Murine hematopoietic stem cells
20. Kunkel TA. Rapid and efficient site-specific mutagenesis without phenotypic selection. Proc Natl Acad Sci U S A. 1985; 82: 488 Tybulewicz VL, Crawford CE, Jackson PK, Bronson RT, Mulligan RC. Neonatal lethality and lymphopenia in mice with a homozygous disruption of the c-abl proto-oncogene. Cell. 1991; 65: 11531163. Labosky PA, Barlow DP, Hogan BL. Mouse embryonic germ EG ; cell lines: transmission through the germline and differences in the methylation imprint of insulin-like growth factor 2 receptor Igf2r ; gene compared with embryonic stem ES ; cell lines. Development. 1994; 120: 31973204. Hogan B, Beddington R, Constantini F, Lacy E. Manipulating the Mouse Embryo. 2nd ed. Cold Spring Harbor, NY: Cold Spring Harbor Press; 1994. 24. Berul CI, Aronovitz MJ, Wang PJ, Mendelsohn ME. In vivo cardiac electrophysiology studies in the mouse. Circulation. 1996; 94: 26412648. Yang T, Wathen MS, Felipe A, Tamkun MM, Snyders DJ, Roden DM. Potassium currents and K channel mRNA in cultured atrial cardiac myocytes AT-1 cells ; . Circ Res. 1994; 75: 870 Yang T, Snyders DJ, Roden DM. Rapid inactivation determines the rectification and [K ]o dependence of the rapid component of the delayed rectifier K current in cardiac cells. Circ Res. 1997; 80: 782789. Wang L, Duff HJ. Developmental changes in transient outward current in mouse ventricle. Circ Res. 1997; 81: 120 Nuss HB, Marban E. Electrophysiological properties of neonatal mouse cardiac myocytes in primary culture. J Physiol. 1994; 479: 265280. Davies MP, An RH, Doevendans P, Kubalak S, Chien KR, Kass RS. Developmental changes in ionic channel activity in the embryonic murine heart. Circ Res. 1996; 78: 1525. Wang L, Feng ZP, Kondo CS, Sheldon RS, Duff HJ. Developmental changes in the delayed rectifier K channels in mouse heart. Circ Res. 1996; 79: Delorme B, Dahl E, Jarry-Guichard T, Marics I, Briand JP, Willecke K, Gros D, Theveniau-Ruissy M. Developmental regulation of connexin 40 gene expression in mouse heart correlates with the differentiation of the conduction system. Dev Dyn. 1995; 204: 358 London B, Trudeau MC, Newton KP, Beyer AK, Copeland NG, Gilbert DJ, Jenkins NA, Satler CA, Robertson GA. Two isoforms of the mouse ether-a-go-go-related gene coassemble to form channels with properties similar to the rapidly activating component of the cardiac delayed rectifier K current. Circ Res. 1997; 81: 870 Lees-Miller JP, Kondo C, Wang L, Duff HJ. Electrophysiological characterization of an alternatively processed ERG K channel in mouse and human hearts. Circ Res. 1997; 81: 719 van Kempen MJ, Fromaget C, Gros D, Moorman AF, Lamers WH. Spatial distribution of connexin43, the major cardiac gap junction protein, in the developing and adult rat heart. Circ Res. 1991; 68: 1638 Wessels A, Vermeulen JL, Viragh S, Kalman F, Morris GE, Man NT, Lamers WH, Moorman AF. Spatial distribution of "tissue-specific" antigens in the developing human heart and skeletal muscle. I. An immunohistochemical analysis of creatine kinase isoenzyme expression patterns. Anat Rec. 1990; 228: 163176. Wessels A, Vermeulen JL, Viragh S, Kalman F, Lamers WH, Moorman AF. Spatial distribution of "tissue-specific" antigens in the developing human heart and skeletal muscle. II. An immunohistochemical analysis of myosin heavy chain isoform expression patterns in the embryonic heart. Anat Rec. 1991; 229: 355368. Moorman AFM, Lamers WH. Molecular anatomy of the developing heart. Trends Cardiovasc Med. 1994; 4: 257264. Wessels A, Vermeulen JL, Verbeek FJ, Viragh S, Kalman F, Lamers WH, Moorman AF. Spatial distribution of "tissue-specific" antigens in the developing human heart and skeletal muscle. III. An immunohistochemical analysis of the distribution of the neural tissue antigen G1N2 in the embryonic heart: implications for the development of the atrioventricular conduction system. Anat Rec. 1992; 232: 97111. Freeman LC, Kass RS. Expression of a minimal K channel protein in mammalian cells and immunolocalization in guinea pig heart. Circ Res. 1993; 73: 968 Brahmajothi MV, Morales MJ, Liu SG, Rasmusson RL, Campbell DL, Strauss HC. In situ hybridization reveals extensive diversity of K channel mRNA in isolated ferret cardiac myocytes. Circ Res. 1996; 78: 10831089. Olgin JE, Kalman JM, Lesh MD. Conduction barriers in human atrial flutter: correlation of electrophysiology and anatomy. J Cardiovasc Electrophysiol. 1996; 7: 11121126. McGuire MA, Janse MJ, Ross DL. "AV nodal" reentry. Part II. AV nodal, AV junctional, or atrionodal reentry? J Cardiovasc Electrophysiol. 1993; 4: 573586.
