Glioblastoma cells spreading through a fly brain. A poxvirus evading detection by its host cell. Novel synthetic materials self-assembling into molecular superstructures.

These images — and many more like them — helped bring to life the high-impact scientific discoveries made at Feinberg this year.

As 2018 comes to a close, we’re sharing a selection of some of the most stunning images of the year:

New Bio-Inspired Dynamic Materials Transform Themselves

Scanning electron micrograph revealed self-assembled superstructures (colored regions) formed by the surprising dynamics of molecules containing peptide and DNA segments. The superstructures are embedded in a matrix of peptide filaments.

Northwestern University scientists developed soft materials that autonomously self-assemble into molecular superstructures and remarkably disassemble on demand, changing the properties of materials and opening the door for novel materials in applications ranging from sensors and robotics to new drug delivery systems and tools for tissue regeneration.

The findings were published in the journal Science.

“We are used to thinking of materials as having a static set of properties,” said Samuel Stupp, PhD, director of the Simpson Querrey Institute for BioNanotechnology and co-corresponding author of the paper. “We’ve demonstrated that we can create highly dynamic synthetic materials that can transform themselves by forming superstructures and can do so reversibly on demand, which is a real breakthrough with profound implications.”

DNA Methylation Plays Key Role in Stem Cell Differentiation

Northwestern Medicine scientists discovered how the process of DNA methylation regulates the development of spinal cord motor neurons, in a study published in the journal Cell Stem Cell.

DNA methylation, an epigenetic mechanism that determines whether or not a gene is expressed, guides stem cells as they transform from blank slates into specialized cells. Motor neurons are highly specialized neuronal cells that connect the central nervous system to muscle and degenerate in amyotrophic lateral sclerosis (ALS).

Evangelos Kiskinis, PhD, assistant professor of Neurology in the Division of Neuromuscular Disease and of Physiology, was senior author of the study.

Caption: Neural progenitors cells differentiated from human embryonic stem cells.

Origin of Neuromodulator in the Retina Pinpointed

A single cell type in the inner retina controls the release of nitric oxide, a neuromodulator that impacts synaptic transmission and regulates blood vessel dilation, according to a study published in Neuron.

Nitric oxide’s role in blood vessel regulation means those cells, a specific kind of amacrine cell called nNOS-2, could be used to help diagnose blood vessel disorders or even as targets for future therapies

Gregory Schwartz, PhD, assistant professor of Ophthalmology, was senior author of the study.

Caption: This image shows a dense gap-junction network formed between nNOS-2 amacrine cells, the main source of the neuromodulator nitric oxide in the mouse retina. Here, a single nNOS-2 amacrine cell was patched and filled with Alexa Fluor 488 to reveal this network when imaged with a multiphoton laser. The large molecule fluorescent dye Alexa Fluor 488 readily passes through nNOS-2 amacrine cell gap junctions when they are in the most open state in dark conditions.

Regenerative Bandage Accelerates Healing in Diabetic Wounds

For diabetic patients, an untreated scratch can turn into an open wound that could potentially lead to a limb amputation or even death. A Northwestern University team developed a new device, called a regenerative bandage, that quickly heals these painful, hard-to-treat sores without using drugs.

A study published in Proceedings of the National Academy of Sciences found that Northwestern’s bandage healed diabetic wounds 33 percent faster than one of the most popular bandages currently on the market.

Guillermo Ameer, ScD, professor in the McCormick School of Engineering and of Surgery in the Division of Vascular Surgery, led the study.

Caption: The secret behind the regenerative bandage is laminin, a protein that sends signals to cells, encouraging them to differentiate, migrate and adhere to one another. Ameer’s team identified a segment of laminin called A5G81 that is critical for the wound-healing process. The image shows stained epidermis cells cultured on the A5G81 peptide.

Chromosome Domain Inherits Information Without Using DNA Sequence

The centromeric nucleosomes, containing CENP-A (red), must be retained in the preceding S-phase for the centromere to correctly assemble and segregate chromosomes during mitosis. Loss of centromere function leads to chromosome instability, which is a common characteristic of cancer cells.

