A new research project at the New Jersey Institute of Technology is taking a closer look at a strange but important behavior in rubber-like materials: their properties can depend on what happened to them before. With a $125,000 New Directions grant from the American Chemical Society Petroleum Research Fund, chemical and materials engineering professor Gennady Gor and his students will investigate how petroleum-derived polymers absorb fluids, swell, contract and change their elasticity over time. The work could improve predictions of how elastomers perform in everything from industrial seals to oil and gas equipment.

Elastomers are polymers capable of undergoing large, reversible deformations. Silicone, neoprene and natural or synthetic rubber are familiar examples. Their molecular chains can stretch, rearrange and return toward their original configuration, giving these materials their characteristic flexibility. Yet exposure to liquids or vapors can dramatically alter that behavior. Hydrocarbon molecules may enter the polymer network, pushing molecular chains apart and causing the material to expand. At the same time, the absorbed fluid can change the polymer’s stiffness, strength and ability to recover its original shape.

Gor’s project focuses on a phenomenon known as hysteresis, in which a material’s current state depends not only on its present conditions but also on the path it took to reach them. For an elastomer, that means the material may respond differently when it is swelling than when it is shrinking, even if its size and surrounding environment are identical. The difference can arise from molecular rearrangements, delayed relaxation or changes in the interactions between polymer chains and absorbed molecules. Such path-dependent behavior is central to understanding why materials sometimes fail to return fully to their previous mechanical state.

The question is especially relevant for petroleum-related technologies. Elastomers are widely used as O-rings, gaskets and seals because they can deform to fill microscopic gaps and maintain a hermetic barrier. In oil and gas environments, however, these components may encounter complex mixtures of hydrocarbons under pressure and at elevated temperatures. If a seal swells excessively, softens or loses its ability to recover after repeated exposure, it can become unreliable. A better understanding of hysteresis could help engineers select materials and operating conditions that reduce leakage and extend component lifetimes.

The new study represents a shift for Gor’s Laboratory for Materials Interfaces. His previous research has largely examined porous adsorbent materials, which collect molecules on their internal surfaces. Elastomers are different: they do not need pores to take up substantial amounts of fluid. Instead, molecules diffuse into the polymer matrix and interact with its flexible chains. The resulting process is more like a sponge absorbing liquid, although the molecular mechanisms are governed by diffusion, thermodynamics and the elasticity of the polymer network.

Günel Nabiyeva, a fourth-year doctoral student, will lead much of the experimental effort with undergraduate chemical engineering student Elitsa Mileva and second-year doctoral student Supun Rangana. The team has already begun collecting data on how rubber deforms in the presence of liquids and vapors. For Mileva, who has spent considerable time reviewing the scientific literature, the grant will provide an opportunity to move deeper into laboratory work. Nabiyeva describes the project as a new system for the research group because the laboratory has not previously studied elastomers in this way.

The researchers will expose polymer samples to controlled concentrations of hydrocarbon vapors and track how the materials respond. Their measurements will combine swelling, fluid uptake and elasticity rather than treating these properties separately. This approach is essential because a polymer can gain mass and volume while simultaneously becoming softer or, under some conditions, displaying a more complicated mechanical response. Different hydrocarbons may produce different results because their molecular size, chemical structure and compatibility with the polymer influence how quickly they enter the material and how strongly they interact with its chains.

Rangana will contribute expertise in ultrasonic sensing, which can measure subtle changes without physically contacting or damaging the sample. Ultrasonic waves travel through a material in ways that depend on its density, structure and mechanical properties. By analyzing changes in wave transmission or reflection, scientists can detect variations in stiffness and internal condition with high precision. Coupling these measurements to vapor exposure could reveal how quickly elasticity changes as molecules enter the polymer and whether the material follows the same path during desorption as it did during absorption.

The team hopes its results will fill a gap in the fundamental understanding of polymer hysteresis. Although hysteresis is well known in many areas of physics and engineering, relatively few studies have examined how history-dependent elasticity develops in swollen elastomers. The new measurements may help distinguish reversible molecular motions from more persistent structural changes and improve models used to predict polymer performance. Ultimately, the researchers aim to make elastomer behavior less mysterious and more reliable, helping engineers design seals and flexible components that remain dependable across repeated cycles of chemical exposure, swelling and recovery.

Subject of Research: Elastomers, petroleum-derived polymers, polymer swelling, elasticity and hysteresis

Article Title: Ultrasonic Experiments Aim to Reveal Why Rubber Remembers Its History

Web References: Gennady Gor’s NJIT profile; NJIT Laboratory for Materials Interfaces

Image Credits: Courtesy of New Jersey Institute of Technology

Keywords

Elastomers, polymers, hysteresis, rubber, polymer swelling, ultrasonic sensors, materials science, chemical engineering, petroleum research, NJIT

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A new study has brought scientists closer to observing how inflammation during pregnancy may alter the earliest stages of human brain development. Using three-dimensional tissue models made from human fetal brain samples, researchers modeled maternal immune activation and identified the signaling molecule interleukin-17A, or IL-17A, as a major driver of abnormal cortical development. The findings, published in Nature Neuroscience, offer a human-based experimental system for investigating how immune signals outside the brain can influence the formation of neural circuits before birth.

