What is a Loose Leaf Textbook?
Loose leaf textbooks are editions that have no binding. Unlike hardcover and paperback books, which are bound together by glue and stitching, loose leaf books come as a stack of hole-punched pages that can be separated or bound by the owner.
While this format does offer unique advantages compared to other editions, there are also disadvantages to consider before purchasing:
- Cost: Fewer materials and a simpler manufacturing process make loose leaf textbooks a great alternative for students looking for cheap textbooks for school.
- Weight: Rather than carry the entire book to class, loose leaf editions provide additional flexibility by allowing individual chapters or sections to be separated from the rest of the book.
- Value: Some loose leaf textbooks lack a unique ISBN number, meaning they can’t be sold as easily once the semester is over.
- Durability: Unlike a bound hardcover or paperback book, it is easier to lose or damage individual pages of a loose leaf textbook. This is especially true if you don’t bind the book or frequently separate certain chapters for convenience.
- Aesthetics: For anyone planning to keep their textbooks long-term, a hardcover or paperback edition with a spine will be more visually appealing on your shelf than a loose leaf book.
Ultimately, it’s up to you to decide which option makes sense. If keeping upfront costs low and having the ability to separate chapters is important to you, loose leaf textbooks are the way to go.
Loose Leaf Textbook Binding Tips
One way to mitigate some of the disadvantages listed above is by learning how to bind a loose leaf textbook. There are a few different ways to do this, each of which has pros and cons.
- Binder: The most common way to bind loose leaf textbooks is with a three-ring binder. Binders are fairly inexpensive and will help protect your loose leaf textbook from damage while securing the pages so none are lost. They will also allow you to easily remove and replace pages as needed. As an extra tip when deciding what size binder to buy for your loose leaf book, we recommend at least ½ inch per 250 pages. So, for example, you should buy a 2 inch binder for a 1,000 page book.
- Yarn/Thread: Another option is to tie your loose leaf textbook together with yarn or thread in each of the hole punches. While this is a cheaper option and it allows you to customize the look of the book with colored thread, it doesn’t provide the same protection as a binder and makes it much more difficult to remove and replace pages.
- Screw Posts: For a sturdier option, consider installing screw posts. These create a more durable binding for loose leaf textbooks than yarn since they provide a more precise fit. In addition, they come in multiple colors and are easier to take out if you want to remove a section of the textbook.
How to Sell Loose Leaf Textbooks
Loose leaf textbooks often retain less value than hardcover or paperback books, and that makes it unlikely for on-campus bookstores to buy them back. However, you can sometimes still sell loose leaf textbooks online. Here’s how to do it:
- Grab your book and head to our sell textbooks page.
- Locate the ISBN number on your book. This can usually be found on the title page, copyright page, or above the barcode. It’s important to make sure you enter the ISBN number for the loose leaf edition in order to receive the correct quote. This should be distinguished by the label “Loose Leaf,” “A la Carte,” or “Binder Ready” preceding the number.
- Enter the ISBN number on TextbookRush and view your quote. If you entered the correct number, the title of the book on our site should include the label “Loose Leaf,” “A la Carte,” or “Binder Ready” in the quote preview.
- Review our terms and conditions to ensure your loose leaf textbook meets our criteria for buyback.
- Accept your quote and follow the instructions to ship it to our facility.
That’s it! Selling loose leaf textbooks is a great way to further reduce their cost and clear out space for next semester. And if it turns out they don’t have any resale value, you can always donate, trade, or recycle them. Learn how in our post on what to do with old textbooks.
POST LAMINECTOMY SYNDROME | Restore Medical Partners
Post-laminectomy syndrome is a misnomer, as it is not actually a syndrome – it is a very generalized term that is often used to describe the condition of patients who have not had a successful result with back surgery or spine surgery and have experienced continued pain after surgery. There is no equivalent term for post-laminectomy surgery syndrome in any other type of surgery (e.g. there is no failed cardiac surgery syndrome, failed knee surgery syndrome, etc.).
There are many reasons that a back surgery may or may not work, and even with the best surgeon and for the best indications, spine surgery is no more than 95% predictive of a successful result.
Reasons for Failed Back Surgery and Pain after Surgery
Spine surgery is basically able to accomplish only two things:
- Decompress a nerve root that is pinched, or
- Stabilize a painful joint.
