text:
Graduate - Sydney College of Osteopathy - Sydney College of Chiropractic
International College of Applied Kinesiology
Member Chiropractic & Osteopathic College of Australasia (COCA)
Myofascial Trigger Point Dry Needling Neuromuscular Procedures, Biopuncture
Non-Surgical Solutions for Tendinopathy, Tenosynovitis, Bursitis & Knee Cartilage
Article by Dr Peter Richard Pedersen
For decades, European doctors have prescribed diabetic patients a fat-soluble form of vitamin B1 called benfotiamine to treat neuropathies and help prevent complications such as blindness, kidney failure, heart attack, and limb amputation.
Benfotiamine blocks destructive biochemical pathways that enable high blood sugar levels to damage nerves and small blood vessels.
Benfotiamine also inhibits the formation of advanced glycation end products in both diabetic and normal aging organisms. Glycation not only causes kidney, nerve, and retinal damage in diabetics, but is also a significant contributory factor in cardiovascular disease and other aging disorders in adults without diabetes.(1-6)
Here, we'll explore how to use benfotiamine to help protect against the dangers of elevated blood sugar and toxic glycation reactions.
Sugar molecules, in excess quantity or over long periods of time, wreak havoc on human tissues. As the number of people with type 2 diabetes has skyrocketed over the past 20 years, we've learned to recognize strong relationships between blood sugar levels and many chronic conditions previously thought to be purely age-related. The link seems to be the total lifetime exposure to blood sugar that's the culprit. In other words, diabetics develop problems sooner because of their chronic higher sugar levels, but even non-diabetic people eventually suffer tissue injury related to the interaction between blood sugar and tissue proteins.
Studies of diabetic patients have shown that prolonged tissue exposure to elevated glucose levels results in the production of a class of molecules called "advanced glycation end products" (AGEs).(1-4)
These molecules are proteins and lipids that have become bonded to some of the sugar molecules found in high concentrations in diabetics' blood.(5)
Advanced glycation end products are well known for their destructive activities in diabetes, where they contribute to vascular disease, kidney failure, eye damage, and other kinds of dysfunction,(5,6) including the nerve damage known as diabetic peripheral neuropathy.(3,4,7)
In patients with this kind of neuropathy, AGEs directly damage vital components of nerve cells,(8) insidiously reducing their ability to conduct warning sensations such as pain and pressure.
People with peripheral neuropathies may not perceive the need to shift their weight, for example, to allow an even distribution of blood flow to a pressure point such as the buttock or foot.(9) Inadequate blood flow to such areas in turn can result in tissue death (necrosis), producing pressure sores that invite infection.(10) And because AGEs also impair immune function, those infections in vulnerable diabetic patients can rapidly become life- and limb-threatening; in fact, amputation of an entire extremity can often be the only treatment if the condition cannot be prevented (foot infections are the single most common cause of hospitalization and amputations in persons with diabetes).(11)
Our rapidly expanding experience with the diabetic population has taught us that the AGE-related damage to tissues involves a specific chemical receptor that responds to the presence of AGE molecules by inducing inflammation. That receptor molecule is appropriately termed RAGE (for "receptor for AGE").(8)
And we're learning that it's not just diabetics who are affected—with enough time and exposure, we all develop "AGE-related" problems.(6)
Ominously, AGE/RAGE reactions occur even in people without known diabetes or insulin resistance, although those conditions hasten the process.(12)
With advancing age, even normal blood sugar levels, given sufficient time, produce AGEs that act on RAGEs to induce deadly inflammation in blood vessels, nerves, liver, and other vital tissues.(6,13,14)
A growing number of studies are now demonstrating links between levels of AGEs in the blood of non-diabetics and major risk factors for atherosclerosis and heart disease.(15,16)
Credible scientists have even speculated that these AGE-related changes could ultimately contribute to an "upper limit" of the human life span(1,7 ) with the implication that if we could prevent them from happening, we could conceivably extend human life expectancy dramatically!
One of the most important natural anti-AGE compounds is vitamin B1, or thiamine, and its natural derivative, benfotiamine. Thiamine is a well-known nutrient that has myriad roles throughout the body, particularly in maintaining the healthy, normal functioning of nerve cells.18 Thiamine has been shown to interfere with the AGE/RAGE process in meaningful ways.(19,20)
A vivid demonstration of thiamine's ability to block AGE production and its effects in the laboratory was provided in 1996 by researchers in Italy, who subjected cells in culture to high glucose levels both with and without thiamine supplementation.(21)The researchers measured the cells' ability to function normally and also their production of AGE molecules. High glucose inhibited normal cell reproduction and metabolic activity—but the addition of thiamine significantly reduced total AGE formation, increased cell survival, and restored reproductive activity to normal levels.(21)
These findings and those of other laboratory investigators have led to calls for trials of high-dose thiamine to prevent glycation-induced damage to nerve cells8and other tissues such as the liver, where AGE-induced damage plays a key role in the development of cirrhosis.(5,22)
Scientists in Toronto were able to prevent glycation damage to liver cells in culture by supplementing them with thiamine.(23) They also showed that when liver cells were made thiamine-deficient, they were susceptible to damage at much lower levels of glycation products than were normal cells, which suggests that avoiding thiamine deficiency might be an important cirrhosis-prevention strategy.
And Indian researchers recently demonstrated the potential anticancer activity of thiamine.(24) They discovered thiamine to be one of the B vitamins that blocks the production of free radicals by AGE molecules, which in turn prevents dangerous DNA injury that can lead to cancer initiation.
These promising results with thiamine supplementation led to the natural question: why not simply use high-dose thiamine to prevent AGE formation in diabetics, and perhaps even in non-diabetic people as well? The answer is based on the concept of bioavailability—not all beneficial molecules are equally well absorbed from the digestive tract, and once absorbed, they may be extensively metabolized and/or poorly penetrate target tissues. Water-soluble nutrients like thiamine are well absorbed, but tend not to penetrate lipids to any great degree (oil and water don't mix well)—so they aren't as bioavailable to target tissues that are composed of lipids (fats). This is in part because cell membranes themselves are primarily made up of lipid molecules.
Thus, as a water-soluble vitamin, thiamine has an upper dose limit beyond which additional quantities are simply excreted in urine.(25,26) Clearly, for the beneficial anti-AGE effects and related reduction in inflammatory markers to be realized, a better means of delivering thiamine to tissues is needed. Fortunately, thiamine's fat-soluble cousin benfotiamine is a highly bioavailable nutrient that achieves better distribution throughout the body.(27,28)
Advanced glycation end products (AGEs) are produced in most tissues exposed to elevated blood sugar levels, and even in tissues exposed to normal blood sugar for a long enough time.
Advanced glycation end products induce oxidative stress and inflammation, and are responsible for a large amount of tissue damage and dysfunction in diabetic patients. They are increasingly being recognized as harmful in non-diabetic people as well.
The fat-soluble thiamine-derived nutrient benfotiamine blocks three of the major biochemical pathways through which high blood sugar promotes tissues damage—without known side effects. Benfotiamine can reach tissues more than five times more readily than thiamine (vitamin B1) itself, and has been widely used in Europe for decades.
An explosion of laboratory and human data now demonstrate that benfotiamine can block the actual tissue-level effects of AGEs and prevent their potentially deadly consequences in both diabetic and non-diabetic people.
Benfotiamine is better than thiamine at penetrating cell membranes and protecting AGE-vulnerable tissues from harmful glucose-protein and glucose-lipid reactions, helping to protect nerve, retinal, kidney, and other cells. Studies suggest that the benefits of benfotiamine may greatly outpace those of thiamine. Biochemical nutritionists at the Friedrich Schiller University in Germany studied three thiamine preparations in seven healthy volunteers and evaluated the bioavailability of each compound.(29)
Subjects took 100 mg of either benfotiamine, thiamine disulfide, or fursultiamin (another thiamine derivative), and their blood levels of thiamine were measured repeatedly over a 10-hour period, along with biochemical markers of whether cells were actually "seeing" the effects of thiamine. Benfotiamine produced a more rapid and earlier increase in blood and displayed significantly increased bioavailability, compared with either of the other two formulations. These researchers concluded that benfotiamine is the best form of thiamine for therapeutic use.
The same researchers found similar results in a more detailed study of benfotiamine versus thiamine mononitrate in patients with end-stage renal disease (who are frequently thiamine-deficient).(30) Subjects who received 100 mg/day of benfotiamine had faster and higher peak levels than those receiving standard thiamine supplements, achieving nearly double the levels and allowing an amazing 420% increase in total 24-hour tissue exposure after a single dose. These results were interpreted as further justification for the use of benfotiamine in patients who require high intracellular concentrations of thiamine. Later studies from the same group demonstrated that the elevated tissue levels produced by benfotiamine markedly increased the all-important cellular content,(31) providing conclusive evidence of benfotiamine's overall superiority to thiamine in blocking formation of AGEs and the RAGE reactions that follow. Benfotiamine's anti-AGE activity has now been shown to be superior to that of thiamine alone in the treatment of neurodegenerative diseases and cancer,(32) as well as on the kidney, eye, and nerve damage seen in diabetic patients.(4)
It is clear that benfotiamine can reach AGE-vulnerable tissues and cells at high levels. In looking at how benfotiamine performs at actually preventing the AGE/RAGE reactions from taking place, Italian scientists collaborating with the World Health Organization studied its effects in correcting endothelial cell damage caused by elevated glucose levels(33)—just the kind of damage we know is caused by AGEs in both diabetic and non-diabetic people. The researchers cultured human endothelial cells in normal and very high glucose concentrations, treating them with benfotiamine or thiamine, and measuring the cells' survival and rates of healthy reproduction. The high glucose levels predictably impaired cell replication by nearly 30%—and addition of thiamine raised survival to 80% of normal, while benfotiamine raised it to nearly 90%! Benfotiamine also cut AGE production in the high-glucose environment from 160% of normal to similar levels found in healthy glucose-exposed cells. The scientists speculated that these dramatic effects resulted from benfotiamine's ability to help cells use glucose more efficiently, reducing the level of waste products that are most active in producing AGEs.
