCells
{
 public:

  AliESDCaloCells();
  AliESDCaloCells(const char* name, const char* title, VCells_t ttype=kUndef);
  AliESDCaloCells(const AliESDCaloCells & cells);
  AliESDCaloCells & operator=(const AliESDCaloCells& source);
  virtual ~AliESDCaloCells();

  virtual AliVCaloCells * CopyCaloCells(Bool_t all) const;
  virtual void    Copy(TObject &obj) const;
  void            Clear(const Option_t*);
  void            CreateContainer(Short_t nCells);
  void            DeleteContainer();
  void            Sort();

  Bool_t          IsEMCAL()  const { return (fType == kEMCALCell); }
  Bool_t          IsPHOS()   const { return (fType == kPHOSCell) ; }
  Char_t          GetType()  const { return  fType               ; }
  void            SetType(Char_t t){ fType = t                   ; }

  inline Bool_t   GetCell(Short_t pos, Short_t &cellNumber, Double_t &amplitude, Double_t &time, Int_t &mclabel,      Double_t &efrac) const;
  Bool_t          SetCell(Short_t pos, Short_t  cellNumber, Double_t  amplitude, Double_t  time, Int_t  mclabel = -1, Double_t  efrac = 0., Bool_t isHG=kFALSE);

  Short_t         GetNumberOfCells() const  { return fNCells ; }
  void            SetNumberOfCells(Int_t n) { fNCells = n    ; }

  inline Double_t GetCellAmplitude(Short_t cellNumber);
  inline Bool_t   GetCellHighGain(Short_t cellNumber);  //is this cell High Gain
  inline Short_t  GetCellPosition(Short_t cellNumber);
  inline Double_t GetCellTime(Short_t cellNumber);

  inline Double_t GetAmplitude(Short_t pos) const;
  inline Bool_t   GetHighGain(Short_t pos) const;
  inline Double_t GetTime(Short_t pos) const;
  inline Short_t  GetCellNumber(Short_t pos) const;

  // MC & embedding
  inline Int_t    GetCellMCLabel(Short_t cellNumber) ;
  inline Int_t    GetMCLabel(Short_t pos) const ;

  inline Double_t GetCellEFraction(Short_t cellNumber) ;
  inline Double_t GetEFraction(Short_t pos) const ;

  inline void     SetEFraction    (Short_t pos,         Double32_t efrac) ;
  inline void     SetCellEFraction(Short_t cellNumber,  Double32_t efrac) ;

 protected:

  Int_t       fNCells;       ///< Number of cells

  /// If Cell is High Gain or Low Gain
  Bool_t     *fHGLG;         //[fNCells]

  /// Array of cell absolute Id. numbers.
  Short_t    *fCellNumber;   //[fNCells]

  /// Array with cell amplitudes (= energy!).
  Double32_t *fAmplitude;    //[fNCells][0.,0.,16]

  /// Array with cell times.
  Double32_t *fTime;         //[fNCells][0.,0.,16]

  /// Array with fraction of MC energy and data - for embedding.
  Double32_t *fEFraction;    //[fNCells][0.,0.,16]

  ///  Array of MC labels, each label is the highest contributor to the cell signal.
  Int_t      *fMCLabel;      //[fNCells]

  Bool_t      fIsSorted;     //!<! True if cell arrays are sorted by index.

  Char_t      fType;         ///< Cell type.

  /// \cond CLASSIMP
  ClassDef(AliESDCaloCells, 5) ;
  /// \endcond

};

///
/// Given the position index in the array, return the cell parameters.
///
/// \param pos: Index of cell in array
/// \param cellNumber: Absolute cell Id. number
/// \param amplitude: Cell energy
/// \param time: Cell time
/// \param mclabel: MC particle index in kine tree
/// \param efrac: Fraction of energy (embedding)
///
/// \return True if pos is correct not negative or larger than expected.
///
Bool_t AliESDCaloCells::GetCell(Short_t pos, Short_t &cellNumber, Double_t &amplitude,
                                Double_t & time, Int_t & mclabel, Double_t & efrac) const
{
  if (pos>=0 && pos<fNCells)
  {
    cellNumber = fCellNumber[pos];
    amplitude  = fAmplitude[pos];
    time       = fTime[pos];

    if(fMCLabel)   mclabel = fMCLabel[pos];
    else           mclabel =-1 ;
    if(fEFraction) efrac   = fEFraction[pos];
    else           efrac   = 0 ;

    return kTRUE;

