IntroductionDysregulation of the autonomic nervous system has been implicated in nonsuicidal self-injury (NSSI) in laboratory studies of physiological reactivity, but it remains unclear whether self-reported everyday autonomic symptom burden is associated with NSSI severity.MethodsWe conducted a preregistered cross-sectional online survey of N = 1,002 German-speaking adolescents and young adults aged 14–30 years (M = 23.43; 73% women). Autonomic symptoms were assessed with the COMPASS 31; NSSI presence and frequency were measured with the SITBI-R across four reference periods (past week, month, year, lifetime). Data were analyzed using zero-inflated negative binomial models.ResultsThe 12-month NSSI prevalence was 22.6%. Higher COMPASS 31 scores were associated with lower odds of reporting zero NSSI episodes across all reference periods and with higher NSSI episode counts for the past month, past year, and lifetime; the past-week count association was not statistically significant. These associations held after controlling for childhood adversity, perceived stress, medication, and hormonal contraception.DiscussionThese results indicate that self-reported autonomic symptom burden was robustly associated with NSSI involvement, particularly with the likelihood of any NSSI and with episode counts over longer reference periods. These findings suggest that self-reported autonomic symptom burden may represent a clinically relevant somatic correlate of NSSI severity.
Single-Cell Atlas Simultaneously Maps 3D Genome Architecture and DNA Methylation
Scientists at the Salk Institute and the Arc Institute, along with their collaborators, unveiled the first body-wide single-cell atlas of two major epigenetic systems: three-dimensional genome folding and DNA methylation, measured simultaneously in the same cells.
The atlas spans 86,689 cells from 16 human tissues, revealing 35 major cell types and 206 subtypes, and is freely available online. The work is part of the National Institutes of Health’s 4D Nucleome (NIH 4DN) program, which aims to understand how the genome is organized in space and time to regulate gene expression in health and disease.
Because the two epigenetic layers were measured together, the researchers could compare what each layer says about a cell’s identity. And while often the two pictures agree, they found that sometimes they do not.
The Salk paper “Human body single-cell atlas of 3D genome organization and DNA methylation” was published alongside five other NIH 4DN papers in Science, and three others in Science Advances.
The Human Genome Project, completed in 2003, produced a linear read of the three billion DNA letters in the human body. But the letters alone don’t explain how a single genome produces hundreds of different cell types. That information lives in the epigenome in the form of chemical modifications and structural folds layered on top of the DNA sequence, where they can switch genes “on” and “off” in patterns specific to each cell type.
![Caption: Salk scientists Jingtian Zhou (left), Jesse Dixon (center), and Joseph Ecker (right) profiled 86,689 cells across 16 human tissues, linking cell-type-specific epigenetic features to disease risk and revealing that a cell’s 3D genome and DNA methylation don’t always tell the same story. [Salk Institute]](https://www.genengnews.com/wp-content/uploads/2026/07/260723-pr-ecker-dixon-authors-232x300.jpg)
Two of the most consequential epigenetic features are 1) DNA methylation, where small chemical groups called methyl groups are attached to specific DNA bases, and 2) 3D genome organization, where intricate loops, folds, and compartments bring distant stretches of DNA into contact. Both influence gene expression, but they had never been measured together in single cells across the human body.
“There has been an appreciation for trying to understand, at the individual cell level, how the genome is organized, so that we can get a better idea of how genetic variants impact disease,” said co-corresponding author Joseph Ecker, PhD, a professor and Salk International Council Chair in Genetics at Salk and a Howard Hughes Medical Institute investigator. “Some cell types may be more vulnerable than others to genetic variants, because the genome is organized differently in different cell types—and whether a variant matters can depend on that organization.”
Why is noncoding DNA relevant in disease?
Most disease-associated genetic variants fall in the noncoding regions of the genome. That has made it difficult to figure out how a variant contributes to disease, which cell type it acts in, and what gene it ultimately affects.
The new atlas identifies more than 1.36 million differentially methylated regions and 283,606 differential chromatin loops across the human body’s cell types, using tissues from the heart, brain, lungs, stomach, skin, and more. When the researchers overlaid genetic variants known to raise disease risk, specific pairings emerged like variants for blood-glucose regulation concentrated in endocrine cells, atrial fibrillation variants in heart muscle cells, balding variants in skin fibroblasts, and bipolar disorder and schizophrenia variants in excitatory and inhibitory neurons.
