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By: Bertram G. Katzung MD, PhD
- Professor Emeritus, Department of Cellular & Molecular Pharmacology, University of California, San Francisco
Nitrogen buy nitrostat 2.6mg online, present in the form of ammonia nitrostat 2.6mg lowest price, is a deamination product of amino acids generic 2.6 mg nitrostat overnight delivery. The removal of nitrogen is a metabolic process that is part of the Krebs-Henseleit cycle purchase 6.4mg nitrostat otc, also known as the urea or ornithine cycle (illustrated in Figure 3-1). Five key products that perpetuate the cycle are: arginine, urea, ornithine, carbamoyl P(phosphate), and aspartate. The reactions occur intracellularly and are distributed between the mitochondrial matrix and the cytosol. Subsequently, a new urea molecule is produced starting with the ornithine product after it enters the mitochondria. Fumarate is then cleaved by argininosuccinate lyase to form arginine and the cycle begins again. Urea is eliminated from the body primarily through the urinary system and accounts for approximately half of the total urinary solids. Elevated urea levels may be associated with congestive heart disease, urinary obstruction, gastrointestinal disorders, as well as renal disease. Elevated urea levels may also be an indicator of dehydration, starvation, or shock. A protein-rich meal results in increased urea synthesis and plasma urea concentration. Urea levels below the normal physiological range may indicate over hydration, malnutrition, too little dietary protein in the diet, or liver injury/disease. Adaptation may also occur in response to increased or decreased urea concentrations within physiological range of homeostasis. Because urea is a naturally occurring product in mammals and other biological organisms, the majority of the literature identified during the search process pertained to urea production in vivo and factors affecting its production. This section will only present results from studies of exogenously administered urea. Dawes (2006) reported data for the absorption of urea through the oral mucosa in 10 adults (5 males and 5 females; age range 24?68 years; mean age 36 years) who chewed gum that contained urea as an additive. Study participants signed a consent that had been approved by the Health Research Ethics Board of the University of Manitoba and avoided eating, drinking, chewing gum, or any type of oral hygiene activities for at least 1 hour prior to the study. The second group simultaneously chewed two pieces of gum containing only phenol red to establish the endogenous urea concentration in saliva for use as a sham control. Saliva samples were collected from each group at a 5-minute period prior to initiating gum chewing and during a 10-minute chewing time. The investigators suggested the difference was due to the higher rate of saliva production in gum chewers and longer collection time resulting in sample dilution. Urea absorption was determined as the percentage of urea recovered relative to the percentage of unabsorbable phenol red recovered (theoretically 100%) to adjust for sample loss due to swallowing during saliva collection. The results summarized in Table 3-1 show the percentage of phenol red and urea recovered from the saliva samples and the chewed gum residues plus saliva obtained from sham control and urea exposed participants (Dawes, 2006). The percentage of phenol red and urea recovered in the saliva and chewed gum Saliva Chewed gum + saliva a b b b Group Volume Percent recovery Percent recovery (mL) Phenol red Urea Phenol red Urea c Control 26. Based on the observation that the percentage of urea recovery was less than the nonabsorbed marker, phenol red, Dawes (2006) postulated that when the salivary urea concentration is higher than that in the plasma, urea may be absorbed through the oral mucosa. Dawes (2006) noted that calculation of an absorption coefficient was not possible since: (1) saliva urea concentrations were not maintained at a constant level, and (2) the mucosa surface area was not measured. Interpretation of this study is limited as radiolabeled urea was not used to distinguish urea in the chewing gum from endogenous urea. Additionally, information on the 8 actual amount rather than the percent of urea recovered in saliva of the control group would aid in a better understanding of urea absorption. Fasted rats were included in this study design as the authors were interested in the effects of diet on the disposition of urea. Nonfasted rats received food ad libitum, but the food was removed 15 hours prior to dosing and withheld for 8 hours after treatment of the fasted rats. Urine, feces, blood, and/or tissue samples were collected at 30 minutes, and 1, 4, 8, 24, 