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2. What is the Stem Cell
Theory of Renewal? 3. Why do we hear much
in the news about embryonic stem cells and very little
about adult stem cells? 4. What is the effect
of StemEnhance? 5. What is the science
behind StemEnhance?
7. Can StemEnhance deplete
the bone marrow? Do we have a finite number of stem cells? 9. Can stem cells lead
to aberrations such as cancer? 10. Why has StemTech
HealthSciences elected to use the Network Marketing distribution
channel?
Recently, people conducting an Internet search on “stem
cell enhancer” were surprised to find an article
by Stephen Barrett already raising doubts about StemEnhance
and stem cell enhancers. We welcome this opportunity to
provide you with further information on StemEnhance. Barrett also claims that blue-green algae based products might contain dangerous toxins. (See below for reports on microcystin and neurotoxicity) There is no excuse at this point in time, nearly a decade after the industry has developed a stringent quality control program, to still repeat such irrelevant allegations. Whereas infection of beef by E.coli is still responsible for more than 20,000 intoxications and nearly 500 deaths every year, whereas aflatoxin in corn, peanuts, milk products, spices and other foodstuff have been responsible for several deaths, and whereas shellfish toxins are still responsible for several deaths every year, blue-green algae has been linked to no ill effect. Like any other food ingredient, if potential contaminants like heavy metals, pesticides, and shellfish toxins are present in quantity below levels established as safe, then the product is deemed safe. Stating that blue-green algae may be dangerous is akin to stating that eating a shrimp cocktail or a hamburger at your favorite restaurant is dangerous. Such a statement reflects a lack of scientific background and knowledge, or deceptive intent. Barrett states that before taking any product, it is advisable to know whether it has been proven safe and effective for its intended purpose(s), and that with respect to StemEnhance, the following questions would have to be answered. 1. What evidence shows that
taking StemEnhance will improve anyone's health? 1. What evidence shows
that taking StemEnhance will improve anyone's health? As Mr. Barrett must know, given his claimed experience with the FDA, that we cannot make any health claims linked to StemEnhance since it is a dietary supplement and not a drug. Our claims are limited to structure and function claims, which is what we have solidly documented. StemEnhance supports the natural release of stem cells from the bone marrow, thereby assisting the body in maintaining optimal health. We would be delighted to publish the single patient outcomes we have documented, but they could be construed as inferred health claims. Nevertheless, clinical studies are currently in progress involving specific organs and system to further document the mechanics of stem cell physiology, and these studies will be eventually published.
The question may also refer to the safety of increasing the number of circulating stem cells everyday by 25-30%. Here also the safety is unquestionable. The normal range for the number of circulating stem cells is between 1.2 and 5.0 stem cells per µL of blood. An increase of 30% in the number of circulating stem cells would at most mean an increase of 1.5 cells per µL, which is well within normal physiological range. Looking at this from a different angle, Krause et al. [7] reported that one single stem cell was enough to reconstitute the entire hematopoietic (red blood cell) and immune systems. If one single stem cell can do this, then the billions of stem cells left in the bone marrow after taking StemEnhance can maintain a healthy and strong bone marrow. 4. How can users be
certain that long-term use will not cause abnormal tissue
growth?
AFA contains phenylethylamine (PEA), known as the “molecule of love” or the “molecule of joy”. PEA is a natural compound made by the brain whenever one feels content, happy. Deficiency in PEA has been linked to problems of concentration and low mood, and oral intake of PEA has been shown to improve these conditions. StemEnhance concentrates PEA at about 5mg/g. PEA is responsible for the immediate feeling of well-being that one experiences after taking StemEnhance. Because of the effect of PEA in the brain, StemEnhance could be contraindicated for people suffering from severe manic depression.
