Search Results - (Author, Cooperation:J. S. Graham)
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1Latest Papers from Table of Contents or Articles in PressN. Waddell ; M. Pajic ; A. M. Patch ; D. K. Chang ; K. S. Kassahn ; P. Bailey ; A. L. Johns ; D. Miller ; K. Nones ; K. Quek ; M. C. Quinn ; A. J. Robertson ; M. Z. Fadlullah ; T. J. Bruxner ; A. N. Christ ; I. Harliwong ; S. Idrisoglu ; S. Manning ; C. Nourse ; E. Nourbakhsh ; S. Wani ; P. J. Wilson ; E. Markham ; N. Cloonan ; M. J. Anderson ; J. L. Fink ; O. Holmes ; S. H. Kazakoff ; C. Leonard ; F. Newell ; B. Poudel ; S. Song ; D. Taylor ; S. Wood ; Q. Xu ; J. Wu ; M. Pinese ; M. J. Cowley ; H. C. Lee ; M. D. Jones ; A. M. Nagrial ; J. Humphris ; L. A. Chantrill ; V. Chin ; A. M. Steinmann ; A. Mawson ; E. S. Humphrey ; E. K. Colvin ; A. Chou ; C. J. Scarlett ; A. V. Pinho ; M. Giry-Laterriere ; I. Rooman ; J. S. Samra ; J. G. Kench ; J. A. Pettitt ; N. D. Merrett ; C. Toon ; K. Epari ; N. Q. Nguyen ; A. Barbour ; N. Zeps ; N. B. Jamieson ; J. S. Graham ; S. P. Niclou ; R. Bjerkvig ; R. Grutzmann ; D. Aust ; R. H. Hruban ; A. Maitra ; C. A. Iacobuzio-Donahue ; C. L. Wolfgang ; R. A. Morgan ; R. T. Lawlor ; V. Corbo ; C. Bassi ; M. Falconi ; G. Zamboni ; G. Tortora ; M. A. Tempero ; A. J. Gill ; J. R. Eshleman ; C. Pilarsky ; A. Scarpa ; E. A. Musgrove ; J. V. Pearson ; A. V. Biankin ; S. M. Grimmond
Nature Publishing Group (NPG)
Published 2015Staff ViewPublication Date: 2015-02-27Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Adenocarcinoma/drug therapy/genetics ; Animals ; Carcinoma, Pancreatic Ductal/drug therapy/genetics ; *DNA Mutational Analysis ; DNA Repair/genetics ; Female ; Genes, BRCA1 ; Genes, BRCA2 ; Genetic Markers/genetics ; Genome, Human/*genetics ; Genomic Instability/genetics ; *Genomics ; Genotype ; Humans ; Mice ; Mutation/*genetics ; Pancreatic Neoplasms/classification/drug therapy/*genetics ; Platinum/pharmacology ; Point Mutation/genetics ; Poly(ADP-ribose) Polymerase Inhibitors ; Xenograft Model Antitumor AssaysPublished by: -
2Latest Papers from Table of Contents or Articles in PressP. Bailey ; D. K. Chang ; K. Nones ; A. L. Johns ; A. M. Patch ; M. C. Gingras ; D. K. Miller ; A. N. Christ ; T. J. Bruxner ; M. C. Quinn ; C. Nourse ; L. C. Murtaugh ; I. Harliwong ; S. Idrisoglu ; S. Manning ; E. Nourbakhsh ; S. Wani ; L. Fink ; O. Holmes ; V. Chin ; M. J. Anderson ; S. Kazakoff ; C. Leonard ; F. Newell ; N. Waddell ; S. Wood ; Q. Xu ; P. J. Wilson ; N. Cloonan ; K. S. Kassahn ; D. Taylor ; K. Quek ; A. Robertson ; L. Pantano ; L. Mincarelli ; L. N. Sanchez ; L. Evers ; J. Wu ; M. Pinese ; M. J. Cowley ; M. D. Jones ; E. K. Colvin ; A. M. Nagrial ; E. S. Humphrey ; L. A. Chantrill ; A. Mawson ; J. Humphris ; A. Chou ; M. Pajic ; C. J. Scarlett ; A. V. Pinho ; M. Giry-Laterriere ; I. Rooman ; J. S. Samra ; J. G. Kench ; J. A. Lovell ; N. D. Merrett ; C. W. Toon ; K. Epari ; N. Q. Nguyen ; A. Barbour ; N. Zeps ; K. Moran-Jones ; N. B. Jamieson ; J. S. Graham ; F. Duthie ; K. Oien ; J. Hair ; R. Grutzmann ; A. Maitra ; C. A. Iacobuzio-Donahue ; C. L. Wolfgang ; R. A. Morgan ; R. T. Lawlor ; V. Corbo ; C. Bassi ; B. Rusev ; P. Capelli ; R. Salvia ; G. Tortora ; D. Mukhopadhyay ; G. M. Petersen ; D. M. Munzy ; W. E. Fisher ; S. A. Karim ; J. R. Eshleman ; R. H. Hruban ; C. Pilarsky ; J. P. Morton ; O. J. Sansom ; A. Scarpa ; E. A. Musgrove ; U. M. Bailey ; O. Hofmann ; R. L. Sutherland ; D. A. Wheeler ; A. J. Gill ; R. A. Gibbs ; J. V. Pearson ; A. V. Biankin ; S. M. Grimmond
Nature Publishing Group (NPG)