Murine ear drops for earache relief
5. Wallace, R. J., Jr, Dunbar, D., Brown, B. A. et al. 1994 ; . Rifampin-resistant Mycobacterium kansasii. Clinical Infectious Diseases 18, 736 43. Graybill, J. R. & Bocanegra, R. 2001 ; . Treatment alternatives for Mycobacterium kansasii. Journal of Antimicrobial Chemotherapy 47, 417 20. Alcala, L., Ruiz-Serrano, M. J., Perez-Fernandez Turegano, C. et al. 2003 ; . In vitro activities of linezolid against clinical isolates of Mycobacterium tuberculosis that are susceptible or resistant to first-line antituberculous drugs. Antimicrobial Agents and Chemotherapy 47, 4167. 8. Moellering, R. C. 2003 ; . Linezolid: the first oxazolidinone antimicrobial. Drugs and Drug Therapy 138, 13542. 9. Guna, R., Dominguez, V., Garay, A. et al. 2004 ; . Actividad in vitro de linezolid frente a Mycobacterium kansasii. Enfermedades Infecciosas y Microbiologia Clinica 22 Suppl. 1, 191. 10. Brown-Elliott, B. A., Crist, C. J., Mann, L. B. et al. 2003 ; . In vitro activity of linezolid against slowly growing nontuberculous mycobacteria. Antimicrobial Agents and Chemotherapy 46, 17368. 11. Rodriguez Diaz, J. C., Lopez, M., Ruiz, M. et al. 2003 ; . In vitro activity of new fluoroquinolones and linezolid against non-tuberculous mycobacteria. International Journal of Antimicrobial Agents 21, 585 8. Wallace, R. J., Jr, Brown-Elliott, B. A., Ward, S. C. et al. 2001 ; . Activities of linezolid against rapidly growing mycobacteria. Antimicrobial Agents and Chemotherapy 45, 7647. 13. Brown-Elliott, B. A., Wallace, R. J., Jr, Blinkhorn, R. et al. 2001 ; . Successful treatment of disseminated Mycobacterium chelonae infection with linezolid. Clinical Infectious Diseases 33, 1433 4. Kubica, G. P 1984 ; . Clinical microbiology. In The Mycobacteria. A Sourcebook Kubica, G. P. & Wayne, L. G. Eds ; , pp. 133 75. Marcel Dekker Inc, New York, NY, USA. 15. Padilla, E., Gonzalez, V., Manterola, J. M. et al. 2004 ; . Identification of Mycobacterium species from MB BacT liquid cultures artificially inoculated with mycobacterial strains. Journal of Clinical Microbiology 42, 3083 8. Garcia-Garcia, A., Galvez, J., Julian-Ortiz, J. V. et al. 2004 ; . New agents active against Mycobacterium avium complex selected by molecular topology: a virtual screening method. Journal of Antimicrobial Chemotherapy 53, 6573. 17. Franzblau, S. G., Witzig, R. S., McLaughlin, J. C. et al. 1998 ; . Rapid, low-technology MIC determination with clinical Mycobacterium tuberculosis isolates by using the microplate Alamar Blue assay. Journal of Clinical Microbiology 36, 362 6. National Committee for Clinical Laboratory Standards. 2003 ; . Susceptibility Testing of Mycobacteria, Nocardiae, and Other Aerobic Actinomycetes: Approved Standard M24-A. NCCLS, Wayne, PA, USA. 19. National Committee for Clinical Laboratory Standards. 2004 ; . Performance Standards for Antimicrobial Susceptibility Testing: Fourteenth Informational Supplement: Approved Standard M100-S14. NCCLS, Wayne, PA, USA. 20. Wallace, R. J., Jr, Nash, D. R., Steele, L. C. et al. 1986 ; . Susceptibility testing of slowly growing mycobacteria by a microdilution MIC method with 7H9 broth. Journal of Clinical Microbiology 24, 97681. 21. Garros Garcia, J., Garcia Cebrian, F., Martin Saco, G. et al. 2001 ; . Enfermedad pulmonar por Mycobacterium kansasii. Analisis de 39 casos. Archivos de Bronconeumologia 37, 2734. 22. Rooney, G., Nelson, M. R. & Gazzard, B. 1996 ; . Mycobacterium kansasii: its presentation, treatment and outcome in HIV infected patients. Journal of Clinical Pathology 49, 821 3. Evans, S. A., Colville, A., Evans, A. J. et al. 1996 ; . Pulmonary Mycobacterium kansasii infection. Comparison of the clinical features, treatment and outcome with pulmonary tuberculosis. Thorax 51, 1248 52. British Thoracic Society, Research Committee. 1994 ; . Mycobacterium kansasii pulmonary infection: a prospective study of the results of nine months of treatment with rifampicin and ethambutol. Thorax 49, 435 6. Witzig, R. S. & Franzblau, S. G. 1993 ; . Susceptibility of Mycobacterium kansasii to ofloxacin, sparfloxacin, clarithromycin, azithromycin, and fusidic acid. Antimicrobial Agents and Chemotherapy 37, 19979. 26. Brown, B. A., Wallace, R. J., Jr & Onyi, G. O. 1992 ; . Activities of clarithromycin against eight slowly growing species of nontuberculous mycobacteria, determined by using a broth microdilution MIC system. Antimicrobial Agents and Chemotherapy 36, 198790. 27. Yew, W. W., Piddock, L. J., Li, M. S. et al. 1994 ; . In vitro activity of quinolones and macrolides against mycobacteria. Journal of Antimicrobial Chemotherapy 34, 34351. 