Wednesday, November 26, 2025


Do children imitate communication manners of machines? Experiment on children's response to polite vs. commanding robot





SWPS University

Konrad Maj (Ph.D.) and Pepper 

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Konrad Maj (Ph.D.), social psychologist, SWPS University and humanoid robot Pepper

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Credit: Credit: SWPS University





The presence of robots in schools is no longer surprising. How do elementary school children treat humanoid robots? Are they polite to them, and willing to attribute human-like qualities to them? Researchers from SWPS University have shown that in most cases, children treat robots politely, and younger children and girls are more likely to perceive them as possessing human-like qualities.

The fourth edition of the international HumanTech Summit, organized at SWPS by the HumanTech Center, took place in Warsaw on November 20-22, 2025. Interactions with robots were among the topics discussed during the event.

Social robots, ones that support people in everyday life, are increasingly finding roles in educational settings. We already know that robots and virtual assistants can support constructive educational outcomes and healthy social development in children. It also turns out that they can increase children's engagement in learning.

Robots in education can be programmed in a variety of ways. For example, they can adapt teaching methods to individual students' needs, boost students' motivation and engagement through fun, or provide immediate feedback. However, it is important to remember that interactions with robots also raise certain concerns, such as whether prolonged contact with them will negatively impact children's social behaviour, emphasises Konrad Maj, PhD, first author of the study, a social psychologist and head of the HumanTech Center for Social and Technological Innovation.

It is therefore important to understand how children interact with them and in what situations interactions with robots are most beneficial. This is the focus of researchers from SWPS University: Konrad Maj, Ariadna Gołębicka, and Zuzanna Siwińska in a new study described in the paper "How children learn from robots: Educational implications of communicative style and gender in child–robot interaction”, published in Computers & Education.

How do children react to humanoid robots?

In the study, the researchers used a 120-centimeter tall humanoid robot Pepper (created by SoftBank Robotics) with a child-like appearance. Designed for social engagement, the device is equipped with sensors, cameras, and microphones. These features enable Pepper to recognize speech, gestures, and some emotional cues. The study participants included 251 children aged 7-12.

The researchers considered two aspects: the robot's communicative style toward humans (polite or commanding) and its "gender" (female or male), which they determined by giving the robot a name (Adam or Ada). They chose these variables because they directly influence how children interpret the robot’s intentions, warmth, and authority, which affects both engagement and academic performance. This could be important in the future design of social robots.

The researchers wondered, among other things, whether children treated politely by a robot would also be polite to it. They also wanted to find out whether younger children would be more inclined to anthropomorphise the robot (attribute human-like qualities to it) than older children, and whether girls would be more likely to do so than boys.

During the study, children were introduced to a robot that imitated animals for them, observed its reaction to an attempt to take its photo (either polite or with a firm message not to do so), to which they were instructed to respond. They then answered questions about Pepper. They were asked, for example, whether they thought the robot could be happy, whether it could dream or imagine things.  

How will children imitate a robot that politely asks requests or commands?

It turned out that children interacting with a polite robot almost always responded to it politely. Those addressed by the robot in a commanding manner also responded politely in most cases, rather than imitating its authoritarian communication style, indicating that in this case, established social norms prevailed over imitation.

Younger children and girls were significantly more likely to anthropomorphise the robot. It also turned out that polite robots were more likely to be attributed human-like qualities than commanding ones, especially when their tone matched gender expectations. Anthropomorphisation was most likely to occur when the robot was programmed to be polite and female.

Our results suggest that social cues in interactions between children and robots in education are particularly important. Adapting the robot's communication style to children's developmental level and their social expectations can increase student engagement and potentially support positive learning outcomes, Maj believes.

He adds that as robots increasingly enter classrooms, understanding how children perceive and respond to them will be critical to ensuring that in the future they become effective learning partners.

HumanTech Summit 2025

Interactions with robots were among the topics of the international HumanTech Summit 2025 conference (November 20-22, 2025) that took place for the fourth time in Warsaw and online.

One of the speakers was Professor Emily Cross (ETH Zürich, Switzerland), an expert in the neurocognitive foundations of human-robot interaction. Her research focuses on how we learn from others, how embodied experiences (such as dance, movement, and interaction with robots) shape social perception, and how humans interact with social robots and artificial intelligence systems. Another speaker, Jessica M. Szczuka, PhD, from the University of Duisburg-Essen, investigates how digital technologies (artificial intelligence, chatbots, robots, VR) are transforming intimacy, sexuality, and interpersonal relationships, with a particular focus on synthetic relationships and the ethics of digitalized intimacy.

Peng Liu, PhD, (Zhejiang University, China) also attended the conference. His research focuses on machine psychology and human-AI collaboration, particularly in the context of automated vehicles, decision support systems, and generative AI.

At the HumanTech Summit 2025, experts discussed the social and psychological aspects of new technologies, including human-AI relations, artificial intelligence in the workplace, the impact of new technologies on employment policies and the labour market, and the psychological aspects of technology. The event was organized by the HumanTech Center for Social and Technological Innovation at the SWPS University.