48, 72, and/or 96 hours. In both fasted and nonfasted rats given 2 mg urea/kg body weight, plasma concentrations decreased biphasically as a function of time in both the oral and i. The pharmacokinetic parameters for the concentration and t1/2 of urea within the plasma are shown in Table 3-2. The t1/2 calculated for each phase of the curve was also similar at all four doses (see Table 3-2). The authors claim that the disposition of exogenous urea is similar to that of endogenous urea and suggests that rats have a sufficiently large capacity for disposition. Two in vivo studies in rats were conducted to examine the uptake and distribution kinetics of exogenous 14 [ C]-urea administered orally or intraperitoneally. The results from these studies, along with data from a more recent study by 14 Sahin and Rowland (2007) of the hepatic kinetics of [ C]-urea in situ and the effect of erythrocytes on uptake and elimination, are presented here. In general, fasting had little effect on the tissue distribution but did produce a slight increase in the overall concentrations. With the exception of the brain and eyeball, the maximum tissue concentrations were recorded 30 minutes to an hour after urea administration (plasma concentration reached Cmax at 30 minutes in both the nonfasted and fasted animals; 1,231 319 and 1,675 938 ng eq/mL, respectively). Excluding the gastrointestinal tract (site of administration), the tissues with the highest radiolabel concentration were the kidney and urinary bladder (~2. Fat and brain had the lowest urea concentrations (225 138 and 263 182 ng eq/mL, respectively) at this time point. Urea concentrations in the remaining tissues were similar to or below that in the plasma. After 24 hours, all tested tissues, with the exception of the large intestine and the Harderian gland, had below detectable levels of radiolabeled urea after 24 hours.
Conclusion the dose of erythropoietin ranges from 50-150 Currently available hematopoietic growth factors U/kg 3 times weekly for most patients buy nitrostat 6.4mg cheap, although in can improve the production of 3 major blood cell chemotherapy patients and those undergoing elective groups effective nitrostat 6.4 mg. The availability of these growth factors surgery buy generic nitrostat 6.4 mg on line, the dose can be increased to purchase 6.4 mg nitrostat overnight delivery as high as 300 has had a major impact the treatment of a variety U/kg. Studies have demonstrated that erythropoietin of illnesses, both malignant and nonmalignant. This dose with any other therapy, the use of these growth schedule has received approval from the Food and factors must be assessed with regards to their Drug Administration. Once the hematocrit has proven clinical efficacy, side effect profile, and reached the 30% to 36% (0. The side effects of erythropoietin are minimal with References the predominantly reported adverse events being 1. Supportive care in hematologi cal malignancies: hematopoietic growth factors, infections, bone pain, headaches, hypertension, and, rarely, transfusion therapy. High-Dose Cancer Therapy: Pharmacology, tual result of increasing platelet production. Baltim ore, M D: W illiam s & Oprelvekin is indicated for the prevention of W ilkins; 1992: 289-313. A comparative review of colony-stimulating severe thrombocytopenia and to reduce the need factors. Toxicologists and environmental health regulators learned about state-of-the-art stem cell models, including human cells that are derived from embryos, induced pluripotent stem cells, and adult lineage restricted stem cells, which could be used to inform environmental health decisions. Stem cell biologists learned more about the critical questions challenging environmental health scientists. Stem cells have received much attention because self-renew in culture, are also thought to be of their potential therapeutic applications, but in the pluripotent. This is because stem cells have how pluripotent embryonic stem cells can be the special property of being able to differentiate to manipulated to produce more than 200 specifc produce a wide variety of cell types?a property that cell types corresponding to all the major lineages enables them to be used to model aspects of human (types of cells) and to more immature cells that can biology that have been largely inaccessible to study by be used for studying developmental processes. William the cells of the resulting two-cell embryo are thought Lensch (Harvard University). Changing the conditions becomes a blastocyst?a hollow ball of cells with an in which stem cells are cultured, adding components outer layer that will become the placenta and an to or subtracting components from the medium, inner cell mass that is comprised of cells that are can alter