Studies in animals powerfully support these encouraging findings with research from a number of quarters revealing the benefits of benfotiamine in preventing diabetic complications. German researchers working with diabetic rats studied the effects of benfotiamine and thiamine on nerve function and on the formation of AGEs in nerve tissue.(28) In one group of animals, they studied the preventive effects of the supplements, administering them immediately after diabetes was chemically induced. A second group of animals received supplements only two months later, to study the supplements' treatment effects. As expected, nerve conduction speeds dropped off in diabetic animals, while AGE levels increased by up to five-fold. In the prevention group, nerve conduction increased substantially compared with control animals, and was nearly normal by six months in the benfotiamine-supplemented group (no further improvement was seen after three months in the thiamine-supplemented animals). Remarkably, similar results were also found in the benfotiamine treatment group—but not in the thiamine-treated animals. Benfotiamine also dramatically reduced AGE formation in nerve cells, which probably explains its dramatic effects. These researchers concluded that "timely administration of benfotiamine was effective in prevention of functional damage and of AGE formation in nerves of diabetic rats"—a radically promising finding!
In 2003, British researchers treated rats with benfotiamine and thiamine aimed at preventing diabetic nephropathy (kidney disease), a condition that is associated with a very high risk of cardiovascular disease and death.(34) They found that high-dose therapy with benfotiamine and thiamine prevented the accumulation of molecules that trigger the formation of AGEs, oxidative stress, and inflammation—the major factors that ultimately produce kidney damage. They also found that kidney function actually improved in the animals treated with benfotiamine and thiamine, demonstrating not only biochemical but actual whole-organism benefits.
In related studies, German and American physicians showed that treating diabetic rats with high doses of benfotiamine prevented retinopathy, another complication of diabetes.(35) The researchers pointed out that benfotiamine works by simultaneously inhibiting three major pathways by which high sugar levels cause tissue damage, such as retinopathy.(36) Benfotiamine was also shown to stimulate a key enzyme called transkelotase, which converts potentially damaging glucose breakdown products into harmless compounds that are safely eliminated. Together, these actions make benfotiamine a front-runner in preventing the development of diabetic complications.35,36
Another important and life-threatening complication of diabetes is the heart condition known as diabetic cardiomyopathy, in which individual heart muscle cells cannot contract as strongly as they normally would. The reasons for these changes are only partially understood, but appear to be related both to oxidative stress and inflammation at least in part caused by AGEs affecting the contractile proteins that cause heart muscle cells to beat.(37-40)
Cardiovascular and alternative medicine researchers at the University of Wyoming put these ideas to the test, treating mice with benfotiamine therapy 14 days after inducing diabetes in the animals. They then studied characteristic features of heart muscle performance that indicated how strongly the hearts were beating and how well the heart tissue responded to chemical signals. Astonishingly, benfotiamine treatment abolished the muscle cell abnormalities induced by diabetes in these animals! Oxidative stress was also measurably reduced though in this short-term study, the researchers did not find effects on AGEs.(41)
Bizarrely, AGEs are formed by the interaction of glucose and proteins through a specific kind of chemical reaction, called the "Maillard" reaction, that is identical to the so-called "browning reactions" found in ripening fruits and foods cooked at high temperatures.(58,59) Maillard reactions are distinctly unwelcome in human tissues, where their AGE-related products produce powerfully destructive oxidative stress and inflammatory reactions,(6,15,19) which ultimately lead to atherosclerosis and its deadly consequences.(6,15) By "cross-linking" with collagen and other long-lived proteins, AGEs have far-reaching deleterious effects by reducing the elasticity of tissues such as blood vessels where these proteins reside.(60) Furthermore, the biochemical changes induced by AGEs may also damage DNA,(24) which, together with inflammation, can promote the development of cancer.(57)
Clearly, the Maillard "browning" reactions occur all the time in our bodies, gradually adding to our burden of oxidative stress, inflammation, and tissue dysfunction—and ultimately to our cumulative risk of serious chronic age-related diseases.
Further research has also shown that benfotiamine is effective at preventing slow-to-heal pressure sores, which are a major cause of suffering and even death in diabetic patients. A group of researchers in Italy used benfotiamine to speed the healing of such wounds.(42) Diabetic mice were given oral benfotiamine or a control liquid, and then underwent ischemia (restricted blood flow) of one limb. The scientists then measured tissue indicators of cell death and destruction. Remarkably, benfotiamine completely prevented ischemia-induced necrosis (tissue death) in animals' toes, improved blood flow and oxygenation, and restored normal blood vessel relaxation (an important control mechanism that is lost in AGE-induced endothelial injury). But that's not all—closer microscopic examination of the tissue showed substantially improved new blood vessel formation and inhibition of cell death in the affected limbs. Supplementation also prevented accumulation of AGEs in the blood vessels, which probably accounts for the remarkable benefits. The authors were understandably exuberant in their concluding statement, "We have demonstrated, for the first time, that benfotiamine aids the post-ischemic healing of diabetic animals…"
An explosion of convincing animal studies further supports benfotiamine's remarkable benefits. Benfotiamine has now been shown to counteract AGE-related toxicity on endothelial cells,(43) to relieve inflammatory and neuropathic (nerve-induced) pain in both diabetic and non-diabetic rats,(44) and to alleviate diabetes-induced oxidative damage to brain tissue.(45) Interestingly, benfotiamine's protective effect on brain tissue is produced by mechanisms that seem to be unrelated to AGE formation, opening the door to even greater benefits in this area!
There is clearly no doubt that benfotiamine has proven itself in laboratory studies, and research is now yielding convincing evidence from human trials as well. Dramatic results are flowing in from top-level researchers around the world, demonstrating that benfotiamine's potent AGE/RAGE inhibition translates directly into measurable benefits for humans.
Since benfotiamine has such potent anti-AGE and oxidative stress-reducing effects, scientists wondered if it would be helpful in treatment of diabetic neuropathies in humans. To investigate, German researchers conducted a randomized, double-blind, controlled study of benfotiamine plus vitamins B6 and B12 in patients with diabetic polyneuropathy.(46) This study of 24 patients lasted 12 weeks, and demonstrated dramatic improvement in nerve conduction velocity (the speed with which electrical signals move along nerves) in benfotiamine recipients versus controls. There was also an improvement of patients' ability to sense vibration (again, an important measure of the ability to perceive pressure and motion). None of the patients experienced side effects related to treatment. These researchers concluded that benfotiamine (in combination with the B vitamins) "represents a starting point in treatment of diabetic polyneuropathy."
Three years later, Hungarian researchers conducted dose-finding studies of benfotiamine. These scientists treated patients who had painful diabetic neuropathy with a higher-dose benfotiamine treatment of 320 mg/day or with medium-dose treatment of 150 mg/day. This was a six-week-long, open trial among 36 subjects ranging from 40 to 70 years old whose diabetes was under reasonably good control. All patients experienced significant improvements in pain and vibration sensation, as well as in objective measurements of nerve function, with most improvements being evident by the third week of the study. The greatest changes were seen in the high-dose recipients. The researchers concluded that benfotiamine is effective even in the medium-dose range, but that maximum benefits would be found with higher doses. These findings represent a major breakthrough in the management of this heartbreaking and deadly complication of diabetes.(47)
Results such as these have now been confirmed by independent research groups, one of whom studied 40 inpatients with diabetic polyneuropathy of not more than two years' duration.(48) Twenty of their subjects received benfotiamine 100 mg four times daily, while the others got only placebo tablets. The researchers used a standardized neuropathy score that included measurements of vibration perception as well as patients' and their physicians' subjective assessments (it's just as important to know that the patient feels better as it is to know that their "numbers" are improving). Dramatic improvements were seen in benfotiamine patients' scores compared with controls, with the most pronounced effect being a reduction in pain. More benfotiamine patients than placebo patients also felt that their overall condition improved, and no patients in either group experienced side effects. The authors pointed out that their findings confirmed the results of earlier trials, and provided "further evidence for the beneficial effects of benfotiamine in patients with diabetic neuropathy."
Nutritional research on benfotiamine has now expanded, with a growing number of studies evaluating its benefits in areas other than diabetic neuropathy. One important area is the prevention of endothelial dysfunction in both large and microscopic blood vessels, a major contributor to atherosclerosis in diabetic as well as non-diabetic patients.
In the first study of its kind, investigators looked at the effects of benfotiamine in blocking endothelial dysfunction and oxidative stress after consuming a meal rich in dietary AGEs.(49) They provided type 2 diabetic subjects with a heat-processed test meal that had a high AGE content, both before and after a three-day period of supplementation with 1,050 mg/day of benfotiamine. The scientists measured standard indicators of large- and small-vessel function, as well as blood levels of AGEs, oxidants, and markers of endothelial dysfunction throughout the study. The high-AGE meals before the supplement period had a profound effect on capillary blood flow in reaction to a stimulus, reducing it by 60%, while the ability of larger vessels to dilate (relax) in response to increased blood flow was diminished by 35%.(50) These changes are typical of findings in people with early atherosclerosis, which can lead to heart attack or stroke.(51-53)
Remarkably, these detrimental effects on blood vessels were completely prevented by the three-day period of benfotiamine supplementation! Similarly, the AGE-induced post-meal increases in serum markers of endothelial dysfunction and oxidative stress were also significantly reduced after the supplement period. This landmark study, in the authors' own words, "confirms micro- and macrovascular endothelial dysfunction accompanied by increased oxidative stress following a real-life, AGE-rich meal in individuals with type 2 diabetes and suggests benfotiamine as a potential treatment."(50) A follow-up study by the same research team late last year further showed that the vital molecule adiponectin—which promotes glucose uptake into skeletal muscle and increases fat burning(54)— decreases after a similar high-AGE meal. Again, benfotiamine prevented this detrimental effect of a meal rich in AGEs.(55)
Clinical studies to date suggest that the benefits of benfotiamine can be achieved at doses of 150-1,000 mg per day in divided doses. Benfotiamine appears to be highly safe, with no reports of toxicity or drug interactions in the scientific literature.(56)