Northwestern Medicine scientists discovered an epigenetic mechanism that preserves chromatin domains called centromeres during the process of DNA replication. The study was published in the journal Developmental Cell.

According to Daniel Foltz, PhD, associate professor of Biochemistry and Molecular Genetics and senior author of the study, the findings shed light on a system that may lead to cancer when defective.

Increased Cell Recycling Could Treat Aging-Related Conditions

Mice engineered to more quickly recycle their own cells lived longer than their non-engineered siblings, according to a study published in Nature.

These findings suggest that autophagy, the system of cell recycling and housekeeping, may be responsible for functional declines associated with aging, according to CongCong He, PhD, assistant professor of Cell and Molecular Biology and a co-author of the study. In fact, reinstating higher rates of autophagy may be an effective way to treat aging-related diseases.

Caption: Fasting for 24 hours induced dramatic formation of autophagic vesicles (green dots, labeled by a marker protein LC3 tagged with the green fluorescent protein) in skeletal muscle. Blue indicates stained nuclei.

Enzyme Blocker Stops Growth of Deadly Brain Tumor

Investigators were able to halt the growth of glioblastoma, an aggressive form of brain cancer, by inhibiting an enzyme called CDK5. The findings were published in Cell Reports.

The discovery of this enzyme’s regulatory influence on glioblastoma may open the door to a long-awaited improvement upon current therapy options, according to Subhas Mukherjee, PhD, research assistant professor of Pathology and first author of the study. Daniel Brat, MD, PhD, chair and Magerstadt Professor of Pathology, was senior author of the study.

Caption: Glioblastoma cells (orange) spread throughout a fly brain (normal cells in blue), used to model human cancer.

The image was also featured on the cover of the Fall 2018 issue of Northwestern Medicine magazine.

Cellular Mechanism Protects Organs During Iron Deficiency

Scientists discovered a protective cellular mechanism that kicks in during iron deficiency, keeping cells running even in the face of continued iron deprivation, according to a study published in the Proceedings of the National Academy of Sciences.

The protein, called tristetraprolin (TTP), is activated during iron deficiency, and lowers iron usage to match availability and prevents mitochondrial dysfunction. Hossein Ardehali, MD, PhD, professor of Medicine in the Division of Cardiology and of Pharmacology, was senior author of the study.

Caption: Image of mitochondria in heart cells after the levels of TTP (the master regulator of cellular iron conservation) are reduced.

Exploring the Mechanisms of Poxvirus Replication

A study published in the journal Cell uncovered how poxviruses take control of a protein complex called mTOR in order to enhance their replication and counteract a host’s immune response.

The study was led by principal investigator Derek Walsh, PhD, along with Mojgan Naghavi, PhD, both associate professors of Microbiology-Immunology.

The scientists sought to understand how poxviruses exploit mTOR — a protein complex which regulates cellular metabolism and protein synthesis — and evade being sensed by host cells.

Caption: During poxvirus infection, dysregulated mTOR (orange) localizes at the host-cell golgi network resulting in degradation of the DNA sensor, cGAS (green).

Human Stem Cell Model Reveals Mechanisms of Herpes Infection

These images illustrate the difference in susceptibility to HSV-1 infection — indicated by orange staining — between central nervous system neurons (left) and peripheral nervous system neurons (right) in iPSC-derived neurons from a control patient without TLR3 mutations (green staining for neuronal marker and blue for DNA).

A team of scientists developed a novel stem cell model to demonstrate that a pathway protecting neurons in the brain from herpes simplex virus 1 (HSV-1) infection does not exist in neurons throughout the rest of the body.

The study, published in Proceedings of the National Academy of Sciences, helps explain why the virus is common in the peripheral nervous system but rarely infects the brain, and it provides new insights into mechanisms of HSV-1 encephalitis — a rare and deadly viral-induced inflammation of the brain.

Gregory Smith, PhD, professor of Microbiology-Immunology, was a principal investigator of the study. Osefame Ewaleifoh, a PhD/MPH student in the Driskill Graduate Program in Life Sciences (DGP), was a co-first author.

Brat, Foltz, He, Naghavi, Smith, Stupp and Walsh are also members of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.

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