Konrad Maj (Ph.D.), social psychologist, SWPS University and humanoid robot Pepper

Credit
SWPS University

 

The future of type 1 diabetes: Can stem cells provide a cure?



Xia & He Publishing Inc.





Type 1 diabetes (T1D) is an autoimmune disorder characterized by the specific destruction of insulin-producing pancreatic β-cells. While islet transplantation has demonstrated promise, its widespread application is hampered by immune rejection, the necessity for lifelong immunosuppression, and a critical shortage of donor organs. This review posits that regenerative medicine, particularly strategies centered on stem cells and pancreatic progenitor cells, holds the key to a lasting cure. We explore innovative avenues for regenerating functional β-cells, with a focused analysis on the potential of pancreatic progenitor cells, the conversion of resilient α-cells, and the reprogramming of senescent β-cells. Despite persistent challenges such as immune attack and suboptimal cell differentiation, harnessing endogenous regenerative mechanisms and engineering immune-evasive cells present a transformative pathway toward restoring physiological insulin production and liberating patients from exogenous insulin dependence.

Introduction
The pathogenesis of T1D involves a selective autoimmune attack on pancreatic β-cells, sparing other endocrine cells like glucagon-producing α-cells. This selectivity underscores a fundamental opportunity: leveraging the innate resistance of non-β cells for therapeutic regeneration. Current treatments, including islet transplantation, are plagued by the recurrence of autoimmunity and organ donor scarcity. This review critically synthesizes past research to hypothesize that the future of T1D management lies in activating the body's own regenerative potential or creating an inexhaustible source of immune-tolerant β-cells from stem cells.

The Search for Elusive Pancreatic Stem Cells
A central quest in the field is the identification of endogenous pancreatic stem or progenitor cells in adults. While a dedicated stem cell niche akin to the bone marrow is absent in the mature pancreas, evidence points to the ductal epithelium as a reservoir of cells with progenitor-like capabilities. Advances in single-cell transcriptomics are now empowering researchers to identify and characterize these rare, transient cell populations, mapping their potential to differentiate into endocrine lineages. Concurrently, the derivation of β-like cells from pluripotent stem cells (e.g., embryonic or induced pluripotent stem cells) has progressed to clinical trials (e.g., ViaCyte, Vertex Pharmaceuticals), showing restored insulin production in patients. The dual approach—activating endogenous progenitors and transplanting externally differentiated cells—represents a powerful, scalable strategy.

Replicating β-cells and the Potential of Ductal Epithelium
Historically, β-cell mass expansion was thought to occur primarily through the replication of existing β-cells. However, this process is limited and often accompanied by temporary dedifferentiation, compromising function. In contrast, the process of neogenesis—the formation of new islets from progenitor cells—offers a more robust solution. The ductal epithelium exhibits remarkable plasticity, capable of generating new β-cells, especially in response to injury, metabolic stress, or specific signaling cues. Key pathways like Notch and Wnt, along with the inhibition of the Hippo pathway (activating YAP), have been shown to enhance this ductal-to-β-cell conversion, highlighting a viable therapeutic target for regeneration.

Unlocking Secrets from α-Cell Resilience
A pivotal insight for T1D therapy is the inherent resistance of α-cells to autoimmune destruction. This resilience is multi-faceted: α-cells express lower levels of key autoantigens, possess stronger anti-apoptotic signaling, exhibit greater endurance against inflammatory cytokines like interferon-gamma, and may reside in a more protected microenvironment within the islet. This inherent "immune privilege" provides a blueprint for protecting β-cells. Strategies such as molecular mimicry (engineering β-cells to express α-cell protective molecules), immune checkpoint modulation (e.g., introducing PD-1), and anti-inflammatory cytokine therapy (e.g., IL-10) are being explored to shield β-cells from immune attack.

Key Signaling Pathways in β-Cell Regeneration
Reversing T1D requires a deep understanding of the molecular pathways governing β-cell development and identity.

  • NGN3 (Neurogenin 3): A master regulator of endocrine differentiation, NGN3 reactivation in adult ductal or acinar cells can drive the formation of new, glucose-responsive β-like cells.

  • Wnt/β-catenin and Hippo/YAP: These pathways are crucial for progenitor cell proliferation, survival, and differentiation. Their targeted activation promotes the expansion and maturation of β-cell precursors.

  • GLP-1 (Glucagon-like peptide-1): Beyond its insulinotropic effects, GLP-1 enhances β-cell survival, proliferation, and even promotes the transdifferentiation of α-cells into β-like cells.

  • GDF11 (Growth differentiation factor 11): This factor shows promise in stimulating β-cell regeneration and may counteract age-related decline in regenerative capacity.

