Category Archives: Oregon Stem Cells

The Oregon Stem Cell Center conducts basic and applied research in the field of Stem Cell Biology with the long-term goal to harness the properties of stem cells for regenerative medicine and cell therapy.

Our mission

Cell and transplantation therapy have been part of mainstream medicine for decades, but cell therapy has made only limited advances in several years. Cell therapy is currently used in transfusion medicine, bone marrow transplantation, orthopedics and in dermatology. Although clinical trials have clearly documented the potential for novel cell therapies, cell supply has been severely limiting and is the main obstacle to more wide-spread success. Islet transplants have worked for type 1 diabetes, fetal cells were successful for severe Parkinson's disease and hepatocytes have been useful for the treatment of metabolic disease. Stem cell biology promises to solve the problem of limited cell availability by finding ways to isolate cells from living donors, cadavers or immortal stem cell sources.

Our cores

The Oregon Stem Cell Center has 3 cores:

Philip Streeter, Ph.D. is the director of these core laboratories. The main goal of the cores is to generate novel reagents for the isolation of stem cells and their differentiated offspring by generating monoclonal antibodies directed against cell surface antigens of living cells. To date, antibodies useful for cell sorting of living cells are only available for a very limited number of tissues, chiefly blood tissues. It therefore has not been possible to isolate and purify living liver stem cells, pancreas stem cells, cardiac stem cells etc.

The Oregon stem cell cores are poised to embark on a systematic effort to produce novel cell surface antibodies for all tissues of the mouse, rat, primates and humans. The cell sorting core uses a state-of-the-art Cytopeia high speed InFlux instrument and is capable of sorting large and fragile cells without loss of viability. Pamela Canaday is the FACS operator. The cell isolation core will provide cell isolations services including tissue procurement and protease digestion of these tissues.

Center description

The Oregon Stem Cell Center was created on January 1, 2004 and is directed by Markus Grompe, M.D. The center is housed on the top (7th) floor of the Biomedical Research Building.In 2009, the center administratively became part of the Pap Family Pediatric Research Institute.

The center has both primary and affiliate faculty members representing multiple departments and centers at OHSU. Research topics that are covered include pluripotent stem cells, hematopoietic stem cells, leukemia stem cells, hepatic and pancreatic progenitors, mesenchymal stem cells, neural stem cells, muscle stem cells and intestinal stem cells.

The OSCC has 3 cores, a monoclonal antibody production core, a cell sorting core and a cell isolation core. Philip Streeter, Ph.D. is the director of these core laboratories. The main goal of the cores is to generate novel reagents for the isolation of stem cells and their differentiated offspring by generating monoclonal antibodies directed against cell surface antigens of living cells. The cell sorting core uses a state-of-the-art Cytopeia high speed InFlux instrument and is capable of sorting large and fragile cells without loss of viability. The cell isolation core will provide cell isolations services including tissue procurement and protease digestion of these tissues.

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About | OHSU

Saccharomyces cerevisiae () is a species of yeast. It has been instrumental in winemaking, baking, and brewing since ancient times. It is believed to have been originally isolated from the skin of grapes (one can see the yeast as a component of the thin white film on the skins of some dark-colored fruits such as plums; it exists among the waxes of the cuticle). It is one of the most intensively studied eukaryotic model organisms in molecular and cell biology, much like Escherichia coli as the model bacterium. It is the microorganism behind the most common type of fermentation. S.cerevisiae cells are round to ovoid, 510m in diameter. It reproduces by a division process known as budding.[1]

Many proteins important in human biology were first discovered by studying their homologs in yeast; these proteins include cell cycle proteins, signaling proteins, and protein-processing enzymes. S. cerevisiae is currently the only yeast cell known to have Berkeley bodies present, which are involved in particular secretory pathways. Antibodies against S.cerevisiae are found in 6070% of patients with Crohn's disease and 1015% of patients with ulcerative colitis (and 8% of healthy controls).[2] S. cerevisiae, a yeast, have been found to contribute to the smell of bread by Schieberle (1990); proline, and ornithine present in yeast are precursors of 2acetyllpyrroline, a roastsmelling odorant, in the bread crust.[3]

"Saccharomyces" derives from Latinized Greek and means "sugar-mold" or "sugar-fungus", saccharon () being the combining form "sugar" and myces () being "fungus". cerevisiae comes from Latin and means "of beer". Other names for the organism are:

This species is also the main source of nutritional yeast and yeast extract.

In the 19th century, bread bakers obtained their yeast from beer brewers, and this led to sweet-fermented breads such as the Imperial "Kaisersemmel" roll,[5]which in general lacked the sourness created by the acidification typical of Lactobacillus. However, beer brewers slowly switched from top-fermenting (S. cerevisiae) to bottom-fermenting (S. pastorianus) yeast and this created a shortage of yeast for making bread, so the Vienna Process was developed in 1846.[6]While the innovation is often popularly credited for using steam in baking ovens, leading to a different crust characteristic, it is notable for including procedures for high milling of grains (see Vienna grits[7]),cracking them incrementally instead of mashing them with one pass; as well as better processes for growing and harvesting top-fermenting yeasts, known as press-yeast.

Refinements in microbiology following the work of Louis Pasteur led to more advanced methods of culturing pure strains. In 1879, Great Britain introduced specialized growing vats for the production of S. cerevisiae, and in the United States around the turn of the century centrifuges were used for concentrating the yeast,[8]making modern commercial yeast possible, and turning yeast production into a major industrial endeavor. The slurry yeast made by small bakers and grocery shops became cream yeast, a suspension of live yeast cells in growth medium, and then compressed yeast, the fresh cake yeast that became the standard leaven for bread bakers in much of the Westernized world during the early 20th century.

During World War II, Fleischmann's developed a granulated active dry yeast for the United States armed forces, which did not require refrigeration and had a longer shelf-life and better temperature tolerance than fresh yeast; it is still the standard yeast for US military recipes. The company created yeast that would rise twice as fast, cutting down on baking time. Lesaffre would later create instant yeast in the 1970s, which has gained considerable use and market share at the expense of both fresh and dry yeast in their various applications.

In nature, yeast cells are found primarily on ripe fruits such as grapes (before maturation, grapes are almost free of yeasts).[9] Since S. cerevisiae is not airborne, it requires a vector to move.

Queens of social wasps overwintering as adults (Vespa crabro and Polistes spp.) can harbor yeast cells from autumn to spring and transmit them to their progeny.[10] The intestine of Polistes dominula, a social wasp, hosts S. cerevisiae strains as well as S. cerevisiae S. paradoxus hybrids. Stefanini et al. (2016) showed that the intestine of Polistes dominula favors the mating of S. cerevisiae strains, both among themselves and with S. paradoxus cells by providing environmental conditions prompting cell sporulation and spores germination.[11]

The optimum temperature for growth of S. cerevisiae is 3035C (8695F).[10]

Two forms of yeast cells can survive and grow: haploid and diploid. The haploid cells undergo a simple lifecycle of mitosis and growth, and under conditions of high stress will, in general, die. This is the asexual form of the fungus. The diploid cells (the preferential 'form' of yeast) similarly undergo a simple lifecycle of mitosis and growth. The rate at which the mitotic cell cycle progresses often differs substantially between haploid and diploid cells.[12] Under conditions of stress, diploid cells can undergo sporulation, entering meiosis and producing four haploid spores, which can subsequently mate. This is the sexual form of the fungus. Under optimal conditions, yeast cells can double their population every 100minutes.[13][14] However, growth rates vary enormously both between strains and between environments.[15] Mean replicative lifespan is about 26cell divisions.[16][17]

In the wild, recessive deleterious mutations accumulate during long periods of asexual reproduction of diploids, and are purged during selfing: this purging has been termed "genome renewal".[18][19]

All strains of S.cerevisiae can grow aerobically on glucose, maltose, and trehalose and fail to grow on lactose and cellobiose. However, growth on other sugars is variable. Galactose and fructose are shown to be two of the best fermenting sugars. The ability of yeasts to use different sugars can differ depending on whether they are grown aerobically or anaerobically. Some strains cannot grow anaerobically on sucrose and trehalose.

All strains can use ammonia and urea as the sole nitrogen source, but cannot use nitrate, since they lack the ability to reduce them to ammonium ions. They can also use most amino acids, small peptides, and nitrogen bases as nitrogen sources. Histidine, glycine, cystine, and lysine are, however, not readily used. S.cerevisiae does not excrete proteases, so extracellular protein cannot be metabolized.

Yeasts also have a requirement for phosphorus, which is assimilated as a dihydrogen phosphate ion, and sulfur, which can be assimilated as a sulfate ion or as organic sulfur compounds such as the amino acids methionine and cysteine. Some metals, like magnesium, iron, calcium, and zinc, are also required for good growth of the yeast.

Concerning organic requirements, most strains of S. cerevisiae require biotin. Indeed, a S. cerevisiae-based growth assay laid the foundation for the isolation, crystallisation, and later structural determination of biotin. Most strains also require pantothenate for full growth. In general, S. cerevisiae is prototrophic for vitamins.