“A lot of the genetic variation that predisposes someone to disease is in noncoding parts of the genome,” said co-corresponding author Jesse Dixon, MD, PhD, associate professor and Helen McLoraine Developmental Chair at Salk. “By adding in the 3D genome aspect, we can potentially bridge that gap—connecting noncoding variations with the genes they affect in specific cells and tissues.”
What happens when two epigenetic lenses disagree?
One of the study’s most surprising findings is that DNA methylation and 3D genome structure don’t always tell the same story about a cell. In skeletal muscle, the team found fibers that look like mature, differentiated muscle cells by their 3D genome folding, but still carry the methylation signature of muscle stem cells. The reverse almost never happens. The most plausible explanation, they explained, is that these cells are caught mid-differentiation, with 3D architecture updating first and methylation catching up.
Similar mismatches appeared in Schwann cells of the peripheral nervous system and in placental trophoblasts. The pattern suggests that different epigenetic features update on different time scales during cell state transitions—a finding that could reshape how researchers define “cell type” in adult tissues and how they track cells moving between states in disease.
The atlas also revises a long-standing assumption about “non-CG methylation,” an unusual form of methylation previously thought to be largely confined to brain cells and stem cells. The study shows that it carries cell-identity information across many human tissues, including muscle, pancreas, and immune cell types, at lower but biologically meaningful levels.
“The inconsistency between modalities may be further used to determine what cell populations are switching between each other in adult tissues and diseases, which could, for example, expand our understanding of cancer cell dynamics,” said co-first and co-corresponding author Jingtian Zhou, PhD, a former graduate researcher in Ecker’s lab who now leads his own lab at the Arc Institute.
A public resource for scientists and artificial intelligence
To make the atlas broadly usable, the team built an interactive web browser that lets researchers visualize DNA methylation and 3D chromatin contacts across every tissue, cell type, and subtype in the study. The underlying data, including 195 billion methylation measurements and 18 billion chromatin contacts, are freely available.
The resource arrives as artificial intelligence tools are increasingly used to predict the functional impact of genetic variants. Atlases like this one can provide the labeled, cell-type-resolved training data that models need to make accurate predictions—a bottleneck that has historically limited the field.
For example, in a companion paper in the same issue of Science, a study led by Bing Ren, PhD, from the New York Genome Center and Columbia University used the atlas’ cross-tissue methylation data to show that a substantial fraction of the brain’s resident immune cells, called microglia, are replaced by cells resembling blood monocytes between roughly ages 50 and 75. The finding challenges the long-held view that microglia persist from embryonic development throughout the life span.
“DNA methylation patterns are specific to each cell type and analogous to a cellular barcode,” said Ren, who also co-authored the Salk-led study. “The comprehensive cross-tissue DNA methylation atlases show that the aging microglia in the human hippocampus more closely match the monocytes from peripheral blood than microglia from young adults, providing a crucial clue for the biological identity of these cells.”
The NIH 4D Nucleome consortium, of which this study is a part, aims to extend this kind of mapping into the fourth dimension: time. A 4D understanding of the genome—how its structure and chemistry change as cells develop, age, and respond to disease—remains a major goal, and the cross-tissue atlas provides reference scaffolding that future time-course studies will build on.
Along with scientists from the Salk Institute and Arc Institute, investigators from the University of California, San Diego, Columbia University, New York Genome Center, University of California, Los Angeles, Harvard, Henan University in China, Vanderbilt University, Stanford University, Broad Institute, University of Sheffield in the U.K., Yale, University of Florida, University of Freiburg in Germany, University of Graz in Austria, and Nanchang University in China; and Chongyuan Luo also contributed to the Science paper.
The post Single-Cell Atlas Simultaneously Maps 3D Genome Architecture and DNA Methylation appeared first on GEN – Genetic Engineering and Biotechnology News.
Turning Solar Power Into Protein
According to projections from the United Nations, global food demand could increase by around 60 percent by 2050, while only about two percent additional agricultural land is expected to become available. Researchers at the Technical University of Munich (TUM) report that they are exploring new approaches to safeguard food security. A team at the TUM Campus Straubing has developed a process for producing crucial amino acids from carbon dioxide, hydrogen, and renewable energy.
