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Quantum biology studies span multiple disciplines including physics, engineering, and biology with the goal of understanding the quantum underpinnings of living systems. Recent findings have brought wide attention to the role of quantum mechanisms in the function and regulation of biological processes. Moreover, a number of activities have been integral in building a vibrant quantum biology community. Due to the inherent interdisciplinary nature of the field, it is a challenge for quantum biology researchers to integrate and advance findings across the physical and biological disciplines. Here we outline achievable approaches to developing a shared platform—including the establishment of standardized manipulation tools and sensors, and a common scientific lexicon. Building a shared community framework is also crucial for fostering robust interdisciplinary collaborations, enhancing knowledge sharing, and diversifying participation in quantum biology. A unified approach promises not only to deepen our understanding of biological systems at a quantum level but also to accelerate the frontiers of medical and technological innovations. 

Recent studies have furthered our understanding of how dying and living cells interact in different physiological contexts, however the signaling that initiates and mediates apoptosis and apoptosis-induced proliferation are more complex than previously thought. One increasingly important area of study is the biophysical control of apoptosis. In addition to biochemical regulation, biophysical signals (including redox chemistry, bioelectric gradients, acoustic and magnetic stimuli) are also known yet understudied regulators of both cell death and apoptosis-induced proliferation. Mounting evidence suggests biophysical signals may be key targets for therapeutic interventions. This review highlights what is known about the role of biophysical signals in controlling cell death mechanisms during development, regeneration, and carcinogenesis. Since biophysical signals can be controlled spatiotemporally, bypassing the need for genetic manipulation, further investigation may lead to fine-tuned modulation of apoptotic pathways to direct desired therapeutic outcomes. 

Reactive oxygen species (ROS) signaling regulates cell behaviors and tissue growth in development, regeneration, and cancer. Commonly, ROS are modulated pharmacologically, which while effective comes with potential complications such as off-target effects and lack of drug tolerance. Thus, additional non-invasive therapeutic methods are necessary. Recent advances have highlighted the use of weak magnetic fields (WMFs, <1 mT) as one promising approach. We previously showed that 200 μT WMFs inhibit ROS formation and block planarian regeneration. However, WMF research in different model systems at various field strengths have produced a range of results that do not fit common dose response curves, making it unclear if WMF effects are predictable. Here, we test hypotheses based on spin state theory and the radical pair mechanism, which outlines how magnetic fields can alter the formation of radical pairs by changing electron spin states. This mechanism suggests that across a broad range of field strengths (0–900 μT) some WMF exposures should be able to inhibit while others promote ROS formation in a binary fashion. Our data reveal that WMFs can be used for directed manipulation of stem cell proliferation, differentiation, and tissue growth in predictable ways for both loss and gain of function during regenerative growth. Furthermore, we examine two of the most common ROS signaling effectors, hydrogen peroxide and superoxide, to begin the identification and elucidation of the specific molecular targets by which WMFs affect tissue growth. Together, our data reveal that the cellular effects of WMF exposure are highly dependent on ROS, and we identify superoxide as a specific ROS being modulated. Altogether, these data highlight the possibilities of using WMF exposures to control ROS signaling in vivo and represent an exciting new area of research. 

Non-ionizing radiation is commonly used in the clinical setting, despite its known ability to trigger oxidative stress and apoptosis, which can lead to damage and cell death. Although induction of cell death is typically considered harmful, apoptosis can also be beneficial in the right context. For example, cell death can serve as the signal for new tissue growth, such as in apoptosis-induced proliferation. Recent data has shown that exposure to non-ionizing radiation (such as weak static magnetic fields, weak radiofrequency magnetic fields, and weak electromagnetic fields) is able to modulate proliferation, both in cell culture and in living organisms (for example during tissue regeneration). This occurs via in vivo changes in the levels of reactive oxygen species (ROS), which are canonical activators of apoptosis. This review will describe the literature that highlights the tantalizing possibility that non-ionizing radiation could be used to manipulate apoptosis-induced proliferation to either promote growth (for regenerative medicine) or inhibit it (for cancer therapies). However, as uncontrolled growth can lead to tumorigenesis, much more research into this exciting and developing area is needed in order to realize its promise. 

Abstract The COVID‐19 pandemic forced educators to teach in an online environment. This was particularly challenging for those teaching courses that are intended to support bench science research. This practitioner article tells the story of how an instructor transformed their Course‐based Undergraduate Research Experience (CURE) using the Backwards Design Method into a synchronous online course. Research objectives in this transformed course included: conducting a literature review, identifying research questions and hypotheses based on literature, and developing practical and appropriate research methodologies to test these hypotheses. We provide details on how assignments were created to walk students through the process of research study design and conclude with recommendations for the implementation of an online CURE. Recommendations made by the instructor include scaffolding the design, building opportunities for collaboration, and allowing students to fail in order to teach the value of iteration. The Backwards Design framework naturally lends itself to a scaffolded instructional approach. By identifying the learning objectives and final assessment, the learning activities can be designed to help students overcome difficult concepts by filling in the gaps with purposeful instruction and collaborative opportunities. This present course also practiced iteration through the extensive feedback offered by the instructor and opportunities for students to revise their work as their understanding deepened. Anecdotally, based on end of course reviews, students overall had a positive experience with this course. Future work will examine the efficacy of student learning in this online environment and is forthcoming. 

Biological systems are constantly exposed to electromagnetic fields (EMFs) in the form of natural geomagnetic fields and EMFs emitted from technology. While strong magnetic fields are known to change chemical reaction rates and free radical concentrations, the debate remains about whether static weak magnetic fields (WMFs; <1 mT) also produce biological effects. Using the planarian regeneration model, we show that WMFs altered stem cell proliferation and subsequent differentiation via changes in reactive oxygen species (ROS) accumulation and downstream heat shock protein 70 (Hsp70) expression. These data reveal that on the basis of field strength, WMF exposure can increase or decrease new tissue formation in vivo, suggesting WMFs as a potential therapeutic tool to manipulate mitotic activity.