Yeast has two mating types, a and (alpha), which show primitive aspects of sex differentiation.[20] As in many other eukaryotes, mating leads to genetic recombination, i.e. production of novel combinations of chromosomes. Two haploid yeast cells of opposite mating type can mate to form diploid cells that can either sporulate to form another generation of haploid cells or continue to exist as diploid cells. Mating has been exploited by biologists as a tool to combine genes, plasmids, or proteins at will.

The mating pathway employs a G protein-coupled receptor, G protein, RGS protein, and three-tiered MAPK signaling cascade that is homologous to those found in humans. This feature has been exploited by biologists to investigate basic mechanisms of signal transduction and desensitization.

Growth in yeast is synchronised with the growth of the bud, which reaches the size of the mature cell by the time it separates from the parent cell. In well nourished, rapidly growing yeast cultures, all the cells can be seen to have buds, since bud formation occupies the whole cell cycle. Both mother and daughter cells can initiate bud formation before cell separation has occurred. In yeast cultures growing more slowly, cells lacking buds can be seen, and bud formation only occupies a part of the cell cycle.

Cytokinesis enables budding yeast Saccharomyces cerevisiae to divide into two daughter cells. S. cerevisiae forms a bud which can grow throughout its cell cycle and later leaves its mother cell when mitosis has completed.[21]

S. cerevisiae is relevant to cell cycle studies because it divides asymmetrically by using a polarized cell to make two daughters with different fates and sizes. Similarly, stem cells use asymmetric division for self-renewal and differentiation.[22]

For many cells, M phase does not happen until S phase is complete. However, for entry into mitosis in S. cerevisiae this is not true. Cytokinesis begins with the budding process in late G1 and is not completed until about halfway through the next cycle. The assembly of the spindle can happen before S phase has finished duplicating the chromosomes.[21] Additionally, there is a lack of clearly defined G2 in between M and S. Thus, there is a lack of extensive regulation present in higher eukaryotes.[21]

When the daughter emerges, the daughter is two-thirds the size of the mother.[23] Throughout the process, the mother displays little to no change in size.[24] The RAM pathway is activated in the daughter cell immediately after cytokinesis is complete. This pathway makes sure that the daughter has separated properly.[23]

Two interdependent events drive cytokinesis in S. cerevisiae. The first event is contractile actomyosin ring (AMR) constriction and the second event is formation of the primary septum (PS), a chitinous cell wall structure that can only be formed during cytokinesis. The PS resembles in animals the process of extracellular matrix remodeling.[23] When the AMR constricts, the PS begins to grow. Disrupting AMR misorients the PS, suggesting that both have a dependent role. Additionally, disrupting the PS also leads to disruptions in the AMR, suggesting both the actomyosin ring and primary septum have an interdependent relationship.[25][24]

The AMR, which is attached to the cell membrane facing the cytosol, consists of actin and myosin II molecules that coordinate the cells to split.[21] The ring is thought to play an important role in ingression of the plasma membrane as a contractile force.

Proper coordination and correct positional assembly of the contractile ring depends on septins, which is the precursor to the septum ring. These GTPases assemble complexes with other proteins. The septins form a ring at the site where the bud will be created during late G1. They help promote the formation of the actin-myosin ring, although this mechanism is unknown. It is suggested they help provide structural support for other necessary cytokinesis processes.[21] After a bud emerges, the septin ring forms an hourglass. The septin hourglass and the myosin ring together are the beginning of the future division site.

The septin and AMR complex progress to form the primary septum consisting of glucans and other chitinous molecules sent by vesicles from the Golgi body.[26] After AMR constriction is complete, two secondary septums are formed by glucans. How the AMR ring dissembles remains poorly unknown.[22]

Microtubules do not play as significant a role in cytokinesis compared to the AMR and septum. Disruption of microtubules did not significantly impair polarized growth.[27] Thus, the AMR and septum formation are the major drivers of cytokinesis.

When researchers look for an organism to use in their studies, they look for several traits. Among these are size, generation time, accessibility, manipulation, genetics, conservation of mechanisms, and potential economic benefit. The yeast species S. pombe and S. cerevisiae are both well studied; these two species diverged approximately 600to300 million years ago, and are significant tools in the study of DNA damage and repair mechanisms.[29]

S. cerevisiae has developed as a model organism because it scores favorably on a number of these criteria.

S. cerevisiae has been highly studied as a model organism to better understand aging for more than five decades and has contributed to the identification of more mammalian genes affecting aging than any other model organism.[31] Some of the topics studied using yeast are calorie restriction, as well as in genes and cellular pathways involved in senescence. The two most common methods of measuring aging in yeast are Replicative Life Span, which measures the number of times a cell divides, and Chronological Life Span, which measures how long a cell can survive in a non-dividing stasis state.[31] Limiting the amount of glucose or amino acids in the growth medium has been shown to increase RLS and CLS in yeast as well as other organisms.[32] At first, this was thought to increase RLS by up-regulating the sir2 enzyme, however it was later discovered that this effect is independent of sir2. Over-expression of the genes sir2 and fob1 has been shown to increase RLS by preventing the accumulation of extrachromosomal rDNA circles, which are thought to be one of the causes of senescence in yeast.[32] The effects of dietary restriction may be the result of a decreased signaling in the TOR cellular pathway.[31] This pathway modulates the cell's response to nutrients, and mutations that decrease TOR activity were found to increase CLS and RLS.[31][32] This has also been shown to be the case in other animals.[31][32] A yeast mutant lacking the genes sch9 and ras2 has recently been shown to have a tenfold increase in chronological lifespan under conditions of calorie restriction and is the largest increase achieved in any organism.[33][34]

Mother cells give rise to progeny buds by mitotic divisions, but undergo replicative aging over successive generations and ultimately die. However, when a mother cell undergoes meiosis and gametogenesis, lifespan is reset.[35] The replicative potential of gametes (spores) formed by aged cells is the same as gametes formed by young cells, indicating that age-associated damage is removed by meiosis from aged mother cells. This observation suggests that during meiosis removal of age-associated damages leads to rejuvenation. However, the nature of these damages remains to be established.

During starvation of non-replicating S. cerevisiae cells, reactive oxygen species increase leading to the accumulation of DNA damages such as apurinic/apyrimidinic sites and double-strand breaks.[36] Also in non-replicating cells the ability to repair endognous double-strand breaks declines during chronological aging.[37]

S. cerevisiae reproduces by mitosis as diploid cells when nutrients are abundant. However, when starved, these cells undergo meiosis to form haploid spores.[38]

Evidence from studies of S. cerevisiae bear on the adaptive function of meiosis and recombination. Mutations defective in genes essential for meiotic and mitotic recombination in S. cerevisiae cause increased sensitivity to radiation or DNA damaging chemicals.[39][40] For instance, gene rad52 is required for both meiotic recombination[41] and mitotic recombination.[42] Rad52 mutants have increased sensitivity to killing by X-rays, Methyl methanesulfonate and the DNA cross-linking agent 8-methoxypsoralen-plus-UVA, and show reduced meiotic recombination.[40][41][43] These findings suggest that recombination repair during meiosis and mitosis is needed for repair of the different damages caused by these agents.

Ruderfer et al.[39] (2006) analyzed the ancestry of natural S. cerevisiae strains and concluded that outcrossing occurs only about once every 50,000 cell divisions. Thus, it appears that in nature, mating is likely most often between closely related yeast cells. Mating occurs when haploid cells of opposite mating type MATa and MAT come into contact. Ruderfer et al.[39] pointed out that such contacts are frequent between closely related yeast cells for two reasons. The first is that cells of opposite mating type are present together in the same ascus, the sac that contains the cells directly produced by a single meiosis, and these cells can mate with each other. The second reason is that haploid cells of one mating type, upon cell division, often produce cells of the opposite mating type with which they can mate. The relative rarity in nature of meiotic events that result from outcrossing is inconsistent with the idea that production of genetic variation is the main selective force maintaining meiosis in this organism. However, this finding is consistent with the alternative idea that the main selective force maintaining meiosis is enhanced recombinational repair of DNA damage,[44][45][46] since this benefit is realized during each meiosis, whether or not out-crossing occurs.

S. cerevisiae was the first eukaryotic genome to be completely sequenced.[47] The genome sequence was released to the public domain on April 24, 1996. Since then, regular updates have been maintained at the Saccharomyces Genome Database. This database is a highly annotated and cross-referenced database for yeast researchers. Another important S.cerevisiae database is maintained by the Munich Information Center for Protein Sequences (MIPS). The S. cerevisiae genome is composed of about 12,156,677 base pairs and 6,275 genes, compactly organized on 16 chromosomes.[47] Only about 5,800 of these genes are believed to be functional. It is estimated at least 31% of yeast genes have homologs in the human genome.[48] Yeast genes are classified using gene symbols (such as sch9) or systematic names. In the latter case the 16 chromosomes of yeast are represented by the letters A to P, then the gene is further classified by a sequence number on the left or right arm of the chromosome, and a letter showing which of the two DNA strands contains its coding sequence.[49]

Examples:

The availability of the S.cerevisiae genome sequence and a set of deletion mutants covering 90% of the yeast genome[50] has further enhanced the power of S.cerevisiae as a model for understanding the regulation of eukaryotic cells. A project underway to analyze the genetic interactions of all double-deletion mutants through synthetic genetic array analysis will take this research one step further. The goal is to form a functional map of the cell's processes.

