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ABSTRACT Mouse myeloid leukemia cells M1 ; were induced to differ entiate into mature macrophages and granulocytes by gluco corticoids on a protein inducer in ascitic fluid from tumor bearing rats. Addition of nonstenoidal antiinflammatomyagents to Ml cells in suspension cultures inhibited the induction of differentiation by glucocorticoid dexamethasone ; or the pro tein inducer. The inhibition was unrelated to cytotoxicity and was reversible. The nonstenoidal antiinflammatony agent indo methacin inhibited dexamethasone-induced differentiation only when added before the time of commitment of the cells to differentiation. The indomethacin-mediated inhibition was counteracted by prostaglandins E1 or E2 but not by prostaglandins F1 or F26. Prostaglandin E stimulated phagocytosis induced by a subop timal concentration of dexamethasone, but prostaglandin F did not. Moreover, lysozyme activity, which is a typical biochemical marker of macnophages, was induced in Ml cells by prosta glandin E alone, as well as by inducens of differentiation. These results suggest that prostaglandin E may be important in the induction of differentiation of myeloid leukemia cells. INTRODUCTION Some myeloid leukemia cell lines can be induced to undergo differentiation in vitro 1 , 15, 17, 19 ; and in vivo 9 ; . Their differentiation is detected by change in cell morphology, induc tion of locomotive and phagocytic activities, adhesion of cells to the dish, elevation of lysosomal enzyme activities, and the appearance of Fc and C3 receptors on the cell surface 15, 18, 21 , 26, 31 ; . Ml line cells, established from an SL mouse with myeloid leukemia, can be induced to undergo diffementia tion by protein inducers, glucocorticoids, some antibiotics, bacterial lipopolysacchanides, dimethyl sulfoxide, and polyi.

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Eisensamer et al. Colocalization of Drugs and 5-HT3 Receptors in Rafts enriched membrane subdomains during transport to the apical cell surface. Cell 68: 533544. Bruses JL, Chauvet N, Rutishauser U 2001 ; Membrane lipid rafts are necessary for the maintenance of the 7 nicotinic acetylcholine receptor in somatic spines of ciliary neurons. J Neurosci 21: 504 512. Burgi S, Baltensperger K, Honegger UE 2003 ; Antidepressant-induced switch of 1-adrenoceptor trafficking as a mechanism for drug action. J Biol Chem 278: 1044 1052. Calkin PA, Barnes EMJR 1994 ; Agonist-induced internalization and degradation of -aminobutyric acidA GABAA ; receptor polypeptides from the neuronal surface. J Protein Chem 13: 438. Connolly CN, Uren JM, Thomas P, Gorrie GH, Gibson A, Smart TG, Moss SJ 1999 ; Subcellular localization and endocytosis of homomeric 2 subunit splice variants of -aminobutyric acid type A receptors. Mol Cell Neurosci 13: 259 271. Dalskov SM, Immerdal L, Niels-Christiansen LL, Hansen GH, Schousboe A, Danielsen EM 2005 ; Lipid raft localization of GABAA receptor and Na , K ATPase in discrete microdomain clusters in rat cerebellar granule cells. Neurochem Int 46: 489 499. Davies PA, Pistis M, Hanna MC, Peters JA, Lambert JJ, Hales TG, Kirkness EF 1999 ; The 5-HT3B subunit is a major determinant of serotonin-receptor function. Nature 397: 359 363. Di Francesco C, Bickel MH 1977 ; Membrane lipids as intracellular binders of chloropromazine and related drugs. Chem Biol Interact 16: 335346. Donati RJ, Thukral C, Rasenick MM 2001 ; Chronic treatment of C6 glioma cells with antidepressant drugs results in a redistribution of Gs . Mol Pharmacol 59: 1426 1432. Edidin M 2003 ; The state of lipid rafts: from model membranes to cells. Annu Rev Biophys Biomol Struct 32: 257283. Eisensamer B, Rammes G, Gimpl G, Shapa M, Ferrari U, Hapfelmeier G, Bondy B, Parsons C, Gilling K, Zieglgansberger W, Holsboer F, Rupprecht R 2003 ; Antidepressants are functional antagonists at