Search Term: " high-dose "
Exploring the fatty acids that REDUCE your risk of premature death
April 27, 2019 09:55 AM
According to six separate studies published in the Asia Pacific Journal of Clinical Nutrition, the regular consumption of fatty acids substantially decreases the risk of premature death in adults. When the fatty acids are derived specifically from fish oil, the risk of death from any cause is reduced by 14 percent, compared to low or no consumption. Specifically, the risk of dying from a cardiac event is reduced by a whopping 47 percent. Unfortunately, because these studies don't appear in medical journals, most doctors do not advise their patients to take fish oil. There is also evidence that suggests fish oil decreases the risk of stroke and has potent anti-inflammatory properties. A word of caution, if you are on blood-thinners, consult with an integrative physician before taking fish oils regularly.
"In one study, fish oil was associated with better survival rates in heart attack victims, with researchers finding improved heart function and lower levels of inflammatory markers in people who took high-dose fish oil for six months after suffering a heart attack."
Read more: https://www.naturalhealth365.com/fatty-acids-nutrition-news-2790.html
Taking vitamin B6 could help you recall dreams
May 24, 2018 09:16 AM
A study that was recently shown in the journal called Perceptual and Motor Skills proved that vitamin B6 supplements can actually help you recall dreams. They ended up giving 100 participants from Australia the vitamin right before bedtime in order to see if they could recall what they dreamed about the night before. It did not impact the color or vividness of the imagery, but they were clear and easy to remember. The participants each took 240mg of Vitamin B6 before bed.
"The study, published online in the journal Perceptual and Motor Skills, included 100 participants from around Australia taking high-dose vitamin B6 supplements before going to bed for five consecutive days."
Read more: http://www.thesouthasiantimes.info/news-Taking_vitamin_B6_could_help_you_recall_dreams-207247-Health-23.html
High Dose Vitamin C Can Reduce a Cold’s Duration by 20 Percent
May 01, 2017 09:59 AM
When you have a cold, it can be hard to talk, walk, breath, or even crawl out of the bed. They say that a cold must simply run its course, and all that can be done is treat the symptoms. But, there is new evidence that begs to differ. With high doses of Vitamin C, you may be able to kick the cold where it hurts, and reduce the time that you are sick by an average of 20%!
"A huge amount of data has found significant effects for vitamin C in the prevention and alleviation of symptoms of infections, including the common cold."
Read more: http://www.healthnutnews.com/high-dose-vitamin-c-can-reduce-colds-duration-20-percent/
High-dose vitamin C reduces inflammation in cancer patients, study shows
December 07, 2016 04:59 PM
It is was the first time this type of treatment was tested and studied specifically for its effects on inflammation in cancer patients. The results found indicate great promise for the use of high-dose intravenous vitamin C treatments to help reduce inflammation in cancer patients, which is one of the major factors of cancer and its progression. A range of cancers has been proven to benefit from vitamin C treatments, including cancers of the prostate, breast, skin, bladder, lung, pancreas, thyroid, and B-cell lymphoma.
"High levels of inflammation seem to indicate a higher risk of cancer as well as a less hopeful prognosis for healing and recovery."
Antioxidants and your health
May 17, 2010 10:44 AM
There is an impressive amount of scientific evidence supporting the health benefits of supplementing with a wide variety of antioxidants. Consequently, there are many health practitioners who have begun to recommend high dietary intakes of these crucial nutrients in order to prevent against oxidative stress. It was anticipated over two decades ago by leading researchers that high-dose supplementation with antioxidants is developing a significant role in the prevention and treatment of a lot of today’s common illnesses. It should be noted that antioxidants do not work in isolation. When an antioxidant neutralizes a free radical, it, itself, is oxidized and must be regenerated by another antioxidant before it can be used again. Because of this, it is crucial to supplement with a wide variety of antioxidants, in order to reflect what actually occurs in nature.
Vitamin C, an aqueous-phase antioxidant, is the main guard against oxidative attack in the extra-cellular matrix, as well as within the cytoplasm of the cell. Vitamin C happens to be a substrate for eight different enzyme systems that are involved in various cellular functions. Among these functions are collagen synthesis, ATP synthesis in the mitochondria, and hormone biosynthesis. Its main antioxidant partners are vitamin E and beta carotene, both of which help to regenerate vitamin C.