As of 2010[update] a model of genetic interactions is most comprehensive yet to be constructed, containing "the interaction profiles for ~75% of all genes in the Budding yeast".[51] This model was made from 5.4 million two-gene comparisons in which a double gene knockout for each combination of the genes studied was performed. The effect of the double knockout on the fitness of the cell was compared to the expected fitness. Expected fitness is determined from the sum of the results on fitness of single-gene knockouts for each compared gene. When there is a change in fitness from what is expected, the genes are presumed to interact with each other. This was tested by comparing the results to what was previously known. For example, the genes Par32, Ecm30, and Ubp15 had similar interaction profiles to genes involved in the Gap1-sorting module cellular process. Consistent with the results, these genes, when knocked out, disrupted that process, confirming that they are part of it.[51]

From this, 170,000 gene interactions were found and genes with similar interaction patterns were grouped together. Genes with similar genetic interaction profiles tend to be part of the same pathway or biological process.[52] This information was used to construct a global network of gene interactions organized by function. This network can be used to predict the function of uncharacterized genes based on the functions of genes they are grouped with.[51]

Approaches that can be applied in many different fields of biological and medicinal science have been developed by yeast scientists. These include yeast two-hybrid for studying protein interactions and tetrad analysis. Other resources, include a gene deletion library including ~4,700 viable haploid single gene deletion strains. A GFP fusion strain library used to study protein localisation and a TAP tag library used to purify protein from yeast cell extracts.[citation needed]

The international Synthetic Yeast Genome Project (Sc2.0 or Saccharomyces cerevisiae version 2.0) aims to build an entirely designer, customizable, synthetic S. cerevisiae genome from scratch that is more stable than the wild type. In the synthetic genome all transposons, repetitive elements and many introns are removed, all UAG stop codons are replaced with UAA, and transfer RNA genes are moved to a novel neochromosome. As of March2017[update], 6 of the 16 chromosomes have been synthesized and tested. No significant fitness defects have been found.[53]

Among other microorganisms, a sample of living S.cerevisiae was included in the Living Interplanetary Flight Experiment, which would have completed a three-year interplanetary round-trip in a small capsule aboard the Russian Fobos-Grunt spacecraft, launched in late 2011.[54][55] The goal was to test whether selected organisms could survive a few years in deep space by flying them through interplanetary space. The experiment would have tested one aspect of transpermia, the hypothesis that life could survive space travel, if protected inside rocks blasted by impact off one planet to land on another.[54][55][56] Fobos-Grunt's mission ended unsuccessfully, however, when it failed to escape low Earth orbit. The spacecraft along with its instruments fell into the Pacific Ocean in an uncontrolled re-entry on January 15, 2012. The next planned exposure mission in deep space using S. cerevisiae is BioSentinel. (see: List of microorganisms tested in outer space)

Saccharomyces cerevisiae is used in brewing beer, when it is sometimes called a top-fermenting or top-cropping yeast. It is so called because during the fermentation process its hydrophobic surface causes the flocs to adhere to CO2 and rise to the top of the fermentation vessel. Top-fermenting yeasts are fermented at higher temperatures than the lager yeast Saccharomyces pastorianus, and the resulting beers have a different flavor than the same beverage fermented with a lager yeast. "Fruity esters" may be formed if the yeast undergoes temperatures near 21C (70F), or if the fermentation temperature of the beverage fluctuates during the process. Lager yeast normally ferments at a temperature of approximately 5C (41F), where Saccharomyces cerevisiae becomes dormant. A variant yeast known as Saccharomyces cerevisiae var. diastaticus is a beer spoiler which can cause secondary fermentations in packaged products.[57]

In May 2013, the Oregon legislature made S. cerevisiae the official state microbe in recognition of the impact craft beer brewing has had on the state economy and the state's identity.[58]

S. cerevisiae is used in baking; the carbon dioxide generated by the fermentation is used as a leavening agent in bread and other baked goods. Historically, this use was closely linked to the brewing industry's use of yeast, as bakers took or bought the barm or yeast-filled foam from brewing ale from the brewers (producing the barm cake); today, brewing and baking yeast strains are somewhat different.

Owing to the high cost of commercial CO2 cylinder systems, CO2 injection by yeast is one of the most popular DIY approaches followed by aquaculturists for providing CO2 to underwater aquatic plants. The yeast culture is, in general, maintained in plastic bottles, and typical systems provide one bubble every 37 seconds. Various approaches have been devised to allow proper absorption of the gas into the water.[59]

Saccharomyces cerevisiae is used as a probiotic in humans and animals. Especially, a strain Saccharomyces cerevisiae var. boulardii is industrially manufactured and clinically used as a medication.

Several clinical and experimental studies have shown that Saccharomyces cerevisiae var. boulardii is, to lesser or greater extent, useful for prevention or treatment of several gastrointestinal diseases.[60] Moderate quality evidence shown Saccharomyces cerevisiae var. boulardii to reduce risk of antibiotic-associated diarrhea both in adults[61][60][62] and in children[61][60] and to reduce risk of adverse effects of Helicobacter pylori eradication therapy[63][60][62]. Also some limited evidence support efficacy of Saccharomyces cerevisiae var. boulardii in prevention (but not treatment) of travelers diarrhea[60][62] and, at least as an adjunct medication, in treatment of acute diarrhea in adults and children and of persistent diarrhea in children[60].

Administration of S. cerevisiae var. boulardii is considered generally safe[62]. In clinical trials it was well tolerated by patients, and adverse effects rate was similar to that in control groups (i. e. groups with placebo or no treatment)[61]. No case of S. cerevisiae var. boulardii fungemia has been reported during clinical trials[62].

In clinical practice, however, cases of fungemia, caused by Saccharomyces cerevisiae var. boulardii are reported[62][60]. Patients with compromised immunity or those with central vascular catheters are at especial risk. Some researchers have recommended not to use Saccharomyces cerevisiae var. boulardii for treatment of such patients[62]. Others suggest only that caution must be exercised with its use in risk group patients[60].

Saccharomyces cerevisiae is proven to be an opportunistic human pathogen, though of relatively low virulence[64]. Despite widespread use of this microorganism at home and in industry, contact with it very rarely leads to infection[65]. Saccharomyces cerevisiae was found in the skin, oral cavity, oropharinx, duodenal mucosa, digestive tract and vagina of healthy humans[66] (one review found it to be reported for 6% of samples from human intestine[67]). Some specialists consider S. cerevisiae to be a part of normal microbiota of the gastrointestinal tract, the respiratory tract and the vagina of humans[68] while others believes that the species cannot be called a true commensal and originates in food[67][69]. Presence of S. cerevisiae in human digestive system may be rather transient[69], for example experiments show that in the case of oral administration to healthy individuals it is eliminated from the intestine within 5 days after the end of administration[67][65].

Under certain circumstances, however, such as degraded immunity, Saccharomyces cerevisiae can cause infection in humans[65][64]. Studies show that it causes 0.45-1.06% of the cases of yeast-induced vaginitis. In some cases women suffering from S. cerevisiae-induced vaginal infection were intimate partners of bakers, and the strain was found to be the same that their partners used for baking. As of 1999, no cases of S. cerevisiae-induced vaginitis in women, who worked in bakeries themselves, were reported in scientific literature. Some cases were linked by researchers to the use of the yeast in home baking[64]. Cases of infection of oral cavity and pharynx caused by S. cerevisiae are also known.[64]

Occasionally Saccharomyces cerevisiae causes invasive infections (i. e. gets into the bloodstream or other normally sterile body fluid or into a deep site tissue, such as lungs, liver or spleen) that can go systemic (involve multiple organs). Such conditions are life-threatening.[64][69] More than 30% cases of S. cerevisiae invasive infections lead to death even if treated.[69] S. cerevisiae invasive infections, however, are much rarer than invasive infections caused by Candida albicans[64][70] even in patients weakened by cancer[70]. S. cerevisiae causes 1% to 3.6% nosocomial cases of fungemia.[69] A comprehensive review of S. cerevisiae invasive infection cases found all patients to have at least one predisposing condition.[69]

Saccharomyces cerevisiae may enter the bloodstream or get to other deep sites of the body by translocation from oral or enteral mucosa or through contamination of intravascular catheters (e. g. central venous catheters).[68] Intravascular catheters, antibiotic therapy and compromised immunity are major predisposing factors for S. cerevisiae invasive infection.[69]

A number of cases of fungemia were caused by intentional ingestion of living S. cerevisiae cultures for dietary or therapeutic reasons, including use of Saccharomyces boulardii (a strain of S. cerevisiae which is used as a probiotic for treatment of certain forms of diarrhea).[64][69] Saccharomices boulardii causes about 40% cases of invasive Saccharomyces infections[69] and is more likely (in comparison to other S. cerevisiae strains) to cause invasive infection in humans without general problems with immunity[69], though such adverse effect is very rare relative to Saccharomices boulardii therapeutic administration[71].