the serotonin type 3 5-HT3 ; receptor. Mol Psychiatry 8: 994 1007. Fan P 1994 ; Inhibition of a 5-HT3 receptor-mediated current by the selective serotonin uptake inhibitor, fluoxetine. Neurosci Lett 173: 210 212. Fra AM, Williamson E, Simons K, Parton RG 1995 ; De novo formation of caveolae in lymphocytes by expression of VIP21-caveolin. Proc Natl Acad Sci USA 92: 8655 8659. Gimpl G, Fahrenholz F 2000 ; Human oxytocin receptors in cholesterolrich vs. cholesterol-poor microdomains of the plasma membrane. FEBS Lett 267: 24832497. Henry ME, Moore C, Kaufmann M, Michelson D, Schmidt M, Stoddard E Vuckevic AJ, Berreira P, Cohen BM, Renshaw PF 2000 ; Brain kinetics of paroxetine and fluoxetine on the third day of placebo substitution: a fluorine MRS study. J Psychiatry 157: 1506 1508. Hering H, Lin CC, Sheng M 2003 ; Lipid rafts in the maintenance of synapses, dendritic spines, and surface AMPA receptor stability. J Neurosci 23: 32623271. Hermann B, Wetzel CHR, Pestel E, Ziegelgansberger W, Holsboer F, Rupprecht R 1996 ; Functional antagonistic properties of clozapine at the 5-HT3 receptor. Biochem Biophys Res Commun 225: 957960. Hooper NM 1999 ; Detergent-insoluble glycoshingolipid cholesterol-rich membrane domains, lipid rafts and caveolae. Mol Membr Biol 16: 145156. Ilegems E, Pick HM, Deluz C, Kellenberger S, Vogel H 2004 ; Noninvasive imaging of 5-HT3 receptor trafficking in live cells. J Biol Chem 279: 53346 53352. Kinon BJ, Lieberman JA 1996 ; Mechanisms of action of atypical antipsychotic drugs: a critical analysis. Psychopharmacology 124: 234. Korpi ER, Wong G, Luddens H 1995 ; Subtype specificity of gammaaminobutyric acid type A receptor antagonism by clozapine. Naunyn Schmiedebergs Arch Pharmacol 352: 365373. Koshikawa N, Durcan MJ, Weaver K, Lawrence K, Campbell IC 1987 ; Subcellular distribution of -adrenoceptors in brain following administration of antidepressant drugs. Neuropharmacology 26: 13431349. Kurzchalia TV, Parton RG 1999 ; Membrane microdomains and caveolae. Curr Opin Cell Biol 11: 424 431. Lankiewicz S, Lobitz N, Wetzel CHR, Rupprecht R, Gisselmann G, Hatt H 1998 ; Molecular cloning, functional expression, and pharmacological characterization of 5-hydroxytryptamine3 receptor cDNA and its splice variants from Guinea Pig. Mol Pharmacol 53: 202212. Ledesma MD, Simons K, Dotti CG 1998 ; Neuronal polarity: essential role. Mahasandana C, Pung-Amritt P, Treesucon A, Petrarat S, Veerakul G, Visudhiphan S, Yenchitsomanus PT. Carrier detection by DNA linkage analysis in eighty Thai hemophilia A families. Journal of the Medical Association of Thailand. 85: S513-21 Suppl 2 ; , 2002 Aug ; . DNA Linkage Analysis, Hemophilia A, Polymerase Chain Reaction. DNA linkage analysis was performed in Thai hemophilia A families to evaluate its value for carrier detection. Both intragenic and extragenic polymorphic DNA regions of the factor VIII gene, including Bcl I-RFLP in intron 18, microsatellites CA repeats ; in introns 13 and 22, and extragenic Stl4 DXS 52 ; VNTR, were amplified by polymerase chain reaction PCR ; before analyses by appropriate electrophoretic procedures. A total of 80 Thai hemophilia A families 48 with a family history and 32 with a sporadic case ; , containing 349 DNA samples from 90 hemophilia A patients, 143 parents, and 116 relatives, were analyzed. Heterozygosities in the patients' mothers from both families with a family history and with a sporadic case were observed in 71 out of 80 families 88.75% ; for all polymorphic DNA markers analyzed. The carrier status could be identified in 36 females and excluded in 44 females. This result indicates that the DNA linkage analysis can be used for carrier detection or exclusion in the majority of Thai hemophilia A families. It should also be useful for prenatal diagnosis in families at risk of hemophilia A, which is part of the prevention and control of this disease.