We have come a long way in a few short years of nutritional research. Just over a decade ago, the devastating effects of AGE/RAGE reaction products on tissues were believed to be inevitable in people with diabetes, presenting the grim prospects of progressive loss of nerve, blood vessel, and kidney function, and their consequences on quality and quantity of life.(3) Thanks to the discovery of the fat-soluble form of thiamine, benfotiamine, the past decade has witnessed an abundance of promising research to help dispel those ominous predictions and offers new hope for people with diabetes.(7,14) Equally exciting work is now beginning to emerge, suggesting that this is only the beginning. Benfotiamine is currently being studied for its benefits in non-diabetic people as well, where it may help reduce DNA damage in people with end-stage renal disease,(57) ensure protection from the endothelial dysfunction that leads to atherosclerosis and congestive heart failure, and provide relief in a host of additional painful nerve conditions.(18) Benfotiamine's impressive safety record supports its use in both diabetic and non-diabetic people interested in reducing the impact of AGE/RAGE on their longevity and quality of life.
Article compiled by Dr Peter Richard Pedersen
1. Cameron NE, Gibson TM, Nangle MR, Cotter MA. Inhibitors of advanced glycation end product formation and neurovascular dysfunction in experimental diabetes. Ann NY Acad Sci. 2005 Jun;1043:784-92.
2. Giusti C, Gargiulo P. Advances in biochemical mechanisms of diabetic retinopathy. Eur Rev Med Pharmacol Sci. 2007 May;11(3):155-63.
3. Head KA. Peripheral neuropathy: pathogenic mechanisms and alternative therapies. Altern Med Rev. 2006 Dec;11(4):294-329.
4. Karachalias N, Babaei-Jadidi R, Ahmed N, Thornalley PJ. Accumulation of fructosyl-lysine and advanced glycation end products in the kidney, retina and peripheral nerve of streptozotocin-induced diabetic rats. Biochem Soc Trans. 2003 Dec;31(Pt 6):1423-5.
5. Ahmed N, Thornalley PJ. Advanced glycation endproducts: what is their relevance to diabetic complications? Diabetes Obes Metab. 2007 May;9(3):233-45.
6. Vasdev S, Gill V, Singal P. Role of advanced glycation end products in hypertension and atherosclerosis: therapeutic implications. Cell Biochem Biophys. 2007;49(1):48-63.
7. Varkonyi T, Kempler P. Diabetic neuropathy: new strategies for treatment. Diabetes Obes Metab. 2008 Feb;10(2):99-108.
8. Thornalley PJ. Glycation in diabetic neuropathy: characteristics, consequences, causes, and therapeutic options. Int Rev Neurobiol. 2002;50:37-57.
9. Dinh TL, Veves A. A review of the mechanisms implicated in the pathogenesis of the diabetic foot. Int J Low Extrem Wounds. 2005 Sep;4(3):154-9.
10. Brem H, Tomic-Canic M. Cellular and molecular basis of wound healing in diabetes. J Clin Invest. 2007 May;117(5):1219-22.
11. Andersen CA, Roukis TS. The diabetic foot. Surg Clin North Am. 2007 Oct;87(5):1149-77.
12. Koyama H, Yamamoto H, Nishizawa Y. RAGE and soluble RAGE: potential therapeutic targets for cardiovascular diseases. Mol Med. 2007 Nov;13(11-12):625-35.
13. Marsche G, Weigle B, Sattler W, Malle E. Soluble RAGE blocks scavenger receptor CD36-mediated uptake of hypochlorite-modified low-density lipoprotein. FASEB J. 2007 Oct;21
14. Thomas MC, Baynes JW, Thorpe SR, Cooper ME. The role of AGEs and AGE inhibitors in diabetic cardiovascular disease.
Curr Drug Targets. 2005 Jun;6(4):453-74.
15. Yamagishi S, Adachi H, Takeuchi M, et al. Serum level of advanced glycation end-products (AGEs) is an independent determinant of plasminogen activator inhibitor-1 (PAI-1) in nondiabetic general population. Horm Metab Res. 2007 Nov;39(11):845-8.
16. Hartog JW, Voors AA, Schalkwijk CG, et al. Clinical and prognostic value of advanced glycation end-products in chronic heart failure. Eur Heart J. 2007 Dec;28(23):2879-85.
17. Robert L, Robert AM, Fulop T. Rapid increase in human life expectancy: will it soon be limited by the aging of elastin? Biogerontology. 2008 Jan 4.
18. Malecka SA, Poprawski K, Bilski B. Prophylactic and therapeutic application of thiamine (vitamin B1)—a new point of view.
Wiad Lek. 2006;59(5-6):383-7.
19. Booth AA, Khalifah RG, Todd P, Hudson BG. In vitro kinetic studies of formation of antigenic advanced glycation end products (AGEs). Novel inhibition of post-Amadori glycation pathways.
J Biol Chem. 1997 Feb 28;272(9):5430-7.
20. Booth AA, Khalifah RG, Hudson BG. Thiamine pyrophosphate and pyridoxamine inhibit the formation of antigenic advanced glycation end-products: comparison with aminoguanidine. Biochem Biophys Res Commun. 1996 Mar 7;220(1):113-9.
21. La Selva M, Beltramo E, Pagnozzi F, et al. Thiamine corrects delayed replication and decreases production of lactate and advanced glycation end-products in bovine retinal and human umbilical vein endothelial cells cultured under high glucose conditions. Diabetologia. 1996 Nov;39(11):1263-8.
22. Ahmed N, Luthen R, Haussinger D, et al. Increased protein glycation in cirrhosis and therapeutic strategies to prevent it.
Ann NY Acad Sci. 2005 Jun;1043:718-24.
23. Shangari N, Mehta R, O'brien PJ. Hepatocyte susceptibility to glyoxal is dependent on cell thiamin content. Chem Biol Interact. 2007 Jan 30;165(2):146-54.
24. Suji G, Sivakami S. DNA damage during glycation of lysine by methylglyoxal: assessment of vitamins in preventing damage. Amino Acids. 2007 Nov;33(4):615-21.
25. Geyer J, Netzel M, Bitsch I, et al. Bioavailability of water- and lipid-soluble thiamin compounds in broiler chickens. Int J Vitam Nutr Res. 2000 Dec;70(6):311-6.
26. Hilbig R, Rahmann H. Comparative autoradiographic investigations on the tissue distribution of benfotiamine versus thiamine in mice. Arzneimittelforschung. 1998 May;48(5):461-8.
27. Loew D. Pharmacokinetics of thiamine derivatives especially of benfotiamine. Int.J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.
28. Stracke H, Hammes HP, Werkmann D, et al. Efficacy of benfotiamine versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes. 2001;109(6):330-6.
29. Greb A, Bitsch R. Comparative bioavailability of various thiamine derivatives after oral administration. Int J Clin Pharmacol Ther. 1998 Apr;36(4):216-21.
30. Frank T, Bitsch R, Maiwald J, Stein G. Alteration of thiamine pharmacokinetics by end-stage renal disease (ESRD). Int J Clin Pharmacol Ther. 1999 Sep;37(9):449-55.
31. Frank T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfontiamine. Eur J Clin Pharmacol. 2000 Jun;56(3):251-7.
32. Coy JF, Dressler D, Wilde J, Schubert P. Mutations in the transketolase-like gene TKTL1: clinical implications for neurodegenerative diseases, diabetes and cancer. Clin Lab. 2005;51(5-6):257-73.
33. Pomero F, Molinar MA, La SM, et al. Benfotiamine is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol. 2001;38(3):135-8.
34. Babaei-Jadidi R, Karachalias N, Ahmed N, Battah S, Thornalley PJ. Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes. 2003 Aug;52(8):2110-20.
35. Obrenovich ME, Monnier VM. Vitamin B1 blocks damage caused by hyperglycemia. Sci Aging Knowledge Environ. 2003 Mar 12;2003(10):E6.
36. Hammes HP, Du X, Edelstein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.
37. Aragno M, Mastrocola R, Alloatti G, et al. Oxidative stress triggers cardiac fibrosis in the heart of diabetic rats. Endocrinology. 2008 Jan;149(1):380-8.
38. Okoshi K, Guimaraes JF, Di Muzio BP, Fernandes AA, Okoshi MP. Diabetic cardiomyopathy. Arq Bras Endocrinol Metabol. 2007 Mar;51(2):160-7.
39. Aragno M, Mastrocola R, Medana C, et al. Oxidative stress-dependent impairment of cardiac-specific transcription factors in experimental diabetes. Endocrinology. 2006 Dec;147(12):5967-74.
40. Adeghate E. Molecular and cellular basis of the aetiology and management of diabetic cardiomyopathy: a short review. Mol Cell Biochem. 2004 Jun;261(1-2):187-91.
41. Ceylan-Isik AF, Wu S, Li Q, Li SY, Ren J. High-dose benfotiamine rescues cardiomyocyte contractile dysfunction in streptozotocin-induced diabetes mellitus. J Appl Physiol. 2006 Jan;100(1):150-6.
42. Gadau S, Emanueli C, Van LS, et al. Benfotiamine accelerates the healing of ischaemic diabetic limbs in mice through protein kinase B/Akt-mediated potentiation of angiogenesis and inhibition of apoptosis. Diabetologia. 2006 Feb;49(2):405-20.
43. Marchetti V, Menghini R, Rizza S, et al. Benfotiamine counteracts glucose toxicity effects on endothelial progenitor cell differentiation via Akt/FoxO signaling. Diabetes. 2006 Aug;55(8):2231-7.
44. Sanchez-Ramirez GM, Caram-Salas NL, Rocha-Gonzalez HI, et al. Benfotiamine relieves inflammatory and neuropathic pain in rats. Eur J Pharmacol. 2006 Jan 13;530(1-2):48-53.
45. Wu S, Ren J. Benfotiamine alleviates diabetes-induced cerebral oxidative damage independent of advanced glycation end-product, tissue factor and TNF-alpha. Neurosci Lett. 2006 Feb 13;394(2):158-62.
46. Stracke H, Lindemann A, Federlin K. A benfotiamine-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes. 1996;104(4):311-6.
47. Winkler G, Pál B, Nagybéganyi E, Ory I, Porochnavec M, Kempler P. Effectiveness of different benfotiamine dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999 Mar;49(3):220-4.
48. Haupt E, Ledermann H, Kopcke W. Benfotiamine in the treatment of diabetic polyneuropathy—a three-week randomized, controlled pilot study (BEDIP study). Int J Clin Pharmacol Ther. 2005 Feb;43(2):71-7.
49. Negrean M, Stirban A, Stratmann B, et al. Effects of low- and high-advanced glycation endproduct meals on macro- and microvascular endothelial function and oxidative stress in patients with type 2 diabetes mellitus. Am J Clin Nutr. 2007 May;85(5):1236-43.
50. Stirban A, Negrean M, Stratmann B, et al. Benfotiamine prevents macro- and microvascular endothelial dysfunction and oxidative stress following a meal rich in advanced glycation end products in individuals with type 2 diabetes. Diabetes Care. 2006 Sep;29(9):2064-71.
51. Playford DA, Watts GF. Special article: non-invasive measurement of endothelial function. Clin Exp Pharmacol Physiol. 1998 Jul;25
52. Bonetti PO, Pumper GM, Higano ST, et al. Noninvasive identification of patients with early coronary atherosclerosis by assessment of digital reactive hyperemia. J Am Coll Cardiol. 2004 Dec 7;44(11):2137-41.
53. Shimbo D, Grahame-Clarke C, Miyake Y, et al. The association between endothelial dysfunction and cardiovascular outcomes in a population-based multi-ethnic cohort. Atherosclerosis. 2007 May;192(1):197-203.
54. Vu V, Riddell MC, Sweeney G. Circulating adiponectin and adiponectin receptor expression in skeletal muscle: effects of exercise. Diabetes Metab Res Rev. 2007 Nov;23(8):600-11.
55. Stirban A, Negrean M, Stratmann B, et al. Adiponectin decreases postprandially following a heat-processed meal in individuals with type 2 diabetes: an effect prevented by benfotiamine and cooking method. Diabetes Care. 2007 Oct;30(10):2514-6.
56. No authors listed. Benfotiamine. Monograph. Altern Med Rev. 2006 Sep;11(3):238-42.
57. Schupp N, Schmid U, Heidland A, Stopper H. New approaches for the treatment of genomic damage in end-stage renal disease. J Ren Nutr. 2008 Jan;18(1):127-33.
58. Dyer DG, Blackledge JA, Thorpe SR, Baynes JW. Formation of pentosidine during nonenzymatic browning of proteins by glucose. Identification of glucose and other carbohydrates as possible precursors of pentosidine in vivo. J Biol Chem. 1991 Jun 25;266(18):11654-60.
59. Grandhee SK, Monnier VM. Mechanism of formation of the Maillard protein cross-link pentosidine. Glucose, fructose, and ascorbate as pentosidine precursors. J Biol Chem. 1991 Jun 25;266(18):11649-53.
Group Practice since 1977
70 Nerang-Broadbeach Rd
Corner of Warrener Street
Nerang - Gold Coast
Exit 71- East side of the M1
Monday to Friday:
8am - 5:30pm
8am to 4pm...ish
Chiropractic, Osteopathy
Acupuncture and TCM
Nutritional Biochemist,
Naturopath, Herbalist,
Massage, Physiotherapy,
Integrative and Complementary
Traditional Medicine
Trigger Point Dry Needling
while you sleep with
patches using the best facial acupuncture points.
Anti ageing without the chemical consequences.
Experience the intensive
Qi Beauty MingFacial
in our Gold Coast salon.
Copyright © 2014 - Dr. Peter Pedersen - All rights reserved
Your Health Matters Group Practice - since 1977 - 63 Warrener Street Nerang / corner of Broadbeach-Nerang Road. Exit 71 on the Eastern side of the M1
Qi beauty - Anti - Aging System - Lifestyle and Wellness


