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Category: bioengineering

Dental caries (tooth decay) is a common oral health condition that often causes significant pain and discomfort and may even lead to tooth loss. In severe and untreated cases, bacterial infection combined with the host’s immune response can cause bone resorption, or the breakdown of bone tissue in the tooth root. Moreover, traditional treatments for advanced dental caries, such as surgery, can result in bone defects that require complex bone grafting procedures.

Building on this knowledge, bone tissue engineering and dental tissue regeneration have gained the attention of researchers worldwide. Recent reports suggest that microRNAs (miRNAs)—small, non-coding ribonucleic acid sequences—play a key role in bone tissue regeneration. However, the underlying mechanisms and pathways regulated by miRNAs remain unclear.

To investigate the intrinsic processes involved in dental bone repair, a team of researchers led by Associate Professor Nobuyuki Kawashima, graduate student Ziniu Yu, and Professor Takashi Okiji from the Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (Science Tokyo), Japan, has conducted a series of innovative experiments using human dental pulp stem cells (hDPSCs) and mice.

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Birmingham scientists have identified an essential genetic code for a method called plasmid curing, which aims to “displace” antibiotic-resistance genes from bacteria.

Plasmids, which are small, circular strands of DNA, play a crucial role in allowing to share beneficial genes rapidly in a changing environment, most concerningly when they carry genes conferring resistance to antibiotics.

Professor Chris Thomas from Birmingham’s School of Biosciences has investigated plasmid curing for many years, and engineered useful “multi-copy” (many copies in each bacterium) plasmids for this purpose, resulting in a patented, efficient way to displace unwanted plasmids that carry resistance.

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Mitochondrial diseases affect approximately 1 in 5,000 people worldwide, causing debilitating symptoms ranging from muscle weakness to stroke-like episodes. Some of these conditions result from mutations in mitochondrial DNA (mtDNA), the genetic material housed in these organelles. For patients with the common m.3243A>G mutation, which can cause MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) and diabetes mellitus, treatments remain limited.

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Patreon: https://bit.ly/3v8OhY7

Michael Levin is a Distinguished Professor in the Biology Department at Tufts University, where he holds the Vannevar Bush endowed Chair, and he is also associate faculty at the Wyss Institute at Harvard University. Michael and the Levin Lab work at the intersection of biology, artificial life, bioengineering, synthetic morphology, and cognitive science. Michael also appeared on the show in episode #151, which was all about synthetic life and collective intelligence. In this episode, Michael and Robinson discuss the nature of cognition, working with Daniel Dennett, how cognition can be realized by different structures and materials, how to define robots, a new class of robot called the Anthrobot, and whether or not we have moral obligations to biological robots.

The Levin Lab: https://drmichaellevin.org/

OUTLINE
00:00 Introduction.
02:14 What is Cognition?
08:01 On Working with Daniel Dennett.
13:17 Gatekeeping in Cognitive Science.
25:15 The Multi-Realizability of Cognition.
31:30 What are Anthrobots?
39:33 What Are Robots, Really?
59:53 Do We Have Moral Obligations to Biological Robots?

Robinson’s Website: ⁠http://robinsonerhardt.com⁠

Robinson Erhardt researches symbolic logic and the foundations of mathematics at Stanford University. Join him in conversations with philosophers, scientists, weightlifters, artists, and everyone in-between.

Continue reading “Michael Levin: The New Era of Cognitive Biorobotics | Robinson’s Podcast #187” | >

A nice brief paper comparing plasmid multimer formation in different strains of bacteria and identifying conditions under which such multimer formation occurs minimally. #biotech #synbio

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A Kobe University team was able to edit the DNA of Lactobacillus strains directly without a template from other organisms. This technique is indistinguishable from natural variation and enabled the researchers to create a strain that doesn’t produce diabetes-aggravating chemicals.

Humans have improved the microorganisms we rely on for millennia, selecting variants that are better able to produce wine, yogurt, natto and many other products. More recently, direct genetic modification has emerged as a tool to exert more precise and efficient control over the improvement, but also has drawn much public criticism for often using DNA from unrelated organisms in these modifications. Kobe University bioengineer NISHIDA Keiji says, “As a consequence, using such transgenic techniques is not favorable for food products due to legislations being restrictive and social acceptance being low.”

Nishida and his team have developed a technique that gives even more precise control over the genetic content of a microorganism that does not rely on template DNA from other organisms. He says: “We have invented a DNA base editing technology named ‘Target-AID,’ which is superior to conventional techniques such as ‘CRISPR-Cas9’ in several aspects. For example, CRISPR-Cas9 induces DNA breaks and often causes cell death, while our Target-AID inserts precise point mutations without such breaks.”

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A research team has uncovered a previously unknown type of immune signaling molecule—a novel compound combining histidine and ADP-ribose—produced by bacteria’s Thoeris II defense system in response to viral infection. This finding expands our understanding of bacterial immunity and may pave the way for innovative tools in biotechnology, gene editing, and antimicrobial therapy.

The paper, titled “TIR domains produce histidine-ADPR as an immune signal in bacteria,” is published in the journal Nature, and the team includes scientists at Vilnius University’s Life Sciences Centre (VU LSC), together with colleagues from the Weizmann Institute of Science (Israel) and Harvard Medical School.

The discovery sheds light on how bacteria, much like humans, communicate viral threats at the molecular level—in this case, triggering a self-sacrificing response to halt virus spread and protect bacterial populations. Beyond its fundamental significance, the finding opens exciting avenues for rethinking immune mechanisms and virus-host interactions.

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