“Dr. Barrett was offered on several issues by the
Plaintiff, but the Court found that there was substantial
overlap on the issues that he and Dr. Sampson were asked
to address. “Thus, in order to avoid duplicative
or cumulative evidence (see Cal. Evidence Code §§
352, 411, 723), Dr. Barrett's testimony was limited by
the Court to the sole issue of FDA treatment of homeopathic
drugs. The relevancy of this issue was questionable at
best, since the Plaintiff had previously asserted that
its case did not depend on or seek to establish any violation
of federal food and drug laws or regulations. Nevertheless,
Plaintiff elicited testimony from Dr. Barrett on his experience
with the FDA as it relates to regulation of homeopathic
drugs. References [1] Orlic D, Kajstura J, Chimenti S, Limana F, Jakoniuk I, Quaini F, Nadal-Ginard B, Bodine DM, Leri A. & Piero Anversa. (2001) Mobilized bone marrow cells repair the infracted heart, improving function and survival. PNAS 98(18):10344–10349. [2] Werner N, Kosiol S, Schiegl T, Ahlers P, Walenta K, Link A, Bohm M, Nickenig G. (2005) Circulating endothelial progenitor cells and cardiovascular outcomes. N Engl J Med. 8;353(10):999-1007. [3] Bozlar M, Aslan B, Kalaci A, Baktiroglu L, Yanat AN, Tasci A. (2005) Effects of human granulocyte-colony stimulating factor on fracture healing in rats. Saudi Med J. 26(8):1250-4. [4] Kong D, Melo LG, Gnecchi M, Zhang L, Mostoslavsky G, Liew CC, Pratt RE, Dzau VJ. (2004) Cytokine-induced mobilization of circulating endothelial progenitor cells enhances repair of injured arteries. Circulation. 110(14):2039-46. [5] Eroglu E, Agalar F, Altuntas I, Eroglu F. (2004) Effects of granulocyte-colony stimulating factor on wound healing in a mouse model of burn trauma. Tohoku J Exp Med. 204(1):11-6. [6] Tomoda H, Aoki N. Bone marrow stimulation and left ventricular function in acute myocardial infarction. Clin Cardiol. 2003 Oct;26(10):455-7. [7] Krause DS, Theise ND, Collector MI, Henegariu O, Hwang S, Gardner R, Neutzel S, Sharkis SJ. (2001) Multi-organ, multi-lineage engraftment by a single bone marrow-derived stem cell. Cell 105:369-77. [8] Eglitis MA and Mezey VA. (1997) Hematopoietic cells differentiate into both microglia and macroglia in the brains of adult mice. Proc. Natl. Acad. Sci. USA Vol. 94, pp. 4080–4085. [9] Camargo FD, Green R, Capetenaki Y, Jackson KA, and Goodell MA. (2003) Single hematopoietic stem cells generate skeletal muscle through myeloid intermediates. Nature 9(12):1520-27. [10] Ianus A, Holz GG, Theise ND, and Hussain MA. (2003) In vivo derivation of glucosecompetent cells from bone marrow without evidence of cell fusion. J. Clin. Invest. 111:843-850.