Viktoria Lehmann, a doctoral candidate at TUM, describes one potential application for biotechnologically produced amino acids.
“A dairy cow needs far more than the grass growing in its pasture. High milk yields require supplemental protein, which is typically supplied through animal feed. These feeds are enriched with amino acids, the chemical building blocks of proteins,” she explains. “Across livestock production systems worldwide, millions of tons of amino acids are used as feed additives. However, their production consumes large amounts of land, water, and other resources. We wanted to find a more resource-efficient way to meet this protein demand.”
In a recently published study “Plug and Play – Enzymatic Amino Acid Production from Methanol and Carbon Dioxide” in Nature Communications, the team demonstrated its approach. The concept behind it: solar energy is converted into electricity using photovoltaic systems. This electricity is used to generate hydrogen, which, together with carbon dioxide, is converted into methanol—an alcohol widely used in industry as a chemical precursor. Specialized enzymes then convert the methanol step by step into amino acids. Which amino acid is produced depends on the specific enzymes used.
“Plants use sunlight to build biomass, but they are relatively inefficient at doing so. We are investigating an alternative pathway in which renewable energy is first converted into chemical energy carriers and then into valuable protein building blocks,” notes Volker Sieber, PhD, professor of chemistry of Biogenic Resources and Rector of the TUM Campus Straubing. “In the long term, this approach could help make more productive use of available land and enable a more sustainable production of amino acids.”
A modular platform technology
In 2023, the researchers demonstrated the production of the amino acid L-alanine from green methanol. Their latest work expands the approach to a total of seven amino acids. “Our modular plug-and-play concept can be compared to a construction kit,” says Vivian Willers, PhD, whose doctoral research laid the foundation for the study. “What started with a single amino acid is increasingly evolving into a platform technology for producing protein building blocks from renewable energy.”
The team successfully produced the amino acids glycine, serine, L-aspartic acid, L-valine, L-glutamic acid, and L-proline. In the future, this technology could help reduce dependence on protein-rich feed ingredients such as soy, which are not always produced sustainably. These amino acids are also key components of nutrient media used in cultured meat production. As a result, the researchers see applications extending well beyond conventional agriculture.
While the team was able to demonstrate the entire process chain—from carbon dioxide via methanol ultimately to amino acids—the current production volumes are still too low for commercial use. The researchers are working to further improve the performance of the enzymes involved.
“Our work is primarily a proof of technological feasibility,” points out Sieber. “We have shown that a broad range of biologically relevant amino acids can be produced from CO₂-based methanol. This opens up new possibilities for the sustainable production of protein building blocks.”
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Art therapy for depression: a systematic review and meta-analysis
IntroductionDepression is among the leading causes of disability globally. Therefore, exploring the various non-medical treatment options for this condition is particularly important. The aim of the review was to assess the effect of art therapy on depressive symptoms.MethodsThe foundation of this review is a pre-planned, explorative, secondary analysis of a previously published umbrella review, encompassing the databases Cochrane Library, Embase, MEDLINE, CINAHL, ERIC, American Psychological Association PsycArticles, American Psychological Association PsycInfo, PSYNDEX, the German Clinical Trials Register, and ClinicalTrials.gov. Included were all randomized trials with any patient population receiving active visual art therapy. The outcome was depressive symptoms measured by depression assessment instruments. We followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and conducted a bias assessment using a modified Cochrane risk of bias tool. Data was pooled using a random-effects model and visualized in forest plots. A pooled standardized mean difference (SMD) with hedges g was calculated to measure the reduction of depressive symptoms.ResultsOf 3,100 identified reports we included 26 studies. Of these, 19 studies with 997 patients were eligible for inclusion in the meta-analysis. Overall, we found a standardized mean difference of 0.53 (95% CI: 0.30 to 0.76) for depressive symptoms, favoring the intervention group. Main sources of variation were different types of control groups, methodological quality, and patient populations.ConclusionOur results suggest that art therapy is associated with improved depressive symptoms. Therefore, art therapy should be accessible as complementary treatment for patients suffering from depressive symptoms.