Of all the antioxidants, it seems as if vitamin E offers the greatest protection against heart disease because of its ability to protect the cardiovascular system from oxidative damage. It is lipid-soluble, making it an important component of the cell membrane, where it works to protect the cell against lipid peroxidation and control oxidation-induced inflammatory events. Recently, the gamma tocopherol form of vitamin E has shown a great deal of promise in its ability to reduce the risk of several oxidative stress related disease.
Beta-carotene is a member of a diverse group of photosynthetic pigments. It plays a huge role in human nutrition. As an antioxidant, it possesses a double-bond structure that allows it to react effectively with single oxygen radicals, absorbing and diffusing their energy. Beta-carotene also acts as a precursor for vitamin A by supplying a portion of the body’s requirement for the vitamin. This act alone plays a central role in the chemistry of vision. Beta-carotene and vitamin A both prevent the oxidation of cholesterol, reduce oxidative damage to DNA, and disable oxygen free radicals that are produced by exposure to sunlight and air pollution. These antioxidants are also involved in the activation of gene expression and the control of cell differentiation.
When combined together, vitamin C, vitamin E, and beta-carotene produce and important antioxidant trio that plays a huge role in fighting oxidative and inflammatory events. There are several other antioxidants that should be noted due to their ability to work synergistically with the vitamin C, vitamin E, and beta-carotene trio. These include vitamin A, alpha-lipoic acid, lycopene, coenzyme Q10, and the antioxidant mineral, selenium. In order to determine whether a nutrient provides antioxidant support, scientists question whether the product contains vitamin C, vitamin E, vitamin A, beta-carotene, alpha-lipoic acid, lycopene, coenzyme Q10, and selenium and to what strength these vitamins and minerals are per serving.
May 28, 2007 11:50 AM
Decades later, in January 2007, the FDA finally acknowledged the legitimacy of Pauling’s approach by approving the Cancer Treatment Center of America’s investigation of high-dose intravenous vitamin C and its effects on cancer patients. Meanwhile, Korean researchers undertaking a similar investigation reported in February 2007 that cancer patients receiving mega-dose intravenous vitamin C were found to show greater physical, emotional and cognitive function, while reporting less fatigue, nausea, vomiting, pain and appetite loss.
Intravenous mega-dose vitamin C is entirely different league from supplementation—but many studies suggest that vitamin C supplements may help prevent cancer.
In the Nurse’s Health Study, premenopausal women with a family history of breast cancer who consumed an average of 205mg of vitamin C every day (well above the RDA) experienced a 63% lower risk of breast cancer than women who consumed an average of 70mg a day. A prospective study that tracked 870 men over 25 years found that those who consumed over 83mg of vitamin C daily had a 64% reduction in lung cancer. University of California researchers tracking 12,000 adults for an average of ten years found that those with the highest vitamin C intake had the lowest death rates for all cancers. Finally, an analysis of 90 separate studies found that vitamin C and vitamin C rich foods offered significant protective effects against various forms of cancer.
Vitamin C is already a supplement superstar—but, as it turns out, we may just be beginning to understand its far-reaching health benefits. –Patrick Dougherty
Benfotiamine raises the blood level of thiamine pyrophosphate (TPP)
August 02, 2005 03:52 PM
Benfotiamine raises the blood level of thiamine pyrophosphate (TPP), the biologically active co-enzyme of thiamine.4
Thiamine and its Co-enzyme, TPP
Thiamine (vitamin B1) plays an essential part in the metabolism of glucose, through actions of it co-enzyme TPP (thiamine pyrophosphate). TPP is formed by the enzymatically-catalyzed addition of two phosphate groups donated by ATP to thiamine. TPP also goes by the name "thiamine diphosphate." In the cytoplasm of the cell, glucose, a 6-carbon sugar, is metabolized to pyruvic acid, which is converted into acetyl-CoA, otherwise known as "active acetate." Acetyl CoA enters the mitochondrion, where it serves as the starting substrate in the Kreb’s cycle (citric acid cycle). The Krebs cycle is the primary source of cellular metabolic energy. TPP, along with other co-enzymes, is essential for the removal of CO2 from pyruvic acid, which in turn is a key step in the conversion of pyruvic acid to acetyl CoA. CO2 removal from pyruvic acid is called "oxidative decarboxylation," and for this reason, TPP was originally referred to as "cocarboxylase." TPP is thus vital to the cell’s energy supply. Benfotiamine helps maintain healthy cells in the presence of blood glucose. Acting as a biochemical "super-thiamin," it does this through several different cellular mechanisms, as discussed below.