28. Gillespie, S. H. & Billington, O. 1999 ; . Activity of moxifloxacin against mycobacteria. Journal of Antimicrobial Chemotherapy 44, 3935. 29. Fassbender, M., Lode, H., Schiller, C. et al. 1996 ; . Comparative pharmacokinetics of macrolide antibiotics and concentrations achieved in polymorphonuclear leukocytes and saliva. Clinical Microbiology and Infection 1, 23543. 30. Moise, P. A., Birmingham, M. C. & Schentag, J. J. 2000 ; . Pharmacokinetics and metabolism of moxifloxacin. Drugs of Today 36, 22944. 31. Cynamon, M. H., Elliot, S. A., DeStefano, M. S. et al. 2003 ; . Activity of clarithromycin alone and in combination in a murine model of Mycobacterium kansasii infection. Journal of Antimicrobial Chemotherapy 52, 306 7. Conte, J. E., Golden, J. A., Kipps, J. et al. 2002 ; . Intrapulmonary pharmacokinetics of linezolid. Antimicrobial Agents and Chemotherapy 46, 147580. 33. Griffith, D. E., Brown-Elliott, B. A. & Wallace, R. J., Jr 2003 ; . Thrice-weekly clarithromycin-containing regimen for treatment of Mycobacterium kansasii lung disease: results of a preliminary study. Clinical Infectious Diseases 37, 1178 82.
What is murine cytomegalovirus
According to the criteria of Weinshilboum and Sladek 1 ; . The studies were approved by the institutional review board for clinical trials at St. Jude Children's Research Hospital, and informed consent was obtained from the participants or their guardians. Synthesis of cDNA. First-strand cDNA was synthesized, essentially as described 14 ; , from 2 , ug of total cellular RNA. The reaction mixture 100 ul ; contained 10 mM Tris-HCl pH 8.3 at 20C ; , 50 mM KCl, 1.5 mM MgCl2, 0.001% wt vol ; gelatin, 0.2 mM dNTPs, 20 units of RNasin, 200 ng of the random hexamers, and 200 units of Moloney murine leukemia virus reverse transcriptase SuperScript; GIBCO BRL ; and was incubated at 42C for 60 min. PCR of TPMT Coding Region. PCR primers were synthesized on the basis of the published colon carcinoma TPMT cDNA sequence 12 ; . The sequences of primers used for the first round of amplification and all subsequent PCR amplifications are given in Table 1. Each cycle of amplification consisted of denaturation at 94C for 1 min, annealing at 55C for 30 sec, and primer extension at 72C for 2 min 35 cycles ; . After amplification, TPMT PCR products were made blunt and the product was cloned into the Sma I site of plasmid pGEM7Zf + ; Promega ; . The inserts present in positive clones were sequenced by automated fluorescence sequencing. Northern and Southern Blot Hybridization Probes. The wildtype human liver TPMT cDNA, cloned as described above, was used for probe preparation. Oligonucleotide h28S 5'-GCA.
6276 migration, and function of the injected DC. Because maturation of DC in situ resembles more closely the physiological process involved in response to pathogen infection, in situ maturation may lead to enhanced T cell immunity. In addition, the in situ DC maturation approach eliminates an ex vivo cell culture step and dispenses with the use of expensive biologicals maturation agents ; , which are not always available for clinical use. In this study, we show that murine bone marrow-derived immature DC injected into skin exposed to adjuvants are as effective or superior to ex vivo matured DC in migrating to lymph nodes, stimulating CTL responses, and inducing tumor immunity. Furthermore, immature human monocyte-derived DC injected into adjuvant-treated skin of cancer patients acquire migratory capacity and migrate to the draining lymph node as effectively as ex vivo matured DC.
Recombinant murine il 12
Table 1. Demographic and Clinical Characteristics of 161 Patients MITT Sample ; and 62 Normal Controls.
Mad1, Mad2, Mad3, and Mps1 13 ; . Damage to mitotic spindle fibers can activate these mitotic checkpoint genes, whose products arrest mitosis and repair the spindles 13, 14 ; . Mutations in any of these genes result in failure to arrest the cell cycle at G2-M, and cells exit mitosis prematurely 14 ; . Inactivation of murine BUB1 also impairs cell-cycle arrest in the mouse, causing premature cell-cycle progression and aneuploidy 15 ; . These facts suggest that mitotic checkpoint genes may be critical for preventing aneuploidy during chromosomal segregation of mammalian cells. To investigate the function of BRCA2, we have used a yeast two-hybrid system to search for proteins in addition to Rad51 that can interact with BRCA2. Here we report the detection of one such protein, hBUBR1 16 ; . We also demonstrate that this association can lead to phosphorylation of BRCA2 protein. Materials and Methods and muse.