New Target on Tumor Blood Vessels Could Expand Immunotherapy Responses
Immune checkpoint inhibitors have transformed cancer treatment, producing long-lasting—and sometimes curative—responses in patients with advanced malignancies. Yet only a minority of patients benefit, particularly those whose tumors have spread to the liver, where immunotherapy often proves less effective.
A new preclinical study from researchers at the German Cancer Research Center in Heidelberg suggests the answer may lie not within the cancer cells themselves, but in a specialized population of cells lining the tumor’s blood vessels. The findings, published in Cancer Research, identify lipoprotein lipase (LPL)-expressing tumor endothelial cells as critical regulators of T-cell infiltration into liver metastases and point to a new strategy for enhancing immunotherapy in tumors that are otherwise resistant to treatment.
The discovery builds on growing evidence that remodeling tumor blood vessels can improve immunotherapy. Anti-angiogenic agents such as bevacizumab, which targets the VEGF pathway, have already demonstrated clinical benefit when combined with immune checkpoint blockade. In the landmark IMbrave150 trial, atezolizumab plus bevacizumab significantly improved overall survival compared with sorafenib in patients with advanced hepatocellular carcinoma.
Despite that success, durable responses remain relatively uncommon. Approximately 30% of patients experienced an objective response to the combination therapy, while only about eight percent achieved a complete response. Those results suggest that targeting VEGF alone does not fully overcome the barriers preventing immune cells from reaching and attacking tumors.
To better understand those barriers, the investigators analyzed how blood vessel cells within and surrounding liver metastases responded over time after T-cell therapy. Their analyses uncovered a previously unrecognized subgroup of tumor endothelial cells that express LPL, an enzyme best known for its role in fat metabolism but not previously linked to antitumor immunity.
Rather than serving as passive conduits for blood flow, these endothelial cells actively orchestrated the immune response.
The researchers found that LPL-positive endothelial cells helped activated CD8-positive T cells leave the bloodstream and enter metastatic tumors. Once there, the T cells were able to recognize and destroy cancer cells, leading to regression of liver metastases in mouse models.
The study also revealed why these specialized blood vessel cells appear to be so important. Many cancers evade immune attack by reducing expression of major histocompatibility complex class I (MHC-I), the molecular display system that allows T cells to recognize tumor-derived proteins. Without adequate antigen presentation, even activated T cells struggle to identify malignant cells.
The authors found that LPL-positive endothelial cells compensate for this weakness. Instead of relying solely on tumor cells to present antigens, the endothelial cells themselves captured tumor proteins and displayed them through MHC-I, effectively providing T cells with the information needed to locate nearby cancer cells.
As the authors write, “LPL enhanced MHC-I-dependent cross-presentation of tumor antigens on tumor endothelial cells, thereby promoting T-cell infiltration.”
That interaction created a positive feedback loop. Once activated T cells recognized antigens displayed by the endothelial cells, they also targeted those blood vessel cells, further amplifying immune activity within the tumor microenvironment.
Genetic experiments reinforced the importance of the pathway. Increasing LPL expression specifically in endothelial cells enhanced T-cell infiltration into liver metastases, while eliminating LPL from those cells impaired immune cell recruitment and reduced the effectiveness of T-cell–mediated tumor control.
Importantly, the findings extended beyond animal models.
When the investigators examined human liver metastasis samples, they observed that tumors containing higher numbers of LPL-positive blood vessels also contained significantly more infiltrating T cells, suggesting that the mechanism may operate in patients as well.
The authors conclude that “LPL-positive tumor endothelial cells orchestrate activated CD8-positive T-cell homing into immunologically cold tumors with low baseline MHC-I expression.”
The work also helps explain why vascular-targeted therapies benefit only a subset of patients receiving immunotherapy. Previous research has largely focused on normalizing abnormal tumor blood vessels or increasing expression of molecules that help immune cells adhere to vessel walls. While those approaches improve immune cell access, they do not address another fundamental obstacle: many tumors simply fail to present enough antigens for T cells to recognize.
By acting as surrogate antigen-presenting cells, LPL-positive endothelial cells appear capable of overcoming that limitation, enabling T cells to infiltrate tumors that would otherwise remain immunologically “cold.”
The findings suggest that future combination strategies may need to extend beyond VEGF inhibition and instead directly promote the immune-supporting functions of tumor blood vessels.