Benfotiamine and Glucose Metabolism Benfotiamine normalizes cellular processes fueled by glucose metabolites.
As long as glucose remains at normal levels, excess glucose metabolites do not accumulate within the cell. The bulk of the cell’s glucose supply is converted to pyruvic acid, which serves as substrate for production of acetyl CoA, the primary fuel for the Krebs cycle. Of the total amount of metabolic energy (in the form of ATP) released from food, the Krebs cycle generates about 90 percent.5 In the presence of elevated glucose levels, the electron transport chain, the final ATP-generating system in the mitochondrion, produces larger than normal amounts of the oxygen free radical "superoxide." This excess superoxide inhibits glyceraldehyde phosphate dehydrogenase (GAPDH), as key enzyme in the conversion of glucose to pyruvic acid, resulting in an excess of intermediate metabolites known as "triosephosphates." Increase triosephophate levels trigger several cellular mechanisms that result in potential damage to vascular tissue. Cells particularly vulnerable to this biochemical dysfunction are found in the retina, kidneys and nerves.
Benfotiamine has been shown to block three of these mechanisms: the hexosamine pathway, the diaglycerol-protein kinease C pathway and the formation of Advanced Glycation End-poducts. As discussed below, benfotiamine does this by activating transketolase, a key thiamin-dependent enzyme.6 Benfotiamine stimulates tranketolase, a cellular enzyme essential for maintenance of normal glucose metabolic pathways.* Transketolase diverts the excess fructose-6-phosphate and glyceraldehydes-3-phosphate, (formed by the inhibition of GAPDH, as mentioned above), into production of pentose-5-phosphates and erythrose-4-phosphate and away from the damaging pathways. Benfotiamine activates transketolase activity in bovine aortic endothelial cells incubated in glucose.6 To test benfotiamine’s ability to counteract these metabolic abnormalities caused by elevated blood glucose, studies have been done in diabetic rats. Benfotiamine increases transketolase activity in the retinas of diabetic rats, while concomitantly decreasing hexosamine pathway activity, protein kinase C activity and AGE formation.6
Benfotiamine and Protein glycation Benfotiamine controls formation of Advanced Glycation End-products (AGEs).
AGEs have an affinity for proteins such as collagen, the major structural protein in connective tissue. AGEs are formed through abnormal linkages between proteins and glucose. This occurs via a non-enzymatic glycosylation reaction similar to the "browning reaction" that takes place in stored food.7 At high glucose concentrations, glucose attaches to lysine, forming a Schiff base, which in turn forms "early glycosylation products." Once blood glucose levels return to normal levels, the amount of these early glycosylation products decreases, and they are not particularly harmful to most tissue proteins. On long-lived proteins such as collagen, however, early glycosylation products are chemically rearranged into the damaging Advanced Glycation End-products. AGE formation on the collagen in coronary arteries causes increased vascular permeability. This vessel "leakiness" allows for abnormal cross-linking between plasma proteins and other proteins in the vessel wall, comprising vascular function and potentially occluding the vessel lumen. A number of other potentially harmful events may also occur, including production of cytokines that further increase vascular permeability. Endothelin-1, a strong vasoconstrictor, is over produced, increasing the possibility of thrombosis and generation of oxygen free radicals is stimulated.8 It is vitally important to support normal glucose metabolic pathways so that formation of AGEs is minimized. Benfotiamine, in the test tube (in vitro) prevents AGE formation in endothelial cells cultured in high glucose by decreasing the glucose metabolites that produce AGEs.9 Endothelial cells make up the membranes that line the inner walls of organs and blood vessels. In a rat study comparing the effects of Benfotiamine with water-soluble thiamin, Benfotiamine inhibited AGE formation in diabetic rats while completely preventing formation of "glycooxidation products," which are toxic by products of chronic elevated blood glucose. AGE levels were not significantly altered by thiamin.10 Benfotiamine also normalized nerve function in the animals. After three months of administration, "nerve conduction velocity (NCV)," a measure of nerve function, was increased by both benfotiamine and thiamin; at six months, NCV was normalized by benfotiamine, whereas thiamin produced no further increases in this parameter.