Murine ear wax remover
Member must simultaneously write the date he she signed the consent form in his her own and writing when signing the consent form; 10. Member should write in the time they signed the consent form. This is only important in cases where the thirty 30 ; -day period has not lapsed and the 72-hour period has passed between the time the Member signed the consent form and the time the sterilization procedure was performed 11. Race and ethnicity designation optional 12. Language used to explain the consent form if an interpreter is used; 13. Signature of the interpreter and the date the interpreter signed the consent form. The interpreter must sign his her name and simultaneously write the date in his her own handwriting. If an interpreter is not used, write "NA" in blanks; 14. Name of the individual to be sterilized; 15. Type of sterilization operation to be performed Procedure must be written out - Do Not Abbreviate 16. Signature of person obtaining consent and date he she signed the consent form. The person who obtained consent must sign and date the consent form simultaneously in his her own handwriting. To avoid possible claim denial, the person obtaining consent should sign the same day as the Member. 17. Name of the facility where the person obtaining consent is located; 18. Address of the facility where the person obtaining consent is located; 19. Name of the individual to be sterilized; 20. The exact date the sterilization was performed. The date of service on the claim requesting payment must be the same date on the sterilization consent form. a ; Thirty 30 ; calendar days must have lapsed between the date the Member signed the consent form and the date the sterilization procedure was performed. Start counting day one 1 ; the day after the Member signs the consent form and then the sterilization can be performed on the 31st day except in the case of premature delivery or emergency abdominal surgery. b ; In case of premature delivery, at least 72 hours must have passed between the day and time the Member signed the consent form before the sterilization procedure can be performed. At least thirty 30 ; calendar days would have had to lapse between the date the Member signed the consent form and the individual's expected date of delivery. c ; In the case of emergency abdominal surgery, at least 72 hours must have passed between the day and time the Member signed the consent form before the sterilization procedure can be performed. d ; The consent form expires 180 calendar days from the date of the Member's signature. Start counting day one 1 ; on the day after the Member signs the consent form. The procedure must be performed within 180 calendar days. 21. Type of sterilization procedure to be performed Procedure must be written out - Do Not Abbreviate ; . 22. Alternative final paragraph instruction: Cross out paragraph two 2 ; if at least thirty 30 ; calendar days have lapsed between the date of the Member's signature on the consent form and the date the sterilization operation was performed. Cross out paragraph one 1 ; if this sterilization was performed less than thirty 30 ; calendar days but more than 72 hours after the date of the Member's signature on the consent form because of premature delivery or emergency abdominal surgery. Check the appropriate boxes for premature delivery and individual's expected date of delivery and fill in the Member's expected date of delivery. If emergency abdominal surgery, check appropriate box and describe circumstances. 23. Physician's signature * . 24. Time Physician signed the consent form. 25. Date of Physician's signature. * The Physician who performed the sterilization procedure must sign his her name and date he she signed the consent form simultaneously in his her own handwriting. The Physician must sign the consent form after surgery. Typed or stamped signatures, initials, or dates are not acceptable. If the Physician signs the consent form the same day as surgery, he she must specify what time he she signed the consent form. a ; If the Physician signs the consent form the same day as surgery and signs the time he she signed the consent form as 8 a.m.or earlier, the time surgery ended must be specified. b ; If the Physician signs the consent form the day after surgery or later, the time the Physician signed the consent form may be omitted. Note: Incomplete information on the Sterilization Consent Form will result in denial of claim. All fields on consent form must be legible.
Define murine calvaria
| Murine bone marrow transplantationWould be mediated by other kinds of recombination mechanisms that do not specifically target the Ig loci but could involve an Ig locus. In contrast to primary translocations, secondary translocations usually are complex, unbalanced translocations or insertions, often involving 3 different chromosomes and sometimes with associated inversion, deletion, duplication, or amplification. Primary translocations should be present in all tumor cells in both MGUS and MM, whereas secondary translocations are expected to be less frequent in MGUS than in MM, and might be present in only a subset of MGUS or MM tumor cells. Obviously, however, the only definitive way to distinguish primary from secondary translocations would be to document the time s ; at which translocations occur during the progression of individual tumors. In the absence of this definitive test, the criteria described above provide some help in distinguishing primary from secondary translocations. Dysregulation of Myc: A Paradigm for Late Secondary Translocations in MM Similar to other kinds of B cell tumors, translocations that dysregulate c-myc represent an important pathogenic event in MM.4 Chromosomal translocations that dysregulate c-myc by juxtaposing it with one of the three Ig loci represent an essentially invariant and apparently primary event in human Burkitt's lymphoma and murine plasmacytoma tumors. The nontranslocated c-myc allele is not expressed, corresponding to the absence of c-myc expression, in resting germinal center B cells and terminally differentiated plasma cells. Strikingly, L-myc 1 HMCL ; or 1 c-myc allele is expressed selectively in all informative HMCL, consistent with cis-dysregulation of L-myc or 1 c-myc allele in all HMCL. In addition, by our analysis of published24, 25 gene expression profiling, N-myc which is not expressed in normal PB or PC ; expressed in 2 of primary MM tumors. Three-color FISH analyses of metaphase chromosomes show that nearly 90% of HMCL and 50% of advanced MM tumors have similar karyotypic abnormalities involving c-myc, L-myc 1 HMCL ; , or N-myc 1 tumor ; . Simple, reciprocal t 8; 14 ; and t 8; 22 ; translocations are infrequent. Most karyotypic abnormalities are complex translocations and insertions that often are nonreciprocal, and frequently involve 3 different chromosomes. Karyotypic abnormalities involving c-, L-, or N-myc often do not include association with an Ig enhancer, which suggests that secondary translocations can dysregulate c-myc by juxtaposition to non-Ig enhancers. By interphase FISH analyses, it is reported that the c-myc locus is rearranged in 3% of MGUS SMM tumors, 10% of MM tumors with a low tumor mass, and 19% of MM tumors with a and mycostatin.
