Lifeboat Foundation

Summary: Researchers developed the world’s first 3D-printed brain tissue that grows and behaves similarly to natural brain tissue, marking a significant leap forward for neurological and neurodevelopmental disorder research.

This novel 3D-printing technique uses a horizontal layering approach and a softer bio-ink, allowing neurons to interconnect and form networks akin to human brain structures.

The ability to precisely control cell types and arrangements provides unparalleled opportunities to study brain functions and disorders in a controlled environment, offering new avenues for drug testing and understanding brain development and diseases like Alzheimer’s and Parkinson’s.

Heartbeat-induced pulsations of cerebral blood vessels can directly entrain neuronal activity.

An AI algorithm outperformed other screening methods in identifying cervical precancer. The approach could be especially valuable in low-resource settings.

A team of molecular engineers have developed a type of plastic that can be shape-shifted using tempering. In their paper published in the journal Science the team, from the University of Chicago, with a colleagues from the US DEVCOM Army Research Laboratory, Aberdeen Proving Ground, the National Institutes of Standards and Technology and the NASA Glenn Research Center, describe how they made their plastic and how well it was able to shape shift when they applied various types of tempering.

Haley McAllister and Julia Kalow, with Northwestern University, have published a Perspective piece in the same issue of Science outlining the work.

Over the past several years, it has become evident that the use of plastics in products is harmful to not only the environment but also human health —bits of plastic have been found in the soil, the atmosphere, the oceans, and the human body.

Some hereditary genetic defects cause an exaggerated immune response that can be fatal. Using the CRISPR-Cas9 gene-editing tool, such defects can be corrected, thus normalizing the immune response, as researchers led by Klaus Rajewsky from the Max Delbrück Center now report in Science Immunology.

Familial hemophagocytic lymphohistiocytosis (FHL) is a rare disease of the immune system that usually occurs in infants and young children under the age of 18 months. The condition is severe and has a high mortality rate. It is caused by various gene mutations that prevent cytotoxic T cells from functioning normally. These are a group of immune cells that kill virus–infected cells or otherwise altered cells.

If a child with FHL contracts a virus—such as the Epstein-Barr virus (EBV), but also other viruses—the cytotoxic T cells cannot eliminate the infected cells. Instead, the immune response gets out of control. This leads to a cytokine storm and an excessive inflammatory reaction that affects the entire organism.

Plant cell-surface receptors that are known to participate in immunity, development, and reproductive processes include the LRR-, G-lectin-, Wall-associated kinase (WAK)-, Domain of Unknown Function 26 (Duf26)-, L-lectin-, Lysin motif (LysM)-, and Malectin-containing RLKs and RLPs (Fig. 1a–h). There are additional RLK families with different ectodomains, such as the proline-rich extensin-like receptor kinases (PERKs) and thaumatin-like protein kinases (TLPKs)^9,13. However, their function in immunity is not well-characterized. Cell-surface receptors with LRR-, G-lectin-, WAK-, and LysM-ectodomains have been reported to recognise PAMPs, while others perceive self-molecules or unidentified ligands (Fig. 1h; Supplementary Fig. 1). Recognition of the diverse array of ligands is likely to be accomplished by variable structures and combinations of different ectodomains (Fig. 1a–g). To trace the origins of different receptor classes within the plant lineage, we first identified RLKs and RLPs in 350 genomes from Glaucophyta, red algae, green algae, Bryophytes, and Tracheophytes. We define here RLKs as any proteins with both 1–2 TMs and KDs, and RLPs as any protein with 1–2 TMs, but lack KDs. In total, we identified 177,645 RLKs, almost up to 70% of which possess either LRR-, G-lectin-, WAK-, Duf26-, L-lectin-, LysM-and Malectin-ectodomains (Fig. 1i). Next, we searched for proteins with these ectodomains and TMs that lack KDs and found 41,144 RLPs (Fig. 1j). We further examined which of the identified RLKs and RLPs families are likely to be involved in immunity. A previous report suggested a positive correlation between the gene family sizes of cell-surface immune receptors and intracellular immune receptors (the NB-ARC family) across the angiosperms⁴. We examined the correlation between the relative size (%; number of identified genes in the family/numbers of searched genes × 100; see methods) of the RLK families, the RLPs families, and the NB-ARC family in each genome. Notably, most RLK families (except for the LysM-RLKs) exhibit positive correlations with the NB-ARC family, while most RLP families (except for the LRR-RLPs) do not exhibit positive correlation with the NB-ARC family (Main Fig. 1k). Furthermore, we checked the expression level of these receptor families in Arabidopsis thaliana during immunity. Notably, the RLKs, except for LRR-and Malectin-RLKs, generally exhibit higher expression levels compared to the RLPs during immunity (Main Fig. 1k; Supplementary Fig. 2). These data collectively suggest that the RLKs are more likely to be involved in immunity than the RLPs.

