Philadelphia University + Thomas Jefferson University
Sidney Kimmel Medical College
Department of Medicine

Facilities & Labs

The Center City Philadelphia urban campus is conveniently located in a three block area between 9th and 11th streets and Locust and Chestnut. In response to anticipated changes in the delivery of health care in the U.S., the Sidney Kimmel Medical College (SKMC) and Thomas Jefferson University Hospitals have announced a realignment and further integration to address the changing environment of health care. The Hospital serves as a major tertiary care referral center for the Delaware Valley and, as a Level I Trauma Center, has more than 45,000 admissions annually.

While studying at Thomas Jefferson University, students will have access to the following facilities and labs:

Research Facilities

Clinical Facilities

  • Ambulatory Patient in the Office

  • Inpatient Medical ICU

  • Pulmonary Fellowship Testing Laboratory

  • Hospital Bronchoscopy Suite

  • Outpatient Services

Summer Laboratory

Dr. Summer's laboratory focuses on lung metabolism and understanding how local and systemic metabolic derangements contribute to the onset and progression of lung diseases.

One major area of investigation is on the relationship between obesity and acute lung injury. Recent epidemiological studies indicate a paradoxical relationship exists between obesity and acute lung injury, in that, obese individuals are at increased risk for developing acute lung injury but outcomes in established disease are improved when compared to lean patients. In these investigations, Dr. Summer's laboratory is utilizing genetic and diet-induced obesity models to understand how injury and inflammatory responses differ during obesity. These studies aim to direct future clinical investigations focusing on the prevention and the treatment of acute lung injury in lean and obese subjects.

In related studies, Dr. Summer's laboratory is investigating the association between hormonal responses from adipose tissue and outcomes in acute lung injury. It is now increasingly apparent that adipose tissue is not just a storage depot for fuel but an important endocrine organ that secretes a multitude of hormones called adipokines. These adipokines act on virtually all tissues, including lung, and serve to regulate diverse biological processes involved in immune, metabolic and vascular regulation. Recent work from Dr. Summer's laboratory has identified a relationship between plasma levels of the adipokine adiponectin and outcomes in patients with respiratory failure from diverse etiologies. In ongoing investigations, his laboratory will investigate whether a similar association exists in patients with respiratory failure from acute lung injury. Adiponectin oligomeric fractions will be measured in plasma samples obtained from patients participating in the National Heart, Lung and Blood Institute ARDS Network Fluid and Catheter Treatment Trial (FACTT). The goal of this study is to determine whether measuring adiponectin oligomers is useful for predicting outcomes in patients with acute lung injury.

Another major focus of Dr. Summer's laboratory is on intermediary metabolism in the lung and understanding how alterations in local metabolic activity contribute to the progression of lung diseases. Our current hypothesis is that metabolic stress resulting from lung injury drives the inflammatory and the reparative responses seen in many pathological lung conditions (e.g. idiopathic pulmonary fibrosis, sarcoidosis, hypersensitivity pneumonitis, acute lung injury). The goal of these studies is to identify novel therapeutic targets of metabolic pathways that can be used for treating lung diseases.

Penn Laboratory

“G protein-coupled receptor (GPCR) signaling in airway smooth muscle."
Studies focus on understanding the mechanisms by which PKA mediates both contractile inhibition and negative feedback regulation of the β2AR in human airway smooth muscle. Protocols include: 1) development of human airway smooth muscle cultures using airway tissue harvested from asthmatic or non-asthmatic subjects; 2) biochemical analysis of pro- and anti- contractile signaling in airway smooth muscle cultures; 3) cloning of recombinant PKA inhibitory constructs and expressing them in cells or tissue; and 4) analysis of regulation of airway smooth muscle contraction using murine trachea or 4th generation human airways ex vivo.

“Arrestin selectivity for GPCRs in airway smooth muscle.”
Studies focus on detailing the role arrestin isoforms play in regulating the signaling capacity and function of different pro- and anti- contractile GPCRs in airway smooth muscle. Protocols include: 1) development of human airway smooth muscle cultures using airway tissue harvested from asthmatic or non-asthmatic subjects, and murine airway smooth muscle cultures derived for airways from beta-arrestin1 and beta-arrestin2 subtype knockout mice ; and 2) characterization of effect of arrestin subtype knockout (mice) or knockdown (human) on signaling and function of pro- and anti- contractile GPCRs. 

“OGR1 is a proton-sensing GPCR in airway smooth muscle.”
Studies focus on characterizing the signaling events elicited by reduced extracellular pH in human airway smooth muscle cells, their dependence on the G protein-coupled receptor OGR1, and associated functional consequences. Protocols involve: 1) assessing signaling by OGR1 in artificial systems (recombinant OGR1 expressed in HEK293 cells) or primary human airway smooth muscle (endogenous OGR1 in cells in culture or 4th generation human airways) by reduced extracellular pH or novel putative OGR1 ligands; 2) effect of reduced extracellular pH or novel putative OGR1 ligands on single cell or human airway smooth muscle tissue contraction both ex vivo (mouse and human) or in vivo (in mice expressing or lacking OGR1).

“Optimizing beta-adrenoceptor signaling bias in asthma.”
Studies explore the capacity of different ligands of the beta-2-adrenoceptor (b2AR) to promote Gs and arrestin-dependent signaling, and regulate the asthma phenotype in murine models of allergic lung inflammation, based on the observation that certain types of b2AR antagonists (“beta-blockers), when administered chronically in mice, strong inhibit the development of allergen-induced inflammation and airway hyperreactivity. Protocols include: 1) characterization of ligand “bias” (the ability to promote Gs- or arrestin-dependent signaling) in multiple cell types (including airway epithelium and smooth muscle); 2)  the effect of these ligands on mucin production in murine and human airway epithelial cultures; and 3) the effect of chronic ligand treatment on the asthma phenotype induced by allergic lung inflammation in wild type mice and mice deficient in beta-arrestin expression in specific cell types.