Dysfunctional glucose metabolic pathways leading to AGE formation occurs in endothelial cells of the kidneys. In a recent animal study, benfotiamine was administered to rats with elevated glucose levels. Benfotiamine increased transketolase activity in the kidney filtration system of these rats, while at the same time shifting triosephophates into the pentose pathway and preventing protein leakage.11
Benfotiamine has an excellent tolerability profile and can be taken for long periods without adverse effects.3,12 The statements in this fact sheet have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
1. Bitsch R, Wolf M, Möller J. Bioavailability assessment of the lipophilic benfotiamine as compared to a water-soluble thiamin derivative. Ann Nutr Metab 1991;35(2):292-6.
2. Schreeb KH, Freudenthaler S, Vormfelde SV, et al. Comparative bioavailability of two vitamin B1 preparations: benfotiamine and thiamine mononitrate. Eur J Clin Pharmacol 1997; 52(4):319-20.
3. Loew D. Pharmacokinetics of thiamine derivatives especially of benfotiamine. Int J Clin Pharmacol Ther 1996;34(2):47-50.
4. 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;56(3):251-7.
5. Pike RL, Brown ML. Nutrition, An Integrated Approach, 3rd Ed. New York:MacMillan; 1986:467.
6. Hammes H-P, Du X, Edlestein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic neuropathy. Nat Med 2003;9(3):294-99.
7. Monnier VM, Kohn RR, Cerami A. Accelerated age-related browning of human collagen in diabetes mellitus. Proc Natl Acad Sci 1984;81(2):583-7.
8. Brownlee M. The pathological implications of protein glycation. Clin Invest Med 1995;18(4):275-81.
9. Pomero F, Molinar Min A, La Selva M, et al. Benfotiamine is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol 2001;38(3):135-8.
10. Stracke H, Hammes HP, Werkman 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):300-6.
11. Babaei-Jadidi R, Karachalias N, Ahmed N, et al. Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes 2003;52(8):2110-20.
12. Bergfeld R, MatsumaraT, Du X, Brownlee M. Benfotiamin prevents the consequences of hyperglycemia induced mitochondrial overproduction of reactive oxygen specifies and experimental diabetic neuropathy (Abstract) Diabetologia 2001; 44(Suppl1):A39.
July 15, 2005 12:58 PM
Glycerylphosphorylcholine -- Supports Cognitive Function in AD ...
May 24, 2005 09:52 AM
Cognitive Improvement in Mild to Moderate Alzheimer's Dementia After Treatment with the Acetylcholine Precursor Choline Alfoscerate: A Multicenter, Double-Blind, Randomized, Placebo-Controlled Trial Maria De Jesus Moreno Moreno, MD Instituto Nacional de la Senectud, Mexico City, Mexico
in both men and woman they consistently improved after 90 and 180 days versus baseline with adiministration of GPC three times a day, whereas in the placebo group they remained unchanged or worsened. Statistically significant differences were observed between treatments after 90 and 180 days.