text:
NRCC to offer handgun safety class
|A handgun safety class will be offered through New River Community College on Tuesday, November 5 and Thursday, November 7.
Both class meetings will take place from 6 to 9 p.m. in Edwards Hall, room 206, at NRCC in Dublin. Range time will be offered on the Saturday following the class.
The cost of the course is $60, which includes a textbook.
The six-hour classroom portion of the course, instructed by Joey Williams, is required. However, range time is optional. The class is intended for individuals who are applying for a handgun permit through the courts and will cover topics such as the nomenclature of revolvers and/or semi-automatic handguns.
Participants will also learn how to care for, maintain and store their handguns.
To register, contact the NRCC Office of Workforce Development at 540-674-3600, ext. 4323.
Other Options:

subset: commoncrawl


text:
|index by Group
|index by Distribution
|index by Vendor
|index by creation date
|index by Name
|Name: antlr-java
|Distribution: openSUSE 11.4
|Version: 2.7.7
|Vendor: openSUSE
|Release: 80.4
|Build date: Tue Feb 22 23:16:31 2011
|Group: Development/Tools/Other
|Build host: build24
|Size: 374842
|Source RPM: antlr-2.7.7-80.4.src.rpm
|Packager: http://bugs.opensuse.org
|Url: http://www.antlr.org/
|Summary: ANother Tool for Language Recognition (Manual)
Java runtime for antlr
GPLv2+ ; Public Domain, Freeware ; MIT
* Mon Aug 23 2010 email@example.com - add missing java requires of antlr-java package * Thu Aug 19 2010 firstname.lastname@example.com - enabled the python (python-antlr) and csharp (antlr-csharp) support - moved jar files to new antlr-java package, which is required by main antlr one. This is to have jar files in noarch package - do not use default make install, but install files manually with a compatibility links to /usr/share/antlr-2.7.7 * Wed Aug 18 2010 email@example.com - Ensure that the development files are build too. The package is now a build requirement for the KDESDK4 package. - Removed the structure to build just the native version. * Mon Mar 03 2008 firstname.lastname@example.com - updated to 2.7.7 * updated BaseAST.java to make the doWorkForAll method static. Same behaviour, except no ClassCastExceptions when sibling.getFirstChild() happens to return an AST that doesn't extend BaseAST. Oliver Wong contributed the patch. * updated TokenStreamRewriteEngine.java to reflect bug fixes discovered in v3 counterpart. * Wed Feb 20 2008 firstname.lastname@example.com - do not PreReq files to fix build env setup for other packages - remove SL-9.1 traces * Fri May 04 2007 firstname.lastname@example.com - added unzip to BuildRequires * Sat Oct 07 2006 firstname.lastname@example.com - added check that checks whether deleted files ShowString.java and StreamConverter.java are really not in place * Thu Oct 05 2006 email@example.com - deleted antlr-2.7.6/examples/java/unicode.IDENTs/ShowString.java antlr-2.7.6/examples/java/unicode.IDENTs/StreamConverter.java from tar ball due to licensing issues (Bug #207621) * Mon Sep 25 2006 firstname.lastname@example.com - fixes necessary to compile with Java 1.5.0 - set source="1.4" and target="1.4" for ant "javac" tasks - set source="1.4" for ant "javadoc" tasks * Wed Sep 20 2006 email@example.com - Provide: antlr-bootstrap Obsoletes: antlr-bootstrap
/usr/share/antlr-2.7.7 /usr/share/antlr-2.7.7/antlr.jar /usr/share/java/antlr-2.7.7.jar /usr/share/java/antlr.jar
Generated by rpm2html 1.8.1
Fabrice Bellet, Mon Jul 10 03:30:32 2017


text:
LONG BEACH - Importers and exporters who saw their goods stranded on docks and ships during the clerical workers strike earlier this month will receive some financial relief.
The Port of Long Beach Board of Harbor Commissioners on Monday unanimously approved the first reading of an ordinance waiving cargo-related holding and storage fees that were incurred during the strike at the Long Beach port, where three of six terminals were closed from Nov. 28 to Dec. 4.
Port officials said forgoing the cargo fees, which exporters and importers are charged when items sit longer than required, will help customers quickly move the container backlog.
"I think it's the right thing to do," Commissioner Rich Dines said before voting for the waiver. "We need to protect the interest of cargo owners who choose the Port of Long Beach as their port of choice. Competition is more fierce today than ever and we want to keep the cargo coming to Long Beach."
The strike started Nov. 27 at the Port of Los Angeles after more than two years of talks fell apart between the International Longshore and Warehouse Union Local 63 Office Clerical Unit, the union representing more than 600 clerical workers at both ports, and their employers, the Los Angeles/Long Beach Harbor Employers Association, which represents shipping agencies and terminal operators in Southern California.
The strike, which longshore workers honored, spread to the Port of Long Beach a day later, resulting in the shutdown of two-thirds of the twin ports, considered the nation's busiest seaport complex.
The closures prompted ships either to sit idly in the water waiting to dock or head to other ports.
Don Snyder, director of trade development for the Port of Long Beach, said the port was able to recover quickly once the strike was over because there were enough berths and cranes to meet the surge of returning vessels, plus additional night and weekend hours to help with the backlog of cargo.
"With few exceptions, the recovery has been proceeding amazingly fast and smooth when you talk to most parties," Snyder said.
Trade conferences help
Trade-related organizations that will gather in Long Beach for conferences over the next five years will account for 16,885 booked room nights and about $7.5 million in economic impact for the city of Long Beach, a top convention official told Port of Long Beach officials Monday.
They include groups such as Intermodal Association of North America, which is expected to generate $3.8 million to the local economy and 9,120 room nights when it meets in September 2014 and 2017, while Trans Pacific Maritime Conference, whose members will gather March 2013, 2014 and 2015, is estimated to yield $2.7 million to Long Beach and 6,600 room nights, said Steve Goodling, president and CEO of the Long Beach Area Convention and Visitors Bureau.
Conventions also include the California Construction Expo, which will account for 50 room nights and $387,500 in economic impact when it meets in August 2013, the U.S. Grains Council with 830 room nights and $444,330 to the city when it meets in February 2014, and the Footwear Retailers and Distributors of America, which will meet in October 2013 and account for 285 room nights and $236,000 to the local economy, Goodling added.
Goodling credited the bureau's partnership with the port for helping to secure the business.
firstname.lastname@example.com, 562-714-2088, twitter.com/KarenMeeksPT


text:
Christopher Hubbart will live at 17132 Laredo Vista Drive, Palmdale (Lake Los Angeles)
More on this story...
LOS ANGELES (CNS) - Despite objections from
A formal hearing will be held in 45 days by Santa Clara Superior Court Judge Gilbert Brown to finalize the proposed housing of Christopher Hubbart, who admitted raping about 40 women between 1971 and 1982.
Hubbart, who was arrested in 1972 in
Over the next two years, he raped another 15 women in the
Hubbart is being held at
In May, Santa Clara Superior Court Judge Gilbert Brown ruled that Hubbart should be released from prison and housed somewhere in
Lacey's office and Antonovich have strongly opposed plans to allow Hubbart to live in
A prosecutor in
Hubbart, 62, could be released as early as December.
``Our priority is to safeguard our residents and make certain Hubbart is obeying all conditions of his release,'' Lacey said.
Antonovich said in July that Hubbart needs to remain ``behind bars, not released into our neighborhoods.''
``Perhaps the judge should take him, if he wants him out so badly, let him live in
Hubbart was born in


text:
Another year of incident and event photography in Raleigh, Wake County, and a few other places. Thanks
for everyone's support and assistance. Featured agencies include but are not limited to Raleigh FD, Raleigh PD, Wake
County EMS, Durham FD, Bay Leaf FD, Warrenton FD, Warrenton PD, Soul City FD, Morehead City FD, Newport FD,
Fuquay-Varina FD, Rolesville FD, Wake County EM, Six Forks EMS, Wake County FF Association, NC Task Force 8,
Durham Highway FD, Cary FD, Western Wake FD, Stony Hill FD, Apex FD, Raleigh FD Historical Society, Wake-New Hope FD,
NC Forest Service, Wake Forest FD, Cary EMS, Charlotte FD, Morrisville FD, Garner FD, Raleigh-Durham Airport ES,
Selma FD, Selma EMS, Fairview FD, and the Dragon Slayers,
Mike Legeros photographs.


