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The next software revolution: programming biological cells | Sara-Jane Dunn

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The cells in your body are like computer software: they’re “programmed” to carry out specific functions at specific times. If we can better understand this process, we could unlock the ability to reprogram cells ourselves, says computational biologist Sara-Jane Dunn. In a talk from the cutting-edge of science, she explains how her team is studying embryonic stem cells to gain a new understanding of the biological programs that power life — and develop “living software” that could transform medicine, agriculture and energy.

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Vitamin B6: Increase NAD Without NR, NMN, or Niacin?

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The factory making bionic arms for Ukrainian soldiers — BBC News

Thousands of people in Ukraine have lost their limbs in the war against Russia, according to World Health Organisation estimates.

The Ukrainian charity Superhumans and the UK-based company Open Bionics have partnered to create bionic arms for the wounded.

The BBC visited the factory in Bristol, England, responsible for creating the prosthetics.

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#Ukraine #BionicArm #Bristol

A newly discovered pathway could prevent kidney failure in masses

Researchers have recently made a groundbreaking discovery in the field of kidney disease. They have found a new pathway that could potentially prevent kidney failure in thousands of people. Dr. Carl May and his team at Bristol Medical School, with funding from Kidney Research UK, have discovered a new treatment pathway for non-genetic nephrotic syndrome.

This targets the unknown factor that leads to kidney failure. Nephrotic syndrome is a rare kidney condition that causes protein to leak into the urine, affecting around 10,000 people annually in the UK. The discovery offers hope for patients, especially children, who may develop kidney failure.

Researchers from Bristol Renal have identified a receptor called PAR-1 that works in conjunction with an unknown factor to cause kidney failure in patients with idiopathic nephrotic syndrome (INS). They found that anti-PAR-1 treatments could block the effect of the factor and prevent kidneys from failing, potentially making transplantation a more viable option for more patients.

Inhibition of Rho-kinase ameliorates decreased spine density in the medial prefrontal cortex and methamphetamine-induced cognitive dysfunction in mice carrying schizophrenia-associated mutations of the Arhgap10 gene

Reversing schizophrenia with gene therapy year 2023.

Copy-number variations in the ARHGAP10 gene encoding Rho GTPase–activating protein 10 are associated with schizophrenia. Model mice (Arhgap10 S490P/NHEJ mice) that carry “double-hit” mutations in the Arhgap10 gene mimic the schizophrenia in a Japanese patient, exhibiting altered spine density, methamphetamine-induced cognitive dysfunction, and activation of RhoA/Rho-kinase signaling. However, it remains unclear whether the activation of RhoA/Rho-kinase signaling due to schizophrenia-associated Arhgap10 mutations causes the phenotypes of these model mice. Here, we investigated the effects of fasudil, a brain permeable Rho-kinase inhibitor, on altered spine density in the medial prefrontal cortex (mPFC) and on methamphetamine-induced cognitive impairment in a touchscreen‑based visual discrimination task in Arhgap10 S490P/NHEJ mice. Fasudil (20 mg/kg, intraperitoneal) suppressed the increased phosphorylation of myosin phosphatase–targeting subunit 1, a substrate of Rho-kinase, in the striatum and mPFC of Arhgap10 S490P/NHEJ mice. In addition, daily oral administration of fasudil (20 mg/kg/day) for 7 days ameliorated the reduced spine density of layer 2/3 pyramidal neurons in the mPFC. Moreover, fasudil (3–20 mg/kg, intraperitoneal) rescued the methamphetamine (0.3 mg/kg)-induced cognitive impairment of visual discrimination in Arhgap10 S490P/NHEJ mice. Our results suggest that Rho-kinase plays significant roles in the neuropathological changes in spine morphology and in the vulnerability of cognition to methamphetamine in mice with schizophrenia-associated Arhgap10 mutations.