Though far from satisfactory. Further research on pharmacological treatment stimulating the brain in conjunction with SLT is warranted.

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Soma - buy soma soma - buy soma online. TABLE OF CONTENTS INDEX OF AUTHORITIES . ii STATEMENT REGARDING ORAL ARGUMENT . 1 STATEMENT OF THE CASE . 1 STATEMENT OF PROCEDURAL HISTORY . 2 STATEMENT OF FACTS. 3 STATE'S REPLY TO APPELLANT'S POINT OF ERROR NUMBER TWO . 3 The trial court's denial of Appellant's motion to sever Count Two from that of Count One and Count Three did not affect Appellant's substantial rights under Tex. R. App. Proc. 44.2 b and testosterone. Cutaneous fungal infections are among the most prevalent dermatologic conditions in the elderly and among the most commonly self-treated medical conditions.138, 139 Fungal infections mycoses ; of the skin are most frequently caused by microorganisms called dermatophytes and yeast, though they can infrequently be caused by nondermatophyte molds.140 Some cutaneous fungal infections, such as mycoses of the nails i.e., tinea unguium ; , 141 are increasing in incidence, while others, such as tinea barbae i.e., infection of the beard ; , remain rare.142.
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Biochemical features different from calciferol nutritional deficiency and are now classified as hypophosphatemic rickets. In 1961 Prader et al. characterized a distinctive form of hereditary rickets, which they called pseudodeficiency rickets.20 Features that clearly distinguished pseudodeficiency rickets from X-linked hypophosphatemia were hypocalcemia, the potential for complete remission with high doses of calciferols, and an autosomal transmission pattern. In 1971 1, 25 OH ; 2D3 was shown to be the active metabolite of vitamin D3 that accumulated in the nuclei of target tissues.21-23 This discovery led quickly to the development of methods to measure active metabolites in blood, characterization of defects in 1, 25 OH ; synthesis and action, and an understanding of the roles of 1 hydroxylated and other analogues for therapy. Fraser and associates24 showed that pseudodeficiency rickets in one patient was corrected with physiologic doses of 1, 25 OH ; 2D3; they suggested that this disorder represented a defect in 25 OH ; hydroxylase enzyme. Subsequently Brooks and coworkers described a patient with similar clinical features but high serum levels of 1, 25 OH ; before and during treatment; they suggested that pseudodeficiency rickets be classified as type 1 deficient production of 1, 25 OH ; type II impaired end-organ response to 1, 25 OH ; .25 Pathology. Rickets and osteomalacia are disorders of bone mineralization in which osteoblastic activity and the production of bone matrix continue, but the rate of mineralization is impaired leading to an accumulation of unmineralized matrix. These changes result in rickets in the growing child with open epiphyses and osteomalacia in the adult. The most important physiological alteration in rickets and osteomalacia is a deficiency of inorganic phosphate in the extracellular fluids with or without an associated deficiency of calcium. The morphological changes of rachitic bones occur primarily at the epiphyses of growing long bones, where there is proliferation and maturation of the cartilage cells. The columns of cartilage cells are surrounded by matrix in which mineral is deposited resulting in a uniform zone of calcified cartilage at the junction of the bone and cartilage. Capillaries from the bony side invade the degenerating cartilage cells forming tunnels in the calcified matrix, and osteoblasts, which accompany the capillaries, deposit a protein-rich matrix termed osteoid. The osteoid is mineralized as the calcified cartilage matrix is resorbed. This coupled process of endochondral bone formation continues, with orderly deposition of layer upon layer of new bone with continuous resorption and remodeling of bone until a final structure is achieved. In rickets the sequence of events is markedly disturbed, beginning with a failure of the cartilage matrix to mineralize. Capillary invasion of the degenerating cartilage is haphazard, and osteoblasts proliferate in an irregular pattern, forming osteoid that accumulates without mineralizing. A broad zone of proliferative cartilage and osteoid develops in which bone mineral is irregularly deposited. The rachitic intermediate zone or metaphysis is a bulky mass consisting of cartilage, invading blood vessels, osteoblasts, fibroblasts, and marrow elements. The rachitic intermediate zone lacks the rigidity of the normal bone cartilage junction, and becomes compressed and deformed laterally by pressure. The bending and twisting of the soft and yielding rachitic metaphysis can explain much of the deformity of the long bones in rickets. In the shaft of the bone trabeculae are covered with layers of unmineralized osteoid, and lacking rigidity, the shaft is bent by muscle pull or weight bearing and in severe rickets may be easily fractured. Over time, the bone shaft can become considerably thickened by deposition of excess osteoid that is partially mineralized. A similar defect in mineralization occurs in the intramembranous bones of skull and pelvis and vertebral bodies, causing a characteristic coarse and almost cystic structure. Radiological Findings. The anatomical changes described above produce characteristic radiological findings, which are visible relatively late. Among the radiological changes are: increased width of the uncalcified portion of the bone between the center of ossification in the epiphyses and the end of the bony and valium.