Although additional studies will be needed to determine whether therapies can safely increase LPL activity in patients, the work identifies the protein as both a potential biomarker and a therapeutic target. Measuring LPL-positive blood vessels could help identify patients most likely to benefit from immunotherapy combinations, while therapies that enhance this endothelial cell program could potentially expand responses among patients whose tumors currently resist immune attack.
As the authors conclude, enhancing antigen presentation by tumor endothelial cells “presents a promising approach to compensate the intrinsic inability of tumor cells and boost antitumor immunotherapy,” offering a potential new avenue for turning immunologically cold liver metastases into tumors that respond to immune-based treatment.
The post New Target on Tumor Blood Vessels Could Expand Immunotherapy Responses appeared first on Inside Precision Medicine.
A 2-Tiered Rescue Protocol to Mitigate Difficulty-Based Failures of ChatGPT (GPT-5) and Gemini on the German M2 Medical Examination: Evaluation Study
Background: Large language models (LLMs) have demonstrated expert-level performance on medical licensing examinations, but most benchmarks focus on final accuracy. Critical gaps remain in understanding model efficiency (latency), the efficacy of tiered “rescue” protocols for error correction, and the systematic correlation between performance and human-rated question difficulty. The German M2 examination, paired with the AMBOSS platform’s user data–driven difficulty ratings, provides an opportunity to map AI performance against human cognitive load. Objective: This study aimed to move beyond singular accuracy scores by (1) evaluating and comparing the baseline (tier 1; T1) accuracy and response latency of next-generation rapid-response LLMs, (2) analyzing the efficacy of a 2-tiered rescue (tier 2; T2) protocol in correcting initial errors, and (3) correlating model performance with the user data–driven AMBOSS difficulty rating. Methods: We evaluated 4 LLMs (Gemini 2.5 Flash, Gemini 2.5 Pro, GPT-5 Instant, and GPT-5 Thinking) on the complete 316-item German M2 (Fall 2024) medical examination, including all multimodal (image-based) questions. A zero-shot copy-paste prompting strategy was used, and outputs were evaluated against ground-truth answers using a strict exact-match criterion. A 2-tiered protocol was used: T1 (Gemini Flash and GPT-5 Instant) provided baseline responses. If incorrect, a T2 (Gemini Pro and GPT-5 Thinking) model was deployed as a “rescue.” Performance was analyzed using the McNemar test, the Wilcoxon signed-rank test, the Fisher exact test, and logistic regression. Results: Baseline (T1) accuracy was identical at 91.5% (289/316; 95% CI 87.85%‐94.06%) for both Gemini 2.5 Flash and GPT-5 Instant, with 27 errors each. However, Gemini Flash (mean 1.57, SD 1.06 s) was significantly faster than GPT-5 Instant (mean 2.07, SD 1.89 s; <.001). Additionally, GPT-5 Instant expended significantly more time on incorrect answers compared with correct ones (=.002), whereas Gemini Flash showed no such hesitation (=.81). The T2 rescue rate for GPT-5 Thinking (13/27, 48.2%; 95% CI 30.74%‐66.01%) was higher, though not statistically significant (=.41), than that for Gemini 2.5 Pro (9/27, 33.3%; 95% CI 18.64%‐52.18%). This rescue protocol elevated final accuracy to 94.3% (298/316; 95% CI 91.18%‐96.37%) for the Gemini system and 95.6% (302/316; 95% CI 92.70%‐97.34%) for the GPT-5 system (=.48). A strong, inverse relationship with difficulty was found: for every 1-point increase in difficulty, the odds of a correct T1 response decreased by 42.1% (odds ratio 0.579, 95% CI 0.425‐0.788; <.001) for Gemini Flash and 47.7% (odds ratio 0.523, 95% CI 0.379‐0.720; <.001) for GPT-5 Instant. This negative correlation persisted even after the rescue (=.01 and =.006, respectively). Conclusions: Expert-level LLM performance on the German M2 examination masks a critical vulnerability: a decrease in accuracy correlated with increased question difficulty. A 2-tiered “rescue” system is an effective strategy to mitigate these difficulty-based failures and achieve >95% accuracy.