text:
Historian awarded NEH fellowship
University of South Carolina history professor Dr. Marjorie J. Spruill has been awarded a prestigious fellowship from the National Endowment for the Humanities (NEH) to complete her book, "Women's Rights, Family Values, and the Polarization of American Politics."
Marjorie Spruill
The fellowship comes with an award of $50,000. Spruill will spend the academic year 2010 – 11 writing the book, which details the transformation of American political culture during the 1970s.
"I would like to think that this is important to understanding American politics today," Spruill said. "This book will speak to a broad audience and contribute to the national conversation about this prolonged period of partisanship and polarization that has continued now for 30 years and is confounding efforts of our leaders to address the most important problems facing our society.
Spruill, a specialist in U.S. history and leading expert on women's history, focuses her research on both women's rights advocates and the conservative women who challenged them for the right to speak for American women and influence policy.
"The great debates of that era over women's rights and social roles played a crucial and largely unrecognized role in this transformation," Spruill said.
Spruill has been researching this book for 10 years and has interviewed many prominent figures, including President Jimmy Carter and his wife, Rosalynn; women's-rights leader Gloria Steinem and Phyllis Schlafly, a leader of conservative women.
"This is one of the most prestigious grants a historian can receive," said Dr. Lacy Ford, chairman of the history department. "Selections are made from an intensely competitive national pool of applicants. This award is a tribute to Marjorie and is an indication of both how highly her peers regard her work and how important her current project is to the understanding of the modern culture wars."
Spruill joined USC's faculty in 2004. She previously taught at Vanderbilt University and the University of Southern Mississippi. She has written or edited numerous books, including her book, "New Women of the New South: The Leaders of the Woman Suffrage Movement in the Southern States," and the three-volume series, "South Carolina Women: Their Lives & Times," which she co-edited with USC professor Dr. Valinda Littlefield and Dr. Joan Maire Johnson of Northeastern Illinois University.
NEH fellowship
- What: $50,000 award to history professor
- Who: Dr. Marjorie J. Spruill to use fellowship to complete book, "Women's Rights, Family Values, and the Polarization of American Politics"
- When: Academic year 2010 – 11


text:
Install BT5 into a USB stick and try it...Read wiki on how to install BT5 in a USB stick.
Hello, I'm new to the forum, so excuse my "Newness"
I have a Acer Aspire One netbook that's a little over a year and half old.
I replaced it 6 months ago by building a rig, so the netbook isn't doing anything.
It's slow, and laggy, but I was wondering if I DBAN it, would it be able to run backtrack 5 as its main OS?
I know its not designed for that, so what would be the problems?
I realize this question might make no sense, like I said, I'm new to this.
Install BT5 into a USB stick and try it...Read wiki on how to install BT5 in a USB stick.
Netbooks are enough for BackTrack 5's system requirements.
I also use BackTrack 5 on my netbook. But I don't recommend using it as a main OS. As you said, it's not designed for this.
Install it alongside your OS and use with GRUB.
Ps: Technically, you can use it as a main OS but you must make some configurations (adding user, adding repos, installing codecs etc.) before using it.


text:
|Used In
|The Great Gatsby
|Show Multiple Meanings
Go to Book Vocabulary
unspecified meaning
There are no more uses of "positive" in the book.
To see samples from other sources, click a word sense below:
as in: I'm absolutely positive! Define
certain (having no doubt)as in: had a positive effect Define
good or beneficialas in: positive feedback from my boss Define
approval or agreementas in: a positive attitude Define
optimistic or agreeableas in: The test came back positive. Define
found a condition or substance to be presentas in: a positive number Define
greater than zero (of a number)
|Show Multiple Meanings
|Go to Book Vocabulary


text: People get bored. It's what we do. Most are stuck behind a desk all day too bub so reading/posting on this forum is better than doing anything work related. I'd rather talk about a chest high swell than pay attention to the conference call I'm on right now. Yes, this is the new normal.


text:
Let's make one and try to get wide ranging agreement.
Please add to the list or float ideas for discussion. Loads of things that can be added. Even conduct at after parties ha.
1. Ref says 'stop', you stop. (obey ref at all times)
What would you like to add?


