University of Chicago

Jonathan Moss, MD, PhD.

Increased ยต-opioid receptor expression in metastatic lung cancer.

Singleton PA, Mirzapoiazova T, Hasina R, Salgia R, Moss J.

Br J Anaesth. 2014 Jul;113 Suppl 1:i103-8. doi: 10.1093/bja/aeu165. Epub 2014 Jun 11.

PMID: 24920011 [PubMed - indexed for MEDLINE]

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The Mu opioid receptor promotes opioid and growth factor-induced proliferation, migration and Epithelial Mesenchymal Transition (EMT) in human lung cancer.

Lennon FE, Mirzapoiazova T, Mambetsariev B, Poroyko VA, Salgia R, Moss J, Singleton PA.

PLoS One. 2014 Mar 24;9(3):e91577. doi: 10.1371/journal.pone.0091577. eCollection 2014.

PMID: 24662916 [PubMed - in process]

David Glick, MD

The Impact of Competition on Hospital Quality Metric Performance As part of our ongoing look at the value and meaning of surgical quality measure performance across the United States, we published our analysis of the impact of competitive environment (how many other hospitals within a 20 mile radius also perform heart valve surgery or care for acute myocardial infarctions) on quality metric performance and cost of care. We found that competition does not drive improvements in quality metric scores and that costs are higher when competition is greater. Our findings suggest that hospitals do not compete meaningfully on costs or publically reported quality metrics. (Anesthesia & Analgesia 2015;120:220-9) Evaluation of the Correlation Between Bis Readings and Memory Formation in Subjects Who are Sedated but not Unconscious At this year's International Anesthesia Research Society meeting in Montreal our lab presented two abstracts (Anesthesia & Analgesia2014;118; S-143 and S-307) that demonstrated that the ability to recall words either following premedication with midazolam or during the recovery period following a general anesthetic was correlated with the Bis reading recorded when the words were spoken to the subjects. However, the clinical value of this difference in Bis readings is uncertain, as there is tremendous overlap in the ranges of Bis scores among those that did and those that did not recall the words.

Steven Roth, M.D.

Imagine if we could use cells or cell free media derived from patients to reverse the effect of organ damage. This is what Dreixler et al did in a rodent model of retinal ischemia. Conditioned medium (CM) from rat bone marrow stem cells (BMSCs) or unconditioned medium (uCM) was injected into the vitreous 24 hours after the end of ischemia. CM 24 hours after ischemia significantly improved retinal function and attenuated cell loss in the retinal ganglion cell layer. CM attenuated postischemic apoptosis and apoptosis-related gene expression. By mass spectrometry and spectral counting, 19 proteins that met stringent identification criteria were increased in the CM compared to uCM; the majority were extracellular matrix proteins that mapped into an interactional network together with other proteins involved in cell growth and adhesion. By restoring retinal function, attenuating apoptosis, and preventing retinal cell loss after ischemia, CM is a robust means of delayed postischemic intervention. We identified some potential candidate proteins for this effect.

Dreixler JC, Poston JN, Balyasnikova I, Shaikh AR, Tupper KY, Conway S, Boddapati V, Marcet MM, Lesniak MS, Roth S: Delayed Administration of Bone Marrow Mesenchymal Stem Cell Conditioned Medium Significantly Improves Outcome After Retinal Ischemia in Rats. Investigative Ophthalmology & Visual Science 2014; 55: 3785-3796

A unique feature of this study was the collaboration with those in other departments and institutions: Drs. Lesniak and Balyasnikova from Neurosurgery, Dr. Marcet from Ophthalmology, and the Mass Spectrometry Facility at University of Illinois-Chicago. Supported by National Institutes of Health (Rockville, MD, USA) Grants EY10343 and EY10343-16S1 (American Recovery and Reinvestment Act [SR]), CA122930 (MSL), AG029795-02 for the Medical Student Summer Research Program at the Pritzker School of Medicine, UL1RR024999 to the University of Chicago Institute for Translational Medicine; the Illinois Society for the Prevention of Blindness, Chicago, Illinois, United States (JNP); and a Center-Style Grant from the Dean's Research Advisory Committee of the Division of Biological Sciences of the University of Chicago (MSL, SR). JNP was the recipient of a Medical Student Research Fellowship Award from the American Academy of Neurology (St. Paul, Minnesota, USA) and a student scholarship from the Achievement Rewards for College Scientists Foundation (Washington, DC, USA). Proteomics and informatics services were provided by the University of Illinois-Chicago Research Resources Center Mass Spectrometry, Metabolomics and Proteomics Facility which was established in part by a grant from The Searle Funds at the Chicago Community Trust to the Chicago Biomedical Consortium (University of Chicago, Northwestern University, and University of Illinois).