AFA has been on the marketplace as an exceptional dietary supplement for more than two decades. During this time, not one incident remotely linked to microcystin has been reported… or to any other toxin as a matter of fact. But the media has established another perceived reality for AFA, under a unique set of circumstances. In 1996, I was Director of Research and Development of a marketing company centered around the sale of AFA. Soon after my arrival in 1995, I implemented a testing procedure for a then little-known toxin with the collaboration of Dr. Wayne Carmichael of Wright State University. The toxin was microcystin, which is produced by a type of blue-green algae called Microcystis. Since Microcystis is seen at times in Klamath Lake during some parts of the summer and since a new assay had been developed to measure microcystin, we decided to add this testing to our quality control program. In order to have records as complete as possible we tested samples backing as far as 1992. As expected, microcystin was present in small amounts that presented no health concern. However, in the summer of 1996 we observed a bloom of Microcystis that was somewhat larger than the previous years. After much discussion with several experts we elected to be pro-active with the situation and to trigger an education campaign. Similar to the story with aflatoxin in peanuts and corn, we decided to educate the local authorities and to work toward the development of safe limits to ensure quality and safety. We invited officials at the Oregon Health Division (OHD) to visit our facilities and to tell them about microcystin and our Quality Control program. It was the first time they were hearing about microcystin. We showed them the test, the inventory of product on hold, caught by an efficient Quality control program; we showed them everything. We thought we had done our duty and acted responsibly; we were expecting a response from OHD that would honor the approach we had taken. To our surprise, soon after the officials at OHD published an article mentioning that microcystin was a dangerous toxin, that more than 60 people had died in Brazil from microcystin toxicity. What they failed to mention was that this incident was linked to intravenous exposure through dialysis to about 25 gallons of water contaminated with microcystin. There is a world of difference between intravenous and oral exposures. Just think bout having a teaspoon of peanut butter injected in your vein… In the same article they mentioned that product containing as much as 20 ppm of microcystin had been harvested, though they failed to mention that this product had been caught by an effective Quality Control program and never reached any consumer. We were appalled. The moment we tried to defend our position we became the unconscionable corporate entity trying to make money by intoxicating people. Nothing could have been further from the truth. While a safe limit of 20 ppb had been established for aflatoxin, levels as high as 300 ppb have been tolerated at times, like in 1988, when a drought threatened farmers in the Midwest. Salmonella is present in about 0.02% of the eggs consumed by American, which amounts to a few thousand real exposures everyday. Contamination of ground beef by E. coli is responsible for an estimated 20,000 hospitalization and nearly 500 deaths every year. While all of these are tolerated, OHD triggered an unprecedented misleading bad press for a product that had no history of ill effect. Officials at OHD went as far as publishing an appalling paper in the scientific literature reporting that in spite of a ruling limiting the amount of microcystin in AFA at 1 ppm, 85 of the 87 samples taken from the marketplace contained a level of microcystin superior to 1 ppm. As with their previous releases, they failed to mention an important piece of information. The ruling was passed on October 17, 1997. Between the summer of 1996 and the date of the ruling, the industry had adopted the safe limit proposed by two prominent scientists, Dr. Wayne Carmichael, expert in toxic cyanobacteria at Wright State University, and Dr. Gary Flamm, former Head Toxicologist at the FDA in Washington, who both proposed a safe level of 5 ppm. These testimonials are on records at the Oregon Department of Agriculture (ODA). The samples tested by OHD were taken from the marketplace in the months following the ruling of 1 ppm. However, all the samples came from product released on the marketplace prior to the ruling, respecting the interim level of 5 ppm proposed by the experts. So while the industry was playing by the rules and respecting experts’ opinion, OHD once again acted deceptively concluding that the industry ignored the ruling. The situation was like one day changing the speed limit on a street and then accusing someone of having driven too fast the day before. The intent to deceive was obvious for those knowing the situation in details. Supported by experts we proposed to have a moratorium at 5 ppm for 2 years while we would pay for studies showing the safety of low levels of microcystin in AFA. The study that OHD relied upon for their safety assessment consisted of mice gavaged daily with pure toxin dissolved in water. The very process of gavaging a mouse leads to significant liver injury. In that study, at times control groups showed greater “toxicity” than the group receiving the highest level of toxin. The study was obviously flawed. Beside, using pure toxin was inappropriate. For example, AFA contains significant levels of silymarin, a bioflavanoid known to provided 100% protection against microcystin. To establish the safety of microcystin as a contaminant of AFA, we have to test microcystin in AFA. OHD refused any suggestion. Later on, someone close to the one person leading this whole vendetta at OHD, Duncan Gilroy, told me that no reasonable argument could change OHD’s position because Duncan Gilroy did not like blue-green algae and had the clear intention of bringing down this industry. Even after the ruling of 1 ppm, Gilroy kept telling consumer that no level of microcystin was safe and people should avoid consuming from blue-green algae. In any industry if a product is below the level considered safe, the product is deemed pure and safe for consumption, like corn and peanuts with aflatoxin, and beef with E. coli.