S. boulardii may contaminate intravascular catheters through hands of medical personnel involved in administering probiotic preparations of S. boulardii to patients.[69]

Systemic infection usually occurs in patients who have their immunity compromised due to severe illness (HIV/AIDS, leukemia, other forms of cancer) or certain medical procedures (bone marrow transplantation, abdominal surgery).[64]

A case was reported when a nodule was surgically excised from a lung of a man embloyed in baking business, and examination of the tissue revealed presense of Saccharomyces cerevisiae. Inhalation of dry baking yeast powder is supposed to be the source of infection in this case.[72][69]

Not all strains of Saccharomyces cerevisiae are equally virulent towards humans. Most environmental strains are not capable to grow at temperatures above 35C (i. e. at temperatures of living body of humans and other mammalian). Virulent strains, however, are capable to grow at least above 37C and often up to 39C (rarely up to 42C).[66] Some industrial strains are also capable to grow above 37C.[64] European Food Safety Authority (as of 2017) requires that all S. cerevisiae strains capable of growth above 37C that are added to the food or feed chain in viable form must, as to be qualified presumably safe, show no resistance to antimycotic drugs used for treatment of yeast infections[73].

The ability to grow at elevated temperatures is an important factor for strain's virulence but not the sole one.[66]

Other traits that are usually believed to be associated with virulence are: ability to produce certain enzymes such as proteinase[64] and phospholipase[66], invasive growth[66] (i.e. growth with intrusion into the nutrient medium), ability to adhere to mammalian cells[66], ability to survive in the presence of hydrogen peroxide[66] (that is used by macrophages to kill foreign microorganisms in the body) and other abilities allowing the yeast to resist or influence immune response of the host body[66]. Ability to form branching chains of cells, known as pseudohyphae is also sometimes sait to be associated with virulence[64][66], though some research suggests that this trait may be common to both virulent and non-virulent strains of Saccharomyces cerevisiae[66].

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Saccharomyces cerevisiae - Wikipedia

PRP and Stem Cell Joint Regeneration in Portland Oregon

Oregon Regenerative Medicine is dedicated to empowering our patients to create healthy, active longevity through the use of PRP and Stem Cell joint regeneration, Prolotherapy, Platelet Rich Plasma PRP, condition-specific nutritional programs, hormone optimization, education, and inspiration. We live and practice what we preach. We are the experts in Regenerative Medicinein the Portland and Lake Oswego region. Since 1978, we have pioneered the use of safe, effective natural medicine in Oregon.

Regenerative Medicine includes the use of non-surgical injection procedures for the repair of damaged tendons, ligaments, joints and skin. Our regenerative and biological treatments include Prolotherapy, Platelet Rich Plasma PRP, and Adult Stem Cell Therapies. These treatments enhance the natural cycles of repair in aging and chronically injured joints, ligaments, tendons, and skin. Regenerative orthopedic injections are an effective treatment for all manner of acute and chronic pain in any joint. We specialize in back and neck injuries,as well as osteoarthritis and injuries of thehip, knee, shoulder, elbow, wrist, hand, TMJ, foot and ankle. For our patients who have been told that their only solution is surgery or a lifetime on pain medications, the vast majority have been able to achieve drug-free, pain-free function without surgery or joint replacement.

At Oregon Regenerative Medicine, we useAdipose-Derived Stem Cell Therapy to treat a wide range of orthopedic and degenerative diseases, including inflammatory and rheumatoid arthritis. We use adult stem cells that are harvested from your own adipose tissue. Unlike embryonic stem cells, adult stem cells are approved by the FDA for research and treatment of a wide variety of conditions. Adult adipose tissue is the most abundant source of stem cells in the human body and has shown great promise in the treatment of a host of conditions.

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PRP and Stem Cell Joint Regeneration | Portland Oregon

Adult Stem Cell Orthopedics is a powerful form of regenerative injection therapy and can be an effective alternative to major surgery and joint replacement procedures. We are the stem cell therapy experts in Oregon and the Portland area. In this procedure,we harvest Mesenchymal Stem Cells (MSCs) from your own body. The tissue we harvest is known as AD-SVF, orAdipose Derived-Stromal Vascular Fraction. AD-SVF provides the richest source of your own mesenchymal stem cells. These specific tissue fractions are located within the adipose bed, whichserves to nurture and protect your stem cell population. This combination of stem cells,native tissue matrix and bio-scaffolding act together torepair and regenerate affected tissues. When harvested along with the stem cells, and mixed with your own platelet rich plasma, these tissue products provide the potent combination of cytokines, cell signals, and scaffolding necessary for MSCsto differentiate and repair the target injury.

Your adipose is the ideal harvest tissue for MSCs because the stem cell concentration in your fat is at least1000 times higherthan it is in bone marrow aspirate. In fact, up to 45% of the nucleated cells within adipose tissue are Mesenchymal stem cells. Another advantage is that AD-SVF contains the full complement of matrix tissue fractions necessary for cartilage, ligament, tendon and fascia regeneration. Bone marrow contains very fewof these matrix tissues. Therefore, your adipose tissue is the most ideal site for harvesting stem cells.

The harvesting procedureis minimally invasive. Our modern clinic in Lake Oswego Oregon is renowned for its caring staff and comfort. From start to finish the procedure will take about 2.5 hours. First, a small incision is made in the skin and a patented tissue harvester is inserted and used to extract your adipose derived stem cells.We then separate and concentrate the AD-SVF that contains the stem cells and tissue matrix. Next,a 4-ounce quantity of blood is drawnand yourplatelet rich plasma (PRP) is concentrated. The PRP is combinedwith the Stromal Vascular Fraction (AD-SVF) to activate the Mesenchymal stem cells.The PRP and the AD-SVF concentrates activate the stem cells and are immediately injected under ultrasound guidance into your affected area: hip joint, knee joint, lumbar spine, shoulder, etc.

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Adult Stem Cell Orthopedics - Oregon Regenerative Medicine

What exactly are stem cells and why is everyone talking about them? What effect do they have on our health?

A very simple understanding is that stem cells are a neutral cell and theyre capable of differentiating into every other cell in the body. In other words, you have a universal cell; its like a universal part that can become anything else. So, if you needed stem cells to make parts for your brain, your nervous system, your heart, your liver, your kidneysthats what stem cells do.

Stem cells can divide into other cells in the body and they are part of our bodys repair system.

So as were growing over time and as were repairing damage, thats all stem cells doing that job. When a stem cell divides it can take two different paths: it can either become more stem cells, or it can divide into highly specialized cells like muscle, tissue, liver, heart, kidneys and so forth. And so this is just another way of saying that these stem cells are universal and they can become whatever your body needs them to become.

Another important thing to know about stem cells is that theyre found throughout the entire body. Formerly, scientists thought that stem cells were located in the bone marrow and thats how you get to them. Then it was discovered that youd find stem cells in fatty tissue, so you could extract them from there, but now really what were understanding is that adult stem cells are located throughout the body. This is because that these stem cells become specialized and theyre needed at locations throughout the body for normal and for normal repair.

So what if there was a way to stir up these stem cells and make them active again where you could heal the way that you did when you in your 20s? How could we do that? This approach would obviously be very safe, be highly effective, and also inexpensive compared to other methods available.

Thats what the X-39 Patch is all about. X-39 elevates a peptide in the body that will activate stem cells. When you look at the information that we have on the X 39 you are only seeing 5% of the picture. This is an extraordinarily powerful product and it has far-reaching health benefits. See the latest video about the LifeWave X39 patch on vimeofor more.

How does the LifeWave X39 stimulate production of stem cells?In brief, X39 elevates GHK-cu peptide.What does GHK-cu do?

Copper Peptide GHK-Cu BenefitsIf you look at the wikipedia page and youll see why this peptide is considered the Holy Grail of Health!

A little more about Copper Peptide GHK-CuGHK-Cu occurs naturally in humans and is released when the body has an injury. The immediate benefit at the site of the injury is that its copper content makes it powerful at fighting infection. Next the peptide activates stem cells, promotes wound healing, attraction of immune cells, antioxidant and anti-inflammatory effects, stimulation of collagen and glycosaminoglycan synthesis in skin fibroblasts and promotion of blood vessels growth. GHK-Cu also can modulate expression of a large number of human genes, generally reversing gene expression to a healthier state.

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DISCLAIMERThe information presented on the pages of Oregon Light Therapy is for educational purposes only. It is not intended to diagnose or treat disease, nor does it replace the 1-on-1 relationship with your health care provider.

