MRI helps reveal rare spread of cervical cancer into the uterine corpus
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Updates every hour. Last Updated: 23-Oct-2026 01:16 ET (23-Oct-2026 05:16 GMT/UTC)
A new study introduces a novel injectable composite microsphere that combines cells and biomaterials to significantly accelerate bone healing.
This is the first unequivocal record of the species outside its type locality in Dorset, UK, and the largest specimen known to date.
Scientists at Peking University have identified a mitochondrial protein that is essential for protecting motor neurons, offering new insight into how amyotrophic lateral sclerosis (ALS) may develop. The study, led by Dr. Xianhua Wang and Dr. Heping Cheng at the College of Future Technology, Peking University, shows that loss of the mitochondrial protein ROMO1 causes progressive damage to motor neurons and muscles in mice, closely resembling key features of human ALS. The findings were published online in Science Bulletin.
A new study in Science Bulletin reveals that maternal PAN2 protein is essential for early embryonic development by regulating mRNA poly(A) tail length. Using an oocyte-specific conditional knockout mouse model, researchers found that PAN2 deficiency causes embryos to arrest at the two-cell stage due to abnormal poly(A) tail elongation, maternal mRNA accumulation, and impaired zygotic genome activation. PAN2 recognizes substrates via the PAN3-PABPC1 complex, preferring tails lacking guanosine but enriched in uridine.
A research team led by Prof. Yi Sun at Zhejiang University, reported a unexpected finding that the combination of KrasG12D activation and genetic inactivation of UBE2M in the lung triggers the cGAS-STING-NF-κB signal to form a inflammatory tumor microenvironment (TME). Mechnistically, KrasG12D promotes the mitochondrial biogenesis, whereas UBE2M depletion inhibits Parkin neddylation and mitophagy, together causing the cytoplasmic release of damaged mitochondrial DNA. The STING antagonist H-151 rescues TME, indicating a causal role of the cGAS-STING signal. The study therefore demonstrates a unexpected role of UBE2M in prevention TME induced by Kras mutant.
A comprehensive in silico scan of human respiratory viruses identified 3CLpro cleavage motifs within influenza NP and PA. Experimental validation confirmed that 3CLpro-mediated cleavage triggers rapid protein degradation and cytoplasmic mislocalization. Consequently, both ectopic 3CLpro expression and SARS-CoV-2 replication effectively inhibit replication across diverse influenza virus strains, revealing a broad-spectrum antiviral mechanism.