In 1995, Dr. Wayne Carmichael from Wright State University and Dr. Don Anderson from Woodshole Oceanographic Institute became consultants for a member of the Klamath Lake Algae industry, on the specific issue of algal toxicity. During the summer of 1996 a substantial bloom of Microcystis was unexpectedly observed that started in early July and continued into the third week of September. In collaboration with Dr. Jake Kann, Dr. Wayne Carmichael and Dr. Don Anderson, the situation was brought to the public’s attention, because of the industry’s commitment to public safety and public education, which led to the Oregon Health Division's awareness of the situation. Because of the existence of only a few proposed guidelines based on single studies and the uncertainties surrounding these studies, an unrestricted grant was given to the University of Illinois for the completion of a comprehensive risk assessment, reviewing more than 300 scientific articles, aimed at accurately evaluating the risk associated with microcystin as a possible contaminant of blue-green algae products. This risk assessment determined that 10 µg/g was considered a safe level. A similar safe level (5 µg/g) was later confirmed by a risk assessment performed by Dr. Gary Flamm, former head toxicologist at the FDA in Washington, DC. This safe level of 5 µg/g was also supported by Dr. Wayne Carmichael in a written testimonial. Despite the written opinions of many experts and the significant amount of data indicating that levels of 5 µg/g and even 10 µg/g were safe for human consumption, even children, the Oregon Department of Agriculture decided to pass a regulation establishing 1 µg/g as the maximum acceptable concentration (MAC). The actual safe level determined by animal studies was between 2,500 and 6,000 µg of microcystin per day. To add a margin of safety, this safe level was further divided by a factor of 1,000. The adopted safe level of 1 µg/g is therefore 1,000 times lower than level established as safe in animal studies, ensuring complete safety for children. Microcystin is indeed a liver toxin, however, it is completely safe at the levels currently found in blue-green algae products. Liver damage only occurs at levels that exceeds 10,000 times the adopted safe level of 1 µg/g. One would have to eat more than 5,000 capsules per day to reach such levels. The industry nonetheless welcomed the regulation and went immediately into compliance. During the entire process and after the adoption of the regulation the relationship between ODA and the blue-green algae industry has been one of collaboration. One of the unresolved elements of this regulatory process was the development of a validated assay to quantify microcystin. It was believed that such an assay could be developed in the year following the adoption of the regulation. However, collaboration between ODA and FDA in Washington State, as well as with independent universities and institutions, has failed to produce a validated test for the precise measurement of microcystin at low levels. Nevertheless, the tests currently utilized that have been developed and refined over the past 5 years, an enzyme linked immunosorbent assay (ELISA) and a protein phosphatase inhibition assay (PPIA), are precise enough to monitor compliance, even though levels found in a same sample analyzed on different occasions, or by different laboratories, can at times show significant variations. In conclusion, the blue-green algae industry has been
extremely pro-active with the problem of the presence
of Microcystis in Klamath Lake. Members of the Klamath
Lake Algae industry have worked with the Oregon Department
of Agriculture to raise the regulated level to 5 µg/g.
However, DLT’s position has been to fully integrate
the regulatory level of 1 µg/g, and to develop ways
to reduce microcystin content. As stated before, DLT has
developed and implemented a method to separate Microcystis
for Aphanizomenon flos-aquae. Lots of AFA harvested since 2000 all tested at less than 1 µg/g.