their fate. This is in contrast with somatic embryonic stem cells, which are collected cells that make up almost all the body and have a from the inner cell mass and continuously limited life span. Lebkowski pointed out that the this newsletter refects the views of individuals and ideas presented at the meeting?they do not represent either formal consensus conclusions of the attendees or positions necessarily endorsed by the National Research Council. Research by ChanTest, a company that from embryos or via cloning technologies, so their performs screening for drug development, shows use sidesteps the ethical issues discussed above. Hence, it is possible to test effects of Cells that are given specifc factors? can be repro chemicals directly by measuring their effects on grammed to behave more like embryonic stem contractility with methods similar to those used cells. In contrast with many of the that cell lines generated from different kinds of screening approaches used currently, some scien tists envision that those panels of cells will be much better barometers of potential toxic effects in humans. In reviewing stem cell basics, Michael Roberts (University of Missouri) summarized two nonsci entifc concerns that have been expressed. Another concern involves the derivation of human stem cells via cloning tech niques similar to the ones that produced Dolly the sheep. The idea of using cloning technologies to 2 somatic cells behave and differentiate differently, have a rare genetically mediated form of autism possibly because they carry an epigenetic called Timothy syndrome. In this regard, different Although the Stanford researchers have not lineages have different potential. There is also evidence that the made in large quantities, are good candidates for reprogramming process does not completely this kind of screening. Nonetheless, these that researchers can use these cells to produce cells have many interesting applications. In summarizing, Dolmetsch cautioned complex genetic diseases, such as using them to that the goal is complicated by the fact that identify genes that make people who have Down researchers are still trying to identify genetic syndrome more or less susceptible to some links with autism. Role of Environmental Chemicals Breast cancer in Disease Zena Werb (University of California, San francisco) Autism researches the role of stem cells in breast cancer. Ricardo Dolmetsch (Stanford University) is using She is using many experimental systems, including human stem cells to investigate autism-spectrum mouse models and human tissue grown in mice. Dolmetsch told two kinds of pluripotent stem cells: (1) the actively conference attendees that the incidence of autism proliferating population (more numerous) and has been rising and that, although some circum (2) the quiescent type (much rarer). The quiescent cells are some important classes of neurons exist only in called on under more acute circumstances, in primates. Quiescent stem cells are calcium-signaling defcits found in patients who also involved in generation of secretory tissue. This might other issues that toxicologists and stem cell biolo warrant studying stem cell lines from different gists might bear in mind as they develop stem cell genetic backgrounds. Many appear to express genes that are associated with pumping out various types of toxic chemi We have to figure out how we are going cals (drug-transporter genes) and thereby to include metabolism in these assays. Food and Drug Wood Johnson Medical School) pointed out Administration, National Center for that stem cells may use repair enzymes differ Toxicological Research ent from those used by developing cells. Maintaining them in a agreed, noting that he was very concerned that high-oxygen environment in vitro may change Tox 21 is now testing tens of thousands of chemi how they function by mechanisms that include cals with no provision for metabolic activation. Scientists are just beginning to understand Administration Center for biologics Evaluation the mechanisms that control these switches, and Research) pointed out that scientists will which may be important for understanding need to validate the utility of stem-cell?based carcinogenesis. This is something Trosko models for assessing chemicals by comparing the thought should be taken into consideration; data that they yield with the relevant existing indeed, Max Wicha (University of Michigan) bodies of knowledge. He said the Interagency noted that research is beginning to show that Coordinating Committee on the Validation of many oncogenes that cause cancer trigger Alternative Methods has validation paradigms that imbalances between symmetric and asymmetric may prove helpful although they may need to be cell division.