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1. 2. Medco projection based on IMS data and current patent expiration dates. Federal Trade Commission. Pharmacy Benefit Managers: Ownership of Mail-Order Pharmacies. Washington, DC: Federal Trade Commission; 2005. Available at: : ftc.gov opa 2005 09 pharmbenefit . Accessed March 23, 2006. Teagarden JR, Nagle B, Aubert RE, et al. Dispensing error rate in a highly automated mail-service pharmacy practice. Pharmacotherapy. 2005; 25: 1629-1635. Stewart WF, Shechter A, Lipton RB. Migraine heterogeneity: disability, pain, intensity, and attack frequency and duration. Neurology. 1994; 44 suppl 4 ; : S24-S39. Biotechnology Industry Organization. R&D investment is the lifeblood of the biotechnology industry. Available at: : bio healthcare archive medicare biotecrd . Accessed April 5, 2006. Skinner N. Case Management Resource Path for the Patient With Hemophilia. Little Rock, Ark: Case Management Society of America; 2000. Huskamp HA, Deverka PA, Epstein AM, et al. The effect of incentive-based formularies on prescription-drug utilization and spending. New England Journal of Medicine. 2003; 349: 2224-2232, for example, porn star soma.
Immune-mediated hemolytic anemia IMHA ; is a rare but frequently fatal blood disorder affecting mainly middle-aged female dogs. With IMHA, a dog's body produces antibodies that attack its own red blood cells, which leads to red blood-cell destruction and anemia. As anemia develops, the dog's gums become pale, and the whites of the eyes may become yellow with jaundice. IMHA often develops suddenly, makes the dog extremely weak and lethargic, and may, in some cases, lead rapidly to death. "We lose half our patients within their first week of diagnosis, " says Dr. Steven Dow, a Morris Animal Foundation-funded scientist. Standard treatment consists of high doses of steroids that need a few weeks to take effect, creating a race against time. Dr. Dow's team at Colorado State University is testing a new drug called liposomal clodronate that temporarily stops the red blood-cell destruction in dogs with IMHA, which buys muchneeded time for standard treatments to start working. The preliminary results of this study look promising, and Dr. Dow plans to submit a pre-proposal to the Foundation for funding a larger clinical trial to test the effects of the drug in more dogs with IMHA and viagra. Without vigilant policing of a brand to prevent others from misusing or diluting the brand, passing off a product as the brand, or counterfeiting the brand so as to confuse consumers into thinking that they are purchasing a genuine branded product, a brand can flounder and even die. If a brand has lost its distinctiveness, its owner has no competitive advantage. When a brand name means nothing to consumers, it is worthless. It has no selling strength and it lacks the ability to draw in the consumer and tip the balance in the purchasing decision. Consumers who cannot identify a brand generally have no particular reason to buy it. Often, brands do not carry recognition because they are unsuccessfully promoted or marketed. Some previously famous brands are distant memories of the past, or even altogether unknown today. For example, today's generation does not shop for STUDEBAKER LARK convertibles; they buy BMW convertibles. They are not in search of COMMODORE or FRANKLIN computers. Instead, they buy DELL, COMPAQ or APPLE computers. When brands receive negative publicity, their value can decline to the point that their owners decide to "retire" them. After numerous cases of exploding gas tanks, Ford Motor Company stopped using the PINTO brand name because few people were willing to buy a car bearing that name. Similarly, as a result of potential harmful side effects, the REDUX brand diet pill was removed from the market. Some companies have successfully recovered their brand equity through successful marketing, promotion and perseverance. In the 1980s, AUDI brand automobiles suffered from negative publicity in the U.S. because of, for example, soka 350mg!