Published 2016Staff ViewPublication Date: 2016-02-26Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Carcinoma, Pancreatic ; Ductal/classification/genetics/immunology/metabolism/pathology ; Cell Line, Tumor ; DNA Methylation ; DNA-Binding Proteins/genetics ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Genes, Neoplasm/*genetics ; Genome, Human/*genetics ; *Genomics ; Hepatocyte Nuclear Factor 3-beta/genetics ; Hepatocyte Nuclear Factor 3-gamma/genetics ; Histone Demethylases/genetics ; Homeodomain Proteins/genetics ; Humans ; Mice ; Mutation/*genetics ; Nuclear Proteins/genetics ; Pancreatic Neoplasms/*classification/*genetics/immunology/metabolism/pathology ; Prognosis ; Receptors, Cytoplasmic and Nuclear/genetics ; Survival Analysis ; Trans-Activators/genetics ; Transcription Factors/genetics ; Transcription, Genetic ; Transcriptome ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Proteins/geneticsPublished by: -
3Articles: DFG German National LicensesGraham, J. S. ; Martin, J. L. ; Zallnick, J. E. ; Nalls, C. R. ; Mitcheltree, L. W. ; Lee, R. B. ; Logan, T. P. ; Braue, E. H.
Oxford, UK : Blackwell Publishing Ltd
Published 1999Staff ViewISSN: 1600-0846Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: The euthymic hairless guinea pig was the animal model of choice at this laboratory for vesicant injury research. The supply of these animals, however, was interrupted in 1993 by an outbreak of Lisferia monocyfogenes at the commercial supplier's breeding facility, thereby forcing a search for alternative animal models. This report describes the development of a weanling pig model for use in evaluating the severity of skin lesions induced by sulfur mustard [bis(2-chloroethyl)sulfide; SM] using a variety of bioengineering techniques. These methods include reflectance colorimetry (erythema response), high frequency ultrasound imaging (edema response) and a modified dermal torque meter procedure to test for Nikolsky's sign (damage at the dermal-epidermal junction). The time course and exposure time-dependence of SM-induced lesions for these parameters were characterized in this model and compared with previous results in the haired and hairless guinea pig.〈section xml:id="abs1-2"〉〈title type="main"〉Methods:Six male Yorkshire Cross pigs (7–10 kg) were used in this study. The hair on the dorsal surface of each animal was shaved the afternoon prior to SM exposure. Twenty-four dorsal skin sites on each pig were exposed to saturated SM vapor (1.4 mg/l) using 14-mm diameter vapor cups for 0 (control), 5, 10, 15, 20, or 25 min, with four sites per exposure level. Control and exposure sites were rotated to prevent site-specific biases. Lesions were evaluated for erythema (reflectance colorimeter) at 4, 6, 12, 24 and 48 h post-exposure, and for edema (high frequency ultrasound) at 6, 12, 24, and 48 h post-exposure. Evaluations for Nikolsky's sign and histopathology were conducted at 48 h post-exposure.〈section xml:id="abs1-3"〉〈title type="main"〉Results:Maximum erythema responses occurred at 24 h postexposure for all SM exposure times (5, 10, 15, 20 and 25 min). The overall maximum response occurred with a 15-min SM vapor exposure at 24 h post-exposure. Exposures longer than 15 min did not induce significantly greater erythema at any of the time points examined. The earliest time point at which significant edema was noted was at 12 h for the 15- and 25-min SM vapor groups. Maximum edema occurred at 48 h following a 15-min exposure. No significant increase in edema was noted at any observation time point with exposures longer than 15 min. Allsites showed a weakening of the dermal-epidermal junction (positive Nikolsky's sign) 48 h after a 15-min or longer SM vapor challenge. The histologic severity of the lesions did not significantly worsen as the vapor exposure was increased beyond 15 min. (Following a 15-min SM exposure, incidences of epidermal necrosis, pustular epidermitis, microblisters and vascular damage had reached 100%, with maximum mean severity scores.) The weanling pig is more resistant to the effects of SM vapor than either the haired or hairless guinea pig, showing a delayed response and requiring a longer exposure time to generate the same (quantitative and qualitative) response in erythema, Nikolsky's sign and microblister formation. SM vapor-induced edema formation in the weanling pig is not as severe as in the guinea pig models.