Upper Klamath Lake has sometimes been referred to as polluted because of the lake’s incredible bounty of Aph. flos-aquae. The most observable influence of this blue green algae is the change in the chemical properties of the water around the blooming algal masses, namely dissolved oxygen, pH and ammonia. Given summer conditions and a large algal bloom, water chemistry can change drastically and these parameters can reach levels that can directly impact fish species (Monda and Saiki, 1993). Fish will congregate near inflow areas of better water quality, yet their density and stressed condition renders them susceptible to outbreaks of disease and die-offs. In Upper Klamath Lake such fish kills (1971, 1986, 1995) are generally attributed to outbreaks of “Columnaris” disease (Logan and Markle, 1993). These outbreaks have been common in fish hatcheries under crowded, high temperature conditions (Piper et al. 1982). Such impact on the survival of fish has led people unaware of this natural chemistry to state that Klamath Lake is polluted. Various testing for pesticides, petro-chemicals and other contaminants over the past 10 years failed to reveal the presence of any such contaminants. Aph. flos-aquae and the issue of neurotoxicity Klamath Lake The second article concerning Klamath Lake was a preliminary summary of a toxicity test on Upper Klamath Lake Aph. flos-aquae published by Gentile (1971) in a review article on blue-green and green algal toxins. A mouse assay (n=1) was performed on a colony isolate of Aph. flos-aquae cultured for a short period of time in a laboratory. Signs of poisoning in the mouse were reported as similar to that of a Kezar Lake, New Hampshire (see below) Aph. flos-aquae sample later shown to produce a toxin with similarities to saxitoxin and its derivatives. In both articles, several elements did cast significant
uncertainty concerning this possible neurotoxicity of
Upper Klamath Lake Aph. flos-aquae. These include: For these reasons, it could not be concluded that Aph. flos-aquae from Upper Klamath Lake produced a neurotoxin. As quoted by Gentile (personal communication to W.W.C., March 27, 1996), “This anecdotal toxicity test on Upper Klamath Lake Aph. flos-aquae should be rigorously restudied before it can be concluded that the alga produces a toxin”. Periodic toxicity tests in the 1980’s plus frequent regular testing since 1991 have failed to reveal any neurotoxins in Upper Klamath Lake Aph. flos-aquae (Carmichael et al., 2000). Aph. flos-aquae samples from other locations Court Cases In the first one a man, Mr. Fineman, claimed that consumption
of Aph. flos-aquae triggered neuropathy. The case revealed
that Mr. Fineman had been suffering from diabetes since
early childhood and had had many episodes of developing
neuropathy. After two years of contracting with various
laboratories throughout the world to detect and identify
a neurotoxin in Aph. flos-aquae, Mr. Fineman had to withdraw
the suit because of lack of evidence. The court obliged
Mr. Fineman to published the following statement: In a second case, the aforementioned company Cell Tech
filed a lawsuit against an individual, Mark Thorson, who
had relentlessly published over the Internet that Aph.
flos-aquae from Klamath Lake contained a neurotoxin similar
to cocaine and dangerous to consumers. Once again, after
considerable effort to prove his allegations, Mr. Thorson
lost his case. He was also asked to published the following
statement over the Internet: These two cases are interesting as they both relied on the explicit demonstration that Aph. flos-aquae from Klamath Lake contained a neurotoxin. In both cases, many laboratories throughout the world with the capability and the expertise to detect and quantify neurotoxins were contracted to find neurotoxins in Aph. flos-aquae from Klamath Lake, with no success.