Flu Virus Interaction with Host Cell Machinery Mapped Inside Infected Cells
Researchers at EMBL Hamburg and collaborators at the Leibniz Research Institute for Molecular Pharmacology (FMP) have mapped in unprecedented detail how the influenza A virus (AIV) rewires infected human cells. The researchers developed a customized experimental workflow that used in-cell cross-linking mass spectrometry (XL-MS), combined with AlphaFold-based structural modeling and functional assays, to directly map protein-protein interactions (PPIs) in IAV-infected human cells.
They claim that the study marks the first time that scientists have mapped direct virus-host protein contacts at scale inside intact influenza-infected cells, with enough structural detail to model how the proteins fit together. “Our work provides a new way to study flu-host interactions in their native context and with structural insight,” said Jan Kosinski, PhD, group leader at EMBL Hamburg and the Centre for Structural Systems Biology (CSSB). “The current results are a snapshot of a moment during infection, and it opens the door to studying flu-host interactions across the entire infection cycle.”
Kosinski is co-senior and co-corresponding author of the team’s published paper in Nature Microbiology, titled “Mapping in-cell protein contact sites reveals hijacking of paraspeckles during influenza A virus infection,” stating that their findings “… uncover mechanisms by which IAV exploits and remodels host compartments during infection.”
Every year, seasonal influenza kills up to 650,000 people globally and causes serious illness for 3–5 million individuals. When IAV infects cells, it releases RNA that contains the blueprints for a handful of proteins that spread throughout the host cell and repurpose its molecular machinery to make more viruses. “Its replication relies on protein–protein interactions (PPIs) between up to 14 viral proteins and host factors, often confined to cellular compartments and organelles,” the team stated.
Scientists want to understand this process in detail, as it would help in designing better drug therapies and vaccines against the flu virus. “Understanding these host–IAV PPIs in context is essential for elucidating viral strategies and therapeutic targets,” they added.
Studying protein-protein interactions in action during infection is challenging. Most previous studies relied on biochemical methods that required the cell to be broken open before the interactions could be measured. Once the cell’s compartments were gone, proteins that were never in contact inside the cell could meet in the test tube, and fragile or location-specific contacts could be lost. It was then hard to know which interactions actually happened inside an infected cell.
“This is when we learned that our collaborators—Boris Bogdanow and Fan Liu—at FMP Berlin had developed a specialized version of cross-linking mass spectrometry (XL-MS), a long-established technique for mapping protein contacts, tailored specifically to virus-infected cells,” said Kosinski. This was the critical breakthrough. It allowed researchers to do what previous methods couldn’t, including capturing short-lived and location-specific interactions.
“XL-MS allows us to capture protein-protein interactions directly in infected intact cells, while also providing structural information about how these interactions are happening,” explained Bogdanow, who is now a junior research group leader at the Institute of Virology, Charité—Universitätsmedizin Berlin. “This gives us insight into the interface between the virus and the human cell and may, through structural modelling, help identify actionable targets for future pharmaceutical interventions.”
By combining the results obtained through XL-MS with computational structural modeling, the researchers could identify which viral and human proteins interact and also predict how they physically fit together. For this, they used a modified version of the protein structure prediction algorithm AlphaFold.
“The key advantage of the modified AlphaFold approach is that it allowed us to feed our experimental cross-linking data directly into the structural modeling,” explained Kosinski. “This tells the model which parts of the viral and host proteins are close to each other inside infected cells. This was especially useful for virus-host complexes, which are often difficult to predict reliably.”
The study findings revealed two important ways in which the virus hijacks the cell. One involves hemagglutinin, a protein on the virus’s surface that it uses to bind and enter host cells. Tracing how hemagglutinin moves through the cell’s internal transport and processing system revealed how host proteins, some with previously unknown functions, helped the virus correctly fold and modify hemagglutinin during infection.
The other involves paraspeckles, small droplet-like compartments in the nucleus. The researchers found that infection by the influenza A virus causes these organelles to dissolve, releasing the RNA-binding proteins bound within them, which the virus can then use to replicate. “We identified host factors linked to the maturation of distinct glycoforms of the viral surface glycoprotein haemagglutinin through the membrane-bound endoplasmic reticulum–Golgi system,” the scientists wrote in summary. “In the nucleus, we observed the progressive disassembly of paraspeckles (phase-separated membraneless compartments) across multiple cell lines.”