[0287] dd. Nitric oxide donors as disclosed in U.S. Pat. No. 5, 714, 511 or acids, salts, enantiomers, analogs, esters, amides, prodrugs, active metabolites, and derivatives thereof; [0288] ee. Nitric oxide donors as disclosed in U.S. Pat. No. 6, 511, 911 or acids, salts, enantiomers, analogs, esters, amides, prodrugs, active metabolites, and derivatives thereof; and [0289] ff. Nitric oxide donors as disclosed in U.S. Pat. No. 5, 814, 666. [0290] The identification of further compounds that have nitric oxide donor activity and would therefore be useful in the present invention can be determined by release profile andlor induced vasospasm studiesas described in U.S. Pat. Nos. 6, 451, 337 and 6, 358, 536, as well as Moon 2002 ; ZBJU Znt. 89: 942-9 and Fathian-Sabet et al. 2001 ; J. Uvol. 165: 1724-9. [0291] Subject, as used herein, refers to animals such as mammals, including, but not limited to, primates e.g., humans ; , cows, sheep, goats, horses, pigs, dogs, cats, rabbits, guinea pigs, rats, mice or other bovine, ovine, equine, canine, feline, rodent or murine species. [0292] As used herein, treating and treatment refer to a reduction in at least one symptom selected from urinary frequency, urinary urgency, urinary urge incontinence, nocturia and enuresis, which is associated with lower urinary tract disorder. [0293] As used herein, therapeutically effective amount refers to an amount sufficient to elicit the desired biological response. In the present invention the desired biological response is a reduction complete or partial ; of at least one symptom associated with the lower urinary tract disorder being treated wherein the symptom is selected from urinary frequency, urinary urgency, urinary urge incontinence, nocturia and enuresis. As with any treatment, particularly treatment of a multi-symptom disorder, for example, overactive bladder, it is advantageous to treat as many disorder-related symptoms which the subject experiences. [0294] Pharmaceutically acceptable carrier, includes pharmaceutical diluents, excipients or carriers suitably selected with respect to the intended form of administration, and consistent with conventional pharmaceutical practices. For example, solid carriersldiluents include, but are not limited to, a gum, a starch e.g., corn starch, pregelatinized starch ; , a sugar e.g., lactose, mannitol, sucrose, dextrose ; , a cellulosic material e.g., microcrystalline cellulose ; , an acrylate e.g., polymethylacrylate ; , calcium carbonate, magnesium oxide, talc, or mixtures thereof. [0295] Pharmaceutically acceptable carriers can be aqueous or non-aqueous solvents. Examples of non-aqueous solvents are propylene glycol, polyethylene glycol, and injectable organic esters such as ethyl oleate. Aqueous carriers include water, alcoholic aqueous solutions, emulsions or suspensions, including saline and buffered media. [0296] Modes of Adminstration [0297] The compounds for use in the method or kits of the invention can be formulated for administration by any suitable route, such as for oral or parenteral, for example, transdermal, transmucosal e.g., sublingual, lingual, trans.
Chronic murine pneumonia
Am J Physiol Gastrointest Liver Physiol 286: 102-109, 2004. First published Jul 24, 2003; doi: 10.1152 ajpgi.00092.2003 You might find this additional information useful. This article cites 45 articles, 26 of which you can access free at: : ajpgi.physiology cgi content full 286 1 G102#BIBL This article has been cited by 7 other HighWire hosted articles, the first 5 are: Regulatory Binding Partners and Complexes of NHE3 M. Donowitz and X. Li Physiol Rev, July 1, 2007; 87 ; : 825-872. [Abstract] [Full Text] [PDF] PAT-1 Slc26a6 ; is the predominant apical membrane Cl- HCO3- exchanger in the upper villous epithelium of the murine duodenum J. E. Simpson, C. W. Schweinfest, G. E. Shull, L. R. Gawenis, N. M. Walker, K. T. Boyle, M. Soleimani and L. L. Clarke J Physiol Gastrointest Liver Physiol, April 1, 2007; 292 ; : G1079-G1088. [Abstract] [Full Text] [PDF] Epithelial carbonic anhydrases facilitate PCO2 and pH regulation in rat duodenal mucosa M. Mizumori, J. Meyerowitz, T. Takeuchi, S. Lim, P. Lee, C. T. Supuran, P. H. Guth, E. Engel, J. D. Kaunitz and Y. Akiba J. Physiol., June 15, 2006; 573 ; : 827-842. [Abstract] [Full Text] [PDF] Mechanism of augmented duodenal HCO3- secretion after elevation of luminal CO2 O. Furukawa, M. Hirokawa, L. Zhang, T. Takeuchi, L. C. Bi, P. H. Guth, E. Engel, Y. Akiba and J. D. Kaunitz J Physiol Gastrointest Liver Physiol, March 1, 2005; 288 ; : G557-G563. [Abstract] [Full Text] [PDF] Evolutionary origins of eukaryotic sodium proton exchangers C. L. Brett, M. Donowitz and R. Rao J Physiol Cell Physiol, February 1, 2005; 288 ; : C223-C239. [Abstract] [Full Text] [PDF] Updated information and services including high-resolution figures, can be found at: : ajpgi.physiology cgi content full 286 1 G102 Additional material and information about AJP - Gastrointestinal and Liver Physiology can be found at: : the-aps publications ajpgi and mysoline.