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What are stem cells? Oregon Light Therapy

An inhibitory postsynaptic potential (IPSP) is a kind of synaptic potential that makes a postsynaptic neuron less likely to generate an action potential.[1] The opposite of an inhibitory postsynaptic potential is an excitatory postsynaptic potential (EPSP), which is a synaptic potential that makes a postsynaptic neuron more likely to generate an action potential. IPSPs can take place at all chemical synapses, which use the secretion of neurotransmitters to create cell to cell signalling. Inhibitory presynaptic neurons release neurotransmitters that then bind to the postsynaptic receptors; this induces a change in the permeability of the postsynaptic neuronal membrane to particular ions. An electric current that changes the postsynaptic membrane potential to create a more negative postsynaptic potential is generated, i.e. the postsynaptic membrane potential becomes more negative than the resting membrane potential, and this is called hyperpolarisation. To generate an action potential, the postsynaptic membrane must depolarizethe membrane potential must become more positive than the resting membrane potential. Therefore, hyperpolarisation of the postsynaptic membrane makes it less likely for depolarisation to sufficiently occur to generate an action potential in the postsynaptic neurone.

Depolarization can also occur due to an IPSP if the reverse potential is between the resting threshold and the action potential threshold. Another way to look at inhibitory postsynaptic potentials is that they are also a chloride conductance change in the neuronal cell because it decreases the driving force.[2] This is because, if the neurotransmitter released into the synaptic cleft causes an increase in the permeability of the postsynaptic membrane to chloride ions by binding to ligand-gated chloride ion channels and causing them to open, then chloride ions, which are in greater concentration in the synaptic cleft, diffuse into the postsynaptic neurone. As these are negatively charged ions, hyperpolarisation results, making it less likely for an action potential to be generated in the postsynaptic neurone. Microelectrodes can be used to measure postsynaptic potentials at either excitatory or inhibitory synapses.

In general, a postsynaptic potential is dependent on the type and combination of receptor channel, reverse potential of the postsynaptic potential, action potential threshold voltage, ionic permeability of the ion channel, as well as the concentrations of the ions in and out of the cell; this determines if it is excitatory or inhibitory. IPSPs always want to keep the membrane potential more negative than the action potential threshold and can be seen as a "transient hyperpolarization".[3] EPSPs and IPSPs compete with each other at numerous synapses of a neuron. This determines whether or not the action potential at the presynaptic terminal regenerates at the postsynaptic membrane. Some common neurotransmitters involved in IPSPs are GABA and glycine.

This system[1] IPSPs can be temporally summed with subthreshold or suprathreshold EPSPs to reduce the amplitude of the resultant postsynaptic potential. Equivalent EPSPs (positive) and IPSPs (negative) can cancel each other out when summed. The balance between EPSPs and IPSPs is very important in the integration of electrical information produced by inhibitory and excitatory synapses.

The size of the neuron can also affect the inhibitory postsynaptic potential. Simple temporal summation of postsynaptic potentials occurs in smaller neurons, whereas in larger neurons larger numbers of synapses and ionotropic receptors as well as a longer distance from the synapse to the soma enables the prolongation of interactions between neurons.

GABA is a very common neurotransmitter used in IPSPs in the adult mammalian brain and retina.[1][4] GABA receptors are pentamers most commonly composed of three different subunits (, , ), although several other subunits (,, , , ) and conformations exist. The open channels are selectively permeable to chloride or potassium ions (depending on the type of receptor) and allow these ions to pass through the membrane. If the electrochemical potential of the ion is more negative than that of the action potential threshold then the resultant conductance change that occurs due to the binding of GABA to its receptors keeps the postsynaptic potential more negative than the threshold and decreases the probability of the postsynaptic neuron completing an action potential. Glycine molecules and receptors work much in the same way in the spinal cord, brain, and retina.

There are two types of inhibitory receptors:

Ionotropic receptors (also known as ligand-gated ion channels) play an important role in inhibitory postsynaptic potentials.[1] A neurotransmitter binds to the extracellular site and opens the ion channel that is made up of a membrane-spanning domain that allows ions to flow across the membrane inside the postsynaptic cell. This type of receptor produces very fast postsynaptic actions within a couple of milliseconds of the presynaptic terminal receiving an action potential. These channels influence the amplitude and time-course of postsynaptic potentials as a whole. Ionotropic GABA receptors are used in binding for various drugs such as barbiturates (Phenobarbital, pentobarbital), steroids, and picrotoxin. Benzodiazepines (Valium) bind to the and subunits of GABA receptors to improve GABAergic signaling. Alcohol also modulates ionotropic GABA receptors.

Metabotropic receptors, or G-protein-coupled receptors, do not use ion channels in their structure; they, instead, consist of an extracellular domain that binds to a neurotransmitter and an intracellular domain that binds to G-protein.[1] This begins the activation of the G-protein, which then releases itself from the receptor and interacts with ion channels and other proteins to open or close ion channels through intracellular messengers. They produce slow postsynaptic responses (from milliseconds to minutes) and can be activated in conjunction with ionotropic receptors to create both fast and slow postsynaptic potentials at one particular synapse. Metabotropic GABA receptors, heterodimers of R1 and R2 subunits, use potassium channels instead of chloride. They can also block calcium ion channels to hyperpolarize postsynaptic cells.

There are many applications of inhibitory postsynaptic potentials to the real world. Drugs that affect the actions of the neurotransmitter can treat neurological and psychological disorders through different combinations of types of receptors, G-proteins, and ion channels in postsynaptic neurons.

For example, studies researching opioid receptor-mediated receptor desensitizing and trafficking in the locus cereleus of the brain are being performed. When a high concentration of agonist is applied for an extended amount of time (fifteen minutes or more), hyperpolarization peaks and then decreases. This is significant because it is a prelude to tolerance; the more opioids one needs for pain the greater the tolerance of the patient. These studies are important because it helps us to learn more about how we deal with pain and our responses to various substances that help treat pain. By studying our tolerance to pain, we can develop more efficient medications for pain treatment.[5]

In addition, research is being performed in the field of dopamine neurons in the ventral tegmental area, which deals with reward, and the substantia nigra, which is involved with movement and motivation. Metabotropic responses occur in dopamine neurons through the regulation of the excitability of cells. Opioids inhibit GABA release; this decreases the amount of inhibition and allows them to fire spontaneously. Morphine and opioids relate to inhibitory postsynaptic potentials because they induce disinhibition in dopamine neurons.[5]

IPSPs can also be used to study the input-output characteristics of an inhibitory forebrain synapse used to further study learned behaviorfor example in a study of song learning in birds at the University of Washington.[6] Poisson trains of unitary IPSPs were induced at a high frequency to reproduce postsynaptic spiking in the medial portion of the dorsalateral thalamic nucleus without any extra excitatory inputs. This shows an excess of thalamic GABAergic activation. This is important because spiking timing is needed for proper sound localization in the ascending auditory pathways. Songbirds use GABAergic calyceal synaptic terminals and a calcyx-like synapse such that each cell in the dorsalateral thalamic nucleus receives at most two axon terminals from the basal ganglia to create large postsynaptic currents.

Inhibitory postsynaptic potentials are also used to study the basal ganglia of amphibians to see how motor function is modulated through its inhibitory outputs from the striatum to the tectum and tegmentum.[7] Visually guided behaviors may be regulated through the inhibitory striato-tegmental pathway found in amphibians in a study performed at the Baylor College of Medicine and the Chinese Academy of Sciences. The basal ganglia in amphibians is very important in receiving visual, auditory, olfactory, and mechansensory inputs; the disinhibitory striato-protecto-tectal pathway is important in prey-catching behaviors of amphibians. When the ipsilateral striatum of an adult toad was electrically stimulated, inhibitory postsynaptic potentials were induced in binocular tegmental neurons, which affects the visual system of the toad.

Inhibitory postsynaptic potentials can be inhibited themselves through a signaling process called "depolarized-induced suppression of inhibition (DSI)" in CA1 pyramidal cells and cerebellar Purkinje cells.[8][9] In a laboratory setting step depolarizations the soma have been used to create DSIs, but it can also be achieved through synaptically induced depolarization of the dendrites. DSIs can be blocked by ionotropic receptor calcium ion channel antagonists on the somata and proximal apical dendrites of CA1 pyramidal cells. Dendritic inhibitory postsynaptic potentials can be severely reduced by DSIs through direct depolarization.

Along these lines, inhibitory postsynaptic potentials are useful in the signaling of the olfactory bulb to the olfactory cortex.[10] EPSPs are amplified by persistent sodium ion conductance in external tufted cells. Low-voltage activated calcium ion conductance enhances even larger EPSPs. The hyperpolarization activated nonselective cation conductance decreases EPSP summation and duration and they also change inhibitory inputs into postsynaptic excitation. IPSPs come into the picture when the tufted cells membranes are depolarized and IPSPs then cause inhibition. At resting threshold IPSPs induce action potentials. GABA is responsible for much of the work of the IPSPs in the external tufted cells.

Another interesting study of inhibitory postsynaptic potentials looks at neuronal theta rhythm oscillations that can be used to represent electrophysiological phenomena and various behaviors.[11][12] Theta rhythms are found in the hippocampus and GABAergic synaptic inhibition helps to modulate them. They are dependent on IPSPs and started in either CA3 by muscarinic acetylcholine receptors and within C1 by the activation of group I metabotropic glutamate receptors. When interneurons are activated by metabotropic acetylcholine receptors in the CA1 region of rat hippocampal slices, a theta pattern of IPSPs in pyramidal cells occurs independent of the input. This research also studies DSIs, showing that DSIs interrupt metabotropic acetylcholine-initiated rhythm through the release of endocannabinoids. An endocannabinoid-dependent mechanism can disrupt theta IPSPs through action potentials delivered as a burst pattern or brief train. In addition, the activation of metabotropic glutamate receptors removes any theta IPSP activity through a G-protein, calcium ionindependent pathway.

