Northwestern University Feinberg School of Medicine

Jacob Sznajder Lab

Lab Members

Meet the Lab team members. We welcome requests for information about our work and collaboration opportunities.

Principal Investigator

JacobSznajder

Jacob Sznajder, MD
Professor, Division of Medicine-Pulmonary
312-908-7737
MD: Israel Institute of Technology (1978); Internship: Rambam Medical Center, Israel (1980); Residency: Rambam Medical Center, Israel (1982); Fellowship: University of Chicago Hospitals (1986)
View Northwestern University Feinberg School of Medicine faculty profile

Research Interests: Asthma, Chronic obstructive pulmonary disease (COPD), Interstitial lung disease

Research Professors

Laura ADada

Laura A Dada, PhD
lauradada( at )northwestern.edu
Research Associate Professor
312-503-5397
Undergrad: School of Sciences, University of Buenos Aires, Buenos Aires, Argentina; PhD: School of Sciences, University of Buenos Aires, Buenos Aires, Argentina
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EmiliaLecuona

Emilia Lecuona, PhD
e-lecuona( at )northwestern.edu
Research Associate Professor
312-503-5397
Undergrad: University of La Laguna, Spain; PhD: University of La Laguna, Spain
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Graduate Students

PatriciaBrazee

Patricia Brazee
pbrazee( at )u.northwestern.edu
DGP Graduate Student
312-503-1685
Undergrad: Smith College

Project Summary: Seasonal influenza virus A (IAV) infection can cause severe pneumonitis and have negative effects on patients’ health. As the primary target for IAV replication, alveolar epithelial cells (AEC) are important in releasing innate immune mediators that contribute to recruitment of monocytes and macrophages to the site of infection to orchestrate the host response. We are assessing the role of linear ubiquitination assembly complex (LUBAC) in modulating the inflammatory response of IAV-infection in the lungs.

Lab Manager

Lynn C.Welch

Lynn C. Welch
L-welch2( at )northwestern.edu
Research Laboratory Manager
312-503-1685
Undergrad: University of Evansville

Research Staff

ErmelindaCeco

Ermelinda Ceco, PhD
ermelinda.ceco( at )northwestern.edu
Postdoctoral Research Fellow
312-503-1685
Undergrad: Cleveland State University; PhD: University of Chicago

My project focuses on understanding the direct effect of high CO2 on muscle dysfunction, particularly diaphragm muscle wasting which is relevant to patients with lung diseases. Currently, I am exploring the role of high CO2 on diaphragmatic myofiber integrity, regeneration, contractile force and metabolic profile following acute and chronic high CO2 exposure. Understanding the mechanism/s by which high CO2 leads to diaphragm muscle dysfunction and muscle wasting is of biologic and potentially clinical significance.

NataliaMagnani

Natalia Magnani, PhD
nmagnani( at )northwestern.edu
Postdoctoral Research Fellow
312.503.1685
Undergrad: University of Buenos Aires PhD: University of Buenos Aires

During acute lung injury (ALI) there is alveolar epithelium damage resulting in edema in the alveolar space. The alveolar Na,K-ATPase, is essential for edema clearance. Organisms have evolved adaptive mechanisms to promote cellular survival during hypoxic stress. The aim of this project is to evaluate the role of linear ubiquitination assembly complex (LUBAC) in protein kinase C zeta (PKCζ) and Na,K-ATPase regulation in alveolar epithelial cells during prolonged hypoxia.

Luciano Amarelle Ruffinatti

Luciano Amarelle Ruffinatti, MD
luciano( at )northwestern.edu
Postdoctoral Research Fellow
312.503.1685
MD: Universidad de la República, School of Medicine

To determine whether during influenza virus infection mild Na,K-ATPase inhibition serves as a protective mechanism by preventing viral replication in the alveolar epithelium. I am investigating the role of the Na,K-ATPase modulation in the regulating host defense against influenza A infection in human lung epithelial cells and a murine model.

MasahikoShigemura

Masahiko Shigemura, PhD
Masahiko.shigemura( at )northwestern.edu
Postdoctoral Research Fellow
312-503-1685
Undergrad: Hokkaido University; PhD: Hokkaido University School of Medicine

I am studying about effects of high CO2 condition (hypercapnia) on airways and lung function. We are observing that hypercapnia contributes to airway smooth muscle contraction in rodents and primary airway smooth muscle cells. Data from these experiments will inform and provide new insights into pathophysiology of lung diseases such as COPD and asthma.

PritinSoni

Pritin Soni
Research Technologist
Undergrad: University of Wisconsin-Madison