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And tumor response to photodynamic therapy. Photochem Photobiol 1993; 58: 393 Henderson BW, Sitnik-Busch TM, Vaughan LA. Potentiation of photodynamic therapy antitumor activity in mice by nitric oxide synthase inhibition is fluence rate dependent. Photochem Photobiol 1999; 70: 64 Busch TM, Hahn SM, Evans SM, Koch CJ. Depletion of tumor oxygenation during photodynamic therapy: detection by the hypoxia marker EF3 [2 2-nitroimidazol-1[H]-yl ; -N- 3, 3-trifluoropropyl ; acetamide]. Cancer Res 2000; 60: 2636 Wang L, Cull G, Cioffi GA. Depth of penetration of scanning laser Doppler flowmetry in the primate optic nerve. Arch Ophthalmol 2001 ; 119: 1810 4. Chang HY, Chen CR, Hussain SN. Diaphragmatic microcirculation measured by laser-Doppler flowmetry in the rat. J Appl Physiol 1995; 78: 1225 Pogue BW, Braun RD, Lanzen JL, Erickson C, Dewhirst MW. Analysis of the heterogeneity of pO2 dynamics during photodynamic therapy with verteporfin. Photochem Photobiol 2001 ; 74: 700 6. Tang SJ, Gordon ML, Yang VX, et al. In vivo Doppler optical coherence tomography of mucocutaneous telangiectases in hereditary hemorrhagic telangiectasia. Gastrointest Endosc 2003; 58: 591 Chen Z, Milner TE, Wang X, Srinivas S, Nelson JS. Optical Doppler tomography: imaging in vivo blood flow dynamics following pharmacological intervention and photodynamic therapy. Photochem Photobiol 1998; 67: 56 Bizheva K, Unterhuber A, Hermann B, et al. Imaging ex vivo and in vitro brain morphology in animal models with ultrahigh resolution optical coherence tomography. J Biomed Opt 2004; 9: 719 Gee MS, Saunders HM, Lee JC, et al. Doppler ultrasound imaging detects changes in tumor perfusion during antivascular therapy associated with vascular anatomic alterations. Cancer Res 2001 ; 61: 2974 82. Culver JP, Durduran T, Furuya D, Cheung C, Greenberg JH, Yodh AG. Diffuse of optical tomography cerebral blood flow, oxygenation and metabolism in rat during focal ischemia. 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Chance B, Alfano RR, Tromberg BJ, Tamura M, and Sevick-Muraca EM, editors. In: Proceedings of SPIE; 2003 Jan 26-29; San Jose CA ; : SPIE; 2003. 4955: p. 164 74. 28. Yu G, Durduran T, Lech G, et al. Time-dependent blood flow and oxygenation in human skeletal muscles measured with noninvasive near-infrared diffuse optical spectroscopies. J Biomed Opt. 2005, in press. 29. Maret G, Wolf PE. Multiple light scattering from disordered media.The effect of Brownian motion of scatterers. Z Phys B 1987; 65: 409 Pine DJ, Weitz DA, Chaikin PM, Herbolzheimer. Diffusing-wave spectroscopy. Phys Rev Lett 1988; 60: 1134 Boas DA, Campbell LE, Yodh AG. Scattering and imaging with diffusing temporal field correlations. Phys Rev Lett 1995; 75: 1855 van Staveren HJ, Moes CJM, van MarleJ, Prahl SA, van Gemert MJC. Light scattering in Intralipid-10% in the wavelength range of 400-1100 nm. Appl Opt 1991 ; 30: 4507 14. Wang HW, Zhu TC, Putt ME, et al. Broadband reflectance measurements of light penetration, blood oxygenation, hemoglobin concentration, and drug concentration in human intraperitoneal tissues before and after photodynamic therapy. J Biomed Opt 2005; 10: 014004. Wang HW, Putt ME, Emanuele MJ, et al. Treatmentinduced changes in tumor oxygenation predict photodynamic therapy outcome. Cancer Res 2004; 64: 7553 Sehgal CM, Arger PH, Rowling SE, Conant EF, Reynolds C, Patton JA. Quantitative vascularity of breast masses by Doppler imaging: regional variations and diagnostic implications. J Ultrasound Med 2000; 19: 427 quiz 41 2. 36. Sehgal CM, Arger PH, Silver AC, et al. Renal blood flow changes induced with endothelin-1and fenoldopam mesylate at quantitative Doppler US: initial results in a canine study. Radiology 2001 ; 219: 419 26. Pinheiro JC, Bates DM. Mixed-effects models in S and S-plus. NewYork: Springer; 2000. 38. Harrell FE. Regression modeling strategies: with applications to linear models, logistic regression, and survival analysis. NewYork: Springer-Verlag; 2001. 