REFERENCES Carmichael, W.W., Drapeau, C., and Anderson, D.M. (2000) Harvesting of Aphanizomenon flos-aquae Ralfs ex Born. & Flah. Var. flos-aquae (Cyanobacteria) from Klamath Lake for human dietary use, J. App. Phyco., vol. 12, pp. 585-595. Carmichael, W.W., and P.R. Gorham. (1980) Freshwater cyanophyte toxins, In: Algae Biomass, Elsevier, New York, pp. 437-448. Gearheart, R.A., J.K Anderson, M.G. Forbes, M. Osburn, and D. Oros. (1995) Watershed strategies for improving water quality in Upper Klamath Lake, Oregon. Humboldt State University, Environmental Resources Engineering Department. 3 Volumes. Gentile, J.H., and T.E. Maloney. (1969) Toxicity and environmental requirements of a strain of Aphanizomenon flos aquae (L.) Ralfs, Can. J. Microbiol., vol. 15 (2), pp. 165-173. Gentile, J.H. (1971) Blue green and green algal toxins. In: Microbial Toxins, Vol. 7, Academic Press, New York, pp. 27-67. Gorham, P.R. (1964) Toxic Algae. In: Algae and Man, Plenum Press, New York, pp. 307-306. Logan, D.J., and D.F. Markle (1993) Fish faunal survey of Agency Lake and northern Upper Klamath Lake, Oregon. In Environmental research in the Klamath Basin, Oregon - 1992 Annual Report. S.G. Campbell (ed.) p. 341. Monda, D.P. and M.K. Saiki. (1993) Tolerance of Juvenile Lost River and Shortnose suckers to high pH, ammonia concentration, and temperature, and to low dissolved oxygen concentration. In Environmental research in the Klamath Basin, Oregon - 1992 Annual Report. S.G. Campbell (ed.) p. 341. Piper, R.G, I.B. McElwain, L.E. Orme, J.P. McCraren, L.G. Fowler, and J.R. Leonard. (1982) Fish Hatchery Management. U.S. Department of the Interior, Fish and Wildlife Service. Washington D.C. p. 517. Phinney, H.K. and Peek, C.A. (1961) Klamath Lake, an instance of natural enrichment. In Transactions of the seminar on Algae and Metropolitan Wastes. U.S. Public Health Service, pp. 22-27. Rapala, J., Sivonen, K., Luukkainen, R., and S.I. Niemela. (1993) Anatoxin-a concentration in Anabaena and Aphanizomenon under different environmental conditions and comparison of growth by toxic and non-toxic Anabaena strains - a laboratory study, J. Applied Phycol., vol. 5, pp. 581-591. Li, R., Carmichael, W.W., Liu, Y., and Watanabe, M.M. (2000) Taxonomic re-evaluation of Aphanizomenon flos-aquae NH-5 based on morphological and 16 rRNA gene sequences, Hydrobiologica, vol. 438, pp. 99-105. Sawyer, P.J., Gentile J.H., and J.J. Sasner. (1968) Demonstration of a toxin from Aphanizomenon flos-aquae (L.) Ralfs, Can. J. Microbiol., vol. 14, pp. 1199-1204. Overview Klamath Lake Algae from Upper Klamath Lake is absolutely non-toxic. However, like many other agricultural products, Klamath Lake Algae may contain naturally occurring compounds, microorganisms or by-products of human activity that need to be monitored and controlled. Each batch (lot) of Klamath Lake Algae is subjected to a battery of scientific tests to ensure that the algae consistently meets the highest standards of safety and purity. As a result of these tests, Klamath Lake Algae is one of the purest and safest foods available.
