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The rise of antimicrobial resistance has rendered many treatments ineffective, posing serious public health challenges. Intracellular infections are particularly difficult to treat since conventional antibiotics fail to neutralize pathogens hidden within human cells. However, designing molecules that penetrate human cells while retaining antimicrobial activity has historically been a major challenge. Here, we introduce APEXDUO, a multimodal artificial intelligence (AI) model for generating peptides with both cell-penetrating and antimicrobial properties. From a library of 50 million AI-generated compounds, we selected and characterized several candidates. Our lead, Turingcin, penetrated mammalian cells and eradicated intracellular Staphylococcus aureus. In mouse models of skin abscess and peritonitis, Turingcin reduced bacterial loads by up to two orders of magnitude. In sum, APEXDUO generated multimodal antibiotics, opening new avenues for molecular design.

CFN provides consulting services to Invaio Sciences and is a member of the Scientific Advisory Boards of Nowture S.L., Peptidus, European Biotech Venture Builder and Phare Bio. CFN is also a member of the Advisory Board for the Peptide Drug Hunting Consortium (PDHC). The de la Fuente Lab has received research funding or in-kind donations from United Therapeutics, Strata Manufacturing PJSC, and Procter & Gamble, none of which were used in support of this work. An invention disclosure associated with this work has been filed. All other authors declare no competing interests.

Dana-Farber Cancer Institute researchers report that all nine patients in a clinical trial being treated for stage III or IV clear cell renal cell carcinoma (a form of kidney cancer), generated a successful anti-cancer immune response after initiation of a personalized cancer vaccine.

The vaccines were administered after surgery to remove the tumor and are designed to train the body’s immune system to recognize and eliminate any remaining tumor cells. At the time of data cut-off (median of 34.7 months), all patients remained cancer-free.

The results of this Phase I trial were reported in Nature.

The motivation behind the new study was to address these gaps in our understanding by leveraging the power of large-scale data. The researchers recognized that investigating the connection between genetic predisposition to dyslexia and brain structure in a very large sample could provide more robust and reliable insights than smaller, more traditional studies. They aimed to identify specific brain regions and white matter tracts that are associated with genetic risk for dyslexia, and to explore whether different genetic variants might influence distinct neural pathways.

“Thirty-five genetic variants that influence the chance of having dyslexia were already known from a very large study by the company 23andMe in the USA, carried out in over one million people. However, that study did not include brain MRI data. The new aspect of our study was to investigate the genetic variants in relation to brain structure in MRI data from thousands of people,” explained Clyde Francks (@clydefrancks), a professor at the Max Planck Institute for Psycholinguistics in Nijmegen and senior author of the study.

The researchers used two large datasets: the genetic data 23andMe and brain imaging data from over 30,000 adults in the UK Biobank. The 23andMe dataset helped identify genetic variants associated with dyslexia by comparing individuals who reported a dyslexia diagnosis to those who did not. These genetic variants were then used to calculate “polygenic scores” for individuals in the UK Biobank, reflecting their genetic predisposition to dyslexia.

DNA-nanoparticle motors are exactly as they sound: tiny artificial motors that use the structures of DNA and RNA to propel motion through enzymatic RNA degradation. Essentially, chemical energy is converted into mechanical motion by biasing the Brownian motion.

The DNA-nanoparticle motor uses the “burnt-bridge” Brownian ratchet mechanism. In this type of movement, the motor is propelled by the degradation (or “burning”) of the bonds (or “bridges”) it crosses along the substrate, essentially biasing its motion forward.

These nano-sized motors are highly programmable and can be designed for use in molecular computation, diagnostics, and transport.

Tags; #science #neuroscience #happiness #happiness #neurodegenerativediseases #disease #health #mentalhealth #sleep #neuroscientist #disease #education #success.
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About me:
I am Shambhu Yadav, Ph.D., a research scientist at Harvard Medical School (Boston, MA, USA). I also work (for fun) as a Science Journalist, editor, and presenter on a YouTube channel. Science Communication is my passion.

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*Credits and thanks**
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Music source: Epidemic sound.

I shared this already. Here it is from Cell reversing diabetes type 1 with stem cells, reducing need for insulin shots.


Chemically induced stem-cell-derived islets were transplanted beneath the abdominal anterior rectus sheath in one patient with type 1 diabetes, resulting in tolerable safety and promising restoration of exogenous-insulin-independent glycemic control at 1-year follow-up.

Colorectal cancer (CRC) is a serious public health concern worldwide. Immune checkpoint inhibition medication is likely to remain a crucial part of CRC clinical management. This study aims to create new super paramagnetic iron oxide nano-carrier (SPION) that can effectively transport miRNA to specific CRC cell lines. In addition, evaluate the efficiency of this nano-formulation as a therapeutic candidate for CRC. Bioinformatics tools were used to select a promising tumor suppressor miRNA (mir-497-5p). Green route, using Fusarium oxyporium fungal species, manipulated for the synthesis of SPION@Ag@Cs nanocomposite as a carrier of miR-497-5p. That specifically targets the suppression of PD1/PDL1 and CTLA4pathways for colorectal therapy. UV/visible and FTIR spectroscopy, Zeta potential and MTT were used to confirm the allocation of the miR-497 on SPION@Ag@Cs and its cytotoxicity against CRC cell lines. Immunofluorescence was employed to confirm transfection of cells with miR-497@NPs, and the down-regulation of CTLA4 in HT29, and Caco2 cell lines. On the other hand, PDL1 showed a significant increase in colorectal cell lines (HT-29 and Caco-2) in response to mir497-5p@Nano treatment. The data suggest that the mir-497-loaded SPION@Ag@Cs nano-formulation could be a good candidate for the suppression of CTLA4in CRC human cell lines. Consequently, the targeting miR-497/CTLA4 axis is a potential immunotherapy treatment strategy for CRC.


Elfiky, A.M., Eid, M.M., El-Manawaty, M. et al. Sci Rep 15, 4,247 (2025). https://doi.org/10.1038/s41598-025-88165-3

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Cardiomyocytes can be implanted to remuscularize the failing heart1,2,3,4,5,6,7. Challenges include sufficient cardiomyocyte retention for a sustainable therapeutic impact without intolerable side effects, such as arrhythmia and tumour growth. We investigated the hypothesis that epicardial engineered heart muscle (EHM) allografts from induced pluripotent stem cell-derived cardiomyocytes and stromal cells structurally and functionally remuscularize the chronically failing heart without limiting side effects in rhesus macaques. After confirmation of in vitro and in vivo (nude rat model) equivalence of the newly developed rhesus macaque EHM model with a previously established Good Manufacturing Practice-compatible human EHM formulation8, long-term retention (up to 6 months) and dose-dependent enhancement of the target heart wall by EHM grafts constructed from 40 to 200 million cardiomyocytes/stromal cells were demonstrated in macaques with and without myocardial infarction-induced heart failure. In the heart failure model, evidence for EHM allograft-enhanced target heart wall contractility and ejection fraction, which are measures for local and global heart support, was obtained. Histopathological and gadolinium-based perfusion magnetic resonance imaging analyses confirmed cell retention and functional vascularization. Arrhythmia and tumour growth were not observed. The obtained feasibility, safety and efficacy data provided the pivotal underpinnings for the approval of a first-in-human clinical trial on tissue-engineered heart repair. Our clinical data confirmed remuscularization by EHM implantation in a patient with advanced heart failure.


Epicardial engineered heart muscle allografts from induced pluripotent stem cell-derived cardiomyocytes can safely and effectively remuscularize chronically failing hearts in rhesus macaques, leading to improved cardiac function and paving the way for human clinical trials.