Maternal immune activation refers to the biological response triggered when a pregnant individual experiences infection or significant inflammation. Epidemiological studies have associated certain prenatal inflammatory exposures with an increased likelihood of neurodevelopmental conditions, including autism spectrum disorder, schizophrenia, and intellectual disability. Yet the mechanisms behind these associations have remained difficult to study. Animal models have provided important clues, but differences between species can limit their ability to reproduce the timing, cellular organization, and molecular environment of the developing human cortex.

The researchers addressed this challenge with “brain cerebroids,” three-dimensional, ex vivo models that preserve features of developing human fetal brain tissue. Unlike simplified cultures composed of a single cell type, these structures retain a more complex arrangement of neural progenitors, immature neurons, and supporting cells. Their three-dimensional architecture allows cells to communicate and organize in ways that more closely resemble the fetal cortex, including the production and movement of neurons that ultimately establish the layered structure of the brain’s outer region.

To recreate aspects of maternal immune activation, the team exposed the fetal brain cerebroids to inflammatory conditions associated with immune signaling during pregnancy. The central focus was IL-17A, a cytokine produced primarily by activated immune cells, particularly a subset of T cells known as T helper 17 cells. Cytokines are small signaling proteins that coordinate immune responses, but they can also affect tissues beyond the immune system. In the developing brain, inappropriate or excessive exposure to such signals may influence cell proliferation, migration, differentiation, and the formation of connections between neurons.

The study found that IL-17A exposure was linked to disruptions in cortical development within the human cerebroids. These effects are described as “IL-17A-driven,” indicating that the cytokine was not merely associated with the developmental changes but played a functionally important role in producing them. The disturbances affected the organization and behavior of developing neural cells, processes that are essential for building the cortex. During normal development, neural progenitor cells generate new neurons in tightly regulated sequences, while young neurons migrate to their appropriate positions. Interference with either process can alter the structure and connectivity of later-forming brain tissue.

The results are especially significant because they were observed in human fetal brain material rather than inferred only from animal studies. Previous research in mice has implicated maternal immune activation and IL-17A in changes to cortical organization and behavior in offspring. However, the human cerebroid model provides an opportunity to examine whether similar immune mechanisms operate in human tissue, where the timing of neurogenesis, cell-type composition, and cortical architecture differ from those of rodents. The approach may also help reveal human-specific responses that conventional laboratory animals cannot capture.

The findings do not mean that IL-17A exposure during pregnancy inevitably causes a neurodevelopmental condition, nor do they establish that prenatal inflammation is a single explanation for such conditions. Brain development is shaped by a combination of genetic factors, immune signals, environmental influences, and developmental timing. The experiments also took place in an ex vivo model, outside the full physiological environment of a living pregnancy. Cerebroids cannot reproduce the placenta, maternal circulation, hormonal changes, or the complete immune system, all of which influence how inflammatory signals reach the fetus and how long they remain active.

Nevertheless, the model could become a powerful platform for testing mechanisms and potential interventions. Researchers may use it to determine how IL-17A changes gene activity in neural progenitors, whether it alters communication between neurons and glial cells, and which molecular pathways make some developing cells more vulnerable than others. Because the tissue is human and three-dimensional, it may also support studies of patient-specific genetic risk, allowing investigators to compare how different backgrounds respond to the same inflammatory signal.

The work also highlights a broader shift in neuroscience toward experimental systems that combine human tissue with controlled laboratory manipulation. Understanding prenatal inflammation is difficult in clinical studies because immune exposure cannot be ethically assigned or precisely timed in pregnant people. Brain cerebroids offer a way to isolate individual components of that complex biology while preserving more of the developing tissue’s natural organization than conventional two-dimensional cell cultures. As these models improve, they may help distinguish temporary developmental changes from persistent alterations in cortical circuitry and identify when immune signaling is most consequential.

By showing that IL-17A can disrupt human cortical development in a three-dimensional ex vivo system, the study gives researchers a clearer biological target in the search for links between prenatal inflammation and later neurodevelopment. Its most immediate contribution is not a new diagnosis or treatment, but a more precise experimental framework: one that connects maternal immune signaling to cellular events in the developing human cortex. That connection could guide future work on prevention, therapeutic timing, and the complex origins of developmental differences long before the first symptoms become visible.

Subject of Research: Maternal immune activation and IL-17A-driven disruption of human fetal cortical development in 3D ex vivo brain cerebroids.

Article Title: Modeling maternal immune activation in 3D ex vivo human fetal brain cerebroids reveals IL-17A-driven disruption of cortical development.

Article References: Assir, M.Z.K., Yanakiev, M., Gim, D.H. et al. Modeling maternal immune activation in 3D ex vivo human fetal brain cerebroids reveals IL-17A-driven disruption of cortical development. Nature Neuroscience (2026). https://doi.org/10.1038/s41593-026-02400-2

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41593-026-02400-2

Keywords: maternal immune activation, IL-17A, fetal brain development, cortical development, brain cerebroids, neurodevelopment, prenatal inflammation, human brain models, cytokines, neuroscience

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