First author Iuliia Kotova, PhD, former predoctoral fellow at the Kosinski group at EMBL Hamburg, and currently at ETH, said, “What surprised us most was the paraspeckles. Watching these tiny organelles in the nucleus dissolve, consistently across every cell line and every flu strain we tested, told us this isn’t a side effect of infection—it might be a strategy.”
Kosinski added, “There may also be a second benefit for the virus: some evidence suggests paraspeckles contribute to cellular stress responses and antiviral gene regulation, so disrupting them could also weaken parts of the cell’s defense response.”
The researchers believe that their “mapping in context” approach can be used to understand the mechanism of action of other viruses that act similarly. “While the exact host factors and mechanisms often differ from virus to virus, we think our overall approach—combining in-cell cross-linking, structural modeling, and targeted cell-biology follow-up to map native virus-host interactions at specific stages of infection—remains broadly applicable,” Kosinski said.
Bogdanow further commented, “Although this study has focused on a lab-adapted strain, this study lays the groundwork to apply the methodology to viruses of potential pandemic relevance, such as H5N1, and for uncovering the interaction networks that support their multiplication in human cells.”
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New €25 Million BioReliance Testing Facility Opens at Merck KGaA Global Headquarters in Germany
MilliporeSigma opened a new €25 million BioReliance® testing facility at the company’s global headquarters in Darmstadt, Germany. The facility expands access to commercial drug substance and drug product release testing as well as stability testing for biopharmaceutical companies developing and commercializing therapies in Europe, according to the company.
“As demand for biologics and novel therapies continues to grow, our customers need reliable, compliant testing capabilities closer to where their products are developed and commercialized,” said Paolo Carli, head of advanced solutions for the life science business of Merck KGaA. “Our new testing facility combines best-in-class analytical characterization services with more than 75 years of BioReliance expertise to help our European customers move critical therapies toward patients with greater speed and confidence.”
The 2,000-square-meter facility is designed to help customers meet European requirements for in-region drug substance and drug product release testing and to expand the company’s ability to support customers from drug development through commercialization. The site will also offer GMP-compliant stability studies for monoclonal antibodies and cell therapies, addressing the growing demand for biologics testing across Europe.
Located close to major clinical trial sites in Germany, France, Spain, the Netherlands, Belgium and Italy, the Darmstadt facility is strategically positioned to support biopharmaceutical companies seeking to release drug products into European markets, pointed out Carli. By adding these capabilities in the heart of Europe, the company is strengthening its support for customers managing increasingly complex development, quality and regulatory requirements, he added.
A MilliporeSigma spokesperson noted that the BioReliance sites form a global testing network that allows customers to scale across geographies and work with the company across continents. Among the company’s leading technologies is the Blazar® platform, which moves the biosafety testing paradigm from traditional methods to rapid molecular approaches to significantly reducing testing timelines for virus detection.
The Aptegra® CHO genetic stability testing streamlines a previously complex and time-intensive process into a single assay, continued the spokesperson.
MilliporeSigma lists the opening of the Darmstadt facility as one of several significant investments the company has made to grow its global contract testing footprint. In 2024, the company opened a €290 million biosafety testing facility in Rockville, MD, and expanded biosafety testing capacity by 40% across its Glasgow and Stirling sites through a €22 million investment. The company also cites the new BioReliance facility as reflecting the firm’s continued commitment to its global headquarters in Darmstadt, where €2.5 billion has been invested since 2015.
The post New €25 Million BioReliance Testing Facility Opens at Merck KGaA Global Headquarters in Germany appeared first on GEN – Genetic Engineering and Biotechnology News.
Why heat pumps are still so hot in the US
It feels as if it should be illegal to even think about heating appliances during the height of summer—seriously, these heat waves in New York have been brutal—but we need to talk about heat pumps.
The appliances use electricity for heating, they’re incredibly efficient, and they’re on the rise. (For what it’s worth, many heat pumps can also be run in reverse to cool buildings.) In the US, heat pump sales have doubled over the past 15 years, according to a new report. And they’re winning the heating race against fossil fuels, outpacing natural-gas furnaces by 32% during the first quarter of 2026.
