As the world shifts towards greener transportation solutions, electric vehicles (EVs) are at the forefront of this transformation. However, one of the significant challenges facing EVs is the reliability and longevity of their lithium-ion batteries. A recent study by researchers from the Department of Electrical Engineering at Amirkabir University of Technology introduces a novel method for detecting faults in both new and aged lithium-ion battery cells, ensuring the safety and efficiency of EVs throughout their lifespan.

As the demand for electric vehicles (EVs) continues to surge, ensuring the efficiency and safety of their battery systems has become a critical focus for researchers. A groundbreaking study from the Training and Workshops Center at the University of Technology, Baghdad, Iraq, introduces an innovative approach to predicting thermal heat flux distribution in EV battery cells. By combining finite element analysis (FEA) with neural network (NN) models, this research promises to enhance battery performance and longevity, paving the way for more reliable and sustainable electric transportation.

New research identifies the liver protein PTPRD as a key regulator of metabolic liver disease. Reduced levels of PTPRD disrupt glucose and lipid metabolism, promote liver fat accumulation, and impair insulin signaling. The findings indicate the potential of restoring PTPRD function as a novel treatment strategy for non-viral liver conditions such as MASLD and MASH.

A Chinese research team has successfully developed a triplex real-time quantitative fluorescence PCR method capable of simultaneously detecting three critical drug resistance genes—mcr-1, vanA, and bla_NDM-1. This method demonstrates high sensitivity, strong specificity, and excellent reproducibility, offering an efficient tool for rapid detection of drug resistance genes in clinical and food safety applications.

Bone adapts according to the mechanical environment, and this adaptation can be visualized by altering its shape, size, and microarchitecture. Bone adaptation was recognized more than a century ago, with a description presented in The Law of Bone Remodeling. Furthermore, the conceptual model of “The Mechanostat” provides a quantitative relationship between the magnitude of bone tissue deformation (strain) and bone adaptive responses. However, upon maintaining a constant strain magnitude, various bone responses were observed experimentally under different loading parameters (e.g., frequency, rate, number of load cycles, rest insertion, and waveform). Nevertheless, the precise relationship between mechanical signals and bone adaptation remains unclear. Accordingly, we reviewed in vivo loading studies to determine the quantitative relationships between various mechanical signals and bone adaptive responses in various animal loading models. Additionally, we explored how these relationships are influenced by pathophysiological factors, such as age, sex, and estrogen deficiency. Moreover, mechanistic studies that consider cellular mechanical microenvironments to explain these quantitative relationships are discussed. A general formula that considers the bone adaptive response as a function of different loading parameters was proposed. This review may enhance our understanding of bone adaptation and offer guidance for clinicians to develop effective mechanotherapies to prevent bone loss.

Aged individuals and astronauts experience bone loss despite rigorous physical activity. Bone mechanoresponse is in-part regulated by mesenchymal stem cells (MSCs) that respond to mechanical stimuli. Direct delivery of low intensity vibration (LIV) recovers MSC proliferation in senescence and simulated microgravity models, indicating that age-related reductions in mechanical signal delivery within bone marrow may contribute to declining bone mechanoresponse. To answer this question, we developed a 3D bone marrow analog that controls trabecular geometry, marrow mechanics and external stimuli. Validated finite element (FE) models were developed to quantify strain environment within hydrogels during LIV. Bone marrow analogs with gyroid-based trabeculae of scaffold volume fractions (SV/TV) corresponding to adult (25 ​%) and aged (13 ​%) mice were printed using polylactic acid (PLA). MSCs encapsulated in migration-permissive hydrogels within printed trabeculae showed robust cell populations on both PLA surface and hydrogel within a week. Following 14 days of LIV treatment (1 ​g, 100 ​Hz, 1 ​h/day), cell proliferation, type-I collagen (Collagen-I) and filamentous actin (F-actin) were quantified for the cells in the hydrogel fraction. While LIV increased all measured outcomes, FE models predicted higher von Mises strains for the 13 ​% SV/TV groups (0.2 ​%) when compared to the 25 ​% SV/TV group (0.1 ​%). While LIV increased collagen-I volume 34 ​% more in 13 ​% SV/TV groups when compared to 25 ​% SV/TV groups, collagen-I and F-actin measures remained lower in the 13 ​% SV/TV groups when compared to 25 ​% SV/TV counterparts, indicating that both LIV-induced strains and scaffold volume fraction (i.e. available scaffold surface) affect cell behavior in the hydrogel phase. Overall, bone marrow analogs offer a robust and repeatable platform to study bone mechanobiology.