Next, we examined the presence or absence of ectodomains (LRR-, G-lectin-, WAK-, Duf26-, L-lectin-, LysM-and Malectin-ectodomains lacking TM or KD; ectodomain-only proteins), RLPs (TM-bound ectodomains) and RLKs (ectodomains encompassing both TM and KD) in the plant lineage (Fig. 2; Supplementary Fig. 3; Supplementary Data 1a–c). Ectodomains exhibit an ancient heritage, with LRR-, WAK-, LysM-, Malectin-, and L-lectin-domains dating back to the era of Glaucophyta. Similarly, relatively ancient counterparts such as LRR-RLPs, WAK-RLPs, LysM-RLPs, Malectin-RLPs, and L-lectin-RLPs are found in both Glaucophyta and Rhodophyta. In contrast, RLKs emerged more recently. Green algae harbour WAK-RLKs, Malectin-RLKs, and G-lectin-RLKs, and LysM-RLKs, L-lectin-RLKs, and Duf-26-RLKs are exclusive to Embryophytes (Fig. 2). Except for LRR-RLPs, all six families of RLP are basal to the RLK families.

ERS Genomics discusses how gene editing is transforming the future of food.

We are in the middle of a data-driven science boom. Huge, complex data sets, often with large numbers of individually measured and annotated ‘features’, are fodder for voracious artificial intelligence (AI) and machine-learning systems, with details of new applications being published almost daily.

But publication in itself is not synonymous with factuality. Just because a paper, method or data set is published does not mean that it is correct and free from mistakes. Without checking for accuracy and validity before using these resources, scientists will surely encounter errors. In fact, they already have.

In the past few months, members of our bioinformatics and systems-biology laboratory have reviewed state-of-the-art machine-learning methods for predicting the metabolic pathways that metabolites belong to, on the basis of the molecules’ chemical structures¹. We wanted to find, implement and potentially improve the best methods for identifying how metabolic pathways are perturbed under different conditions: for instance, in diseased versus normal tissues.

Cancer treatments, including chemotherapy, in addition to killing a large number of tumor cells, also result in the generation of senescent tumor cells (also called “zombie cells”). While senescent cells do not reproduce, they do, unfortunately, generate a favorable environment for the expansion of tumor cells that may have escaped the effects of the chemotherapy and eventually result in tumor regrowth.

An international team of researchers led by Dr. Manuel Serrano at IRB Barcelona has described in Nature Cancer how cancer cells that have become senescent after chemotherapy activate the PD-L2 protein to protect themselves from the immune system while recruiting immune suppressor cells. The latter creates an inhibitory environment that impairs the ability of lymphocytes to kill cancer cells.

Based on these findings, scientists wondered what would be the effect of inactivating PD-L2. Interestingly, senescent cells lacking PD-L2 are rapidly eliminated by the immune system. This intercepts the capacity of senescent cells to create an immunosuppressive environment and, as a result, lymphocytes retain their full capacity to kill those cancer cells that may have escaped the effects of chemotherapy.