39. Fingar VH, Wieman TJ, Wiehle SA, Cerrito PB. The role of microvascular damage in photodynamic therapy: the effect of treatment on vessel constriction, permeability, and leukocyte adhesion. Cancer Res 1992; 52: 4914 Garbo GM, Vicente MG, Fingar V, Kessel D. Effects of ursodeoxycholic acid on photodynamic therapy in a murine tumor model. Photochem Photobiol 2003; 78: 407 Kelleher DK, Thews O, Scherz A, Salomon Y, Vaupel P. Perfusion, oxygenation status and growth of experimental tumors upon photodynamic therapy with Pdbacteriopheophorbide. Int J Oncol 2004; 24: 1505 Leach RM, Hill HS, Snetkov VA, Ward JP. Hypoxia, energy state and pulmonary vasomotor tone. Respir Physiol Neurobiol 2002; 132: 55 JarmT, Podobnik B, Sersa G, Miklavcic D. Effect of hydralazine on blood flow, oxygenation, and interstitial fluid pressure in subcutaneous tumors. Adv Exp Med Biol 2003; 510: 25 Fingar VH, Wieman TJ, Park YJ, Henderson BW. Implications of a pre-existing tumor hypoxic fraction on photodynamic therapy. J Surg Res 1992; 53: 524.
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Ctivation of the tumor suppressor protein p53 as a transcription factor in response to DNA damage is postulated to be a critical event in preventing cancer. In response to DNA damage or other cellular stresses, p53 protein levels and its activity as a transcription factor increase. The stabilization and activation of p53 results in the arrest of cell-cycle progression in late G1 or in apoptosis in a manner that depends on cell type and the severity of cellular damage; however, our understanding of the mechanisms by which these responses occur is incomplete 1, 2 ; . Recent studies show that DNA damage-activated signaling pathways lead to the phosphorylation of p53 at both N- and C-terminal sites, and accumulating evidence suggests that p53 phosphorylation plays an important role in regulating both the stability and activity of p53 3 ; . One event that is postulated to be critical for p53-mediated DNA damage responses is phosphorylation of serine 15 Ser15 ; in human p53 4, 5 ; . Ser-15 is an evolutionarily conserved residue, corresponding to Ser-18 in murine p53, that can be phosphorylated in vitro by several related protein kinases belonging to the ataxia-telangiectasia mutated ATM ; family 8 these include DNA-PK 6 ; , ATR 7 ; , and ATM itself 8 11 ; . ATM is the product of a tumor suppressor gene that is mutated in the autosomally recessive human genetic disease ataxia-telangiectasia A-T ; . A-T patients exhibit pleiotropic defects, including hypersensitivity to ionizing radiation IR ; and a high incidence of cancer 8 ; . Cells derived from A-T patients, as well as those from ATM-deficient mice, exhibit delayed or reduced responses to IR, including defects in both S-phase and G2 M cell-cycle checkpoints 12, 13 ; . Recent studies have shown that the rapid phosphorylation of human p53 at Ser-15 after IR-induced DNA damage requires the ATM protein kinase 9 11 ; . Furthermore, cells lacking the ATM kinase are hypersensitive to IR 8 ; contrast, ATMdeficient cells respond normally to DNA damage caused by exposure to UV light and to other physical and physiological stresses; however, Ser-15 may be phosphorylated by another ATM family member, ATR, in response to UV treatment 7 ; . These findings suggest that Ser-15 phosphorylation may be a master regulator of p53's responses to DNA damage.
Abstract The combination of high level of beta-2-microglobulin 2m ; and chromosome 13 deletion allows to identify a high-risk subgroup of patients with de novo multiple myeloma MM ; . In this population of patients, we have evaluated the impact of a murine anti-IL6 monoclonal antibody BE-8 ; as part of the second conditioning regimen in a multicenter prospective randomized trial of tandem autologous stem cell transplantation ASCT ; . The first ASCT was prepared by melphalan 200 mg m2, and the second one by melphalan 220 mg m2 plus dexamethasone with or without BE-8 infusion. Two hundred and nineteen patients were included in this trial and 166 were randomized, 85 without BE-8 arm A ; and 81 with BE-8 arm B ; . The median overall survival OS ; and even-free survival EFS ; of the whole group of patients were 41 and 30 months, respectively. Response rates, OS and EFS were not different between the 2 arms of the trial: OS at 54 months 46% in arm A vs 51% in arm B p .90 ; , median EFS 35 months in arm A vs 31 arm B p .39 ; . In high-risk patients the dose-intensity of melphalan 420 mg m2 leaded to encouraging results, but the addition of anti-IL6 monoclonal antibody to the second conditioning regimen did not improve neither OS nor EFS and nafcillin.
