Karger Publishers Expands Open Access Portfolio for 2025 with Subscribe to Open
'It is exciting to explore the potential of Subscribe to Open to enable Open Access (OA) without APCs...we are thrilled to make more journals OA without costs for readers or authors.' — Beth Bayley, Open Science Manager at Karger Publishers
BASEL, SWITZERLAND, March 25, 2025 / EINPresswire.com / -- In the third year of the publisher's S2O pilot, the journal Developmental Neuroscience has again met its sustainability threshold, while the two new journals in the S2O pilot, European Addiction Research and Neurodegenerative Diseases, have also met their criteria for this Open Access model for 2025.
Subscribe to Open refers to a publishing model in which a journal volume can become Open Access if it reaches a certain number of subscriptions or renewals in a given year. In the program's first year at Karger, the 2023 volumes for Developmental Neuroscience and Pediatric Neurosurgery met their targets for OA, while the 2024 and 2025 volumes of Pediatric Neurosurgery did not meet that threshold and are subscription-based, with a paid option to publish any paper as Open Access.
Instead of charging authors an APC, publishing costs under S2O are sustained by subscriptions from libraries, leveraging existing funds and infrastructure. If subscriptions are renewed to a level that ensures the journals' sustainability, Karger converts that year's volume to Open Access, making it completely free of barriers to read, share and re-use under the terms of the Creative Commons Attribution license (CC BY).
'It is exciting to explore the potential of Subscribe to Open to enable OA without APCs,' states Beth Bayley, Open Science Manager at Karger Publishers. 'APCs are one of the greatest challenges to making life-changing information globally accessible, so we are thrilled to make more journals OA without costs for readers or authors.'
With its 'Open for Open' approach, Karger continues to seek ways to publish more Open Access in a way that is sustainable and accessible for all stakeholders.
For more information, please visit Subscribe to Open | Karger Publishers.
About Karger Publishers
Connecting people and science since 1890, Karger provides scientists, healthcare professionals, patients, and the broader public with reliable and tailored information in Health Sciences. Building upon a publishing portfolio of more than 100 reputable scholarly journals and the award-winning Fast Facts medical info series, Karger excels in medical education and omnichannel HCP engagement in multiple formats, including 3D animations, podcasts, AR/VR environments, and more. Academic institutions and both medical affairs and pharma marketing teams in the corporate space entrust Karger with their most demanding communication challenges. Independent and family-led in the fourth generation by Chairwoman Gabriella Karger, Switzerland-based Karger is present in 15 countries with a team of 200 dedicated professionals worldwide.
For more information, please visit karger.com
Christine Hohlbaum
Hohlbaum PR & Social Media
+49 177 8638661
Legal Disclaimer:
Hashtags
Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
Gizmodo
2 days ago
- Gizmodo
Brain Scans Reveal Why Waking Up Is Sometimes Such a Difficult Experience
Want to wake up feeling great? The secret might not be so simple as a multi-step nighttime routine, early bedtime, or a no-device rule. A new study suggests that how we fall asleep and how we wake up the next day may not be so similar as we once thought. Neuroscientists tracked 20 people's brain activity as they woke up from sleep—sometimes naturally, sometimes by setting off an alarm—recording more than 1,000 awakenings in total. They found a pattern of neural activity signaled waking, but that the pattern was slightly different in people who were deep in dream-laden REM sleep as opposed to those in non-REM sleep. And people woken from REM sleep were more likely to say they felt tired on waking. 'The surprise is how consistent [this pattern] was across every awakening and also how it related to the subjective measures,' Francesca Siclari, the study's senior author and neuroscientist at the Netherlands Institute for Neuroscience, told Nature. The results were published this week in Current Biology. Each participant had 256 sensors attached to their scalps, which allowed the researchers to track their brain activity at a second-to-second timescale. From there, the researchers were able to reconstruct a visual map of each participant's brain activity and compared it to how sleepy each participant said they were on waking. They found that when people were roused during REM sleep, a neural 'wave of activation' moved from the front to the back of the brain: the prefrontal cortex, which manages executive function and decision-making, fired up first, followed by a slow 'wave' of alertness that ended at the region associated with vision. During non-REM sleep, the wave started in a central 'hotspot' and then progressed along the same front-to-back pattern. The findings could help researchers tease out why some people who struggle with sleep find it hard to wake up feeling refreshed, although more work is needed to understand whether other issues during sleep, like movement, may be at play. Less subjective measures of wakefulness could also help refine the results. 'Knowing exactly how brain activity is characterized during a normal awakening [means] we can better compare it to these abnormal awakenings,' Siclari told Nature.