Zhang (Jimmy) Xie, MD, PhD

Wang Q, Fong R, Mason P, Fox AP and Xie Z: Caffeine Accelerates Recovery from General Anesthesia. Journal of Neurophysiol. 111: 1331-1340, 2014

This report provided a novel finding on the potential mechanisms of general anesthetic emergence. It demonstrated that drugs, which increase cAMP level or antagonize adenosine receptors, could facilitate the emergence of general anesthesia. The article will provide a deeper insight into the mechanisms of anesthetic actions. From the clinical stand point, caffeine, one of the most common use substances in the world, may have a significant clinical use.


General anesthetics inhibit neurotransmitter release from both neurons and secretory cells. If inhibition of neurotransmitter release is part of an anesthetic mechanism of action, then drugs that facilitate neurotransmitter release may aid in reversing general anesthesia. Drugs that elevate intracellular cAMP levels are known to facilitate neurotransmitter release. Three cAMP elevating drugs (forskolin, theophylline, and caffeine) were tested; all three drugs reversed the inhibition of neurotransmitter release produced by isoflurane in PC12 cells in vitro. The drugs were tested in isoflurane-anesthetized rats. Animals were injected with either saline or saline containing drug. All three drugs dramatically accelerated recovery from isoflurane anesthesia, but caffeine was most effective. None of the drugs, at the concentrations tested, had significant effects on breathing rates, O2 saturation, heart rate, or blood pressure in anesthetized animals. Caffeine alone was tested on propofol-anesthetized rats where it dramatically accelerated recovery from anesthesia. The ability of caffeine to accelerate recovery from anesthesia for different chemical classes of anesthetics, isoflurane and propofol, opens the possibility that it will do so for all commonly used general anesthetics, although additional studies will be required to determine whether this is in fact the case. Because anesthesia in rodents is thought to be similar to that in humans, these results suggest that caffeine might allow for rapid and uniform emergence from general anesthesia in human patients.

Ming Xu, PhD. Neuroscience 278 (2014) 154-164 (attached)



a Department of Anesthesia and Critical Care, The University of Chicago, Chicago, IL, USA

b Medicinal Chemistry Section, National Institute on Drug Abuse-Intramural Research Program, National Institutes of Health, Baltimore, MD, USA


Memories of drug experience and drug-associated environmental cues can elicit drug-seeking and taking behaviors in humans. Disruption of reconsolidation of drug memories dampens previous memories and therefore may provide a useful way to treat drug abuse. We and others previously demonstrated that dopamine D1 and D3 receptors play differential roles in acquiring cocaine-induced behaviors. Moreover, D3 receptors contribute to the reconsolidation of cocaine-induced conditioned place preference. In the present study, we examined effects of manipulating D1 or D3 receptors on reconsolidation of cocaine memories in mouse models of drug self-administration. We found that pharmacological blockade of D1 receptors or a genetic mutation of the D3 receptor gene attenuated reconsolidation that lasted for at least 1 week after the memory retrieval. In contrast, with no memory retrieval, pharmacological antagonism of D1 receptors or the D3 receptor gene mutation did not significantly affect reconsolidation of cocaine memories. Pharmacological blockade of D3 receptors also attenuated reconsolidation in wild-type mice that lasted for at least 1 week after the memory retrieval. These results suggest that D1 and D3 receptors and related signaling mechanisms play key roles in reconsolidation of cocaine memories in mice, and that these receptors may serve as novel targets for the treatment of cocaine abuse in humans. 2014 IBRO.

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