These stats are especially striking at this moment, because a key tax credit for heat pumps just ended with the close of 2025. But you wouldn’t know it from looking at the data. Why are heat pumps still so hot?
In case you need a quick refresher, heat pumps use electricity to essentially move heat from one spot to another. A refrigerant moves around a loop in the device, expanding and compressing, gathering and releasing heat at different points in the cycle. (For a more in-depth look at the thermodynamics, this explainer I wrote in 2023 still holds up.)
The result is an appliance that can be incredibly efficient. Once you pay for and install a heat pump, it’s generally significantly cheaper to run than a gas or oil furnace or other types of electric heating systems. And because they’re more efficient and don’t involve burning fossil fuels, heat pumps can be a major help in decarbonizing buildings.
One of the major hurdles to wider use of heat pumps is the appliances’ cost: They tend to be more expensive to buy and install than gas furnaces. For this reason, many governments offer incentives to encourage their adoption. In the US, people who installed heat pumps between 2023 and 2025 were eligible for up to $2,000 in tax credits.
Last year, though, the Trump administration slashed those tax credits, along with many of the other incentives that were part of the 2022 Inflation Reduction Act. Effective January 1, 2026, no more financial help for heat pumps.
I think I’ve seen this film before, and I didn’t like the ending. Tax credits of up to $7,500 for new EVs ended on September 30, 2025. In the quarter leading up to that deadline, sales spiked as people rushed to take advantage of the incentive. Then they fell off a cliff. Things are starting to normalize now, but clearly the tax credit’s sunset had a major effect.
But as it turns out, heat pumps are an entirely different story. In the first few months of 2026, sales have actually gone up, as Lucas Davis, an energy economist and UC Berkeley professor, points out in a new analysis.
Heat pump shipments were flat from December to January and have seen a gradual rise since then, according to data from the Air Conditioning, Heating, and Refrigeration Institute, a trade group that represents about 90% of the US market. This increase from winter into spring follows a seasonal trend seen in previous years—and it’s actually a bit stronger in 2026.
This data isn’t what you’d expect to see if losing the tax credit were hurting demand. As Davis lays out in his post, it seems the credit wasn’t really convincing people to install heat pumps, or at least the case for doing so was sufficient without the added incentive.
“It appears that the U.S. market for heat pumps is strong enough that it does not depend on tax credits,” Davis writes.
In 2024, MIT Technology Review put heat pumps on our annual list of breakthrough technologies. “We’ve entered the era of the heat pump,” I wrote at the time.
While heat pump sales have been up and down over the last few years, the era is going strong. The appliances have outsold gas furnaces in the US for the last four years. It’s not just the US, either. Countries including China and Germany have seen strong movement to heat pumps in recent years.
There’s rarely a straight path to adoption for new technology, especially something that requires so many individual households to make a significant change. But it’s encouraging that a major decarbonization tool is going strong, even when roadblocks pop up.
This article is from The Spark, MIT Technology Review’s weekly climate newsletter. To receive it in your inbox every Wednesday, sign up here.
STAT+: Pharmalittle: We’re reading about bigger drug discounts in Germany, drugmakers embracing secrecy, and more
Good morning, everyone. Damian Garde here, filling in for Ed Silverman at Pharmalot’s satellite campus along the East River, where today’s cup of stimulation is filled not with coffee but rather a smoothie of curious color and questionable contents (what exactly is an “adaptogen”?). Anyway it’s Friday, as you’re almost certainly aware, and here are some tidbits to help you through the waning hours of another working week. …
German lawmakers passed a bill that would more than double the discount on branded medicines drugmakers must provide to the government, Reuters reports. The policy, part of an effort to plug a sizable budget gap in the country’s health insurance system, would increase the mandatory rebate from 7% to 15.5%. Industry groups have said the bill, if it clears Germany’s upper chamber, would deter investment and imperil the country’s access to new medicines.
The rapid rise of China’s biotech industry has led some American drug developers to do their work in near total secrecy, the Wall Street Journal observes. U.S. startups are increasingly loath to publish early data, disclose their scientific ambitions, or even publicize which diseases they hope to treat, all in fear that nimble Chinese firms will use that information to whip up competing drugs and beat them to the punch of starting clinical trials.