Nanomachines for direct penetration of cancer cells

Proteins are involved in every biological process, and use the energy in the body to alter their structure via mechanical movements. They are considered biological ‘nanomachines’ because the smallest structural change in a protein has a significant effect on biological processes. The development of nanomachines that mimic proteins has received much attention to implement movement in the cellular environment. However, there are various mechanisms by which cells attempt to protect themselves from the action of these nanomachines. This limits the realization of any relevant mechanical movement of nanomachines that could be applied for medical purposes.

The research team led by Dr. Youngdo Jeong from the Center for Advanced Biomolecular Recognition at the Korea Institute of Science and Technology (KIST, President Seok-Jin Yoon) has reported the development of a novel biochemical nanomachine that penetrates the cell membrane and kills the cell via the molecular movements of folding and unfolding in specific cellular environments, such as cancer cells, as a result of a collaboration with the teams of Prof. Sang Kyu Kwak from the School of Energy and Chemical Engineering and Prof. Ja-Hyoung Ryu from the Department of Chemistry at the Ulsan National Institute of Science and Technology (UNIST, President Yong Hoon Lee), and Dr. Chaekyu Kim of Fusion Biotechnology, Inc.

The joint research team focused on the hierarchical structure of proteins, in which the axis of the large structure and the mobile units are hierarchically separated. Therefore, only specific parts can move around the axis. Most existing nanomachines have been designed so that the mobile components and axis of the large structure are present on the same layer. Thus, these components undergo simultaneous movement, which complicates the desired control of a specific part.

Dr Andrew McMahon & Lewis Kleinberg — Pushing The Boundaries Of Research To Build A Synthetic Kidney

Pushing The Boundaries Of Research To Build A Synthetic Kidney — Dr. Andrew McMahon, Ph.D. & Lewis Kleinberg, University Kidney Research Organization (UKRO)

The University Kidney Research Organization (UKRO — https://ukrocharity.org/) is a Los Angeles-based nonprofit charity, co-founded prominent entertainment attorney Kenneth Kleinberg, inspired by his personal journey with kidney disease, focused on supporting medical research and education related to the causes, treatment, and eradication of all forms of kidney disease.

Dr. Andrew McMahon, Ph.D. (https://keck.usc.edu/faculty-search/andrew-p-mcmahon/) is Director of the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC, Provost Professor and the inaugural holder of the W. M. Keck Professorship of Stem Cell Biology and Regenerative Medicine, and is responsible for overseeing UKRO’s Synthetic Kidney Project. In addition, Dr. McMahon chairs the recently created Department of Stem Cell Biology and Regenerative Medicine at the Keck School. He also holds an appointment in the Department of Biological Sciences in the USC Dornsife College of Letters, Arts, and Sciences.

Previously Dr. McMahon served as professor in the Department of Stem Cell and Regenerative Biology, Department of Molecular and Cellular Biology and principal faculty member in the Harvard Stem Cell Institute, as well as led the Department of Cell and Developmental Biology at the Roche Institute for Molecular Biology.

Dr. McMahon received his bachelor’s degree from St. Peter’s College, Oxford University and his Ph.D. from University College in London. He subsequently worked for three years as a postdoctoral fellow at the California Institute of Technology.

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NF-κB Decoy ODN-Loaded Poly(Lactic-co-glycolic Acid) Nanospheres Inhibit Alveolar Ridge Resorption

Residual ridge resorption combined with dimensional loss resulting from tooth extraction has a prolonged correlation with early excessive inflammation. Nuclear factor-kappa B (NF-κB) decoy oligodeoxynucleotides (ODNs) are double-stranded DNA sequences capable of downregulating the expression of downstream genes of the NF-κB pathway, which is recognized for regulating prototypical proinflammatory signals, physiological bone metabolism, pathologic bone destruction, and bone regeneration. The aim of this study was to investigate the therapeutic effect of NF-κB decoy ODNs on the extraction sockets of Wistar/ST rats when delivered by poly(lactic-co-glycolic acid) (PLGA) nanospheres.

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