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The individual i.e., there are no other feasible options ; , or that the imposition of a guardianship is the least restrictive alternative for addressing the proven substantial risk of harm.14.
26-year-old recovering cocaine addict Snorting cocaine is a self-limiting method of using cocaine. This occurs because cocaine constricts the capillaries that absorb the drug, so the more that is snorted, the slower the absorption. The blood level of cocaine is much less than when used intravenously. As the constricting effect of cocaine wears off, the nasal tissues swell, causing a runny sniffling nose characteristic of cocaine snorters. In addition chronic use can kill nasal tissues and in a few cases perforate the and naloxone.
May not express the targeted antigen, and or may be resistant to the effects of the unlabeled antibody 9 ; . The clinical experience with murine CD20 MAbs conjugated to iodine-131 Iodine I 131 Tositumomab or Bexxar ; or yttrium 90 Y90-ibritumomab tiuxetan or Zevalin ; is quite extensive. Both agents have demonstrable efficacy in patients with relapsed or refractory indolent B-cell NHL 7, 8, 10 ; , even after the use of rituximab 13 ; and are approved by the United States Food and Drug Administration. Tositumomab and Iodine I 131 Tositumomab was introduced into clinical trials for the treatment of relapsed or refractory low-grade NHL in 1990. The regimen consists of the sequential administration of a dose of the "cold" or unlabeled MAb, Tositumomab, to improve tumor localization 14, 15 ; of the subsequent Iodine I 131 Tositumomab. The regimen includes a dosimetric dose to enable the calculation of a patientspecific therapeutic dose. This two-step regimen has been given the trade name BEXXAR Corixa Corporation, South San Francisco, CA; GlaxoSmithKline, Philadelphia, PA ; but is referred to herein by the generic name "Iodine I 131 Tositumomab." Use of this regimen has resulted in significant durable clinical responses in some patients, supporting its approval for marketing in 2003. Approval was based on a study in 40 patients with relapsed refractory disease after rituximab therapy and supported by the demonstration of durable responses in four other studies enrolling 190 patients with disease relapsed refractory after chemotherapy. Tumor responses were documented in 60% of patients, with complete responses in 30%. Median response durations have been in excess of 12 months, with occasional durable complete tumor control 10 12, 16 ; . Marrow suppression has been the dose-limiting toxicity. Several observations led to interest in the possibility that the unlabeled Tositumomab could have innate antitumor effects. Clinical regressions have been observed after the imaging portion of the regimen but before the therapeutic dose of radiolabeled antibody. Because the radiation provided in the imaging dose is thought to be too small a dose to induce tumor regressions, it was hypothesized that the murine antibody alone might have significant antitumor effects. Additionally, in vitro testing has shown that Tositumomab can mediate growth suppression and apoptosis in CD20 expressing cell lines 2, 4 ; , and the chimeric anti-CD20 antibody, rituximab, has significant antitumor activity 1, 17, 18 ; . In addition, Tositumomab showed tumor growth inhibition in a human lymphoma xenograft model 3 ; . Clinical and regulatory concerns provided the imperative to determine that the therapeutic benefit provided by radioconjugation justifies the increased toxicity, and to additionally document the activity of unlabeled Tositumomab. This study randomized patients with relapsed or refractory, indolent or transformed, CD20-positive NHL between unlabeled Tositumomab and Iodine I 131 Tositumomab, with each arm receiving identical doses of antibody. A unilateral crossover from unlabeled to radiolabeled Tositumomab was allowed and murine.
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PGE2 production was also investigated in guinea pig macrophages. As observed with mouse macrophages, S-ketoprofen could markedly enhance LPS-induced TNF release also in guinea pig macrophages fig. 4A ; . Conversely, R-ketoprofen was unable to increase TNF production, again in agreement with data obtained on mouse cells. No detectable levels of TNF were induced by ketoprofen enantiomers in control groups data not shown ; . On LPS-induced PGE2 production, the effect of the two enantiomers on guinea pig cells was fully comparable to data obtained in murine macrophages. In fact, the R isomer was 100-fold less inhibitory than S-ketoprofen, inducing a complete inhibition of PGE2 production only at the highest concentration tested fig. 4B ; . Amplification of cytokine production by R- and S-ketoprofen was also investigated in vivo. Guinea pigs received a single dose of ketoprofen enantiomers or racemate and were subsequently injected with LPS. The ketoprofen dose 390 mol kg ; was chosen from previous experiments for its antiinflammatory effect. As shown in table 1, S-ketoprofen could significantly increase the LPS-induced TNF serum level and naltrexone.
18. Volpi I, Perruccio k, Tosti A, Capanni M, Ruggeri L, Posati S, Aversa F, Tabilio A, Romani L, Martelli MF, Velardi A. Postgrafting admionistration of granulocyte colonystimulating factor impairs functional immune recovery in recipients of human leukocyte antigen haplotype-mismatched hematopoietic transplants. Blood 2001; 97: 514-21
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