The optic nerve has been partly regenerated in mice, raising hopes for treating blindness caused by conditions such as glaucoma.
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Scientists at The University of Texas at Austin have discovered how an aggressive and deadly form of leukemia fuels its growth. In an experimental study, they were able to curb the cancer’s growth without harming healthy cells. The finding provides clues for future drug developers about how to increase the effectiveness of one type of chemotherapy.
The study, led by Xiaolu Cambronne of the Department of Molecular Biosciences, in collaboration also with researchers at Dell Medical School and in the Department of Nutritional Sciences, is published in Cell Metabolism.
Acute myeloid leukemia (AML) is an aggressive cancer that starts in the blood-forming cells of the bone marrow. Known for rapid expansion, the cancer kills approximately 11,000 Americans each year. Most of the cases of AML occur in adults over 65, a population that often responds poorly to aggressive treatments, such as bone marrow transplants, and thus has limited options.
Two RNA-editing therapies for genetic diseases have recently gained approval for clinical trials, raising hopes for safer treatments.
The challenge is huge: There’s a lot we don’t understand about Alzheimer’s disease, but we do know that patient’s brains tend to accumulate toxic tau and amyloid-beta proteins, so most research has focused on those targets.
That approach has led to new drugs that can slow the progression of Alzheimer’s to a small degree, but we’ve yet to find anything that can reverse the damage the disease does to the brain.
The big idea: Synapses — the connections between brain neurons — need a protein called “KIBRA” in order to form memories, and there’s a link between certain variants of the KIBRA gene and developing Alzheimer’s.
Nanotechnology is intimately intertwined with efforts to bring bottom-up synthetic cell research to the forefront, and only strengthening these bonds will expand the scope of what this might achieve.
This Review explores the development of ingestible electronics and provides a step-by-step guide for the design of ingestible electronic capsules at the system level.
Near-gapless and haplotype-resolved genome assemblies of the dwarfing ‘M9’ and semi-vigorous ‘MM106’ rootstocks and a major apple cultivar ‘Fuji’ provide insights into the genetic basis of rootstock-induced dwarfing traits.
To construct a pan-genome that encompasses the full range of genetic diversity in B. ole racea, we analyzed the resequencing data of 704 globally distributed B. ole racea accessions covering all different morphotypes and their wild relatives (Supplementary Tables 1 and 2). We identified 3,792,290 SNPs and 528,850 InDels in these accessions using cabbage JZS as reference genome22. A phylogenetic tree was then constructed using SNPs, which classified the 704 accessions into the following three main groups: wild B. ole racea and kales, arrested inflorescence lineage (AIL) and leafy head lineage (LHL; Fig. 1a and Supplementary Note 2). The phylogenetic relationship revealed in our study was generally consistent with those reported previously4,5,24,25. Based on the phylogeny and morphotype diversity, we selected 22 representative accessions for de novo genome assembly (Table 1).
We assembled genome sequences of the 22 accessions by integrating long-reads (PacBio or Nanopore sequencing), optical mapping molecules (BioNano) or high-throughput chromosome conformation capture data (Hi-C) and Illumina short-reads (Methods; Supplementary Note 2 and Supplementary Tables 3–7). The total genome size of these assemblies ranged from 539.87 to 584.16 Mb with an average contig N50 of 19.18 Mb (Table 1). An average of 98% contig sequences were anchored to the nine pseudochromosomes of B. ole racea. The completeness of these genome assemblies was assessed using benchmarking universal single-copy orthologs (BUSCO), with an average of 98.70% complete score in these genomes (Supplementary Table 8).
To minimize artifacts that could arise from different gene prediction approaches, we predicted gene models of both the 22 newly assembled genomes and the five reported high-quality genomes5,21,22,23 using the same annotation pipeline (Methods). Using an integrated strategy combining ab initio, homology-based and transcriptome-assisted prediction, we obtained a range of 50,346 to 55,003 protein-coding genes with a mean BUSCO value of 97.9% in these genomes (Table 1). After gene prediction, a phylogenetic tree constructed based on single-copy orthologous genes clustered the 27 genomes into three groups, similar to the results observed in the population (Fig. 1a and b).
Diagnosing schizophrenia as early as possible helps minimize the toll the neurological disorder takes on the body and the mind. Unfortunately the condition’s signs can be difficult to spot in the early stages.
That’s why researchers led by a team from the Indiana University School of Medicine have developed a test which offers a relatively simple and reliable way to check for current schizophrenia severity and future risk.
“Psychosis usually manifests in young adulthood – a prime period of life,” says neuroscientist Alexander Niculescu from the Indiana University School of Medicine. “Stress and drugs, including marijuana, are precipitating factors on a background of genetic vulnerability.”
