2015 in Scientific Imagery

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From the junctions that hold cells together to the bacteria that cause pneumonia, fascinating scientific images provide a window into the wide range of research that Feinberg faculty, trainees and students published in 2015.

A scientific illustration depicts upper motor neurons, which send messages from the brain to the spinal cord to activate voluntary movement and play a major role in ALS pathology.
A scientific illustration depicts upper motor neurons, which send messages from the brain to the spinal cord to activate voluntary movement and play a major role in ALS pathology.

Exploring Upper Motor Neuron Degeneration in ALS

For the first time, scientists revealed a mechanism underlying the cellular degeneration of upper motor neurons, a small group of neurons in the brain recently shown to play a major role in ALS pathology.

In a study supported by the Les Turner Foundation and published in Cerebral Cortex, Northwestern Medicine scientist Hande Ozdinler, PhD, assistant professor of Neurology, developed a new mouse model for studying upper motor neurons and found that increased stress in the endoplasmic reticulum is one culprit of the cells’ death.

Read the full story here.


This image shows infected neural cells (brown) in the lab’s model of herpes simplex virus encephalitis.
This image shows infected neural cells (brown) in the lab’s model of herpes simplex virus encephalitis.

Studying Age-Related Differences in Herpes Encephalitis

Newborns are more susceptible to severe disease from herpes simplex virus (HSV) infection than adults, often leading to encephalitis or swelling of the brain.

By comparing the disease in adults and newborns, a team of Northwestern Medicine scientists led by William J. Muller, MD, PhD, associate professor of Pediatrics in the Division of Infectious Disease, have revealed age-related differences in the development of encephalitis and the role of autophagy, the cellular mechanism for degradation of unnecessary cellular components, in the newborn brain. The findings were published in PLoS Pathogens.

Read the full story here.


A mutation in desmoplakin (green) delays assembly of the intermediate filament cytoskeleton (red) at cell-cell junctions.
A mutation in desmoplakin (green) delays assembly of the intermediate filament cytoskeleton (red) at cell-cell junctions.

Protein that Helps Cells Stick Together May Explain Heart Disease Development

Northwestern Medicine scientists have uncovered novel regulatory mechanisms behind desmosomes, important junctions that hold cells together. The findings, published in the Journal of Cell Biology, may help explain how some diseases of the skin and heart develop.

Senior author Kathleen Green, PhD, Joseph L. Mayberry, Sr., Professor of Pathology and Toxicology and of Dermatology, and first author Lauren Albrecht, a student in the Driskill Graduate Program in Life Sciences (DGP), focused on a key protein component of desmosomes called desmoplakin.

Read the full story here.


The lattice-like structure of tight junctions (stained green) in the epithelial barrier break down after Oncostatin M exposure (bottom) in bronchial (left) and nasal (right) cultures. Cell nuclei are stained in blue.
The lattice-like structure of tight junctions (stained green) in the epithelial barrier break down after Oncostatin M exposure (bottom) in bronchial (left) and nasal (right) cultures. Cell nuclei are stained in blue.

Mechanism Behind Asthma and Chronic Rhinosinusitis Proposed

A Northwestern Medicine study suggests that a protein called Oncostatin M (OSM) may compromise the airway’s epithelial barrier, a wall of cells that blocks pathogens, environmental factors and allergens from entering tissue and triggering the body’s immune system.

The study’s findings, published in the Journal of Allergy and Clinical Immunology, may have implications for patients with mucosal diseases such as allergic asthma, eosinophilic esophagitis and chronic rhinosinusitis, a type of sinus inflammation that persists for 12 weeks or more.

First author Kate Pothoven, a doctoral student in the Driskill Graduate Program in Life Sciences (DGP), worked with senior author Robert Schleimer, PhD, chief of Medicine-Allergy-Immunology, on the study.

Read the full story here.


