Degradation rate is an important property to evaluate bioabsorbable metallic material; however, values vary depending on the method of measurement. In this study, three different methods of measuring corrosion rate are compared. The degradable samples to analyze corrosion rates include pure magnesium (Mg), lab produced Mg–Zn–Ca alloy (47-7-2), Mg–Zn–Zr–RE (rare earth) alloys (60-13, 60-14), Mg–Zn–Ca–RE alloy (59B), and pure zinc (Zn). A eudiometer was used to measure hydrogen evolution from the reaction of degradable alloys in Hank’s Balanced Salt Solution (HBSS). Corrosion rates based on volume loss of tested alloys in 30 days were calculated using Micro-computed tomography (micro-CT). Final mass change due to corrosion and corrosion removal was measured with a scale. We observed that the corrosion rates indicated by hydrogen evolution were high initially, and slowed down sharply in the following measurements. The corrosion rates of tested alloys calculated by volume loss and mass loss from high to low are: 60–13 ≈ 60–14 ≈ 47–7–2 > 59B > Mg > Zn (p < 0.05). The results provide instruction to experimental methodology to measure corrosion rates of degradable alloys.

The biodegradable ability of magnesium alloys is an attractive feature for tracheal stents since they can be absorbed by the body through gradual degradation after healing of the airway structure, which can reduce the risk of inflammation caused by long-term implantation and prevent the repetitive surgery for removal of existing stent. In this study, the effects of bicarbonate ion (HCO₃⁻) and mucin in Gamble’s solution on the corrosion behavior of AZ31 magnesium alloy were investigated, using immersion and electrochemical tests to systematically identify the biodegradation kinetics of magnesium alloy under in vitro environment, mimicking the epithelial mucus surfaces in a trachea for development of biodegradable airway stents. Analysis of corrosion products after immersion test was performed using scanning electron microscopy (SEM), energy dispersive X-ray spectroscopy (EDX) and X-ray diffraction (XRD). Electrochemical impedance spectroscopy (EIS) was used to identify the effects of bicarbonate ions and mucin on the corrosion behavior of AZ31 magnesium alloys with the temporal change of corrosion resistance. The results show that the increase of the bicarbonate ions in Gamble’s solution accelerates the dissolution of AZ31 magnesium alloy, while the addition of mucin retards the corrosion. The experimental data in this work is intended to be used as foundational knowledge to predict the corrosion behavior of AZ31 magnesium alloy in the airway environment while providing degradation information for future in vivo studies.

The influence of diet on the development of osteoporosis is significant and not fully understood. This study investigated the effect of diets of varying lipid profiles and ω-3, ω-6 and ω-9 composition on the structural and mechanical properties of bone. The hypothesis studied was that a diet high in saturated fat would induce osteoporosis and produce an overall increased detrimental bony response when compared with a diet high in unsaturated ω-6, or ω-9. Male C57BL/6J mice were fed either a control diet, 50:50 mix (saturated:unsaturated) high in ω-9 (HFD^50:50), a diet high in saturated fat (HSF) or a polyunsaturated fat diet high in ω-6 (PUFA) over an 8-week duration. Tibiae were retrieved and evaluated using DMA, 3-point-bending, histomorphometry, and microCT. Mice fed a HSF diet displayed key features characteristic of osteoporosis. The loss tangent was significantly increased in the HFD^50:50 diet group compared with control (p = 0.016) and PUFA-fed animals (p = 0.049). HFD^50:50-fed mice presented with an increased viscous component, longer tibiae, increased loss modulus (p = 0.009), and ultimate stress, smaller microcracks (p < 0.001), and increased trabecular width (p = 0.002) compared with control animals. A diet high in ω-9 resulted in an overall superior bone response and further analysis of its role in bone health is warranted.

The disruption of the blood–brain barrier (BBB) in Alzheimer’s Disease (AD) is largely influenced by amyloid beta (Aβ). In this study, we developed a high-throughput microfluidic BBB model devoid of a physical membrane, featuring endothelial cells interacting with an extracellular matrix (ECM). This paper focuses on the impact of varying concentrations of Aβ_1–42 oligomers on BBB dysfunction by treating them in the luminal. Our findings reveal a pronounced accumulation of Aβ_1–42 oligomers at the BBB, resulting in the disruption of tight junctions and subsequent leakage evidenced by a barrier integrity assay. Additionally, cytotoxicity assessments indicate a concentration-dependent increase in cell death in response to Aβ_1–42 oligomers (LC50 ~ 1 µM). This study underscores the utility of our membrane-free vascular chip in elucidating the dysfunction induced by Aβ with respect to the BBB.

Few studies have investigated the effect of a monosaturated diet high in ω-9 on osteoporosis. We hypothesized that omega-9 (ω-9) protects ovariectomized (OVX) mice from a decline in bone microarchitecture, tissue loss, and mechanical strength, thereby serving as a modifiable dietary intervention against osteoporotic deterioration. Female C57BL/6J mice were assigned to sham-ovariectomy, ovariectomy, or ovariectomy + estradiol treatment prior to switching their feed to a diet high in ω-9 for 12 weeks. Tibiae were evaluated using DMA, 3-point-bending, histomorphometry, and microCT. A significant decrease in lean mass (p = 0.05), tibial area (p = 0.009), and cross-sectional moment of inertia (p = 0.028) was measured in OVX mice compared to the control. A trend was seen where OVX bone displayed increased elastic modulus, ductility, storage modulus, and loss modulus, suggesting the ω-9 diet paradoxically increased both stiffness and viscosity. This implies beneficial alterations on the macro-structural, and micro-tissue level in OVX bone, potentially decreasing the fracture risk. Supporting this, no significant differences in ultimate, fracture, and yield stresses were measured. A diet high in ω-9 did not prevent microarchitectural deterioration, nevertheless, healthy tibial strength and resistance to fracture was maintained via mechanisms independent of bone structure/shape. Further investigation of ω-9 as a therapeutic in osteoporosis is warranted.

Traumatic brain injury (TBI) presents a major biomedical challenge due to its complex biomechanics and the heterogeneous cellular responses it elicits, including neuronal death, glial activation, and blood–brain barrier disruption. Traditional in vitro models, including 2D neuronal cultures, brain slices and transwell systems, have provided valuable insights into molecular and cellular biology but remain limited by their lack of human-specific architecture, vascularization, and neurovascular interactions. The purpose of this review is to systematically examine advances in in vitro TBI modeling, with particular attention to studies leveraging human induced pluripotent stem cell (iPSC)-derived neural and vascular tissues, organoids, hydrogel scaffolds, microfluidic platforms, and mechanical injury. We highlight how the integration of neurovascular unit (NVU) components has improved the physiological and functional relevance of these models. Finally, we identify key limitations, including variability in organoid maturation, incomplete vascularization, and lack of methodological standardization, and outline future directions for improving translational fidelity. Therefore, this review contributes to a critical evaluation of emerging technologies and their potential to advance neurotrauma research and therapeutic discovery.