Bench-to-Bedside Strategies and Technical Hurdles
The translational pipeline is rich with diverse approaches, including stem cell-derived β-cells, autologous iPSC therapies, drug-induced endogenous regeneration (e.g., glucagon receptor antagonists), cellular reprogramming, and encapsulation technologies. However, significant hurdles remain. These include the functional immaturity of stem cell-derived β-cells, the risk of immune rejection even with matched cells, challenges in scaling up production under Good Manufacturing Practice, and the risk of tumorigenicity from residual pluripotent cells. Encapsulation devices face issues with fibrosis and limited nutrient diffusion, while gene-editing strategies like CRISPR, though promising for creating immune-evasive cells, raise concerns about off-target effects.

Future Directions and Conclusion
The future of T1D cure lies in integrated, systems-level approaches. This includes employing biomimetic scaffolds and organ-on-chip systems to improve β-cell maturation, using multi-omics to precisely map cell fates, and combining regenerative therapies with antigen-specific immunomodulation to create a tolerant microenvironment. Furthermore, research must address the neuroendocrine integration of regenerated β-cells and leverage artificial intelligence for personalized treatment strategies.

In conclusion, while challenges in scalability, safety, and immune compatibility are substantial, the convergence of stem cell biology, regenerative signaling, and immunoengineering is paving a concrete path toward a cure for T1D. The vision is shifting from lifelong insulin management to the restoration of endogenous, functional β-cell mass, offering the genuine prospect of insulin independence for patients.

 

Full text:

https://www.xiahepublishing.com/2472-0712/ERHM-2024-00002

 

The study was recently published in the Exploratory Research and Hypothesis in Medicine.

Exploratory Research and Hypothesis in Medicine (ERHM) publishes original exploratory research articles and state-of-the-art reviews that focus on novel findings and the most recent scientific advances that support new hypotheses in medicine. The journal accepts a wide range of topics, including innovative diagnostic and therapeutic modalities as well as insightful theories related to the practice of medicine. The exploratory research published in ERHM does not necessarily need to be comprehensive and conclusive, but the study design must be solid, the methodologies must be reliable, the results must be true, and the hypothesis must be rational and justifiable with evidence.

 

UBC researchers uncover how statins harm muscles—and how to stop it



Study reveals how cholesterol-lowering drugs can trigger muscle damage—and point to a way to make them safer.




University of British Columbia

Statins binding to muscle protein 

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This illustration, based on what researchers were able to observe using high-resolution macromolecular cryo-electron microscopy, shows statin moelcules in black binding to the RyR1 protein.

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Credit: The Bioelectricity Lab, UBC Life Sciences Institute




Statins have transformed heart health, saving millions of lives by lowering cholesterol and reducing the risk of heart attacks and strokes. But for many patients, these drugs come with a troubling downside: muscle pain, weakness and, in rare cases, severe muscle breakdown that can lead to kidney failure. 

University of British Columbia researchers and their collaborators at the University of Wisconsin-Madison have now pinpointed the cause. Their findings, published last week in Nature Communications, could pave the way for a new generation of statins without these side effects. 

The team used cryo-electron microscopy, a powerful imaging technique that reveals proteins at near-atomic detail, to capture how statins interact with a critical muscle protein called the ryanodine receptor (RyR1). This protein acts like a gatekeeper for calcium inside muscle cells, opening only when muscles need to contract. When statins bind to it, they force the gate open, causing calcium to leak continuously—a toxic effect that can damage muscle tissue. 

“We were able to see, almost atom by atom, how statins latch onto this channel,” said lead author Dr. Steven Molinarolo, a postdoctoral researcher in UBC’s department of biochemistry and molecular biology. “That leak of calcium explains why some patients experience muscle pain or, in extreme cases, life-threatening complications.” 

The study focused on atorvastatin, one of the most widely prescribed statins, but the findings suggest the effect may be common across the drug class. The researchers discovered that statins bind in a highly unusual way: Three molecules cluster together inside a pocket of the protein. The first molecule attaches when the channel is closed, priming it to open. Two more molecules then wedge in, forcing the channel wide open. 

“This is the first time we’ve had a clear picture of how statins activate this channel,” said Dr. Filip Van Petegem, senior author and professor at UBC’s Life Sciences Institute. “It’s a big step forward because it gives us a roadmap for designing statins that don’t interact with muscle tissue.” 

By adjusting only those parts of the statin molecule that are responsible for the negative effects, scientists could preserve the part that lowers cholesterol while reducing the risk. 

While severe muscle damage affects only a small fraction of over 200 million statin users worldwide, milder symptoms like aches and fatigue are far more common, and often lead patients to stop treatment. The new findings could help prevent those problems and improve adherence to life-saving therapy. 

The research underscores the importance of advanced imaging technology in driving medical breakthroughs. Using the UBC faculty of medicine’s high-resolution macromolecular cryo-electron microscopy facility, the team was able to visualize the statin-protein interaction in extraordinary detail—turning a fundamental question about drug safety into practical insights that could shape the next generation of therapies. 

“Statins have been a cornerstone of cardiovascular care for decades,” Dr. Van Petegem said. “Our goal is to make them even safer, so patients can benefit without fear of serious side effects.” 

For millions of people who rely on statins, that could mean fewer muscle problems—and a better quality of life.