text:
|Thread Tools
|Display Modes
You mention alot about bubbles but you are unclear. Where were the bubbles coming from.
Did you continuously feed the expansion tank with a slow running hose ? Why ?
Fill up the expansion tank and remove the rad cap and bleed screw. Start the engine and let it idle. Since it does not overheat when its not being driven, you can come back 15-30 minutes later.
Bubbles coming out through the bleed screw is ok, and even then, they wouldn't come out for like 30 minutes unless you've completely drained your block and radiator and are filling everything up from scratch.
If you are getting bubbles IN THE EXPANSION TANK, then you've got a serious problem.
The auxiliary water pump only controls hot water running through the dashboard i.e. cabin heater. It plays no functional role in the cooling system. Please ignore it for now, but do ask your friend to reconnect it back on Monday, its just a 2 minute job for someone who knows his way around this car.
There's a good possibility that its your water pump or thermostat that is busted. But, if you are getting bubbles IN THE EXPANSION TANK, you've got a very serious problem.
You should go back and ask your son what he did to the car (or what others might have done to the car) in the days leading up to this situation.
Good luck.
Last edited by robertobaggio20; 10-12-2012 at 09:24 PM.
M50s are not that tough to bleed. No doubt you did it properly. If the car overheats your best bet would be to replace the thermostat - even if it is not the original problem. Make sure you drill a bleed hole at 12oclock on the new one. Makes bleeding a cinch.
I believe the fluid should travel from the upper to the lower rad hose. Therefore if the tstat and water pump are working properly the rad should cool it down towards the lower hose. From everything I read not sure I could rule out water pump/fan clutch/aux. fan/rad blockage.
You can run a head gasket test pretty easy. Go to autozone or other and borrow their fluid reservoir. By a bottle of HG fluid, stick it on the rad and it will change colors if gas is in the coolant. Great for peace of mind.
Also, you can jump the aux fan with a paper clip and leave it on high when you drive to keep the engine cool. (No it is not a fix).
Here is a great test procedure. I rewrote it into a flow chart which I keep in my Bentley.
Well, here we are, something old that's actually new to me and no doubt many others. The HG colour change fluid test. Brilliant ! Larrick please do that right away sir.
And I'd like to say, with respect to 525it, that drilling holes in the thermostat is completely unnecessary. I've never done it and it has never made anything difficult. You don't have to be worried if you don't do it. Its another myth for the modern age, that may have had a relevance in an earlier era.
I agree that you should change your thermostat and water pump. Oreilly's sells a composite impeller thermostat for around $50, with a lifetime warranty. If the HG fluid test checks out and your HG is ok, then please change both the thermostat and the water pump. They both have approximately the same life span, if I'm not mistaken.
Just remembered. Another way to check for HG problems is via the compression test.
Well if you're gonna use your wife as an excuse, then you should use that "safety issue" blank check for all it's worth. If you're gonna pay that much for the diagnosis and there's a dealership around, you can get it at the dealership for that much or less and might have better diagnostic equipment, probably have better diagnostic equipment than your guy's shop and more importantly, if any of it is under factor recall, the dealership has to tell you and do the work for free.
And this is not something I would recommend and don't work for BMW and the dealership is a rip off 99% of the time but sometimes it is worth it just for the diagnosis and information on factory recall that they have in their computer database. And I'm only suggesting this cause I took my 94 530i in to the dealership for an engine diagnosis and the e-prom and thermostat are still under factory warranty in that car so all of the work was done by BMW even though it is a 94 and I am the third owner. Anyway, there's that. Get to tell them exactly what is wrong and see if you can get the parts and work done much more reasonably priced by that guy you know.
I would love to see that database, by the way.
oh, by the way, sorry if that post seemed like it was telling you to do anything. I really don't know what the correct thing to do is for this situation but just having been around a bunch of mechanics shops and different dealerships and observing their behavior in general with fixing my BMWs over like the past 15 years, when I used to be able to afford a mechanic, is also what my comment is based on, more than mechanical knowledge.
So sorry if I came off like I was telling you what to do as I read that post twice it may have seemed overbearing. The wife is a legitimate excuse to pay a mechanic and is my personal favorite so I also did not mean to denigrate that aspect of your dilemma.
And I wish you the best of luck with this.
There are no bubbles in the expansion tank.
The reason that I used a slow running hose was that I was getting tired of hand feeding water every minute or less.
The bleed screw was removed and the rad cap off. Coolant flowed from the bleeder hole with massive amounts of bubbles.
This was endless and the bubble consistency never changed.
The expansion tank needed constant filling or the bleed hole became "dry" and only steam or nothing came out.
I feared that if it were not constantly toped off that air may be being sucked back into the system.
The top hose never felt "full" to me but I do not know how it is supposed to feel.
There is no apparent leak to account for lose of coolant.
Perhaps more coolant was lost in the initial overheating than I know of but that should not matter once it is refilled.
I bled the engine for over 1 1/2 hours.
The engine does not overheat at idle and the temp needle sits at 1/2 or a needle width above or below 1/2 the entire time.
The test procedure the My525it describes is for engines overheating at idle. Mine does not.
I am confused about the fan clutch. My fan comes on immediately and remains on.
The fan clutch seems fine. I did the newspaper test and it stopped and then stared again.
While cold it moves with a little resistance as described in Bentley.
I will start it again and see how long things take to heat up.
Last time the needle was just below 1/2 after 15min. and the top hose was slightly warm, bottom hose was cold.
Bottom hose warmed at about 30min.
The HG test sounds interesting.
After more reading about the newspaper test. I may have done it incorrectly.
I had a wad of rolled up paper and stopped the fan at the end of the blades.
It seems that a single rolled sheet should be used and pressure at the hub.
The fan does not stop but slows and then picks up speed after release.
That seems to indicate the clutch is ok.
According to my reading about the fan clutch:
A bad fan clutch would cause an over heat at idle.
The fan does not play a big roll in cooling the engine once the vehicle is moving and especially at higher speeds.
Since I only over heat once I am moving, I assume the fan is good.
I started the car again today;
No noise. no white vapor.
5 min. needle into blue, top hose warm
15 min. needle just below 1/2, some visible white vapor from exhaust.
20 min. needle at 1/2, some visible smoke. Bottom hose warm.
"Ticking" noise begins. I believe it is the valves. They quiet down when rpms are raised.
run for another 10 minutes and take out for a ride:
needle creeps up near 3/4 and holds for a few minutes and then creeps to near Red.
I pull over and needle comes down a bit.
I drive home and let idle, temp drops to 3/4. NO white vapor is visible.
I turn off engine and temp comes down to just above 1/2 in a few minutes.
I see no leaks.
I will allow to cool and see f I am still getting bubbles when bleeding.
I will allow the BMW mechanic to do a diagnostic on Monday.
You should not be doing bleeding for 1/2 an hour. The longest it has taken me is 5 minutes after the engine has warmed up. Of course, I've done this for 1/2 hour after full warmup, but I realise now that it was an overkill and unnecessary.
I should have put the time interval in my initial instructions on how to bleed the radiator. I'll ammend it now.
If you are still getting tons of bubbles like 60 or 90 minutes after you start bleeding, you've got a different problem.
I'm not exactly sure if there is a way to check if either the water pump or thermostat is working. I would suggest the following (and you should do this yourself) :
1. Try the HG solution. If it doesn't change colour (thus indicating HG failure or worse), then change both the water pump and thermostat. That should fix your problem. Either component is probably screwed or getting near screwed. And if they do need to do a head gasket job on your car, you'll need to change the wp and thermostat as well anyway.
2. Why didn't you try the HG solution already ?
When you change the water pump, change the water pump's pulley as well. They have a new pulley that is made of high temperature plastic and not the original metal. Made my engine go faster...I'm very pleased ! So this is a great way to turn a repair into an upgrade.
Of course, it might be a good idea to change the belt as well at this point.
Good luck.
I did not know about the HG test until last night. I made an appointment for Monday morning with a good BMW mechanic who once owned this model car. He will do a full diagnostic for $128. I am extremely busy right now as I have just returned from a trip and have a back log of work.
There are a lot of possible causes for the overheating. I should (as you and others suggest) do a full overhaul of the cooing system. I have read many, many threads about over heating the past few days and one theme stands out .
People change the thermostat, fan clutch, water pump and still have an overheating problem and more questions.
I am willing to spend $128 to get a professional's input. I appreciate all the help and suggestions that I have received and I know how much easier it would be for you all to help me out if you could actually stand in front of the car.
It is my son's car and he needs it back as soon as possible. If it were mine, I would do it myself. This is the first time that I have not. As I said before not only is the car overheating but I am getting a little heat from my wife.
Depending on the diagnostic and the price of repair, I will decide what to do.
Either do it myself or have them do it.
I will tell you all the out come on Monday night or Tuesday.
I have not done the HG test because I have committed to have it look at and tested in the shop.
I think there are multiple problems and I do not want to risk destroying the engine.
Thanks again for all you help and concern.
No problem Larrick. We hope to hear good news from you in a few days.
I dropped the 1994 525it at the shop this morning. I had my wife follow me and watch the exhaust for white vapor.
The cat started and ran fine without overheating. Only 3 miles.
My wife did say that she saw more white vapor form the BMW than from other cars.
I left the car with a written history of what happened and what I had done and experienced the past few days.
I got a call a few hours later. There was no circulation of coolant. So the water pump was not working.
I am going to change the water pump, fan clutch (it is a little weak), thermostat, hoses and belts.
My great concern is doing all this work with a bad head gasket.
The shop said that there was NO exhaust contamination in the coolant and pretty much assured me that the head gasket was fine.
They said that the M50 will show this amount of vapor.
Does any one have any comments?
I'm glad the news was good relative to the HG.
Good luck.
As I expected, this was a thermostat or water pump issue. I was quite sure that you were wrong when you said that most of the online posts that you've read suggest that these problems are more serious.
However, if there is no coolant circulation, your engine should be overheating even at idle. Perhaps there is coolant circulation, but it is very poor.
However, I do not like the extra vapour in your tailpipe. This is not normal for an E34, expecially if another vehicle does not exhibit the same amount of vapour (which eliminates environmental issues). If i were you, I would purchase a compression tester for $30 on ebay and do the compression test myself (its easy, check youtube) to be absolutely sure that nothing is up. Also, ask the mechanic to explain the extra vapour, see what he says.
Finally, my suggestion is that you get a composite impeller water pump, instead of a cast iron or stainless steel one. Composite pumps do not corrode, are tougher than plastic, as strong as steel, and almost as light as plastic. Thus, the load on your wp's bearings is reduced, greatly extending its service life and reducing its likelihood for sudden failure. O reilly sells one for $50 before shipping, with a lifetime warranty. Turner sells a BMW pump for around twice that price, but with no lifetime warranty.
Furthermore, I suggest that you pick up a new water pump pulley that's made of thermoplastic these days. It is much lighter than the existing metal wp pulley and your car will be faster. I just did this and am very pleased with the results. Since the pulley needs to be removed to access the fan clutch, you're not going to pay extra for labour. The pulley should cost under $50 and is worth paying for. Please confirm the material of the pulley with customer service if you're buying it online.
I would not bother to replace the fan clutch. If your car did not overheat with a busted water pump and a possibly busted fan clutch, then I think your system would be flawless with a good pump and existing clutch. In fact, I would recommend that you remove the fan clutch, fan and fan shroud entirely. I've been doing that for 2 weeks with no problems. Confirm using Bentley's test procedures first that your auxiliary cooling fan is working well at both low and high speeds, before you delete the fan clutch.
Unless you have already done so, I would suggest that you change the bleed screw and rad cap to new ones. They should only run you $15 in total.
Please purchase the compression test kit and conduct that test on your car.
Perhaps you should do the compression test first. You can even do this yourself while at their workshop, so there will be no extra charges. The extra water vapour in your tailpipe is not right. Your mechanic may have misdiagnosed the issue. Please ask him to describe the exact steps he took to arrive at the conclusion that the wp is busted.
Last edited by robertobaggio20; 10-15-2012 at 08:01 PM.
I will. I am a bit skeptical myself.
It is possible that your HG leak is minor, which is why they couldn't really identify it. In which case, this might be all that you need to get rolling :
This might be the best first option for you.
If it fixes the problem, it will mean that there's no need for you to change the WP and thermostat and all the expense of that, although it is the intelligent thing to do. Perhaps you could postpone that till later when you feel like doing a full head job.
If this is the problem, you are fully justified in demanding a refund from the dealership, even if you fix it some time later. They should bloody well do a compression test on your car for that amount of water vapour shown, and for such a high price for a mere diagnostic.
And while you're there to collect the car, please double check to see if you can get them to show you how the stomp test works. And if it doesn't, they should fix it under warranty or recall or whatever.
Last edited by robertobaggio20; 10-15-2012 at 10:05 PM.
The more I read this - particularly the original: car boiled and continuous bubbles from the bleed - the more I've got to go with HG or worse. Nothing else makes sense. I presume the radiator, water pump and thermostat all tested good?
Good - Fast - Cheap: Pick any two.
3 x E32 735iL (Alpine White, Glacier Blue & Kashmir Beige); 2 X E38 735iL (Oxford Green & Alpine White); E53 X5 4.4i (Pearl Beige); R50 Cooper; R55 Cooper Clubman (Both Pure Silver).
E38 Parts Car
E21 318i; E23 735i; E30 318i; E32 735iL; E34 535i; E38 730iL; E53 4.4i
I've just changed my wiper blades and now my reverse lights don't work. Should I change my fuel pump relay?
The 1994 525it is back on the road and seemingly fine.
The water pump's plastic impeller was completely missing. There was NO coolant circulating except for what may have moved due to heat convection.
That is why it took so long for any heat to reach the valves for the heater core
That is why it could not be bled.
Roberto, I did read My525it's thread but did not see a test for the water pump.
You had written me that if the water pump failed, the engine should overheat at idle.
That makes sense to me too, so what is a definitive test for a water pump short of examining it out of the engine?
There must have ben a blade left on the pump while I was trying to bleed it because I removed the upper hose at the radiator and di see some movement.
But the lack of volume in the hose made me suspect the water pump.
THe thermostat seemed to operate properly.
The water vapor was the scary part but there had always been more vapor than I liked to see.
SO...This is what happened
NEW water pump, thermostat and housing, upper and lower radiator hoses, fan clutch and both serpentine belts.
The cooling system was flushed and filled.
I , on recommendation form the mechanic, changed from Mobil 1 synthetic to Castrol GTX 20W50.
This oil is good for short distance urban driving.
It seems to have quieted the valves, which had always been making a little noise.
This morning the car was showing water vapor but so where most other cars.
7:30 am and 52 degrees with dew.
I will closely monitor the coolant level and exhaust.
The mechanic assured me that the head gasket was fine.
There were zero hydrocarbons in the coolant and he can detect 1 part per million.
The oil was pure and clean.
I quizzed him on the possibility of water only entering a cylinder and not contaminating the oil or the coolant.
His contention is that would be impossible because on the compression stroke of the engine, gasses would pass into the coolant due to high pressure
if coolant were able to enter the cylinder.
He is saying that the "Hydrocarbon" test is the definitive test for a blown head gasket.
He also stated that this model car will show a bit more vapor than most cars.
It runs very smooth and very strong.
I put blue tape at the current cooling level and will watch it closely.
I would say that if there is no coolant lose after a few weeks then all is well.
The most striking thing was the condition of the water pump, absolutely tripped clean.
The heater now blows very warm air out of both passenger and driver side.
This is without benefit of a missing auxiliary pump.
THe needle now sits a needle width below 1/2.
Love a story with a happy ending! Glad it was not the HG or worse.
Good - Fast - Cheap: Pick any two.
3 x E32 735iL (Alpine White, Glacier Blue & Kashmir Beige); 2 X E38 735iL (Oxford Green & Alpine White); E53 X5 4.4i (Pearl Beige); R50 Cooper; R55 Cooper Clubman (Both Pure Silver).
E38 Parts Car
E21 318i; E23 735i; E30 318i; E32 735iL; E34 535i; E38 730iL; E53 4.4i
I've just changed my wiper blades and now my reverse lights don't work. Should I change my fuel pump relay?
In rereading my last entry,I realized that a statement is unclear.
If the water pump had indeed failed,why did the engine not overheat at idle.
It could run for hours with the needle at the 1/2 mark.
So...what is a definitive test for a bad water pump?
How about (for a good pump) - 'One that circulates sufficient coolant for the engine under all conditions'? BTW did you find bits of the old impeller? Where did they go? When the air is cool and the thermostat fully open your water pump was able to keep up. Had the air been hotter and running the air con I guess it would boil, given time.
Good - Fast - Cheap: Pick any two.
3 x E32 735iL (Alpine White, Glacier Blue & Kashmir Beige); 2 X E38 735iL (Oxford Green & Alpine White); E53 X5 4.4i (Pearl Beige); R50 Cooper; R55 Cooper Clubman (Both Pure Silver).
E38 Parts Car
E21 318i; E23 735i; E30 318i; E32 735iL; E34 535i; E38 730iL; E53 4.4i
I've just changed my wiper blades and now my reverse lights don't work. Should I change my fuel pump relay?
Last edited by BMWFatherFigure; 10-17-2012 at 09:28 PM.
Yes there were bits of the old impeller in the box of parts which the shop gave me. I did not do the job.
I did not have the time and my son needed his car back immediately for work.
The system has been flushed so I assume the rest if the bits are out.
In diagnosing an overheating problem, could you assume:
If the upper hose gets hot when the engine is at operating temperature then the thermostat is working.
If the engine overheats with a good thermostat, that means a bad water pump.
But mine did not over heat at idle and the outside temperature was not cool and it could idle for hours.
It only overheated under load and when moving.
Since it did not overheat at idle, the fan was doing a good cooling job.
The fan is not needed at speed.
The question is, does an engine operate at higher temperature when at idle or at speed.
I would have thought that a bad water pump would have made it overheat at idle faster that at speed.
But it was the opposite.
|See More Related BMW Stories
|Forum Navigation
|Today's Posts Search
|Thread Tools
|Display Modes
Linear Mode