  } else
  {
    return kFALSE;
  }
}

///
/// \return Cell amplitude (GeV).
/// \param cellNumber: Cell absolute Id.
///
Double_t AliESDCaloCells::GetCellAmplitude(Short_t cellNumber)
{
  if (!fIsSorted) {
    Sort();
    fIsSorted=kTRUE;
  }

  Short_t pos = TMath::BinarySearch(fNCells, fCellNumber, cellNumber);
  if (pos>=0 && pos < fNCells && fCellNumber[pos] == cellNumber ) {
    return fAmplitude[pos];
  } else {
    return 0.;
  }
}

///
/// \return True for high gain, False for low gain.
/// \param cellNumber: Cell absolute Id.
///
Bool_t AliESDCaloCells::GetCellHighGain(Short_t cellNumber)
{
  if (!fIsSorted) {
    Sort();
    fIsSorted=kTRUE;
  }

  Short_t pos = TMath::BinarySearch(fNCells, fCellNumber, cellNumber);
  if (pos>=0 && pos < fNCells && fCellNumber[pos] == cellNumber ) {
    if(fHGLG)
      return fHGLG[pos];
    else{
      if(fMCLabel)//old version of ESD, for data HG flag stored in MCLabel
        return !(fMCLabel[pos]==-2) ;
      else
	return kTRUE ;
    }
  } else {
    return kFALSE;
  }
}

///
/// \return Cell time (s).
/// \param cellNumber: Cell absolute Id.
///
Double_t AliESDCaloCells::GetCellTime(Short_t cellNumber)
{
  if (!fIsSorted) {
    Sort();
    fIsSorted=kTRUE;
  }

  Short_t pos = TMath::BinarySearch(fNCells, fCellNumber, cellNumber);
  if (pos>=0 && pos < fNCells && fCellNumber[pos] == cellNumber) {
    return fTime[pos];
  } else {
    return -1.;
  }
}

///
/// \return Cell amplitude (GeV).
/// \param pos: Cell position in array.
///
Double_t AliESDCaloCells::GetAmplitude(Short_t pos) const
{
  if (pos>=0 && pos<fNCells) {
    return fAmplitude[pos];
  } else {
    return 0.;
  }
}

///
/// \return True for high gain, False for low gain.
/// \param pos: Cell position in array.
///
Bool_t AliESDCaloCells::GetHighGain(Short_t pos) const
{
  if (pos>=0 && pos<fNCells) {
    if(fHGLG)
      return fHGLG[pos];
    else{
      if(fMCLabel)//old version of ESD, for data HG flag stored in MCLabel
        return !(fMCLabel[pos]==-2) ;
      else
	return kTRUE ;
    }
  } else {
    return kFALSE;
  }
}

///
/// \return Cell time (s).
/// \param pos: Cell position in array.
///
Double_t AliESDCaloCells::GetTime(Short_t pos) const
{
  if (pos>=0 && pos<fNCells) {
    return fTime[pos];
  } else {
    return -1.;
  }
}

///
/// \return Cell absolute Id. number.
/// \param pos: Cell position in array.
///
Short_t AliESDCaloCells::GetCellNumber(Short_t pos) const
{
  if (pos>=0 && pos<fNCells) {
    return fCellNumber[pos];
  } else {
    return fNCells;
  }
}

///
/// \param cellNumber: Cell absolute Id. number.
/// \return Cell position in array.
///
Short_t AliESDCaloCells::GetCellPosition(Short_t cellNumber)
{
  if (!fIsSorted) {
    Sort();
    fIsSorted=kTRUE;
  }

