Toggle light / dark theme

Get the latest international news and world events from around the world.

Log in for authorized contributors

A simple shot shows promise to reverse osteoarthritis within weeks

A research team including scientists and engineers from University of Colorado Boulder, CU Anschutz and Colorado State University has developed a suite of new therapies that prompt aging or damaged joints to repair themselves within weeks, according to animal studies.

The new osteoarthritis treatments include a single, regenerative injection to a joint and a biomaterial repair kit that recruits the body’s own cells to patch holes in damaged cartilage.

To expedite the research, the federal Advanced Research Projects Agency for Health (ARPA-H) announced this week that the multidisciplinary team will advance to the next phase of the project.

The sun is tearing an asteroid to pieces, and Earth is now flying through the fallout

Across Earth, every night, thousands of automated stargazers are waiting to take pictures of shooting stars. I am one of the scientists who study these meteors.

Most movies and news alerts focus on large asteroids that could destroy Earth. And your phone notifies you every few months that an object nine washing machines wide is going to just narrowly skim past. However, the small dust and rubble that enter our atmosphere daily tell an equally interesting story.

My planetary science colleagues and I use camera observations of the night sky to better understand dust, car-sized asteroids and debris from comets in our solar system.

Targeting KRAS G12C Mutation in Colorectal Cancer, A Review: New Arrows in the Quiver

Kirsten rat sarcoma virus oncogene homolog (KRAS) is the most frequently mutated oncogene in human cancer. In colorectal cancer (CRC), KRAS mutations are present in more than 50% of cases, and the KRAS glycine-to-cysteine mutation at codon 12 (KRAS G12C) occurs in up to 4% of patients. This mutation is associated with short responses to standard chemotherapy and worse overall survival compared to non-G12C mutations. In recent years, several KRAS G12C inhibitors have demonstrated clinical activity, although all patients eventually progressed. The identification of negative feedback through the EGFR receptor has led to the development of KRAS inhibitors plus an anti-EGFR combination, thus boosting antitumor activity. Currently, several KRAS G12C inhibitors are under development, and results from phase I and phase II clinical trials are promising.

Frontiers: As a significant mental health disorder worldwide

The treatment of depression has long faced the challenges of a low treatment rate, significant drug side effects and a high relapse rate. Recent studies have revealed that the gut microbiota and neuronal mitochondrial dysfunction play central roles in the pathogenesis of depression: the gut microbiota influences the course of depression through multiple pathways, including immune regulation, HPA axis modulation and neurotransmitter metabolism. Mitochondrial function serves as a key hub that mediates mood disorders through mechanisms such as defective energy metabolism, impaired neuroplasticity and amplified neuroinflammation. Notably, a bidirectional regulatory network exists between the gut microbiota and mitochondria: the flora metabolite butyrate enhances mitochondrial biosynthesis through activation of the AMPK–PGC1α pathway, whereas reactive oxygen species produced by mitochondria counteract the flora composition by altering the intestinal epithelial microenvironment. In this study, we systematically revealed the potential pathways by which the gut microbiota improves neuronal mitochondrial function by regulating neurotransmitter synthesis, mitochondrial autophagy, and oxidative stress homeostasis and proposed the integration of probiotic supplementation, dietary fiber intervention, and fecal microbial transplantation to remodel the flora–mitochondrial axis, which provides a theoretical basis for the development of novel antidepressant therapies targeting gut–brain interactions.

Depression is a disorder that severely affects the mental health of the global population and is characterized by persistent low mood, loss of interest and cognitive dysfunction (GBD 2017 Disease and Injury Incidence and Prevalence Collaborators, 2018; COVID-19 Mental Disorders Collaborators, 2021; Salari et al., 2020). Globally, depression is one of the leading causes of mental disability. According to the World Health Organization (WHO), the global prevalence of depression is approximately 4.4%, which means that more than 300 million people worldwide suffer from depression (Xu et al., 2024). In addition, depression is one of the major causes of suicide deaths, with nearly 800,000 people worldwide dying by suicide each year (World Health Organization, 2021).

How multiple sclerosis kills neurons

MS is typically diagnosed when clinicians see lesions in the myelin-rich white matter of the brain on MRI scans. White matter is made of the nerves that link brain cells and it looks white on a brain scan.

The brain’s grey matter, which houses the “bodies” of the brain cells, can also have MS lesions, especially in its outer layers. These lesions are less common — and harder to see on a brain scan — but they are a sign of chronic and disabling MS.

The scientists wanted to learn more about the neurons that died in these grey-matter lesions, which express a gene called CUX2. In the first study, they looked at developing mouse brains to see how CUX2 neurons are born. This occurs early in life, when the brain is growing quickly, putting cells under tremendous stress.

The cells relied on a mechanism to repair their DNA as they rapidly multiplied, fanned out into the far reaches of the brain and wired up with one another. The mechanism depends on a stress-response gene called ATF4 to keep chromosomes intact. When the team removed ATF4, the growing neurons were rife with DNA damage, and this prevented the frontal part of the brain from forming.

In the second study, the team found DNA damage in grey matter lesions from people with MS involving the same neurons.

In mouse models of MS, the researchers saw that inflammation sparked chemical reactions that damaged DNA in CUX2 neurons. The repair systems that protect these neurons from the stresses of development could no longer keep up; and this led to brain damage.

Together, the two studies outline the natural way the brain’s outer layer neurons cope with DNA damage — and how that system breaks down in MS. ScienceMission sciencenewshighlights.

Scientists uncover brain circuits for impulsivity

Scientists from the Lee Kong Chian School of Medicine at Nanyang Technological University, Singapore, have uncovered how different brain regions work together to enable self-control—the ability to suppress impulsive behaviors and wait for the right moment to act. Their findings advance the understanding of conditions such as attention-deficit hyperactivity disorder (ADHD) and addiction, and could lead to more effective management of these disorders.

According to the researchers, this is the first time that this interplay underlying self-control has been found in the brain. The findings were reported in Science Advances.

Safety Profile of the Trastuzumab-Based ADCs: Analysis of Real-World Data Registered in EudraVigilance

Trastuzumab (T) and tyrosine kinase inhibitors (TKIs) are among the first-line treatments recommended for HER2-positive breast cancer. More recently, antibody-drug conjugates (ADCs) such as trastuzumab deruxtecan (T-DXd) and trastuzumab emtansine (T-DM1) have been authorized, and they represent the second-line therapy in this type of cancer. The present study aimed to evaluate adverse drug reactions (ADRs) associated with T-based ADCs that were spontaneously reported in EudraVigilance—the European pharmacovigilance database. Out of 42,272 ADRs reported for currently approved ADCs on the market, 24% of ADRs were related to T-DM1, while 12% of ADRs were related to T-DXd.

/* */