Vimentin intermediate filaments (green), responsible for the mechanical support of cells, are organized by their transport along microtubules (red). Northwestern Medicine scientists used images like this, acquired using super-resolution microscopy, to discover and measure vimentin filament transport.
Vimentin intermediate filaments (green), responsible for the mechanical support of cells, are organized by their transport along microtubules (red). Northwestern Medicine scientists used images like this, acquired using super-resolution microscopy, to discover and measure vimentin filament transport.

Understanding a Cell Component Integral for Mechanical Stability 

A human cell’s cytoskeleton – the protein network that supports its shape and function – is made of three components. Scientists know a lot about two of them, microfilaments and microtubules, but they’ve only recently had the technological advances to study the dynamics of the third in detail.

In a pair of studies, Northwestern Medicine scientists helped explain how this third component – slender, threadlike structures called intermediate filaments – moves and assembles to protect cells.

The work, led by Vladimir Gelfand, PhD, Leslie B. Arey Professor of Cell, Molecular, and Anatomical Sciences in the Department of Cell and Molecular Biology, may someday have applications for patients with genetic mutations that affect intermediate filaments and their important mechanical properties.

Read the full story here.


mouse lung with pseudomonas aeruginosa pneumonia
This image shows a section of mouse lung following infection with a strain of Pseudomonas aeruginosa (red). This bacterium infects cells by injecting them with a toxin called ExoS. Cells injected with ExoS are blue. Cells that have not been injected are green.

Uncovering the Spread of Bacteria in Pneumonia

Northwestern Medicine scientists have discovered the role a toxin produced by a pneumonia-causing bacterium plays in the spread of infection from the lungs to the bloodstream in hospitalized patients.

“Prior to this study, it was a mystery how the bacteria escaped from the lungs into the bloodstream,” said Alan Hauser, MD, PhD, professor of Microbiology-Immunology and Medicine in the Division of Infectious Diseases. “These findings lay the foundation for future studies to further understand the mechanisms for how the escape to the bloodstream occurs.”

The study was published in PLOS Pathogens.

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There are 30 to 40 different output neurons in the retina called ganglion cells that stream information through the optic nerve to the brain, but many of them have not yet been functionally characterized.
There are 30 to 40 different output neurons in the retina called ganglion cells that stream information through the optic nerve to the brain, but many of them have not yet been functionally characterized.

Reverse Engineering the Retina

The retina is not simply the innermost layer of the eye; it’s also a tissue with more than a hundred types of neurons that help the brain process visual surroundings.

“The retina we see in textbooks is a glorified camera,” said Gregory Schwartz, PhD, assistant professor of Ophthalmology and Physiology. “But that’s not even close to right. The retina is actually the most advanced image-processing machine in the world.”

With a recent five-year, $2.3 million grant from the National Institutes of Health, Schwartz aims to map out all the neural circuits through which the retina transmits information such as color, contrast, motion, direction and location. His findings could eventually inform clinical interventions for blindness, including sophisticated retinal prosthetics to restore vision.

Read the full story and watch a video here.


The cerebellum from an animal early in the demyelinating phase of late-onset multiple sclerosis. The green marks myelinated axons and the red highlights areas of inflammation and demyelination.
The cerebellum from an animal early in the demyelinating phase of late-onset multiple sclerosis. The green marks myelinated axons and the red highlights areas of inflammation and demyelination.

How Multiple Sclerosis Can Be Triggered By Brain Cell Death

Multiple sclerosis (MS) may be triggered by the death of brain cells that make the insulation around nerve fibers, a surprising new view of the disease reported in a study from Northwestern Medicine and The University of Chicago. An experiment in the study also showed that a specially developed nanoparticle prevented MS even after the death of those brain cells.

The nanoparticles are being developed for clinical trials that could lead to new treatments – without the side effects of current therapies – in adults.

Stephen Miller, PhD, Judy Gugenheim Research Professor of Microbiology-Immunology, led the study, which was published in Nature Neuroscience.

Read the full story here.