A technique based on modulating quantum processes inside human cells could improve treatment for glioblastoma.
Half a century after its foundation, the neutral theory of molecular evolution continues to attract controversy. The debate has been hampered by the coexistence of different interpretations of the core proposition of the neutral theory, the ‘neutral mutation–random drift’ hypothesis. In this review, we trace the origins of these ambiguities and suggest potential solutions. We highlight the difference between the original, the revised and the nearly neutral hypothesis, and re-emphasise that none of them equates to the null hypothesis of strict neutrality. We distinguish the neutral hypothesis of protein evolution, the main focus of the ongoing debate, from the neutral hypotheses of genomic and functional DNA evolution, which for many species are generally accepted. We advocate a further distinction between a narrow and an extended neutral hypothesis (of which the latter posits that random non-conservative amino acid substitutions can cause non-ecological phenotypic divergence), and we discuss the implications for evolutionary biology beyond the domain of molecular evolution. We furthermore point out that the debate has widened from its initial focus on point mutations, and also concerns the fitness effects of large-scale mutations, which can alter the dosage of genes and regulatory sequences. We evaluate the validity of neutralist and selectionist arguments and find that the tested predictions, apart from being sensitive to violation of underlying assumptions, are often derived from the null hypothesis of strict neutrality, or equally consistent with the opposing selectionist hypothesis, except when assuming molecular panselectionism. Our review aims to facilitate a constructive neutralist–selectionist debate, and thereby to contribute to answering a key question of evolutionary biology: what proportions of amino acid and nucleotide substitutions and polymorphisms are adaptive?
Half a century after its foundation, the neutral theory of molecular evolution continues to attract controversy. The debate has been hampered by the coexistence of different interpretations of the core proposition of the neutral theory, the ‘neutral mutation–random drift’ hypothesis. In this review, we trace the origins of these ambiguities and suggest potential solutions. We highlight the difference between the original, the revised and the nearly neutral hypothesis, and re-emphasise that none of them equates to the null hypothesis of strict neutrality. We distinguish the neutral hypothesis of protein evolution, the main focus of the ongoing debate, from the neutral hypotheses of genomic and functional DNA evolution, which for many species are generally accepted. We advocate a further distinction between a narrow and an extended neutral hypothesis (of which the latter posits that random non-conservative amino acid substitutions can cause non-ecological phenotypic divergence), and we discuss the implications for evolutionary biology beyond the domain of molecular evolution. We furthermore point out that the debate has widened from its initial focus on point mutations, and also concerns the fitness effects of large-scale mutations, which can alter the dosage of genes and regulatory sequences. We evaluate the validity of neutralist and selectionist arguments and find that the tested predictions, apart from being sensitive to violation of underlying assumptions, are often derived from the null hypothesis of strict neutrality, or equally consistent with the opposing selectionist hypothesis, except when assuming molecular panselectionism. Our review aims to facilitate a constructive neutralist–selectionist debate, and thereby to contribute to answering a key question of evolutionary biology: what proportions of amino acid and nucleotide substitutions and polymorphisms are adaptive?
Previous research has implicated fungi in chronic neurodegenerative conditions such as Alzheimer’s disease, but there is limited understanding of how these common microbes could be involved in the development of these conditions.
Working with animal models, researchers at Baylor College of Medicine and collaborating institutions discovered how the fungus Candida albicans enters the brain, activates two separate mechanisms in brain cells that promote its clearance, and, important for the understanding of Alzheimer’s disease development, generates amyloid beta (Ab)-like peptides, toxic protein fragments from the amyloid precursor protein that are considered to be at the center of the development of Alzheimer’s disease. The study appears in the journal Cell Reports.
“Our lab has years of experience studying fungi, so we embarked on the study of the connection between C. albicans and Alzheimer’s disease in animal models,” said corresponding author Dr. David Corry, Fulbright Endowed Chair in Pathology and professor of pathology and immunology and medicine at Baylor. He also is a member of Baylor’s Dan L Duncan Comprehensive Cancer Center. “In 2019, we reported that C. albicans does get into the brain where it produces changes that are very similar to what is seen in Alzheimer’s disease. The current study extends that work to understand the molecular mechanisms.”