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusions:Erythema, Nikolsky's sign and microblisters all appear to be excellent parameters for evaluating SM vapor-induced cutaneous damage in the weanling pig. Even though the exposure time-dependent response of cutaneous exposure to SM vapor in humans more closely parallels those of the haired and hairless guinea pig with respect to dermal-epidermal separation, weanling pig skin shares many more similarities to human skin and has the potential to be a useful model for antivesicant research. This model should prove valuable in 1) efficacy testing of pretreatments, treatments and topical skin protectants; 2) wound healing studies; 3) evaluationlof skinlwound decontamination systems; and 4) basic vesicant research.Type of Medium: Electronic ResourceURL: -
4Articles: DFG German National LicensesStaff View
ISSN: 1476-4687Source: Nature Archives 1869 - 2009Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsNotes: [Auszug] Pinus ponderosa pollen was germinated for 15 hr. at 29 C. in 0.01 M calcium-potassium phosphate buffer, pH. 5.9, in the presence of the fungistat-bacteriostat mixture Mysteclin (an antibiotic -antifungal mixture composed of tetracycline and mystatin ; kindly supplied by the Medical Division, E. ...Type of Medium: Electronic ResourceURL: -
5Articles: DFG German National LicensesStaff View
ISSN: 1432-2048Keywords: Leaf (proteinase inhibitors) ; Lycopersicon (proteinase inhibitor mRNAs) ; mRNA (proteinase inhibitors) ; Wound-induced proteinase inhibitorsSource: Springer Online Journal Archives 1860-2000Topics: BiologyNotes: Abstract Levels of two wound-inducible serine proteinase inhibitors, called Inhibitor I and Inhibitor II, and their mRNAs were quantified in leaves of tomato (Lycopersicon escululentum (L.) Mill.) plants after wounding the leaves with a hemostat. A single wound on a lower leaf of 25-old tomato plants caused the accumulation of the two inhibitor proteins in wounded and non-wounded leaves beginning about 4–6 h following wounding. The rate of inhibitor accumulation was maximal in leaves for the next 4 h and then declined. By 20 h the accumulation had nearly ceased. Following a single wound, Inhibitor I mRNA [600 bases in length] and Inhibitor II mRNA (760 bases) began to accumulate in wounded leaves about 2 h before the inhibitor proteins could be detected. The levels of mRNA for both inhibitors reached a maximum at about 8 h following wounding and then decayed, both with apparent half lives of about 10 h. Four consecutive wounds, inflicted hourly, increased the levels of mRNA for both inhibitors to over twice the levels induced by a single wound. Within 4 h following multiple wounds, Inhibitor I mRNA represented about 0.5% of the total polyadenylated mRNA (poly(A+)mRNA) and Inhibitor II mRNA about 0.15% of the total. The rates of accumulation of the two inhibitor proteins varied depending upon the age of the plants and their environment during growth, and ranged between 3 and 10 μg Inhibitor I·h-1·(g tissue)-1 for Inhibitor I and about half of these rates for Inhibitor II. Nuclei were isolated from leaves of wounded and non-wounded plants, and in mRNA runoff experiments using specific inhibitor copy DNAs (cDNAs) as probes the synthesis of Inhibitor I and II mRNAs were shown to be regulated, at least in part, at the level of transcription.Type of Medium: Electronic ResourceURL: