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What Are Block Copolymer Micelles?

Block copolymer micelles are generally formed by the self-assembly of either amphiphilic or oppositely charged copolymers in aqueous medium. The hydrophilic and hydrophobic blocks form the corona and the core of the micelles, respectively. Block copolymer micelles can be classified according to the type of intermolecular forces driving the segregation of the core segment from the aqueous milieu. In the past few decades, at least three main categories were identified, viz. amphiphilic micelles (formed by hydrophobic interactions), polyion complex micelles (PICM; resulting from electrostatic interactions), and micelles stemming from metal complexation. Generally, when the hydrophilic segment is longer than the core block, the shape of the resulting micelles is spherical. Conversely, increasing the length of the core segment beyond that of the corona-forming chains may generate various non-spherical structures, including rods and lamellae. 1. What Is Block Polymer? Block copolymers consist of two or more chemically distinct polymer blocks covalently bonded together. These blocks may be thermodynamically incompatible with each other because the entropy of mixing per unit volume is small and varies inversely with molecular weight. In the bulk, block copolymers (BCPs), achieved simply by joining polymer chains together, microphase separate on the molecular scale (5–100 nm), producing complex nanostructures with various morphologies. 2. What Are Polymeric Micelles?

Revealing the mechanism by which brain cholesterol regulates beta-amyloid plaque production

In a new study, researchers from the Scripps Research Institute, the University of Virginia and the University of Washington used advanced imaging methods to reveal how production of the Alzheimer's disease-associated protein amyloid beta (Aβ) in the brain is tightly regulated by cholesterol. These findings advance the understanding of how Alzheimer's disease arises and highlight the long-underappreciated role of cholesterol in the brain, in addition to helping explain why genetic studies have linked Alzheimer's disease risk to a cholesterol transporter protein called apolipoprotein E (apoE). Related findings are published in the Aug. 17, 2021 issue of PNAS. Dr. Hansen said, "We found that cholesterol essentially functions as a signal in neurons that determines how much Aβ is made. So it should be no surprise that apoE, which carries cholesterol to neurons, affects Alzheimer's disease risk." Aβ Aβ in the brains of people with Alzheimer's disease can form large, insoluble aggregates and collect into large clumps or plaques, one of the most prominent features of the disease. Genetic evidence suggests that the production of a subtype of Aβ is associated with Alzheimer's disease, yet the role of Aβ in healthy brains and disease remains a topic of debate, and many previous clinical trials of treatments to clear Aβ have not shown them to be beneficial. In this new study, these researchers took a closer look at the relationship between cholesterol and Aβ production. The role of cholesterol has been hinted at in various previous studies, but never directly confirmed due to technical limitations. They used an advanced microscopy technique called super-resolution imaging to look in cells and in the brains of mice models and track how cholesterol regulates Aβ production. They focused on cholesterol produced in the brain by helper cells called astrocytes and observed that it is carried by the apoE protein to the outer membrane of neurons. It appears to contribute to the maintenance of cholesterol and related molecular clusters, commonly known as lipid rafts that are not well understood, partly because they are too small to be imaged with ordinary light microscopy. As technology improves, they are increasingly recognized as hubs where signaling molecules come together to perform critical cellular functions.

Structure biology will continue to use artificial intelligence

Nature issued an editorial on July 27, 2021, reflecting on recent topical reporting on AlphaFold. Our understanding of protein folding will be altered as a result of machine learning. It is important that all data be made available to the public. "I never imagined we'd make it this far in my lifetime." So said a structural biology expert in response to AlphaFold's results. Artificial intelligence (AI) was used in this work to predict the structures of over 20,000 human proteins, as well as the structures of almost all known proteins generated by 20 model organisms, including E. coli, Drosophila, yeast, soybean, and Asian rice. That's roughly 365,000 structures projected. Researchers from DeepMind, a London-based artificial intelligence company owned by Google parent company Alphabet, and the European Bioinformatics Institute at the European Molecular Biology Laboratory (EBI-EMBL) near Cambridge, UK, released the data online on July 22 (https://alphafold.ebi.ac.uk). AlphaFold is a machine learning tool developed by the DeepMind team, which was trained using DNA sequences (including their evolutionary history) and the known structures of thousands of proteins in the EBI-EMBL protein database that is open to the public. DeepMind also published the source code for AlphaFold and comprehensive instructions on how it was developed a week ago, while academics from the University of Washington in Seattle disclosed another protein structure prediction algorithm (called RoseTTAFold, inspired by AlphaFold).

Stroke Cats Happily and Stay Away from Allergies

For cat lovers, the most tragic thing is probably the cat allergy. As soon as you get close to the cat, you sneeze, have a runny nose, or itchy eyes, skin rashes, and even asthma attacks. There are many people who are allergic to cats, with about 1 in 10 in the population. In some areas, as many as 30% of the population are allergic to cats. While enduring allergies, there are many cat slaves who insist on keeping cats. However, there are also some people who have to send their cats away due to severe allergies of themselves or their family members. Either way is painful. Many people think cat hair is the culprit, but it is not. The real allergen is mainly a protein called Fel d 1 that is secreted through cat's saliva and sebaceous glands. When licking their hair, cats smear this protein all over the body, which is spread into the air through hair and dander, and attaches to carpets, curtains, bed sheets, and clothes and people's hair. Fel d 1 is so sticky that it is difficult to eradicate even after a thorough cleanup. Finding an anti-allergic method targeting Fel d 1 can help most people. Allergen-specific immunotherapy (AIT) is a tolerance–inducing treatment that changes the natural course of allergic diseases through immune regulation mechanisms. Recently, researchers from the Luxembourg Institute of Health published an article titled "Comprehensive mapping of immune tolerance yields a regulatory TNF receptor 2 signature in a murine model of successful Fel d 1-specific immunotherapy using high-dose" in the journal Allergy, clarifying that high-dose specific adjuvant molecule CpG oligonucleotides can modulate the immune system's allergic response to the major cat allergen Fel d 1, thereby promoting human tolerance to cat allergic reactions.

CAR-T Goes Hot: Laser Pulses-heated CAR-T Cells Show Better Efficiency

CAR T-cell therapy has been lauded as a feasible solution for several cancers by patients, clinical researchers, investors, and the media. As a fact, it is now one of the most intriguing research fields in life sciences, as well as a growing research field of immunotherapy, with over 500 clinical trials studying CAR T-cell therapies as possible cancer treatments. A group of researchers lead by scientists at the Georgia Institute of Technology claimed an improvement in the accuracy and capability of CAR T-cell therapy. The study, which was just published in Nature Biomedical Engineering, titled Enhanced intratumoral activity of CAR T cells engineered to produce immunomodulators under photothermal control, is changing the research on oncology. In CAR T-cell treatment, a patient's T cells, a kind of white blood cell, are genetically modified in a laboratory. The patient's immune cells are then given a chimeric antigen receptor (CAR) and reintroduced to the body, where they target out and destroy cancer cells. That's how they work. The senior study investigator Gabe Kwong, author of this paper, said that these therapies have proven to be effective for patients with liquid tumors, but for solid tumors, such as sarcomas, carcinomas, they don’t work well since CAR T-cells are immunosuppressed by the tumor microenvironment. To improve the way CAR T-cells attack cancer, Kwong and his collaborators are altering the environment and introducing cell changes. They engineered T cells with a genetic on-off switch and created a remote-control system that sends the modified T cells on a precise invasion of the tumor microenvironment, where they destroy the tumor and prevent recurrence. The new discovery expands on the lab's previous research into remotely controlled cell treatment strategy. Researchers can precisely target tumors using localized heat deposition, wherever they are in the body. The heat stimulates the CAR T-cells inside the tumors, thus overcoming immunosuppressive problems. The researchers did not treat tumors clinically in the previous trial, but they are doing so now with the novel technology. They used laser pulses from outside the animal's body to produce heat in the tumor of a mouse. Gold nanorods transported to the tumor convert light waves into localized, medium heat, elevating the temperature to 40-42 °C, which is just hot enough to activate the T cells' on-switch without killing healthy tissue or T cells. The cells can boost the expression of cancer-fighting proteins once they are turned on.

Combination of Viral Therapy and T Cell Therapy to Improve The Cure Rate of Cancer

Although the cure rate of several cancers has increased significantly, the prognosis of patients with advanced solid tumors has remained severe in the past few decades. Therefore, there is a need for new therapies that can improve the outcome of patients whose current therapies have failed. Oncolytic (cancer-destroying) vaccinia virus (VV) will be an attractive supplement to current cancer therapy because it can infect, replicate, and lyse tumor cells, and spread to other tumor cells in successive rounds of replication. Although clinical studies have proven their safety, the anti-tumor efficacy of oncolytic VV is not ideal. Oncolytic VV's main mode of action is to destroy tumor cells, which can then activate components of the immune system called T cells, which can spread to remote sites and target any tumors they find. Currently, the spread of the virus in tumors and the activation of tumor-specific T cells are limited, which explains the poor anti-tumor activity of current oncolytic VVs observed. Therefore, it is hoped that by activating the resident T cells in the tumor, oncolytic VV can become a more powerful immunostimulant, thereby killing tumor cells and preventing the growth of new tumors. T cell is a type of white blood cell that plays a central role in cell-mediated immunity. T cells express membrane receptors on their surface and recognize their targets by binding to target molecules related to MHC class I molecules expressed on the surface of tumor cells. Reminded by this tumor target molecule, T cells are activated and then produce cytokines and killer molecules, such as perforin, granzyme A, and granzyme B, which cause tumor cell lysis. More and more evidences show that T cells can effectively control tumor growth and prolong the survival of cancer patients in the early and late stages of the disease. Tumor-specific T cells have been produced in vitro and then reinjected into cancer patients, which is called adoptive T cell therapy. It can be assumed that oncolytic VV and bispecific T cell cements have a strong synergistic therapeutic effect, because T cells can induce bystanders to kill tumor cells that are not infected with the virus, and the cytokines released when they are activated will produce promotor The inflammatory microenvironment inhibits tumor growth, while killing tumor cells through oncolytic VV overcomes the tumor heterogeneity that limits the participation of bispecific T cells in the therapeutic efficacy. In order to activate T cells in tumors, a new T cell involved in the strategy of armed vaccinia virus (TEA-VV) expresses secreted bispecific antibodies that bind to CD3 and the tumor cell surface antigen EphA2 (EphA2-TEA-VV).