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Angiogenic proteins in a subcutaneous B16.F10 melanoma model. The angiogenic protein array monitored both pro- and anti-angiogenic proteins. 17 out of 24 proteins are pro-angiogenic factors. The majority of them G-CSF, GM-CSF, IGF-II, IL-1, IL-1, Il-6, IL-9, TNF , MCP1, eotaxin, bFGF, VEGF, leptin, and thrombopoietin ; are involved in all tumor angiogenesis steps [1326]. Most of these factors, such as G-CSF, GM-CSF, MCSF, IL-1, IL-1, IL-6, IL-9, TNF , MCP1, have proinflammatory effects that strengthen their pro-angiogenic effects and support tumor growth [13, 14, 1620, 27, Moreover, IL-6 has an anti-apoptotic effect on cancer cells by inhibition of p53 induced-apoptosis [29]. On the other hand, FasL helps tumor cells to escape immune surveillance by inducing apoptosis of T cells [30]. The most important effect of liposomal and free PLP on tumor angiogenesis was a strong reduction of most proangiogenic protein levels, whereas the levels of the majority of anti-angiogenic proteins were not affected. As shown in Table 1 and Fig. 3, the reduction of pro-angiogenic protein levels from tumors treated with liposomal PLP was much stronger than that from tumors treated with free PLP. This strong effect is related to the tumor-targeting property of the liposome formulation. The enhanced permeability of blood vessels in solid tumor tissue enables long-circulating liposomes, like those used in this study, to extravasate into the malignant tissue, leading to preferential intratumoral localization of PLP. Once extravasated into the tumor, liposomes appear to accumulate in the surrounding area of capillaries and in macrophages, further increasing effects on two major cell types driving angiogenesis, the endothelial cells and macrophages [3134]. In contrast, when PLP is administered in free form, it is rapid cleared from the circulation and therefore it is not able to localize in the tumor to a substantial degree, with consequently lower antitumor activity as a result [1]. These findings are supported by our previous observations of intratumoral accumulation of long-circulating liposomes in the immediate vicinity of tumor blood vessels and strong uptake of liposomes by intratumoral macrophages [1]. Reduction of pro-angiogenic factors produced principally by macrophages and endothelial cells may shift the balance between pro- and anti-angiogenic proteins in favor of inhibition of angiogenesis Fig. 3, Tables 1 and 2 and zyban.

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In 1989, the World Health Assembly adopted the goal of reducing measles morbidGlobal Measles Control -- Continued ity and mortality by 90% and 95%, respectively, by 1995, compared with estimates of the disease burden in the prevaccine era 1 ; . In 1990, the World Summit for Children adopted a goal of vaccinating 90% of children against measles by 2000. Three regions of the World Health Organization WHO ; have targeted elimination: in 1994, the American Region AMR ; targeted elimination by 2000; in 1997, the Eastern Mediterranean Region EMR ; targeted elimination by 2010; and in 1998, the European Region EUR ; targeted elimination by 2007. This report updates progress since 1997 2 ; toward global measles control and regional elimination of measles, and includes vaccination coverage and disease surveillance data received by WHO as of August 14, 1999. Data for 1998 suggest that routine measles vaccination coverage has declined in some regions, the number of countries reporting cases and coverage to WHO has decreased, and measles continues to be an important cause of morbidity and mortality. Reported Routine Measles Vaccination Coverage Global reported coverage with one dose of measles vaccine declined from 79% in 1997 to 72% in 1998 Table 1 ; . In 1998, 14 countries reported measles coverage below 50%: 10 in the African Region AFR ; Burundi, Cameroon, Central African Republic, Chad, Democratic Republic of Congo, Ethiopia, Liberia, Nigeria, Togo, and Uganda ; , one in AMR Haiti ; , two in EMR Afghanistan and Somalia ; , and one in the South-East Asia Region SEAR ; Democratic People's Republic of Korea ; . Among regions focusing on measles control, AFR and SEAR reported the lowest routine vaccination coverage rates, 49% and 67%, respectively Table 1 ; . These regions reported the greatest decrease