Historically, Upper Klamath Lake was a highly productive
(eutrophic) and diverse ecosystem due to a naturally high
inflow of nutrients (Gearheart et al. 1995). Though the
term eutrophic is often associated with adverse water
quality conditions, in reality, a body of water may be
ecologically “healthy” and eutrophic. In their
1967 report, Miller and Tash described a nutrient-rich
sediment layer many feet deep in Upper Klamath Lake. They
reported that the principal nutrients in Upper Klamath
Lake were supplied through natural geological processes
in quantities sufficient to maintain dense algal blooms,
however they did not include nutrient loading which resulted
from either local or upper watershed non-point sources
(mostly poor forestry and agricultural land management;
Gearheart et al. 1995). Current information indicates
that human activities have increased nutrient loading
to the lake over historical background levels (Bortleson
and Fretwell 1993; Gearheart et al. 1995). However, much
of the current debate centers on the effect of additional
nutrients on an already productive environment. Both internal
and external nutrient loading can influence nutrient concentrations
in the lake (Bortleson and Fretwell 1993) and probably
the composition of the planktonic community, however the
paucity of long-term scientific data makes it difficult
to determine actual causes. Kaffka et al. (1995) remarked
that phosphorous concentrations in available studies were
above levels that many limnologists think are limiting
to algal growth, and concluded that anthropogenic (human)
influences in the Basin were of little consequence compared
to natural enrichment processes. However, during periods
of intense algal blooms in Upper Klamath Lake, dissolved
phosphorus concentrations are reduced to levels which
are known to be limiting (Gearheart et al. 1995). Other
biologists (Gearheart et al. 1995; Bortleson and Fretwell
1993; Kann and Smith 1993; Miller and Tash 1967) have
documented increases in productivity and algal growth
over the past century. Bortleson and Fretwell (1993) noted
that these increases in productivity were detrimental
to fish populations and that such productive systems have
the potential to increase the magnitude of algal blooms,
furthering the detriments to fish. To counteract these
potential changes, most Klamath Basin biologists have
expressed support for efforts to restore natural conditions
through wetland restoration and initiation of appropriate
land management practices in the watershed. REFERENCES Bortleson G.C., and M.O. Fretwell. 1993. A review of possible causes of nutrient enrichment and decline of endangered sucker populations in the Upper Klamath Lake, Oregon. U.S.G.S. Water-Resources Investigations Report 93-4087, p. 24. Gearheart, R.A., J.K Anderson, M.G. Forbes, M. Osburn, and D. Oros. 1995. Watershed strategies for improving water quality in Upper Klamath Lake, Oregon. Humboldt State University, Environmental Resources Engineering Department. 3 Volumes. Kaffka, S.R., Lu, T.X., and H.L. Carlson. 1995. An assessment of the effects of agriculture on water quality in the Tule lake Region of California. Research Progress Report 108. Univ. Of California. p. 85. Kann, J. and V.H. Smith. 1993. Chlorophyll as a predictor of elevated pH in a hypertrophic Lake: Estimating the probability of exceeding critical values for fish success. Klamath Tribes Research Report: KT-93-02. The Klamath Tribes, Chiloquin, Oregon. p. 22. Logan, D.J., and D.F. Markle 1993. Fish faunal survey of Agency Lake and northern Upper Klamath Lake, Oregon. In Environmental research in the Klamath Basin, Oregon - 1992 Annual Report. S.G. Campbell (ed.) p. 341. Matsunaga, S., Moore, R.E., Niernezura, W.P., and W.W. Carmichael. 1989. Anatoxin-a(s) a potent anticholinesterase from Anabaena flos-aquae, J. Amer. Chem. Soc., vol. 111, pp. 8021-8023. Miller, W.F, and J.C. Tash. 1967. Interim report: Upper Klamath Lake Studies, Oregon, Federal Water Pollution Control Administration. p. 37. Monda, D.P. and M.K. Saiki. 1993. Tolerance of Juvenile Lost River and Shortnose suckers to high pH, ammonia concentration, and temperature, and to low dissolved oxygen concentration. In Environmental research in the Klamath Basin, Oregon - 1992 Annual Report. S.G. Campbell (ed.) p. 341. Oshima, Y., Sugino, K., and T. Yasumoto. 1989. Latest advances in HPLC analysis of paralytic shellfish toxins. In: Mycotoxins and phycotoxins, Natoris, S., Hashimoto, K., and Ueno, T. [Eds], Elsevier, New York, pp. 319-326. Piper, R.G, I.B. McElwain, L.E. Orme, J.P. McCraren, L.G. Fowler, and J.R. Leonard. 1982. Fish Hatchery Management. U.S. Department of the Interior, Fish and Wildlife Service. Washington D.C. p. 517.
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