Light is critical for transmitting visual information to the brain; but light also impacts non-visual processes in the body, such as circadian rhythms, hormone secretion, pupil size and sleep cycles, for example. Exposure to blue light is known to stimulate alertness and enhance cognitive performance, but the neural processes underlying this effect are not well understood. Now, researchers at the University of Liège in Belgium have used ultrahigh-field MRI to find out more about how light stimulates our brains, reporting their findings in Communications Biology.
Non-visual responses to light are mainly mediated by photosensitive retinal ganglion cells that express melanopsin, a photopigment that’s most sensitive to blue light at around 480 nm. These retinal neurons transfer light information to several areas of the brain associated with light-mediated behaviour. In particular, the pulvinar (a region of the posterior thalamus involved in attention control) is consistently activated in response to light, suggesting that the thalamus, a subcortical region, may play a key role in relaying non-visual light information to the cortex.
To investigate this hypothesis, first author Ilenia Paparella and colleagues in the GIGA-CRC laboratory used 7T functional MRI to record the brain activity of 19 healthy young participants while they completed an auditory oddball task known to elicit response in the posterior thalamus. During the task, in which random rare deviant tones were sounded amongst frequent standard tones, the volunteers were either in darkness or exposed to 30 s blocks of blue-enriched polychromatic or control orange light.
Summary: Scientists have successfully determined the genomic composition of octopuses, unveiling a whopping 2.8 billion base pairs across 30 chromosomes. This was a result of comprehensive, computer-assisted genome studies and comparisons with other cephalopod species.
This high-quality reference sequence paves the way for understanding octopus biology and tracing its evolutionary trajectory.
The findings, which shine a light on the dynamic evolutionary history of the octopus genome, will enrich research in neurobiology, behavior, and development.
Amazon is getting into the business of prescription drug delivery via drone to doorsteps, promising to do it within an hour from when an order is placed.
We need to ķeep up with china in human enhancement and biotechnology.
Tristan Harris and Aza Raskin discuss how existing A.I. capabilities already pose catastrophic risks to a functional society, how A.I. companies are caught in a race to deploy as quickly as possible without adequate safety measures, and what it would mean to upgrade our institutions to a post-A.I. world.
What is the impact of treatment interruptions during courses of adjuvant radiation therapy for breast cancer?
The impact of treatment interruptions during courses of adjuvant radiation therapy for breast cancer has not been investigated. To address this issue, investigators conducted a study of 35,845 triple-negative breast cancer (TNBC) patients in the National Cancer Database who received external beam radiation and had overall survival (OS) of at least 12 months. Among these patients, 76% had grade III–IV disease and 68% had N0 cancer.
Multivariable Cox proportional hazard models were used to determine the association between interrupted treatment days and OS. The number of interrupted treatment days was defined as the total number of days from the start to the end of treatment minus the number of expected days of treatment. OS was defined as the time between the date of diagnosis and the date of death.
As the number of interrupted treatment days increased, OS progressively worsened. Compared with 0–1 interrupted treatment days, hazard ratios for poorer OS were 1.069 for 2–5 interrupted treatment days, 1.239 for 6–10 interrupted treatment days, and 1.265 for 11–15 interrupted treatment days. Other factors significantly associated with poorer OS were Black versus white race (HR, 1.278), other nonwhite versus white race (HR, 1.337), grade III–IV versus grade I disease (HR, 1.743), and stage N1–N3 versus N0 disease (HR, 2.534–4.992).
Continue reading “Interrupting Radiation Therapy for Triple-Negative Breast Cancer” »
Researchers are attempting to uncover the basics of how fat tissue is structured and, specifically, inflammation associated with obesity, in the hopes of unlocking the connection between the accumulation of fat and poor health outcomes. Now, a new study by researchers at the University of Michigan revealed previously unrecognized immune cell types and interactions within adipose tissue using single-cell analysis of gene expression combined with spatial transcriptomics.
The findings are published in JCI Insight in an article titled, “A lipid-associated macrophage lineage rewires the spatial landscape of adipose tissue in early obesity.”
“Adipose tissue macrophage (ATM) infiltration is associated with adipose tissue dysfunction and insulin resistance in mice and humans,” wrote the researchers. “Recent single-cell data highlight increased ATM heterogeneity in obesity but do not provide a spatial context for ATM phenotype dynamics. We integrated single-cell RNA-Seq, spatial transcriptomics, and imaging of murine adipose tissue in a time course study of diet-induced obesity. Overall, proinflammatory immune cells were predominant in early obesity, whereas nonresident antiinflammatory ATMs predominated in chronic obesity.”