Atlantic tomcod hepatocellular carcinoma shows anaplastic hepatocytes with extreme nuclear pleomorphism and some multinuclear cells discount nitrostat 2.6mg fast delivery. Pantothetic Acid Deficiency Rainbow trout with classic nutritional gill disease due to discount 2.6 mg nitrostat pantothenic acid deficiency generic 6.4 mg nitrostat fast delivery. Note fusion of lamellae at tips of filaments; more normal lamellae towards bases (bar = 100?m) nitrostat 2.6 mg cheap. Pyridoxine Deficiency Pyridoxine deficient pancreatitis and mild degeneration of pancreatic acinar cells. Vitamin E decfiency severe necrosis, fibrosis and atrophy of muscle fibers in trout. Phosphorus deficiency pancreatic acinar cells are swollen, lack zymogen & show mild degeneration. In particular, the Committee addresses questions related to the safety and allergenic properties of cosmetic products and ingredients with respect to their impact on consumer health, toys, textiles, clothing, personal care products, domestic products such as detergents and consumer services such as tattooing. Scientific Committee members Claire Chambers, Gisela Degen, Ruta Dubakiene, Bozena Jazwiec-Kanyion, Vassilios Kapoulas, Jean Krutmann, Carola Liden, Jean-Paul Marty, Thomas Platzek, Suresh Chandra Rastogi, Jean Revuz, Vera Rogiers, Tore Sanner, Gunter Speit, Jacqueline Van Engelen, Ian R. The opinions are published by the European Commission in their original language only. Kojic dipalmitate is mentioned in the Inventory of Cosmetic Ingredients, but derivative esters of Kojic acids are also used. The Commission received a request from a Member State for a safety evaluation of the use of Kojic acid. Stability No data submitted General Comments on physico-chemical characterisation No data were provided on Log Pow No data were provided on the stability of Kojic acid in the test solutions and in the marketed product. It has been shown to act as a competitive and reversible inhibitor of animal and plant polyphenol oxidases, i. Spectrophotometric and chromatographic methods demonstrated that Kojic acid was capable of reducing o-quinones to diphenols to prevent the final pigment (melanin) from forming. Kojic acid might have the property of an insecticide due to its inhibitory effect on tyrosinase as well as its ability to interact with o-quinones of catecholamines, thus preventing the sclerotization process. Kojic oleate, Kojic stearate), in adhesives, in chelate-forming resins and as a plant growth regulating agent to increase production, early maturing and increase sweetness. In the main experiment lethargy, piloerection, abnormal body carriage, ataxia and depressed respiration rate were observed shortly after dosing. Bodyweight increases of rats treated at 16000 mg/kg bw were slightly depressed during the first week. Bodyweight increases of rats treated at 1600 mg/kg bw were slightly depressed during the first week. Animals were weighed before administration of test substance (day 0), and on day 1, 8 and 15. Results In the treated group sedation or hypoactivity, dyspnea and lateral recumbency were observed in all animals on day 1. The body weight gain of the surviving animals of the treated group was similar to that of the control group. The control animals received 2 ml of purified water under the same experimental conditions. Clinical signs, mortality and body weight gain were checked for a period of 14 days following treatment. Results No mortality, clinical signs, cutaneous reactions or apparent abnormalities at necropsy were observed. Body weight gain was reduced slightly between day 1 and day 8 in treated animals compared to the control animals. All mice were examined macroscopically when they had died or at the end of observation period. In the main experiment lethargy, piloerection, ataxia and depressed respiration rate were observed shortly after dosing. Autopsy revealed pallor of the liver, haemorrhage of the lungs and injection of the blood vessels of the abnormal viscera in animals died after treatment. All rats were examined macroscopically when they had died or at the end of observation period. In the main experiment lethargy, piloerection, ataxia, abnormal body carriage and depressed respiration rate were observed shortly after dosing. These signs were accompanied by increased salivation, diuresis, coarse body tremors, gasping and convulsions prior to death in rats treated above 1000 mg/kg bw. One female of the 1000 mg/kg bw group developed persisting paralysis of the hind limp on day three. Autopsy revealed haemorrhage of the lungs, pallor of the liver and injection of the blood vessels of the abnormal viscera as well as opacities of one or both eyes in animals died after treatment. All mice were examined macroscopically when they had died or at the end of the observation period. Haemorrhage at the site of injection was observed immediately after dosing time in all mice. In the main experiment lethargy, piloerection, diuresis, abnormal body carriage and depressed respiration rate were observed shortly after dosing. Autopsy revealed haemorrhage of the lungs, pallor of the liver and haemorrhage at the injection site. In the additional group investigated for effects on the eyes, evidence of lenticular opacities was observed in both eyes of two male rats. After 24 h patches were removed and the skin was evaluated for erythema and oedema. Mucous membrane irritation Guideline: / st Species/strain: rabbit (1 experiment) nd Angora rabbit (2 experiment) Group size: 3 animals (preliminary test) st 5 animals (1 experiment) nd 2 males, 2 females (2 experiment) nd 9 animals (2 experiment, supplementary test) Test substance: Kojic Acid Batch: / Purity: / Dose: 3%, 0.