Unfortunately, back surgery or spine surgery cannot literally cut out a patient’s pain. It is only able to change anatomy, and an anatomical lesion (injury) that is a probable cause of back pain must be identified prior to rather than after back surgery or spine surgery.
By far the number one reason back surgeries are not effective and some patients experience continued pain after surgery is because the lesion that was operated on is not in fact the cause of the patient’s pain.
Predictability of Pain after Surgery
Some types of back surgery are far more predictable in terms of alleviating a patient’s symptoms than others. For instance:
- A discectomy (or microdiscectomy) for a lumbar disc herniation that is causing leg pain is a very predictable operation. However, a discectomy for a lumbar disc herniation that is causing lower back pain is far less likely to be successful.
- A spine fusion for spinal instability (e.g. spondylolisthesis) is a relatively predictable operation. However, a fusion surgery for multi-level lumbar degenerative disc disease is far less likely to be successful in reducing a patient’s pain after surgery.
Therefore, the best way to avoid a spine surgery that leads to an unsuccessful result is to stick to operations that have a high degree of success and to make sure that an anatomic lesion that is amenable to surgical correction is identified preoperatively.
Other Causes of FBSS and Continued Pain after Surgery
In addition to the above-mentioned cause of failed back surgery syndrome, there are several other potential causes of a failed surgery, or continued pain after surgery:
- Fusion surgery considerations (such as failure to fuse and/or implant failure, or a transfer lesion to another level after a spine fusion, when the next level degenerates and becomes a pain generator)
- Lumbar decompression back surgery considerations (such as recurrent spinal stenosis or disc herniation, inadequate decompression of a nerve root, preoperative nerve damage that does not heal after a decompressive surgery, or nerve damage that occurs during the surgery)
- Scar tissue considerations (such as epidural fibrosis, which refers to a formation of scar tissue around the nerve root)
- Postoperative rehabilitation (continued pain from a secondary pain generator).
In addition to the primary reasons for failed back surgery syndrome (FBSS) discussed on the prior page, there are several reasons why a spinal fusion might fail to alleviate a patient’s back pain after surgery, including fusion and implant failures, and transfer lesions.
Failure of Solid Fusion After Spine Surgery
When the fusion is for back pain and/or spinal instability, there is a correlation (although weak) between obtaining a solid fusion and having a better result of the spine surgery. If a solid fusion is not obtained through the spine surgery, but the hardware is intact and there is still good stability to the spine, the patient may still achieve effective back pain relief with the spine surgery. In many cases, achieving spinal stability alone is more important than obtaining a solid fusion from the spine surgery.
On postoperative imaging studies it is often very difficult to tell if a patient’s spine has fused, and it can be even harder to determine if a further fusion surgery is necessary. In general, it takes at least three months to get a solid fusion, and it can take up to a year after the spine surgery. For this reason, most surgeons will not consider further spine surgery if the healing time has been less than one year. Only in cases where there has been breakage of the hardware and there is obvious failure of the spinal construct would back surgery be considered sooner.
Implant Failure in Spine Surgery
An instrumented fusion can fail if there is not enough support to hold the spine while it is fusing. Therefore, spinal hardware (e.g. pedicle screws) may be used as an internal splint to hold the spine while it fuses after spine surgery. However, like any other metal it can fatigue and break (sort of like when one bends a paper clip repeatedly). In very unstable spines, it is therefore a race between the spine fusing (and the patient’s bone then providing support for the spine), and the metal failing.
Metal failure (also called hardware failure, implant failure), especially early in the postoperative course after back surgery, is an indicator of continued gross spinal instability. The larger a patient is and the more segments that are fused, the higher the likelihood of implant failure. Implant failure following spine surgery should be very uncommon in normal sized individuals with a one level fusion.
Transfer Lesion to Another Level after a Spine Fusion
A patient may experience recurrent pain many years after a spine fusion surgery. This can happen because the level above or below a segment that has been successfully fused can break down and become a pain generator.
- This degeneration is most likely to happen after a two-level fusion (e.g. a fusion for L4-L5 and L5-S1 levels) and in a young patient (in the 30-50 year old age range).
- It is much less likely to happen if only the L5-S1 level is fused, as this segment typically does not have much motion and fusing this level does not change the mechanics in the spine all that much.