in coverage during 19971998. The Western Pacific Region WPR ; continued to report the highest routine vaccination coverage 93% ; . Among regions with an elimination target, AMR reported the highest coverage rate 86% ; Table 1 ; . In EMR, regional measles vaccination coverage was 78%, and 14 polio-free countries that began implementing measles elimination strategies reported routine coverage rates 85% 3 ; . EUR reported a routine first dose coverage rate of 71% in 1998; 21 41% ; of 51 EUR countries * did not report vaccination coverage data to WHO. Supplementary Vaccination Campaigns Supplemental vaccination campaigns have been conducted in several countries targeting either measles morbidity and mortality reduction or elimination. In 1998 and 1999, 31 countries in AFR and three countries in EMR Djibouti, Egypt, and Sudan. Of Evidence-Based Medicine in an easily searched compact disc.9 In caring for the patient with cirrhosis and gastrointestinal bleeding a search of The Cochrane Library using the term "variceal bleed" identified the Cochrane review that evaluated the use of somatostatin versus placebo or no treatment in acute bleeding oesophageal varices.10 Some evidence based materials also appear on the internet, including those of the Cochrane Collaboration URL: : hiru master COCHRANE ; and some sites include clinically useful evidence about diagnosis, prognosis, and treatment. For example, the site established by the NHS Research and Development Centre for Evidence-Based Medicine URL given above ; permits browsers to apply the specificity of shifting dullness and the sensitivity of a history of ankle swelling to diagnose patients thought to have ascites; this information could be used to answer some of the questions posed in the diagnosis of the patient with cirrhosis. If the foregoing strategies for gaining rapid access to evidence based medicine fail clinicians can resort to the time honoured and increasingly user friendly systems for accessing the current literature via Medline and Embase, employing methodological quality filters to maximise the yield of high quality evidence and sonata.

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Deteriorate in the diabetic patients." In a highly successful double-blind placebo study of Vinpocetine with 84 elderly patients suffering from chronic vascular senile brain dysfunction, Balestreri et al, found only 12 adverse effect reports in the Vinpocetine group mostly digestive complaints ; versus 17 in the placebo group! No significant adverse laboratory findings were found in either group.35 A major Japanese study by Otomo and colleagues with 207 patients suffering various cerebral disorders found only a 2% incidence of mild adverse side effects- anorexia in 2 patients, hives and stomach pain in 1 and hot flashes in 1. No significant adverse laboratory findings occurred in the 207 Vinpocetine patients.36 In their summary of various animal safety tests, Cholnoky and Domok found the oral LD50 for Vinpocetine the dose lethal for 50% of the test animals ; to be 534mg Kg of bodyweight for mice, 503 mg Kg of bodyweight for rats. This would equate to approximately 35, 000mg for a 150 pound human. The usual therapeutic dose for Vinpocetine for humans is 15-30 mg per day! Because of side effects at high doses when used with pregnant rats uterine bleeding in some ; , Cholnoky and Domok caution against using Vinpocetine in pregnant women, or those trying or expecting to get pregnant.37 Overall, Vinpocetine side effects reported in the literature are rare, usually minor, frequently disappear with prolonged use, and rarely require discontinuance of the drug. Stomach GI upset, dry mouth, rapid heart beat, low blood pressure, and rash hives are the main rarely occurring ; reported side effects.
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After extraction of total RNA from lung with Trizol reagent Life Technologies ; , real-time fluorogenic reverse transcriptionpolymerase chain reaction PCR ; was performed using Assays on Demand gene expression probes for human and mouse SERT Hs00169010 and Mm00439391, respectively; Applied Biosystems ; according to the manufacturer's instructions. Relative mRNA abundance was determined by use of the comparative delta-CT method using 18S ribosomal RNA as internal control.

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