Incidences of nonneoplastic histologic changes in B6C3F1 mice exposed to nitrostat 6.4 mg low price dichloromethane by inhalation (6 hours/day discount 6.4 mg nitrostat visa, 5 days/week) for 2 years discount nitrostat 2.6 mg online. Incidences of neoplastic lesions in male and female B6C3F1 mice exposed to cheap nitrostat 2.6 mg without prescription dichloromethane by inhalation (6 hours/day, 5 days/week) for 2 years. Incidences of selected nonneoplastic and neoplastic histologic changes in male and female Sprague-Dawley rats exposed to dichloromethane by inhalation (6 hours/day, 5 days/week) for 2 years. Incidences of selected nonneoplastic histologic changes in male and female Sprague-Dawley rats exposed to dichloromethane by inhalation (6 hours/day, 5 days/week) for 2 years. Incidences of selected neoplastic histologic changes in male and female Sprague-Dawley rats exposed to dichloromethane by inhalation (6 hours/day, 5 days/week) for 2 years. Summary of studies of reproductive and developmental effects of dichloromethane exposure in animals. Studies of neurobehavioral changes from dichloromethane, by route of exposure and type of effect. Studies of neurophysiological changes as measured by evoked potentials resulting from dichloromethane, by route of exposure. Results from in vitro genotoxicity assays of dichloromethane in nonmammalian systems. Results from in vitro genotoxicity assays of dichloromethane with mammalian systems, by type of test. Comparison of in vivo dichloromethane genotoxicity assays targeted to lung or liver cells, by species. Incidence of liver tumors in male B6C3F1 mice exposed to dichloromethane in a a 2-year oral exposure (drinking water) study. Incidences of liver tumors in male and female F344 rats exposed to dichloromethane in drinking water for 2 years. Incidences of selected neoplastic lesions in B6C3F1 mice exposed to dichloromethane by inhalation (6 hours/day, 5 days/week) for 2 years. Incidences of selected neoplastic lesions in F344/N rats exposed to dichloromethane by inhalation (6 hours/day, 5 days/week) for 2 years. Incidences of mammary gland tumors in two studies of male and female Sprague-Dawley rats exposed to dichloromethane by inhalation (6 hours/day, 5 days/week) for 2 years. Comparison of internal dose metrics in inhalation and oral exposure scenarios in male mice and rats. Results from dichloromethane chromosomal instability assays (in vivo and in vitro), by species. Incidence data for liver lesions and internal liver doses based on various metrics in male and female F344 rats exposed to dichloromethane in drinking water for 2 years. Incidence data for liver lesions (hepatic vacuolation) and internal liver doses based on various metrics in female Sprague-Dawley rats exposed to dichloromethane via inhalation for 2 years. Comparison of oral slope factors derived using various assumptions and metrics, based on tumors in male mice. Summary of uncertainty in the derivation of cancer risk values for dichloromethane. Statistical characteristics of human internal doses for 1 mg/kg-day oral exposures in specific populations. Statistical characteristics of human internal doses for 1 mg/m inhalation exposures in specific subpopulations. Comparison of oral slope factors derived by using various assumptions and metrics, based on liver tumors in male mice. Comparison of inhalation unit risks derived by using various assumptions and metrics. Observations and predictions of total expired dichloromethane resulting from a gavage doses in rats. Mortality risk in Eastman Kodak cellulose triacetate film base production workers, Rochester, New York. Mortality risk by cumulative exposure in Eastman Kodak cellulose triacetate film base production workers, Rochester, New York. Mortality risk in Imperial Chemical Industries cellulose triacetate film base production workers, Brantham, United Kingdom: 1,473 men employed 1946? 