Bartus RT, Dean RL III, Beer B, Lippa AS. The cholinergic hypothesis of geriatric memory dysfunction, Science. 1982;217:408-414. 2. Larson EB, Kukull WA, Katzman RL. Cognitive impairment: Dementia and Alzheimer's disease. Annu Rev Public Health. 1992;13:431-449. 3. Hofman A, Rocca WA, Brayne C, et al, for the European Prevalence Research Group. The prevalence of dementia in Europe: A collaborative study of 1980-1990 findings. Int d Epidemiol. 1991;20:736-748. 4. Blackwood W, Corsellis JAN, eds. Greenfield's Neuropathology. 3rd ed. London: Arnold; 1976. 5. Geldmacher DS. Cost-effective recognition and diagnosis of dementia. 5emin Neurol. 2002;22:63-70. 6. Perry EK, Tomlinson BE, Blessed G, et al. Correlation of cholinergic abnormalities with senile plaques and mental test scores in senile dementia. BMJ. 1978;2:1457-1459. 7. Perry EK. The cholinergic hypothesis--ten years on. Br Med Bull. 1986;42:63-69. 8. Giacobini E. From molecular structure to Alzheimer therapy. Jpn d Pharmacol. 1997;74:225-241. 9. Giacobini E. Invited review: Cholinesterase inhibitors for Alzheimer's disease therapy: From tacrine to future applications. Neurochem Int. 1998;32:413-419. 10. Brinkman SD, Smith RC, Meyer JS, et al. Lecithin and memory training in suspected Alzheimer's disease. J Gerontol. 1982;37:4-9. 11. Davis E, Emmerling MR, Jaen JC, et al. Therapeutic intervention in dementia. Crit Rev Neurobiol. 1993;7:41-83. 12. Amenta E Parnetti L, Gallai V, Wallin A. Treatment of cognitive dysfunction associated with Alzheimer's disease with cholinergic precursors. Ineffective treatments or inappropiate approaches? Mech Ageing Dev. 2001;122:2025-2040. 13. Sigala S, Imperato A, Rizzonelli P, et al. k-Alpha-glycerylphosphorylcholine antagonizes scopolamine-induced amnesia and enhances hippocampal cholinergic transmission in the rat. Eurd Pharmacol. 1992;211:351-358. 14. Govoni S, Battaini E Lucchi L, et al. Effects of alpha-glycerylphosphorylcholine in counteracting drug-induced amnesia: Through cholinergic and non-cholinergic mechanisms [in Italian]. Basi Raz Ter. 1991;21:75-78. 15. Canonico PL, Nicoletti F, Scapagnini U. Neurochemical and behavioral effects of alpha-glycerylphosphorylcholine [in Italian]. Basi Raz Te~ 1990;20: 53-54. 191 CLINICAL THERAPEUTICS ® 16. Parnetti L, Amenta E Gallai V. Choline alphoscerate in cognitive decline and in acute cerebrovascular disease: An analysis of published clinical data. Mech Ageing Dev. 2001;122:2041-2055. 17. Venn RD. The Sandoz Clinical Assessment-Geriatric (SCAG) scale. A general-purpose psychogeriatric rating scale. Gerontology. 1983;29:185-198. 18. Di Perri R, Coppola G, Ambrosio LA, et al. A multicentre trial to evaluate the efficacy and tolerability of alpha-glycerylphosphorylcholine versus cytosine diphosphocholine in patients with vascular dementia. J Int Med Res. 1991;19:330-341. 19. Frattola L, Piolti R, Bassi S, et al. Multicenter clinical comparison of the effects of choline alphoscerate and cytidine diphosphocholine in the treatment of multi-infarct dementia. Curt Ther Res Clin Exp. 1991;49:683-693. 20. Muratorio A, Bonuccelli U, Nuti A, et al. A neurotropic approach to the treatment of multi-infarct dementia using L-c~-glycerylphosphorylcholine. Curt Ther Res Clin Exp. 1992;52:741-75l. 21. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Washington, DC: APA; 1994. 22. McKhann G, Drachman D, Folstein M, et al. Clinical diagnosis of Alzheimer's disease: Report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology. 1984;34:939-944. 23. Folstein ME Folstein SE. "Mini-mental state": A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975; 12:189-198. 24. Loeb C, Gandolfo C. Diagnostic evaluation of degenerative and vascular dementia. Stroke. 1983;14:399-401. 25. Hamilton M. A rating scale for depression.J Neurol Neurosurg Psychiatry. 