text:
The San Antonio Spurs took to the court without three of their top scorers to face Chicago on Monday but still had too much fire power for the Bulls, pulling out a 103-89 victory to pick up their 13th win in 14 games.
Tony Parker (knee), Tim Duncan (knee) and Manu Ginobili (hamstring) all sat out for San Antonio, who own the best record in the NBA at 41-12, but a career-best 26 points from Kawhi Leonard and 18 from Danny Green kept the Spurs machine rolling.
"All of us are basketball players here, we're competitive," Leonard told reporters of the Spurs, who were also without Stephen Jackson for personal reasons.
"That's why we play the game. If we go in doubting ourselves, we're already beat."
San Antonio clung to a 76-75 lead in the fourth quarter before a 19-5 run closed the door on Chicago.
"One would hope you could play with anybody in our system, but it was a tough challenge tonight," said San Antonio coach Gregg Popovich. "I couldn't be more proud of them."
Nate Robinson scored 20 points to pace the Bulls while Joakim Noah added seven and 15 rebounds for the home team, who faded down the stretch.
The Bulls had dominated inside and outrebounded the visitors 49-26 but it did not seem to matter.
San Antonio grabbed a nine-point advantage at halftime and stretched it to 14 in the third before the Bulls closed the quarter strongly to make a game of it.
Chicago (30-21) have now lost three of four.


text:
Short Cuts
Funding may be scarce in the UK, but as public bodies formulate their talent development plans, Screen discovers that the appetite and ambition for short film-making is greater than ever.
It is no coincidence that Bristol Encounters short film festival, which wrapped at the weekend, attracted a record number of delegates and international film-makers. "Festivals for short films have become more relevant again due to lack of broadcast opportunities and the fact that the DVD market for short films just doesn't exist anymore. This is one of the only times you can see films on the big screen," says Encounters managing director Liz Harkman, who revealed that Encounters' dates are to change to an earlier slot in September from 2012.
As a mark of its significance within the industry, the BFI awarded Encounters transition funding worth £50,000 for this year's edition, and while the BFI's future policies are tied up in the impending film policy review it has confirmed that it will be launching a shorts programme in the new year. Film Fund – Shorts 2012 will give filmmakers with "demonstrable experience" the chance to make shorts on budgets of between £25,000 to £50,000.
Looking further ahead, the BFI told Screen that investing in short films is "likely to be part of a holistic approach to talent development going forward."
The BFI scheme may act as a vital route into features, but it's equally important to support those film-makers who are at an earlier stage in their career, says former South West Screen executive Chris Moll, who has recently been appointed as head of talent development at newly created regional body Creative England. "My interest is how we are going to support those film-makers who are just starting to express their voice, and on how we are going to support those earlier shorts as opposed to the one just before the feature".
Peter Carlton, head of Warp Films-Europe, agrees that it is all about small steps. "It's important that people don't assume that if you make two shorts in your garden then you're ready to make a feature. There needs to be that stepping stone, whether that's mid form shorts, or series for the internet or half an hour for TV," says Carlton who also sits on the board of the Encounters Film Festival and was heavily involved in Future Encounters, a new strand at this year's festival. The scheme shines the spotlight on new talent whilst at the same time developing different forms of film-making.
"Instead of trying to find 10 directors who have made award winning shorts, we are looking for diversity of talent. Our line-up this year included people from different backgrounds including TV comedian Matthew Holness, graphic artist Joe Magee and musician Douglas Hart," says Carlton.
Next year there are plans to bring together the participants of Bristol's creative producers' summer school with the 10 film makers in the Future Encounters strand to explore ways that they might be able work together and make new work specifically for the festival. "It might be short films, or outdoor events, or interactive games. It's about broadening film-makers awareness as to how the moving image can be used and showing people from other media what incredible skills film-makers have," says Carlton.
Back in the capital, Film London runs two short films initiatives – a digital filmmaking scheme called PULSE and the London Borough Film Fund Challenge. It has also just launched a special Dickens themed short production scheme to mark the bicentenary of Dickens' birth in 2012.
Elsewhere however, the picture is less rosy, with national short film schemes including the Digital Shorts programme and Cinema Extreme (run by Film4 and the UKFC, which produced Andrea Arnold's Oscar winning short Wasp) coming to an end following the demise of the UKFC. When it comes to Creative England's policy towards shorts in the regions, Moll says he is adopting a "wait and see approach, mainly because it all depends on what comes out of the film policy review.
"But we are pushing towards a national talent strategy where we can all sit down and decide collectively what we want to do with shorts going forward," he adds.
Dan Simmons of Skillset thinks that the key is providing "the right platform to people at different stages in their career, whether that means mentoring or bespoke training. Short films remains a crucial part of the learning curve but I don't think a one-size-fits-all scheme is what's needed. And it's important that things are delivered locally."
Overfunding of shorts might not always be the answer, says the director of the London short film festival Philip Ilson. "It's about getting a balance between heavily funded work and work that is a bit more independent where people play less by the rules," says Ilson who points to France as being an example of a territory that heavily funds shorts, sometimes to the detriment of quality. "A lot of the shorts that come out of France are quite bog standard and mainstream."
Ilson has received over 800 British short film entries for the upcoming London short film festival in January. "That's quite a lot considering there isn't much funding out there," he laughs. Meanwhile, Madeleine Probst who runs Encounters' 90 second film-making competition DepicT! says she was particularly impressed with the British entries this year.
There may be less money on the table than in previous years, but the cost of making short films has also fallen dramatically, with film-makers more able than ever to pick up a camera and shoot a film. "Despite the economic crisis, it's still possible for people to make cool, interesting films using modern digital technology and demonstrate their storytelling to good effect," says Nik Powell, head of the National Film and Television School.
And short film-makers are increasingly thinking outside the box when it comes to funding their projects. British film-maker Mark Gutteridge managed to secure funding from an intercom manufacturer for his award winning short film Intercom, which he is now developing into his first feature with backing from Northern Film & Media.
Despite the internet providing an increasingly accessible platform for short films, it seems that the ultimate prize for many film-makers is still to see their work on the big screen. "Getting a million hits on Youtube is great because it gives you exposure, but nothing will beat being in the cinema with the audience and meeting everyone in the bar afterwards. I think there is room for both," says Ilson.
Gutteridge's latest short, Assessment (which came out of Film London's Borough Film Fund Challenge) is currently playing before screenings of Wuthering Heights at the Curzon Soho, whilst The Virgin Media shorts scheme (which earlier this month hosted a star studded awards ceremony at the BFI), also offers winners the chance to screen their shorts before features at Picturehouse Cinemas.
But the practice of screening shorts before features is no longer widespread, with increasingly lucrative adverts taking their place. "It seems bonkers that there is public money supporting cinemas like Watershed [in Bristol] and Cornerhouse [in Manchester], but we are not asking them to show five minute shorts ahead of the films there. They should be doing that and it's exactly right for those kind of audiences," says Moll. Certainly, when it comes to other forms of distribution, the US seems to be ahead of the game, with channels such as Shorts HD and Dish Network offering alternative platforms.
Looking ahead and Carlton believes there has been a shift in the mind set of many film-makers. "Yes, some want that moment in the cinema and that's great, provided you can get an audience in, and it can justify being on the big screen, both commercially and artistically. But more and more filmmakers understand that different types of films work well in different contexts. If anything it's the funders and distributors who are failing to keep up."
Readers' comments (3)
In response to Chris's cri de coeur, he may like to know that Watershed/Encounters with the grateful help of Arts Alliance digitise the winners of the 90second depict! competition and get them out to cinema servers across the UK to play with features. This has happened over the past four years so makes up an interesting diverse bunch of short film animation and live action content for cinemas to screen. We also work with distributors to identify feature titles that they will play with. At Watershed we indeed screen them in front of features. It's not the whole answer I'm sure but should be noted.
The BFI supports over 150 short films every year through First Light. These films are a valuable training ground for young people to learn the craft of storytelling through film. Young people work alongside professionals and use industry-standard equipment to create high quality work, that, in my opinion deserves a wider audience.
For those interested in pursuing the product placement route for funding which is touched on briefly in the article, this link may be of interest:
It's a video of a "Brands and Filmmakers" panel session from the 2008 Encounters Film Festival. The short film I used as a case study - Amelia and Michael - is available to view online on the BBC Film Network: http://www.bbc.co.uk/filmnetwork/films/p00l3nl0
I'm not sure I agree with the overriding emphasis on "modern digital technology" from Nik Powell and indeed from the UK Film Council's previous approach to short film funding.
Besides the discipline and purposefulness that shooting on film instils, shooting format should also be an aesthetic choice, whether it's Super 8 or IMAX (believe it or not there are a few shorts which have shot on the IMAX format!)
Not only that but often the perceived cost and time implications of shooting on film are not always correct. I know that the filmmakers behind the (feature film) SHIFTY worked out it would be cheaper and quicker for them to shoot on 16mm than HD.
I'm also disagree quite strongly with Phil Ilson's thesis that having a decent budget forces people to "play by the rules" and therefore stifles creativity. His festival shows some interesting and creative work, but I detect a kind of inverse snobbery about budgets and "mainstream" shorts.
"Heavily funded"? The loaded language says it all.
Anyone would think that denying support to filmmakers who aren't "out of touch with the morons who go to the Odeon" (or "BAFTA-chasers" as they are known in the bars of the ICA) is a good thing!
Personally, I think there's room in the world for both types of film, but people involved in short films do seem to get very tribal about it, when surely a catholic commitment to quality would probably better serve audiences and the ecology of new talent coming into the industry.
As much as I love Lynne Ramsay and Andrea Arnold are the audience for their films so unsated that we need to plough resources into bringing through another 10 imitators of their work?
Have your say
You must sign in to make a comment.