Inhibitory postsynaptic potentials have also been studied in the Purkinje cell through dendritic amplification. The study focused in on the propagation of IPSPs along dendrites and its dependency of ionotropic receptors by measuring the amplitude and time-course of the inhibitory postsynaptic potential. The results showed that both compound and unitary inhibitory postsynaptic potentials are amplified by dendritic calcium ion channels. The width of a somatic IPSP is independent of the distance between the soma and the synapse whereas the rise time increases with this distance. These IPSPs also regulate theta rhythms in pyramidal cells.On the other hand, inhibitory postsynaptic potentials are depolarizing and sometimes excitatory in immature mammalian spinal neurons because of high concentrations of intracellular chloride through ionotropic GABA or glycine chloride ion channels.[13] These depolarizations activate voltage-dependent calcium channels. They later become hyperpolarizing as the mammal matures. To be specific, in rats, this maturation occurs during the perinatal period when brain stem projects reach the lumbar enlargement. Descending modulatory inputs are necessary for the developmental shift from depolarizing to hyperpolarizing inhibitory postsynaptic potentials. This was studied through complete spinal cord transections at birth of rats and recording IPSPs from lumbar motoneurons at the end of the first week after birth.

Glutamate, an excitatory neurotransmitter, is usually associated with excitatory postsynaptic potentials in synaptic transmission. However, a study completed at the Vollum Institute at the Oregon Health Sciences University demonstrates that glutamate can also be used to induce inhibitory postsynaptic potentials in neurons.[14] This study explains that metabotropic glutamate receptors feature activated G proteins in dopamine neurons that induce phosphoinositide hydrolysis. The resultant products bind to inositol triphosphate (IP3) receptors through calcium ion channels. The calcium comes from stores and activate potassium conductance, which causes a pure inhibition in the dopamine cells. The changing levels of synaptically released glutamate creates an excitation through the activation of ionotropic receptors, followed by the inhibition of metabotropic glutamate receptors.

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Inhibitory postsynaptic potential - Wikipedia

Puccinia graminisScientific classificationKingdom:Phylum:Class:Subclass:Order:Family:Genus:Species:

P.graminis

Dicaeoma anthistiriaePuccinia albigensisPuccinia anthistiriaePuccinia brizae-maximaePuccinia cerealisPuccinia elyminaPuccinia favargeriPuccinia graminis f. macrosporaPuccinia graminis f.sp. avenaePuccinia graminis f.sp. secalisPuccinia graminis f.sp. triticiPuccinia graminis subsp. majorPuccinia graminis var. graminisPuccinia graminis var. stakmaniiPuccinia graminis var. triticiPuccinia jubataPuccinia linearisPuccinia megalopotamicaPuccinia secalisPuccinia vilisTrichobasis linearis

The stem, black, and cereal rusts are caused by the fungus Puccinia graminis and are a significant disease affecting cereal crops. Crop species that are affected by the disease include bread wheat, durum wheat, barley and triticale.[1] These diseases have affected cereal farming throughout history. Since the 1950s, wheat strains bred to be resistant to stem rust have become available.[2] Fungicides effective against stem rust are available as well.[3]

In 1999 a new virulent race of stem rust was identified that most current wheat strains show no resistance against. The race was named TTKSK (e.g. isolate Ug99), named after the country where it was identified (Uganda) and the year of its discovery (1999).[4] It spread to Kenya, then Ethiopia, Sudan and Yemen, and is becoming more virulent as it spreads.[4] An epidemic of stem rust on wheat caused by race TTKSK is currently spreading across Africa, Asia and the Middle East and is causing major concern due to the large numbers of people dependent on wheat for sustenance. Scientists are working on breeding strains of wheat that are resistant to UG99. However, wheat is grown in a broad range of environments. This means that breeding programs would have extensive work remaining to get resistance into regionally adapted germplasms even after resistance is identified.[4]

An outbreak of another virulent race of stem rust, TTTTF, took place in Sicily in 2016, suggesting that the disease is returning to Europe.[2] Comprehensive genomic analysis of Puccinia graminis combined with plant pathology and climate data has pointed out the potential of the re-emergence of stem wheat rust in UK.[5][6]

There is considerable genetic diversity within the species P. graminis, and several special forms, forma specialis, which vary in host range have been identified.

P. graminis is a member of the phylum Basidiomycota within the kingdom Fungi. The characteristic rust color on stems and leaves is typical of a general stem rust as well as any variation of this type of fungus. Different from most fungi, the rust variations have five spore stages and alternate between two hosts. Wheat is the primary host, and barberry is the alternate host.

There are multiple pathotypes (including QCC and MCC) affecting barley, within forma specialis tritici.[7]

The stem rust fungus attacks the parts of the plant that are above ground. Spores that land on green wheat plants form a pustule that invades the outer layers of the stalk.[4] Infected plants produce fewer tillers and set fewer seed, and in cases of severe infection the plant may die. Infection can reduce what is an apparently healthy crop about three weeks before harvest into a black tangle of broken stems and shriveled grains by harvest.[1]

Stem rust of cereals causes yield losses in several ways:[8]

Stem rust on wheat is characterized by the presence of uredinia on the plant, which are brick-red, elongated, blister-like pustules that are easily shaken off.[1] They most frequently occur on the leaf sheaths, but are also found on stems, leaves, glumes and awns.[1] On leaves they develop mostly on the underside but may penetrate to the upperside.[1] On leaf sheaths and glumes pustules rupture the epidermis, giving a ragged appearance.[1]

Towards the end of the growing season black telia are produced.[1] For this reason stem rust is also known as 'black rust'.[1] The telia are firmly attached to the plant tissue.[1]

The site of infection is a visible symptom of the disease.

Pycnia appear on barberry plants in the spring, usually in the upper leaf surfaces.[8] They are often in small clusters and exude pycniospores in a sticky honeydew.[8] Five to ten days later, cup-shaped structures filled with orange-yellow, powdery aeciospores break through the lower leaf surface.[8] The aecial cups are yellow and sometimes elongate to extend up to 5mm from the leaf surface.[8]

Like other Puccinia species, P. graminis is an obligate biotroph (it colonizes living plant cells) and has a complex life cycle featuring alternation of generations. The fungus is heteroecious, requiring two hosts to complete its life cycle - the cereal host and the alternate host.[8] There are many species in Berberis and Mahonia that are susceptible to stem rust, but the common barberry is considered to be the most important alternate host.[1] P. graminis is macrocyclic[8] (exhibits all five of the spore types that are known for rust fungi[9]).

Animated video of the life cycle of stem rust

P. graminis can complete its life cycle either with or without barberry (the alternate host).[8]

Due to its cyclical nature, there is no true 'start point' for this process. Here, the production of urediniospores is arbitrarily chosen as a start point.

Urediniospores are formed in structures called uredinia, which are produced by fungal mycelia on the cereal host 12 weeks after infection.[8] The urediniospores are dikaryotic (contain two un-fused, haploid nuclei in one cell) and are formed on individual stalks within the uredinium.[8] They are spiny and brick-red.[8] Urediniospores are the only type of spores in the rust fungus life cycle that are capable of infecting the host on which they are produced, and this is therefore referred to as the 'repeating stage' of the life cycle.[8] It is the spread of urediniospores that allows infection to spread from one cereal plant to another.[8] This phase can rapidly spread the infection over a wide area.

Towards the end of the cereal host's growing season, the mycelia produce structures called telia.[8] Telia produce a type of spore called teliospores.[8] These black, thick-walled spores are dikaryotic.[8] They are the only form in which Puccinia graminis is able to overwinter independently of a host.[8]

Each teliospore undergoes karyogamy (fusion of nuclei) and meiosis to form four haploid spores called basidiospores.[8] This is an important source of genetic recombination in the life cycle.[8] Basidiospores are thin-walled and colourless.[8] They cannot infect the cereal host, but can infect the alternative host (usually barberry).[8] They are usually carried to the alternative host by wind.