1988, followed through 2006. Mortality risk in Hoechst Celanese Corporation cellulose triacetate fiber production workers, Rock Hill, South Carolina: 1,271 men and women employed 1954?1977, followed through 1990. Cancer mortality risk in Hoechst Celanese Corporation cellulose triacetate fiber production workers, Cumberland, Maryland: 2,909 men and women employed 1970?1981, followed through 1989. Incidences of histopathologic changes in livers of male and female F344 rats exposed to dichloromethane in drinking water for 90 days. Incidences of histopathologic changes in livers of male and female B6C3F1 mice exposed to dichloromethane in drinking water for 90 days. Incidence data for mammary gland tumors and internal doses based on different dose metrics in male and female F344 rats exposed to dichloromethane via inhalation for 2 years. Exposure response array for oral exposure to dichloromethane (M = male; F = female). Exposure response array for subacute to subchronic inhalation exposure to dichloromethane (log Y axis) (M=male; F=female). Mean value respiration rates for males and females as a function of age [values from Clewell et al. Comparison of model Variation C predictions to dichloromethane exhalation data of McKenna and Zempel (1981) (data not used for model calibration) from bolus oral exposures to 1 and 50 mg/kg dichloromethane, along with 50 mg/kg bolus oral data of Angelo et al. Predicted (logistic model) and observed incidence of noncancer liver lesions in male F344 rats exposed to dichloromethane in drinking water for 2 years (Serota et al.
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Cellular diversity within embryonic stem cells: pluripotent clonal sublines show distinct differentiation potential purchase nitrostat 2.6mg mastercard. Pluripotency governed by Sox2 via regulation of Oct3/4 expression in mouse embryonic stem cells nitrostat 2.6mg cheap. Mitsui K discount 6.4mg nitrostat amex, Tokuzawa Y 6.4mg nitrostat otc, Itoh H, Segawa K, Murakami M, Takahashi K, Maruyama M, Maeda M, Yamanaka S. Simple generation of human induced pluripotent stem cells using poly-beta-amino esters as the non-viral gene delivery system. Nakagawa M, Koyanagi M, Tanabe K, Takahashi K, Ichisaka T, Aoi T, Okita K, Mochiduki Y, Takizawa N, Yamanaka S. Development of Sendai virus vectors and their potential applications in gene therapy and regenerative medicine. Klf4 cooperates with with Oct3/4 and Sox2 to activate the Lefty1 core promoter in embryonic stem cells. Nishimura K, Sano M, Ohtaka M, Furuta B, Umemura Y, Nakajima Y, Ikehara Y, Kobayashi T, Segawa H, Takayasu S, Sato H, Motomura K, Uchida E, Kanayasu-Toyoda T, Asashima M, Nakauchi H, Yamaguchi T, Nakanishi M. Development of defective and persistent Sendai virus vector: a unique gene delivery/expression system ideal for cell reprogramming. Nishino K, Toyoda M, Yamazaki-Inoue M, Fukawatase Y, Chikazawa E, Sakaguchi H, Akutsu H, Umezawa A. Generation of virus-free induced pluripotent stem cell clones on a synthetic matrix via a single cell subcloning in the naive state. Okita K, Matsumura Y, Sato Y, Okada A, Morizane A, Okamoto S, Hong H, Nakagawa M, Tanabe K, Tezuka K, Shibata T, Kunisada T, Takahashi M, Takahashi J, Saji H, Yamanaka S. Ono M, Hamada Y, Horiuchi Y, Matsuo-Takasaki M, Imoto Y, Satomi K, Arinami T, Hasegawa M, Fujioka T, Nakamura Y, Noguchi E. Generation of induced pluripotent stem cells from nasal epithelial cells using a Sendai virus vector. Marked difference in differentiation