Yahoo
3 days ago
- Yahoo
This new study challenges long-standing beliefs about autism
If you purchase an independently reviewed product or service through a link on our website, BGR may receive an affiliate commission. Prior research has shown that people with autism spectrum disorder (ASD) often experience difficulties recognizing faces and even emotional responses. This, many speculate, is what leads individuals with autism to exhibit social communication problems. But the problem with this understanding is that we've never had any clear evidence of how a brain affected by autism perceives the human face and body. This has left us with plenty of questions, but a new study led by Waseda University in Japan could prove this theory wrong and completely change everything we thought we know about how individuals with ASD perceive the faces and bodies of those around them. Today's Top Deals XGIMI Prime Day deals feature the new MoGo 4 and up to 42% off smart projectors Best deals: Tech, laptops, TVs, and more sales Best Ring Video Doorbell deals Challenging long-held beliefs The belief that individuals with ASD often suffer from social communication issues that are driven by how their brains perceive others is a long-standing one. However, as noted above, there's never been any scientific proof to back it up. In this new study from Waseda University, scientists took detailed neuroimages of 23 adults with ASD and compared them to the neuroimages of 23 typically developing (TD) adults. The results were not as different as expected. The researchers note that when looking at the images, they expected to see differences in the lateral occipitotemporal cortex (LOTC). This region of the brain is known to represent the visual information the brain processes to perceive the human body. Until now, it was assumed that individuals with autism, or ASD, would have that information clustered in a different way within their LOTC. However, that isn't the case at all. When looking at the data, the researchers found that individuals in the ASD and TD groups all showed similar structures of activations for their LOTCs. This could disprove the theory that individuals with ASD perceive the human body differently, thus leading to other social communication issues. The researchers also note that there were no significant differences in the size or strength of the activation of the LOTC in either group. 'These results suggest that adults with autism perceive visual body information in much the same way as neurotypical adults,' Professor Hirotaka Kurihara shared in a statement. '[This] challenges long-standing assumptions that differences in body-related perception contribute to social difficulties in ASD.' To double-check the results, the researchers also looked at whether brain patterns could be linked to individual differences. However, they also found no strong connections in this area, either. So, while it is true that individuals with ASD might struggle to read emotions or intentions based on expressions and gestures, that struggle does not seem to be tied to how their brains perceive the human body or face, which could help further research dig deeper into what the actual underlying cause is. We're still a long way from truly understanding autism and the overall affect it has on the individuals affected by it. But researchers are working hard to learn more. We've also seen some pretty amazing breakthroughs in AI development, including an AI that can detect autism just by looking at how you hold objects. More Top Deals Memorial Day security camera deals: Reolink's unbeatable sale has prices from $29.98 See the
Medscape
6 days ago
- Medscape
Why Acute Pain Can Be So Intense for Some and Not Others
Pain is a universal experience, but how it's felt and for how long can vary dramatically from person to person. For some, a surgery or herniated disc is a temporary agony that fades with time. For others, pain can become a chronic, debilitating condition, lingering long after an injury has healed. Scientists are working to understand this complex phenomenon, and new research suggests why some individuals experience pain differently. Our experience of pain relies on a complex network of nerves known as the pain neuroaxis. This system involves both peripheral nerves (those outside the brain and spinal cord) and central neurons (those in the brain, brainstem, and spinal cord). When you feel pain, these neurons fire, sending signals along this pathway to your spinal cord and brain. Many regions of your brain then interpret these signals as pain. 