Once basidiospores arrive on a leaf of the alternative host, they germinate to produce a haploid mycelium that directly penetrates the epidermis and colonises the leaf.[8] Once inside the leaf the mycelium produces specialised infection structures called pycnia.[8] The pycnia produce two types of haploid gametes, the pycniospores and the receptive hyphae.[8] The pycniospores are produced in a sticky honeydew that attracts insects.[8] The insects carry pycniospores from one leaf to another.[8] Splashing raindrops can also spread pycniospores.[8] A pycniospore can fertilise a receptive hypha of the opposite mating type, leading to the production of a dikaryotic mycelium.[8] This is the sexual stage of the life cycle and cross-fertilisation provides an important source of genetic recombination.[8]

This dikaryotic mycelium then forms structures called aecia, which produce a type of dikaryotic spores called aeciospores.[8] These have a worty appearance and are formed in chains - unlike the urediniospores that are spiny and are produced on individual stalks.[8] The chains of aeciospores are surrounded by a bell-like enclosure of fungal cells. The aeciospores are able to germinate on the cereal host but not on the alternative host (they are produced on the alternative host, which is usually barberry).[8] They are carried by wind to the cereal host where they germinate and the germ tubes penetrate into the plant.[8] The fungus grows inside the plant as a dikaryotic mycelium.[8] Within 12 weeks the mycelium produces uredinia and the cycle is complete.[8]

Since the urediniospores are produced on the cereal host and can infect the cereal host, it is possible for the infection to pass from one year's crop to the next without infecting the alternate host (barberry).[8] For example, infected volunteer wheat plants can serve as a bridge from one growing season to another.[8] In other cases the fungus passes between winter wheat and spring wheat, meaning that it has a cereal host all year round.[8] Since the urediniospores are wind dispersed, this can occur over large distances.[8] Note that this cycle consists simply of vegetative propagation - urediniospores infect one wheat plant, leading to the production of more urediniospores that then infect other wheat plants.

Puccinia graminis produces all five of the spore types that are known for rust fungi.[8]

Spores are typically deposited close to the source, but long-distance dispersal is also well documented.[1] The following three categories of long-distance dispersal are known to occur:[1]

This can occur unassisted (the robust nature of the spores allows them to be carried long distances in the air and then deposited by rain-scrubbing) or assisted (typically on human clothing or infected plant material that is transported between regions).[1] This type of dispersal is rare and is very difficult to predict.[1]

This is probably the most common mode of long-distance dispersal and usually occurs within a country or region.[1]

This occurs in areas that have unsuitable conditions for year-round survival of Puccinia graminis - typically temperate regions where hosts are absent during either the winter or summer.[1] Spores overwinter or oversummer in another region and then recolonise when conditions are favorable.[1]

A number of stem rust resistance genes (Sr genes) have been identified in wheat.[10] Some of them arose in bread wheat (e.g. Sr5 and Sr6), while others have been bred in from other wheat species (e.g. Sr21 from T. monococcum) or from other members of the tribe Triticeae (e.g. Sr31 from rye and Sr44 from Thinopyrum intermedium).

None of the Sr genes provide resistance to all races of stem rust. For instance many of them are ineffective against the Ug99 lineage.[10] Notably Ug99 has virulence against Sr31, which was effective against all previous stem rust races. Recently, a new stem rust resistance gene Sr59 from Secale cereale was introgressed into wheat, which provides an additional asset for wheat improvement to mitigate yield losses caused by stem rust (Rahmatov et al., 2016)

Singh et al., [2011] provide a list of known Sr genes and their effectiveness against Ug99.[10]

The fungal ancestors of stem rust have infected grasses for millions of years and wheat crops for as long as they have been grown.[4] According to Jim Peterson, professor of wheat breeding and genetics at Oregon State University, "Stem rust destroyed more than 20% of U.S. wheat crops several times between 1917 and 1935, and losses reached 9% twice in the 1950s," with the last U.S. outbreak in 1962 destroying 5.2% of the crop.[4]

While Ug99 wasn't discovered until 1999, stem rust has been an ongoing problem dating back to Aristotle's time (384-322 B.C).[8] An early ancient practice by the Romans was one where they would sacrifice red animals such as foxes, dogs, and cows to Robigus (fem. Robigo), the rust god. They would perform this ritual in the spring during a festival known as the Robigalia in hopes of the wheat crop being spared from the destruction caused by the rust.[8] Weather records from that time have been observed and it has been speculated that the fall of the Roman Empire was due to a string of rainy seasons in which the rust would have been more harsh, resulting in reduced wheat harvests.[8] Laws banning barberry were established in 1660 in Rouen, France. This was due to the fact that European farmers noticed a correlation between barberry and stem rust epidemics in wheat.[8] The law banned the planting of barberry near wheat fields and was the first of its kind before the parasitic nature of stem rust was discovered in the 1700s.[8]

Two Italian scientists, Fontana and Tozzetti, first explained the stem rust fungus in wheat in 1767.[8] Italian scientist Giuseppe Maria Giovene (1753-1837), in his work Lettera al dottor Cosimo Moschettini sulla ruggine, also thoroughly studied the stem rust.[11] Thirty years later it received its name, Puccinia graminis, by Persoon, and in 1854 brothers Louis Ren and Charles Tulasne discovered the characteristic five-spore stage that is known to some stem rust species.[8] The brothers were also able to make a connection between the red (urediniospore) and black (teliospore) spores as different stages within the same organism, but the rest of the stages remained unknown.[8]

Anton de Bary later conducted experiments to observe the beliefs of the European farmers regarding the relationship between the rust and barberry plants, and after successful attempts to connect the basidiospores of the basidia stage to barberry, he also identified that the aeciospores in the aecia stage reinfect the wheat host.[8] Upon de Bary's discovery of all five spore stages and their need for barberry as a host, John Craigie, a Canadian pathologist, identified the function of the spermogonium in 1927.[8]

Due to the useful nature of both barberry and wheat plants, they were eventually brought to North America by European colonists.[8] Barberry was used for many things like making wine and jams from the berries to tool handles from the wood.[8] Ultimately, as they did in Europe, the colonists began to notice a relationship between barberry and stem rust epidemics in wheat.[8] Laws were enacted in many New England colonies, but as the farmers moved west, the problem with the stem rust moved with them and began to spread to many areas, creating a devastating epidemic in 1916.[8] It wasn't until two years later in 1918 that the United States created a program to remove barberry. The program was one that was supported by state and federal entities and was prompted by the looming fear of food supplies during the war.[8] The "war against barberries" was waged and called upon the help of citizens through radio and newspaper advertisements, pamphlets, and fair booths asking for help from all in the attempt to rid the barberry bushes of their existence.[8] Later, in 1975-1980, the program was reestablished under state jurisdiction.[8] Once this happened, a federal quarantine was established against the sale of stem rust susceptible barberry in those states that were part of the program.[8] A barberry testing program was created to ensure that only the species of barberry and other variations of plants that are immune to stem rust will be grown in the quarantine area.[8]

Excerpt from:
Stem rust - Wikipedia

Note from Ben regarding the Full Body Stem Cell Makeover: I mentioned 30K as total cost on the podcast.That actually is the cost for all the stem cell and exosome injectionsinto the spine and joints.The *cosmetic* and *sexual* add-ons tack 12-15K onto the total cost of this procedure. Just a heads up!

What you are about to discover in this podcast is one of the most advanced, fringe, cutting-edge biohacks and forays into self-experimentation I've ever done

a full body stem-cell makeover at Docere Clinics in Park City, Utahincluding a little-known type of compound called an exosome.

Dr. Harry Adelson, my firstguest on today's podcast,was one of the early adopters of stem cell therapy for the treatment of pain. He began his training in regenerative injection therapy (prolotherapy) in 1998 while in his final year at The National College of Naturopathic Medicine, in Portland, Oregon after having been cured of a rock-climbing injury with prolotherapy. During his residency program in Integrative Medicine at the Yale/Griffin Hospital in Derby, Connecticut, he volunteered after hours in a large homeless shelter in Bridgeport, Connecticut, providing regenerative injection therapies to the medically underserved while gaining valuable experience. He opened Docere Clinics in Park City in 2002 and from day one, his practice has been 100% regenerative injection therapies for the treatment of musculoskeletal pain conditions. In 2006 he incorporated platelet-rich plasma and ultrasound-guided injection into his armamentarium, in 2010, bone marrow aspirate concentrate and adipose-derived stem cells, and in 2013, fluoroscopic-guided injection (motion X-ray).

Since February of 2010, Dr. Adelson has performed over 5,000 bone marrow and adipose-derived adult stem cell procedures and has injected stem cells into over 500 intervertebral discs, placing him among those most experienced in the world with the use of autologous stem cells for the treatment of musculoskeletal pain conditions.

Dr. Amy Killen is also a guest on today's show. She joined Docere Medical after moving to Utah from Portland, Oregon, where she was the Medical Director of an anti-aging and regenerative medicine specialty practice. Dr. Killens medical training began in Dallas, where she attended medical school at UT Southwestern and received her M.D. degree, graduating in the top 10% of her class. She completed a residency in Emergency Medicine at the University of Arizona and served as Chief Resident during her final year. After working as a board-certified emergency physician for more than 7 years, Dr. Killen began studying and training in anti-aging, regenerative, and aesthetic medicine in hopes of approaching patients wellness and beauty from a different perspective and with a new toolbox of innovative and effective treatment options.

