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De novo designed proteins neutralize lethal snake venom toxins.
Nature
January 2025
Department of Biochemistry, University of Washington, Seattle, WA, USA.
Snakebite envenoming remains a devastating and neglected tropical disease, claiming over 100,000 lives annually and causing severe complications and long-lasting disabilities for many more. Three-finger toxins (3FTx) are highly toxic components of elapid snake venoms that can cause diverse pathologies, including severe tissue damage and inhibition of nicotinic acetylcholine receptors, resulting in life-threatening neurotoxicity. At present, the only available treatments for snakebites consist of polyclonal antibodies derived from the plasma of immunized animals, which have high cost and limited efficacy against 3FTxs.
View Article and Find Full Text PDFTargeting transforming growth factor-β1 by methylseleninic acid/seleno-L-methionine in clear cell renal cell carcinoma: Mechanisms and therapeutic potential.
Cancer Treat Res Commun
January 2025
Department of Pharmaceutical Sciences and Experimental Therapeutics, College of Pharmacy, University of Iowa, Iowa City, IA 52242, USA; Holden Comprehensive Cancer Center, University of Iowa, Iowa City, IA 52242, USA. Electronic address:
Clear cell renal cell carcinoma (ccRCC) poses a significant global health challenge as its incidence continues to rise, resulting in a substantial annual mortality rate. Major clinical challenges to current ccRCC treatments include high drug-resistance rates as well as dose-limiting adverse events; underlining the need to identify additional 'druggable' targets. TGF-β1, VEGF, and PD-L1 are potential therapeutic targets in ccRCC.
View Article and Find Full Text PDFPiperine relieves neuropathic pain induced by paclitaxel in mice.
Acta Neurobiol Exp (Wars)
January 2025
Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Piperine is an amide alkaloid isolated from the black pepper plant. This study examined the pain‑relieving activity of piperine against paclitaxel (PTX)‑induced neuropathy. Male mice were divided into 6 groups: Sham‑operated group (remained intact), PTX group (PTX‑treated mice receiving normal saline), PTX+ piperine 10, 25, and 50 mg/kg groups (PTX‑treated mice receiving piperine) and positive control group (PTX‑treated mice receiving imipramine 10 mg/kg).
View Article and Find Full Text PDFDevelopment, Optimization, and Evaluation of Rutin-Loaded Liposomes in the Management of Rheumatoid Arthritis.
Curr Drug Deliv
January 2025
Department of Pharmaceutical Sciences, Gurugram University, Gurugram - 122018, India.
Background: Rheumatoid arthritis is a chronic autoimmune disease, progressively distinctive via cartilage destruction, auto-antibody production, severe joint pain, and synovial inflammation. Nanotechnology represents one of the utmost promising scientific technologies of the 21st century. Nanocarriers could be the key to unlocking its potential by encapsulating Rutin in targeted drug delivery systems, potentially for targeted Rheumatoid arthritis therapy.
View Article and Find Full Text PDFNeuronal mechanisms of nociceptive-evoked gamma-band oscillations in rodents.
Neuron
January 2025
State Key Laboratory of Cognitive Science and Mental Health, Institute of Psychology, Chinese Academy of Sciences, Beijing, China; Department of Psychology, University of Chinese Academy of Sciences, Beijing, China. Electronic address:
Gamma-band oscillations (GBOs) in the primary somatosensory cortex (S1) play key roles in nociceptive processing. Yet, one crucial question remains unaddressed: what neuronal mechanisms underlie nociceptive-evoked GBOs? Here, we addressed this question using a range of somatosensory stimuli (nociceptive and non-nociceptive), neural recording techniques (electroencephalography in humans and silicon probes and calcium imaging in rodents), and optogenetics (alone or simultaneously with electrophysiology in mice). We found that (1) GBOs encoded pain intensity independent of stimulus intensity in humans, (2) GBOs in S1 encoded pain intensity and were triggered by spiking of S1 interneurons, (3) parvalbumin (PV)-positive interneurons preferentially tracked pain intensity, and critically, (4) PV S1 interneurons causally modulated GBOs and pain-related behaviors for both thermal and mechanical pain.
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