propensity among human embryonic stem cell lines. Generation of induced pluripotent stem cells from a small amount of human peripheral blood using a combination of activated T cells and Sendai virus. Seki T, Yuasa S, Oda M, Egashira T, Yae K, Kusumoto D, Nakata H, Tohyama S, Hashimoto H, Kodaira M, Okada Y, Seimiya H, Fusaki N, Hasegawa M. Induced pluripotent stem cell generation using a single lentiviral stem cell cassette. De novo methylation, expression, and infectivity of retroviral genomes introduced into embryonal carcinoma cells. Feeder-free derivation of induced pluripotent stem cells from adult human adipose stem cells. Optimal reprogramming factor stoichiometry increases colony numbers and affects molecular characteristics of murine induced pluripotent stem cells. Recombinant Sendai viruses expressing different levels of a foreign reporter gene. Sox2 is dispensable for the reprogramming of melanocytes and melanoma cells into induced pluripotent stem cells. The histone demethylases Jhdm1a/1b enhance somatic cell reprogramming in a vitamin C-dependent manner. A drug-inducible transgenic system for direct reprogramming of multiple somatic cell types. Present state and future perspectives of using pluripotent stem cells in toxicology research. Harnessing the potential of induced pluripotent stem cells for regenerative medicine. Xiao A, Wang Z, Hu Y, Wu Y, Luo Z, Yang Z, Zu Y, Li W, Huang P, Tong X, Zhu Z, Lin S, Zhang B. Zhao Y, Yin X, Qin H, Zhu F, Liu H, Yang W, Zhang Q, Xiang C, Hou P, Song Z, Liu Y, Yong J, Zhang P, Cai J, Liu M, Li H, Li Y, Qu X, Cui K, Zhang W, Xiang T, Wu Y, Zhao Y, Liu C, Yu C, Yuan K, Lou J, Ding M, Deng H. Gene targeting of a disease-related gene in human induced pluripotent stem and embryonic stem cells. Stem cells are unique cell populations that retained the capability of either self-renewal in nearly infinite cell divisions or to differentiate into one or several cell types. In contrast, adult stem cells are multipotent, harbouring the ability to differentiate into specific cell types of the tissue of origin in which they reside. Thus, adult stem cells are the in vivo source for cell renewal during tissue turnover or in tissue repair. However, broad plasticity of adult stem cells have been described, allowing the cells to differentiate across tissue lineage boundaries to give rise to cell types of other lineages. Embryonic stem cells are isolated from the inner cell mass of mouse or human blastocysts. The generation of human embryonic stem cell lines from preimplantation blastocysts and their use in basic research as well as in future therapeutic application has raised considerable ethical concerns. The source of a human blastocyst are exclusively fertilized eggs that have been grown in vitro for 5 to 6 days. However, the isolation and preparation of cells from the inner cell mass results in the destruction of the blastocysts and is thus considered an embryo-consuming technology, which by this reason is prohibited in many European countries. Alternative technologies, like somatic nuclear transfer, have been developed in order to avoid to waste fertilized human embryos, however, ethical concerns still exist, since enucleated human oocytes are needed. Adult stem cells are easy to obtain, although they reside in low abundance in adult tissues and organs, so-called stem cell niches. Any ethical concerns about harvest and isolation of adult stem cells are neglectable. The sources for adult stem cells are manifold and include easily available human tissue, like blood, bone marrow or adipose tissue, or human material, which is normally unused or even discarded, like umbilical cord, placenta, or deciduous milk teeth.