  Int_t nabove, nbelow, middle;
  Short_t pos = -1;

  nabove = fNCells + 1;
  nbelow = 0;
  while (nabove - nbelow > 1) {
    middle = (nabove + nbelow) / 2;
    if (cellNumber == fCellNumber[middle-1]) {
      pos =   middle - 1;
      break;
    }
    if (cellNumber  < fCellNumber[middle-1]) nabove = middle;
    else                                     nbelow = middle;
  }

  return pos;
}

///
/// \return MC label of highest contributor particle depositing energy in cell.
/// \param pos: Cell position in array.
///
Int_t AliESDCaloCells::GetMCLabel(Short_t pos) const
{
  if (pos>=0 && pos<fNCells && fMCLabel) {
    return fMCLabel[pos];
  } else {
    return -1 ;
  }
}

///
/// \return Fraction of energy in cell from embedding.
/// \param pos: Cell position in array.
///
Double_t AliESDCaloCells::GetEFraction(Short_t pos) const
{
  if (pos>=0 && pos<fNCells && fEFraction) {
    return fEFraction[pos];
  } else {
    return 0.;
  }
}

///
/// \return MC label of highest contributor particle depositing energy in cell.
/// \param cellNumber: Cell position in array.
///
Int_t AliESDCaloCells::GetCellMCLabel(Short_t cellNumber)
{
  if (!fIsSorted) {
    Sort();
    fIsSorted=kTRUE;
  }

  Short_t pos = TMath::BinarySearch(fNCells, fCellNumber, cellNumber);
  if (pos>=0 && fCellNumber[pos] == cellNumber && fMCLabel) {
    return fMCLabel[pos];
  } else {
    return -1;
  }
}

///
/// \return Fraction of energy in cell from embedding.
/// \param cellNumber: Absolute Id number of cell.
///
Double_t AliESDCaloCells::GetCellEFraction(Short_t cellNumber)
{
  if (!fIsSorted) {
    Sort();
    fIsSorted=kTRUE;
  }

  Short_t pos = TMath::BinarySearch(fNCells, fCellNumber, cellNumber);
  if (pos>=0 && pos < fNCells && fCellNumber[pos] == cellNumber && fEFraction) {
    return fEFraction[pos];
  } else {
    return 0.;
  }
}

///
/// Set Fraction of energy in cell from embedding.
/// \param pos: Cell position in array.
/// \param efrac: fraction of energy.
///
void AliESDCaloCells::SetEFraction(Short_t pos,  Double32_t efrac)
{
  if (pos>=0 && pos < fNCells)
  {
    if(!fEFraction) fEFraction = new Double32_t[fNCells];
    fEFraction[pos]  = efrac;
  }
}

///
/// Set fraction of energy in cell from embedding.
/// \param cellNumber: Absolute cell Id. number of cell.
/// \param efrac: fraction of energy.
///
void AliESDCaloCells::SetCellEFraction(Short_t cellNumber, Double32_t efrac)
{
  if (!fIsSorted) {
    Sort();
    fIsSorted=kTRUE;
  }

  Short_t pos = TMath::BinarySearch(fNCells, fCellNumber, cellNumber);
  if (pos>=0 && pos < fNCells && fCellNumber[pos] == cellNumber)
  {
    if(!fEFraction) fEFraction = new Double32_t[fNCells];
    fEFraction[pos] = efrac;
  }
}

#endif

redpajama_set_name: RedPajamaGithub


text:
Q: multiple tables on one template When I render two or more tables on same template I get several deprecations like this one
DEPRECATION: You modified (mut bodyContent) twice in a single render. This was unreliable in Ember 1.x and will be removed in Ember 2.0 [deprecation id: ember-views.render-double-modify]
Furthermore, tables are loading very slow, they are buggy and unreliable - most of the time tables are populated with data, but it even happens that they stay empty - like there is a race condition problem.
Does anyone have an idea what could be a problem?

A: This probably is not a best practice solution, but it does the job. I noticed that when components are rendered at the same time, it takes much more time for rendering. The trick then is to delay rendering of second component, 100ms was enough for me, and after that components are rendered instantly without noticing any lag. I also experienced much longer rendering times in Mozilla Firefox, than in Chrome.

A: you need need probably wrap your code with following:
Ember.run.scheduleOnce('afterRender', this, function(){
// error causing code
})

it insures that it is invoked once after render.