1960;23:56-62. 26. Hamilton M. Development of a rating scale for primary depressive illness. BrJ Soc Clin Psych& 1967;6:278-296. 27. Rosen WG, Mohs RC, Davis KL. A new rating scale for Alzheimer's disease. AmJ Psychiatry. 1984;141:1356-1364. 28. Reisberg B, Ferris SH, De Leon MJ, et al. The Global Deterioration Scale for assessment of primary degenerative dementia. Am J Psychiatry. 1982;139:1136-1139. 29. National Institute of Mental Health. Clinical global impressions. In: Guy W, ed. ECDEU Assessment for Psychopharmacology. Revised edition. Rockville, Md: National Institute of Mental Health; 1976:217-222. 30. Burns A, Russell E, Page S. New drugs for Alzheimer's disease. Br J Psychiatry. 1999;174:476-479. 31. Kumar V, Anand R, Messina J, et al. An efficacy and safety analysis of Exelon in Alzheimer's disease patients with concurrent vascular risk factors. Eur J Neurol. 2000;7:159-169. 32. Knapp MJ, Knopman DS, Solomon PR, et al, for the Tacrine Study Group. A 30-week randomized controlled trial of high-dose tacrine in patients with Alzheimer's disease. JAMA. 1994;271:985-991. 192 M. Moreno 33. Lindstrom MJ, Bates DM. Newton-Rapshon algorithms for linear-mixed effects models for repeated measure data. J Am Stat Assoc. 1998;83:1014-1022. 34. Thai LJ, Carta A, Clarke WR, et al. A 1-year multicenter placebo-controlled study of acetyl-L-carnitine in patients with Alzheimer's disease. Neurology 1996;47:705-711. 35. Rogers SL, Friedhoff LT, for the Donepezil Study Group. The efficacy and safety of donepezil in patients with Alzheimer's disease: Results of a US multicentre, randomized, double-blind, placebo-controlled trial. Dementia. 1996;7:293-303. 36. Rogers SL, Doody RS, Mohs RC, Friedhoff LT, for the Donepezil Study Group. Donepezil improves cognition and global function in Alzheimer disease: A 15-week, double-blind, placebo-controlled study. Arch Intern Med. 1998; 158:1021-1031. 37. Corey-Bloom J, Anand R, Veach J, for the ENA 713 B352 Study Group. A randomized trial evaluating the efficacy and the safety of ENA 713 (rivastigmine tartrate), a new acetylcholinesterase inhibitor, in patients with mild to moderately severe Alzheimer's disease. Int J Geriatr Psychopharmacol. 1998;1:55-65. 38. Rosler M, Anand R, Cicin-Sain A, et al. Efficacy and safety of rivastigmine in patients with Alzheimer's disease: International randomised controlled trial. BMJ. 1999;318: 633-638. 39. Amenta E Bronzetti E, Del Valle M, Vega JA. Effects of alpha-glycerylphosphorylcholine in neuroanatomy of aging brain in experimental animals [in Italian]. Basi Raz Te~: 1990;20:31-38. Address correspondence to: Scientific Department, Italfarmaco SpA, via dei Lavoratori 54, 20092 Cinisello Balsamo, Milan, Italy.
Its not about Ehpedra -- its about DSHEA ...
May 24, 2005 08:58 AM
On april 14th 2005, a federal court in UTAH Ruled against the FDA's ban on low dose ephedra products. The plaintiffs were Nutraceutical Corporation and its subsidiary Solaray. They sued not just to protect their ephedra product, but to protect your access to other supplements. Why did they sue and what does this mean for you?
Media and Political Rhetoric Vs. Real Science
Protecting DSHEA and your access to dietary supplements
Why did Nutraceutical challenge FDA's actions?
Why did FDA Ban Ephedra?
What did the court Decide?
How does the Decision affect me?
Does the ruling mean that ephedra is safe?
What's Next for Ephedra?
What can I do to protect my access to supplements?
Let your congressman and Senators know that access to supplements is important to you. A useful website for contacting them is: www.saveoursupplements.org
contact Nutraceutical by email at: Savesupplements@nutracorp.com
Note: Solaray® Whole herb ephedra was formulated to have 10mg or less ephedrine alkaloids per daily dose(two servings). © Nutraceutical corporation...