Author name: Kristen Hartman

Possible role of CRF peptides in burn-induced hypermetabolism.

Chance WT, Dayal R, Friend LA, Sheriff S (2006) Possible role of CRF peptides in burn-induced hypermetabolism. Life Sci 78(7):694-703. doi: 10.1016/j.lfs.2005.05.083 Summary: Burn trauma has been associated with hypermetabolism and anorexia. Corticotropin releasing factor (CRF) elevates metabolic rate and elicits anorexia, while neuropeptide Y (NPY) reduces metabolic rate while stimulating feeding. After burn treatment, […]

Possible role of CRF peptides in burn-induced hypermetabolism. Read More »

Prenatal glucocorticoid exposure affects learning and vulnerability of cholinergic neurons.

Emgard M, Paradisi M, Pirondi S, Fernandez M, Giardino L, Calza L (2007) Prenatal glucocorticoid exposure affects learning and vulnerability of cholinergic neurons. Neurobiol Aging 28(1):112-121. doi: 10.1016/j.neurobiolaging.2005.11.015 Summary: Women at risk of preterm delivery are commonly treated with synthetic glucocorticoids such as dexamethasone and betamethasone. Here the authors examined adult rats that were prenatally

Prenatal glucocorticoid exposure affects learning and vulnerability of cholinergic neurons. Read More »

LPS Content

Q: In a recent experiment using a saporin-antibody conjugate injected systemically we saw changes in dendritic cells that could be consistent with an LPS effect. Does ATS test for LPS and has this ever been identified as a problem before? A: Yes, this can happen, but we here at ATS will swear innocence. One of

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Featured Article: The biologically active cholecystokinin (26-33) peptide, [Tyr2-SO3]CCK-8, retains high affinity for CCK2 receptors after covalent conjugation to saporin

Lai J, Zhang W, Badghisi H, Hruby VJ, Porreca F (2006) Featured Article: The biologically active cholecystokinin (26-33) peptide, [Tyr2-SO3]CCK-8, retains high affinity for CCK2 receptors after covalent conjugation to saporin. Targeting Trends 7(1) Related Products: CCK-SAP (Cat. #IT-31) Read the featured article in Targeting Trends. See Also: Lai J et al. Featured Article: The

Featured Article: The biologically active cholecystokinin (26-33) peptide, [Tyr2-SO3]CCK-8, retains high affinity for CCK2 receptors after covalent conjugation to saporin Read More »

Cover Article: The Biologically Active Cholecystokinin (26-33) peptide, [Tyr2-SO3]CCK-8, Retains High Affinity for CCK2 Receptors after Covalent Conjugation to Saporin

News Article /

Contributed by Josephine Lai, Wenjun Zhang, Hamid Badghisi, Victor J. Hruby(1) and Frank Porreca, Departments of Pharmacology and Chemistry(1), The University of Arizona, Tucson, AZ 85724. Cholecystokinin (CCK) is widely distributed in the central nervous system and the gastrointestinal tract. The 33-amino acid peptide contains a carboxyl terminal octapeptide sequence Asp-Tyr-Met-Gly-Trp-Met-Asp-Phe-NH2 which confers the biological activity

Cover Article: The Biologically Active Cholecystokinin (26-33) peptide, [Tyr2-SO3]CCK-8, Retains High Affinity for CCK2 Receptors after Covalent Conjugation to Saporin Read More »

Suppression of natural killer cell activity by morphine is mediated by the nucleus accumbens shell.

Saurer TB, Carrigan KA, Ijames SG, Lysle DT (2006) Suppression of natural killer cell activity by morphine is mediated by the nucleus accumbens shell. J Neuroimmunol 173(1-2):3-11. doi: 10.1016/j.jneuroim.2005.11.009 Summary: In this work the authors investigated the role of dopaminergic projections to the nucleus accumbens in modulation of immune parameters such as morphine-induced suppression of

Suppression of natural killer cell activity by morphine is mediated by the nucleus accumbens shell. Read More »

SIRT1 protects against microglia-dependent amyloid-beta toxicity through inhibiting NF-κB signaling.

Chen J, Zhou Y, Mueller-Steiner S, Chen LF, Kwon H, Yi S, Mucke L, Gan L (2005) SIRT1 protects against microglia-dependent amyloid-beta toxicity through inhibiting NF-κB signaling. J Biol Chem 280(48):40364-40374. doi: 10.1074/jbc.M509329200 Usage: To eliminate microglia in mixed cortical cultures, cultures were treated with either Ac-LDL-SAP at 3 ug/ml for 18 h or 5mM

SIRT1 protects against microglia-dependent amyloid-beta toxicity through inhibiting NF-κB signaling. Read More »

Facilitation of conditioned odor aversion by entorhinal cortex lesion in the rat is reversed by cholinergic lesion in the basal forebrain

Ferry B, Herbeaux K, Petoukhova-Traissard N, Galani R, Cassel J, Majchrzak M (2005) Facilitation of conditioned odor aversion by entorhinal cortex lesion in the rat is reversed by cholinergic lesion in the basal forebrain. Neuroscience 2005 Abstracts 881.6. Society for Neuroscience, Washington, DC. Summary: In the rat, conditioned odor aversion (COA) corresponds to the avoidance

Facilitation of conditioned odor aversion by entorhinal cortex lesion in the rat is reversed by cholinergic lesion in the basal forebrain Read More »

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