Advanced training has included completion of the fellowship in Anti-Aging and Regenerative Medicine through the American Association of Anti-Aging Medicine and certification training in Age Management Medicine. Dr. Killen is certified by the National Institute of Medical Aesthetics in both basic and advanced cosmetic injections and trained with Dr. Lisbeth Roy to learn the O-Shot and P-Shot PRP procedures. Further PRP injection training was provided by PRP Life Lift and she completed the Hair Coach certification program with Dr. Alan Bauman in Florida, which taught a comprehensive approach to non-surgical hair loss. Dr. Killen learned how to extract and process stem cells as part of the U.S. Stem Cell Training Course taught by leading stem cell scientist Dr. Kristin Comella. Dr. Amy Killen has also spent many hours in the operating suite learning directly from Harry Adelson N.D.at Docere Clinics.

Dr. Killen has spoken nationally about PRP and stem cell therapies and teaches a physician training course for ApexBiologix outlining current best practices for using regenerative therapies in aesthetics and sexual optimization.

During my discussion with Harry and Amy, you'll discover:

-How Harry got started with prolotherapy and PRP for pain management in farmers and construction workers14:45

-The Stem Cell Theory of Aging, which states that biologic aging is a result of loss function and population of stem cells in musculoskeletal tissues24:00

-How Harry is harvesting stem cells from bone marrow, supplementing them with exosomes (the currency of stem cells, the inter-cellular communication blocks), and then injecting them into all major moving parts as well as skin of face, scalp, and penis28:30

-Why umbilical and amniotic stem cells could potentially be dangerous due to exposing the body to foreign DNA32:30

-What MSC's are, why are they different and better than other stem cell therapies, and how they differentiate into musculoskeletal tissues and have been called medical signaling cells because they trigger the healing of damaged tissues42:00

-Why somebody would undergo a full body stem cell treatment, and whether is it going to rejuvenate all of the cells in my body49:30

-What to expect after a full body stem cell makeover57:00

Interview with Dr. Amy Killen:

-WhatPRP therapy is, and how it differs from stem cells1:07:00

-What happens when you inject stem cells into a mans unit, and why Amy injected Ben1:11:30

-Why Amy injects stem cells and PRP into vaginas, and how the O-Shot improves the power and duration of female orgasms1:15:20

-The secrets of the vampire breast lift and other cosmetic procedures she has done1:18:15

-What causes hair loss, and how to fix it with stem cells1:22:15

-What V-cells are and how they work1:27:00

-Post-treatment care and biohacks to enhance recovery and efficacy of the treatment1:29:00

-And much more!

Click here for the full written transcript of this podcast episode.

Resources from this episode:

Docere Clinics in Park City, Utah

-Video:What Are Exosomes? Ben Greenfield Interviews Dr. Harry Adelson On Full Body Stem Cell Makeover

-Video:Ben Greenfield Interviews Dr. Amy Killen About Stem Cells, PRP, Exosomes & P-Shot

-Video:Ben Greenfield Full Body Stem Cell Makeover With Exosomes: Part 1

-Video:Ben Greenfield Full Body Stem Cell Makeover With Exosomes: Part 2

-All the recovery biohacks I implemented to recover from the stem cell procedures and enhance stem cell production:

Flexpulse PEMFPulsecenters PEMFBiomat InfraredTrusii Hydrogen Rich WaterJoovv Infrared LightNanoVi DNA RepairExogenous HVMN KetonesOmega-3 DHA Superessential Fish OilVielight PhotobiomodulationKion FlexClearlight Sauna

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Do you have questions, thoughts or feedback for Dr. Harry, Amy or me? Leave your comments below and one of us will reply!

Ask Ben a Podcast Question

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How A "Full Body Stem Cell Makeover" Works - Ben ...

What are Stem Cells?

Stem Cells are the basic cells throughout the body that become replacement cells as needed. The cells that make up the structure of our tissues and organs only have a limited lifespan, and therefore a system of replacement, repair, and regeneration takes place for the tissues and organs to survive and function. Stem cells are capable of self-replicating, and can evolve into more cells with specialized function. They are highly active in some parts of the body that naturally need ongoing replacements on a regular basis, like the GI tract and skin. Other parts of the body, however, do not naturally have the ability to regenerate as readily. Some tissues in the body have no ability to repair and regenerate if injured. Stem Cells can be found in high concentrations in fat tissue and bone marrow, and then mobilized to areas in which they are needed. Today, regenerative medicine physicians are trying to utilize these remarkable cells that are able to rejuvenate tissues to help heal injuries. They can be used in addition to other regenerative treatments, such as Platelet Rich Plasma (PRP), to help promote healing.

Stem Cells are currently under intense medical investigation to treat various painful conditions, including discogenic back pain and several different Orthopedic conditions, such as hip and knee pain. Stem cells are aspirated using a minor surgical technique, concentrated much the same way PRP is obtained, and then injected along with PRP into the targeted area. Once in that environment, the cells are able to stimulate growth and regeneration, but at this time the exact mechanism of how this happens remains to be illuminated.

The Stem Cells need to be isolated either from a tissue source, such as bone marrow or fat, or from a commercial source. They are then mixed with Platelet Rich Plasma for injection into an injured area. It is best to restrict activity of the injected area to only mild to moderate activity for the first few weeks. Much like other RIT techniques, healing occurs over the course of 2-4 weeks and the results need to be re-evaluated.

Learn More About Stem Cell Treatmenthttps://en.wikipedia.org/wiki/Mesenchymal_stem_celhttp://cellbanktech.com/wp-content/uploads/2014/02/1.-Caplan-AI.-Mesenchymal-stem-cells-in-JOR-1991.pdf

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Stem Cells | Medford | Ashland | Southern Oregon

The R3 Stem Cell Center of Excellence in Oregon offer treatment both by way of injection or intravenous depending on the condition. This may include degenerative arthritis, a previous stroke, Alzheimers, COPD, an autoimmune condition like Rheumatoid Arthritis and more.

Did you know, for example, that over half of the current knee replacement patients in the US are under the age of sixty five and still working? Therefore, helping those individuals avoid the need for knee replacement and eliminating the time off from work will produce a hefty amount of savings annually when regenerative procedures are used.

The same holds true for hip, shoulder, ankle, wrist and elbow arthritis. Surgery for arthritis is a qualify of life, elective decision and should only be decided on after considerable conservative treatment has been exhausted. This includes regenerative therapy!

R3 Stem Cells Centers offer stem cell treatment using stem cell material obtained from consenting donors after a scheduled c-section through an FDA regulated process. There are no ethical issues since no babies are harmed and no embryonic stem cells are used.

Our Centers nationwide have performed over 10,000 successful procedures to date. As the Nations leaders in regenerative medicine, let R3 help you and your loved ones obtain relief with a complimentary consultation!

Amniotic and Umbilical Cord Stem Cell Therapy

Amniotic fluid and umbilical cord tissue contains a significant amount of regenerative cells such as cytokines, stem cells, growth factors, exosomes, secretomes, mRNA and more. A great analogy is to call it an orchestra since it contains so many different types of regenerative medicine elements that come together to produce an excellent repair process.

Known as the products of conception, amniotic fluid and umbilical cord is acquired from consenting donors after a scheduled c-section. No babies are harmed. Once processing is complete, the material is cryogenically preserved. The lab that R3 works with does NOT radiate the product and uses very little preservative. Therefore cell viability is maximized.

The FDA regulates the process of amniotic/umbical cord acquisition, processing, storage and usage very strictly. This is regulated as a biologic, not a drug, so FDA approval is not possible only regulation.

When it comes to arthritis and soft tissue conditions, outcomes are excellent for over 85% of individuals. These results are very good for even bone on bone arthritis. Patients are typically able to significantly delay or avoid the need for a joint replacement with these therapies.

When it comes to systemic conditions, neurodegenerative, neuropathy, and organ failure, results exceed 75% as well. It has truly been amazing seeing patients achieve a better quality of life after regenerative procedures.

What are the risks?

The risks of these treatments are absolutely minimal. We have not seen any rejection reaction as the DNA antigen factors have been removed. Over 10,000 cases have been performed by R3s Centers over the past 6 years successfully.

There is a typical risk of infection, bleeding, allergic reaction. These are seen in much less than 1% of patients.

PRP Therapy

PRP stands for Platelet Rich Plasma Therapy and involves a simple blood draw from the patient. This will range from 20ccs to 60ccs, which is considerably less than a pint of blood.

This blood is then placed in a kit that goes into a machine called a centrifuge, which spins rapidly for 12 minutes. This separates the blood into three layers, with the middle layer being known as the buffy coat. Thats what is used in PRP and contains the following regenerative materials:

PRP contains minimal stem cells, but does act to call in ones bodys stem cells to assist with repair and regeneration. Not only can PRP therapy help by itself to assist with joint and soft tissue repair, it also can act as a jump start when used in conjunction with amniotic and umbilical tissue.

White blood cells create inflammation, which is the first phase of healing. The bottom line with PRP is that it may be very effective when used either by itself or in conjunction with amniotic/umbilical treatment.

There have been several studies showing the effectiveness of PRP therapy for joint and soft tissue pain. The therapy works very well for:

Since the treatment originates from ones own blood, the risks are minimal to the patient.

If you or a loved one is suffering from joint and/or soft tissue pain and you would like a free consultation to discuss regenerative options, call us at (844) GET-STEM today!

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Stem Cell Therapy Portland Oregon | Stem Cell Therapy