text:
Our African statues selection includes mother and child table sculptures as well as African lady table sculptures. Or, explore our safari statues for animal totem table sculptures, and bring your decor to life.
Beautiful Safari & African Statues
African statues feature richly-ornamented attire as well as the heartfelt moments experienced between a mother and her child. Incorporate one of these expressive table sculptures into your own home decorating. Standing upon your storage cabinet, an African mother sculpture holds her infant close. This loving pair will invite you to reflect on the beauty of the maternal bond. Or, bestow a little glamour on your makeup station. Shop our African table sculptures section, and find an elegant lady statue to hold your earrings and other small jewelry pieces.
Elephant Sculptures, Safari Animal Statues & More
Enrich numerous rooms throughout your abode with safari table sculptures. If your Serengeti-inspired space lacks some oh-so-essential wildlife, turn to our safari animal statues. An elephant totem sculpture portrays pachyderms stacked one on top of the other. Perched on a lotus leaf base, these marvelous animals flaunt a warm brown finish. Or capture the diversity of the savannah, and showcase an animal totem table sculpture. Sustaining a precarious balancing act, an elephant, rhino, zebra and cheetah exhibit brown, black and silver hues. Pair African animal statues with safari-themed throws for visual harmony.
African table sculptures, meanwhile, look quite striking when combined with handcarved wood masks or vibrant wall plaques. Find fashionable African lady sculptures garbed in head wraps, intricate dresses and spangly jewelry. Holding tropical leaves or woven baskets, these captivating sculptures offer a means to display your decorative accents. Also search our African table decorations for mother and child sculptures. Whether cradling her baby or patting her daughter's head, these affectionate moms remind us to appreciate all the little moments of motherhood.
Shop our safari table sculptures for intriguing animals, and uplift your coordinating home accents. Or, turn to African table sculptures for posh style and loving interactions that will refine your surroundings. Arrive at just the right statement for your console table, bookcase shelf or bedroom nightstand.


text:
Frankly speaking it is really important question, there are pluses and minuses in all the systems, tried different ones (emails, tickets, forums).
My choice, at the moment, is a forum. Very easy to manage, users help each other. The only problem I can't get how to have a knowledge base in vBulletin .
Hi everyone, this thread has been really informative! Item support is still something we really want to provide for as part of the marketplaces, and something I'm currently looking at closely, so this is great timing.
Ivor said
tl;dr PEOPLE WANT THEIR SUPPORT FORUM BACK !
When you take something away, people always want it back. We hate change of almost any kind
purethemes said
I use ticket system currently, but I'm planing to switch to forum
What's your reasons for switching over?
kops said
Well the issue with a ticketing system is that the answers are not public…
I've used some great ticket-based systems that are open rather than private, like GitHub's issues system, for example. It's pretty open like a forum (anyone can see the open (and closed) issues, search, comment, answer, etc), but it behaves more like a ticket — it can be marked as resolved, it can be assigned, etc.
kops said
…but since the powers that be decided that a search function is not necessary for a 120-page comments section on an item, then a forum, for me, is the next best thing.
If we wanted to turn the comments into a great way of handling item support, a search function is definitely needed, as is permalinks and a bunch of other stuff the community is asking for. It's not that we don't think search is necessary, it's that the way comments have been structured makes this far from easy. I promise, we're not ignoring requests like this
We could invest the time to make comments work better for item support, but we'd still be cramming item support into a comment system designed for a completely different job.
So, we need to balance that up against the time required to deliver something more appropriate for item support (for as many authors as possible), which is what I'm looking into right now.
kops said
…then adding nothing to the FAQs. That gives me Envato-rage >:|
I think half the problem is that our FAQ system is lacking as well. There's no way for authors to edit or re-order the questions, which must give the authors plenty to "rage" about as well. The good news is this is easy to fix, and I hope we can get to that really soon.
Probably the most important question is: Where are we heading (regarding support)?
Goals: I would say the goals of a new solution, lets call it "Awesome Support Solution (ASS)" should not only have features but should also have some various other goals
- ASS should be useful on all marketplaces and shouldn't vary to much. An author from graphicriver should be able to handle it so as a themeforest author.
- ASS should have a purchase verification implemented.
- ASS should have an integrated search, which just works
- ASS should have a notification system which sends notifications by e-mail or feed (w. API )
- ASS shouldn't be used for pre-sale questions or other kind of conversation ("Good Luck with Sales"...)
- ASS should put the author in more control
- ASS should be based on the Envato API
- ASS should offer the option to turn support requests into customization requests, enabling authors to get also paid for support.
- some things more which other authors already mentioned or mention after my post
Sidenote: Of course I know that the "comments" are already streamlined over all marketplaces and have already a purchase verification included, as well as other solutions have also some features from the above mentioned. The list above should be more of a list where all needed features are collected together.
Another important aspect is to offer more than just "sometimes support, sometimes not". I mean at the moment there is no line between authors which offer free support and authors who don't give any support since it isn't mandatory. Personally I can understand all the authors who are investing so much time into their documentations and even in their FAQ and still having some clients who prefer to just ask. It's annoying. So why not say, with the purchase of an item support isn't included, but offering the option to buy "support packs". Maybe in form as tickets? And authors have the option to opt-out if they don't want to give support (but be honest, who really wants to say no to some bucks?).
On the other hand envato also gets a cut from that – Win / Win / Win, even for the customer since they can expect a better support with better response times.
Authors can even hire staff for support since it would be really easy to determine what income comes through the item itself and what from the "support packs". That goes hand in hand with customization (which is probably the next big thing in this branch > see tweaky for example)
In the end I come to the conclusion that the best solution would be to have a custom stand-alone script (or webapp, you name it) which includes all the features mentioned above, is partly customizeable and fully extensible. It also integrates perfectly with the Envato API (which probably needs also an overhaul as well).
Assuming the above, customers would be able to buy an item with the included documentation and source files. To get some support they simply need to buy a support-pack, with N tickets, which they can spend for their requests.
- Customers can expect a better working support system since it's not only a part of business for authors but instead IT IS their business.
- Authors get some additional money
- Envato gets a cut
- Prices for the items can be lowered again
- Customers who know what they're doing don't need to buy more without the need of support in opposite to a customer who needs support. ("Pay what you get")
- Lots of work for the dev's
- You name it
justinfrench said
I think half the problem is that our FAQ system is lacking as well. There's no way for authors to edit or re-order the questions, which must give the authors plenty to "rage" about as well. The good news is this is easy to fix, and I hope we can get to that really soon.
Personally I think that the majority of customers just give a sh** on FAQ . For some parts it is ok to use FAQ but as soon as it comes to theme-specific FAQ 's it is just useless. Basic Question like how to edit the file can anyway be found in the documentation which is mandatory for every item uploaded.
Re-Ordering would be probably a nice little feature but it wouldn't be hard to "edit" a FAQ . It's just a matter of copy and pasting the whole thing in the editor below and then it can be modified. The old FAQ can be deleted.
To keep it short: If the support forum/ticket solution is good enough there is no need for FAQ at all.
We use a portal based on a theme that was for sale on Themeforest (but is not anymore). It combines a support forum, FAQ and knowledgebase. If anyone wants to see how it looks, you can take a look here.
We also use a support ticket system (Zendesk) which has turned out to be pretty great.
infuse01 said
Goals: [...] I would say the goals of a new solution, lets call it "Awesome Support Solution (ASS)" [...]
That sounds more like a verdict than an abbreviation.
justinfrench said
purethemes saidWhat's your reasons for switching over?
I use ticket system currently, but I'm planing to switch to forum
I'm using http://ticksy.com/ for support, and there are couple things missing (like advanced search engine – it's not very good for users who want to find solution for problem solved 10x before) so I wanted to build my own support forum to have more view on data and more customization options. I decided it's too big task right now and it's not worth it, ticksy is overall great system and for now it's enough for me – it's worth much more than 5$ you have to pay per month to use it. But as all this solution it has one drawback – the verification process. If Envato would bought Ticsky and integrate it with marketplace it would be best thing ever
Anyway, no matter what and when you'll do – the one single most important feature in my opinion is to allow users to reply to other users comments/tickets – many of top elite authors have support teams and now it's impossible for them to use comment section on ThemeForest as only author can reply to comments.
Thanks for taking interest in that matter
justinfrench said
Hi everyone, this thread has been really informative! Item support is still something we really want to provide for as part of the marketplaces, and something I'm currently looking at closely, so this is great timing.
Hi justinfrench,
It's goor to read that Envato is paying attention to it. Improved comments system will be a great help for authors with moderate sales!
However, please don't make support via it compulsory for every author. For those with bigger number of sales it is much more convenient to use their own solutions to provide support. E.g.: we have dedicated support staffs. And we should not give them accesses to TF account to provide support, right? Also authors can have their own support system integrated to knowledge base with dynamical tips and troubleshooter. I'm not sure that Envato can/should develop that.
What wold be a real help – is a dedicated "support" tab on Item page. That will redirect users to authors support system. Or "Item Support" button underneath the item preview right to "Live Preview" and "Screenshots" buttons.
And please please please please bring that * comment paginator back to the top of author dashboard!!!


text:
In a verdict that stunned a nation, a jury found Casey Anthony not guilty in the murder of her 2-year-old daughter Caylee. During that first month that her daughter went missing, Casey Anthony told no one. Not a soul. In fact, when questioned about her daughter's whereabouts – she lied. To her parents. To friends. [Read More…]
Why Casey Anthony lied
July 6, 2011 by Karen Spears Zacharias 39 Comments
Filed Under: Uncategorized Tagged With: Casey Anthony, Caylee Anthony, child abuse, CNN, crime, crime sleuths, Dateline, dateline.com, defense, Dr. Drew, forensics, HLN, Huffington Post, investigators, Jose Baez, jury, Karly Sheehan, murder, Nancy Grace, New York Times, Orlando, prosecutors, Salon, The Daily Beast, the state of Florida, Tot Mom, trial, verdict 39 Comments


text:
Become A Member
Apply For A Loan
Loan Products
Savings Accounts
Checking Accounts
IRA Accounts
Rates, Fees & Calculators
CU Services
Pay Your Credit Card Bill
Insurance Products
Sunbelt Bonus Cash
Become A Member
Become A Select Employee Group
Why Choose A Credit Union?
Affiliations & Partnerships
Central Sunbelt FCU vs Banks
Secure Finances
Improve Your Credit
Hours, Numbers & Locations
Who We Are
For Sale
CSFCU Community
Holiday Schedule
Important Checklist/Changes
ATM/Debit Card Changes
Rewards Checking Changes
What is Advantage Checking?
Changes to Online Services
Changes To Touch Tone Teller
Debit & Online Service Info
New Text Bankng Commands
Phone Number:
(601) 649-7181
Toll Free:
(855) 786-2228
Sunny By Phone:
Option 1
Lost or Stolen Debit Card:
(601) 649-7181
This credit union is federally insured by the
National Credit Union Administration
Privacy Policy
Website Terms
USA Patriot Act