Lifeboat Foundation

A multidrug resistant strain of E. coli, MDR ST131, can readily colonize new hosts, even if those hosts are already have E. coli in their healthy gut.

This work is published in GEN Biotechnology in the paper, “Mapping the Spatial Proteome of Head and Neck Tumors: Key Immune Mediators and Metabolic Determinants in the Tumor Microenvironment.”

HNSCCs are tumors that develop in the lip, oral cavity, larynx, salivary glands, nose, sinuses, or the skin of the face. They are the seventh most common cancer globally causing more than 300,000 deaths annually. Immune checkpoint inhibitors have shown promise in treating recurrent/metastatic cases.

Here, researchers present a framework for single-cell spatial analysis of proteins to analyze HNSCCs. First, they developed an ultra-high plex antibody panel with antibodies for detection of immune cells, cancer cells, and markers that identify cellular metabolism, apoptosis and stress, tumor invasion, and metastasis, as well as cellular proliferation and deregulation.

Data serves as the foundation of today’s biotechnology and pharmaceutical industries, and that foundation keeps expanding. “The appreciation of the value of data and need for quality data has grown in recent years,” says Anastasia Christianson, PhD, vice president and global head of AI, machine learning and data, Pfizer. She notes that the concept of FAIR data—Findable, Accessible, Interoperable, and Reusable data¹—is becoming more widely accepted and more closely achieved.

Part of the transition in data use arises almost philosophically. “There has been a cultural shift or mindset change from data management for the purpose of storage and archiving to data management for the purpose of data analysis and reuse,” Christianson explains. “This is probably the most significant advance. The exponential growth of analytics capabilities and artificial intelligence have probably raised both the expectations for and appreciation of the value of data and the need for good data management and data quality.”

The DNA double helix is composed of two DNA molecules whose sequences are complementary to each other. The stability of the duplex can be fine-tuned in the lab by controlling the amount and location of imperfect complementary sequences.

Fluorescent markers bound to one of the matching DNA strands make the duplex visible, and fluorescence intensity increases with increasing duplex stability. Now, researchers at the University of Vienna succeeded in creating fluorescent duplexes that can generate any of 16 million colors—a work that surpasses the previous 256 colors limitation.

This very large palette can be used to “paint” with DNA and to accurately reproduce any digital image on a miniature 2D surface with 24-bit color depth. This research was published in the Journal of the American Chemical Society.

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.