'Acute pain is beneficial to protecting our bodies, but chronic pain often serves no purpose and outlives its initial purpose and represents a dysfunction,' noted Steve Davidson, PhD, associate director of NYU's Pain Research Center, New York City. Scientists are still learning why normal acute pain sometimes transforms into abnormal chronic pain. New research published in Science Advances challenges a long-held belief: it's not always more neuronal stimulation that causes pain. Instead, the balance between activation and repression in specific neurons is crucial for a normal pain experience. A Surprising 'Volume Control' for Pain This new research focuses on specific neurons called projection neurons found in part of the brainstem called the medullary dorsal horn. These neurons are crucial relay stations, sending pain messages to other parts of the brain, like the parabrachial nucleus, which is involved in processing emotions and motivation alongside pain. To study pain, researchers used mice. For acute pain, they exposed mice to bright ultraviolet light, similar to how a bright light can cause discomfort in your eye at the optometrist. For chronic pain, a loose stitch was tied around the trigeminal nerve below the eye, mimicking a migraine-like pain. Interestingly, during the peak of acute pain, these pain-relay projection neurons became less excitable, explained Alexander Binshtok, PhD, professor in pain research at the Hebrew University of Jerusalem, Jerusalem, Israel, and an author of the study. It's as if their 'volume control' was turned down, causing them to fire fewer signals to the brain even though the pain stimulus was strong. As the mice's behavior indicated they were no longer experiencing pain, the excitability of these neurons returned to normal. After 20 years in the pain field, Binshtok reflected on the long-standing paradigm that pain is linked to increased nerve activity. 'What was surprising is that when we have inflammatory pain, some of the neurons actually decrease the activity in a way to control the level of pain,' he said. Using electrophysiology and computer modeling, the researchers traced the mechanism behind this 'volume control' to an increase in the neuron's potassium A-current (IA). This current acts as a brake on the neuron's activity — when IA increases, it makes it harder for the neuron to fire. This suggests a built-in protective mechanism that helps regulate the intensity of acute pain and prevents the system from being overwhelmed. As Binshtok explained, 'If suddenly these mechanisms are not working, every input from the periphery will be amplified.' The Shift to Chronic Pain The picture changes dramatically when pain becomes chronic. In the mice experiencing long-term pain, researchers observed no such increase in the IA. Instead, these same medullary dorsal horn neurons showed increased excitability and firing. It's as if the protective 'brake' is missing or not working effectively. This suggests a critical difference in how our bodies handle acute vs chronic pain. In acute pain, there appears to be a natural system that helps tune down the pain signals. But if this system isn't functioning properly, or if this tuning mechanism is absent, it could contribute to pain becoming a persistent problem. Davidson summarized the finding that there is a mechanism to reduce activity during acute pain but not in chronic pain with an analogy: 'It's like automatic braking when you are driving too fast in the city — but this mechanism is disabled on the highway, during chronic pain.' Binshtok noted that while it seemed surprising for a neuron to decrease its activity when bombarded with input at first, 'apparently this is not a surprising phenomenon when we look at other systems like the hippocampus or cortex, this adaptation is pretty common.' And this is the first time, Binshtok said, that the same neurons were shown to respond differently in acute vs chronic pain. Looking Ahead The ultimate goal in pain research, noted Patrick Sheets, PhD, associate professor of pharmacology and toxicology at the Stark Neurosciences Research Institute at Indiana University School of Medicine, Indianapolis, is to develop 'some sort of small molecule that then would eliminate aspects of pain that we don't want while preserving the ability of the person to function normally without being overwhelmed by something like addiction or lethargy.' And ultimately, it may be that pain treatment will need a personalized approach. Sheets noted that certain drugs may end up working depending 'primarily on what type of pain you have, and that can be challenging — understanding what sort of pain people are going through, diagnosing it, and then understanding what's happening at the cellular and circuit level so that you can hopefully intervene.' However, whether this IA-driven mechanism could provide relief for chronic pain sufferers is still a long way from being realized. For one thing, the study did not identify the specific potassium channel responsible for changes in IA current, Sheets noted. Davidson also pointed out that, 'ideally, the IA effect would be reversed or blocked experimentally to block the behavioral effect.' Without that, he noted, we don't know whether the increased IA current is the true cause of the change in pain behavior. Additionally, the study focused on male mice — in female mice, they did not observe the same sensitivity to ultraviolet light. Sheets noted that he has also observed sex-linked differences in his own mouse studies. (There is evidence that men and women experience pain differently as well.) And Binshtok noted that even if they find the IA target that could potentially regulate chronic pain in mice, they would still need to confirm the mechanism in humans. There's still a lot left to learn. However, Davidson said, 'Certainly looking into the IA current now looks like a promising avenue for exploration.'