- Most of the motion in the spine is at the L4-L5 level, and to a lesser extent at L3-L4. When the L4-L5 level is included in the spine fusion it transfers a lot of stress to L3-L4. This does not present as much of a problem for elderly patients, since they tend to not be as active nor do they have the fusion for as many years.
- Transfer lesions are far more common in degenerative osteoarthritis conditions ( e.g. degenerative spondylolisthesis) and far less common in disc degeneration problems (e.g. degenerative disc disease or isthmic spondylolisthesis).
The nerve root can take a long time to heal from a lumbar decompression (such as a discectomy, microdiscectomy or laminectomy), making it difficult to gauge the outcome of the surgery.
- In general, if a patient is getting better within three months of the surgery, he or she should continue to get better.
- If there has not been any improvement in the pain approximately three months after the decompression, then the back surgery can be assumed to be unsuccessful, and further work up would be reasonable.
- During the first three months, the success of the back surgery really cannot be judged, and it is often too early to describe the procedure as either a successful or failed back surgery.
Decompression of the lumbar spine will usually relieve the patient’s leg pain directly after the back surgery. However, for 10-20% of patients, the pain will continue until the nerve starts to heal. In some cases, the pain may even be worse for a while after the back surgery because operating around the nerve root creates some increased swelling and this leads to pain.
It usually takes far longer for symptoms of numbness/tingling or weakness to resolve, and sometimes it can take up to a year for these symptoms to subside. If these symptoms persist after a year, they probably represent permanent nerve damage and are unlikely to resolve.
Recurrent Stenosis or Herniation after Decompression
Years after decompression (lumbar laminectomy), lumbar stenosis can come back (the bone can grow back) at the same level, or a new level can become stenotic and cause back pain or leg pain.
Pain that is relieved right after surgery but then returns abruptly is often due to a recurrent lumbar disc herniation. Recurrent lumbar disc herniations happen to about 5% to 10% of patients, and they are most likely to occur during the first three months after back surgery.
Technical Problems after Lumbar Decompression Surgery
Three potential technical problems that cause the pain after surgery to continue include:
- Missed fragment (of the disc or bone) is still pinching the nerve
- The back surgery operation was done at the wrong level of the spine
- Dissection of the nerve root may cause further trauma.
Nerve damage during a discectomy or a lumbar decompression is very uncommon, but has been reported in about 1 in 1,000 cases. When it does occur during back surgeries, a permanent neurological deficit with new weakness in a muscle group is possible, and a postoperative EMG (electromyography) can be helpful to see if there has been nerve damage and if there is any reinnervation (nerve healing) after the back surgery.
At times, decompressing a nerve root through back surgery will cause it to become more inflamed and lead to more pain temporarily until the inflammation subsides.
Inadequate Decompression of a Nerve Root after Surgery
Decompressing a nerve root with back surgery is not always successful, and if a portion of the nerve root is still pinched after the back surgery there can be continued pain. If this is the case, there will usually be no initial pain relief following the back surgery, and subsequent postoperative imaging studies may show continued spinal stenosis in a portion of the lumbar spine.
Scar tissue formation is part of the normal healing process after back surgery. While scar tissue can be a cause of pain, actual scar tissue pain is very rare since the tissue contains no nerve endings.
Rather, the principal mechanism of pain is thought to be the binding of the lumbar nerve root by fibrous adhesions, called epidural fibrosis. Postoperative stretching exercises can help decrease the effects of postoperative scarring around the nerve root.
Scar Tissue Formation after Back Surgery
All patients will heal with scar tissue after back surgeries as this is the only way to heal. The reality is that although scar tissue is often clinically the reason given for continued pain after surgery, it is probably rarely the cause of postoperative pain. Particularly in patients that have similar pain postoperatively to what they had before surgery, it is unlikely that the addition of scar tissue has any clinical relevance.
However, clinicians often use the explanation of scar tissue as the cause of continued pain, whether or not there is any evidence that this is in fact the patient’s pain generator. Often, a better explanation for continued pain after surgery is that either the patient has a secondary problem that needs to be addressed, or that the lesion operated on was not in fact the source of the patient’s pain. These are far more likely scenarios than actual scar tissue pain.
A Possible Exception for Scar Tissue Pain
The one time that scar tissue (epidural fibrosis) may be symptomatic is for a patient who initially does well after a lumbar discectomy or a decompression, only to have recurrent pain come on slowly between 6 to 12 weeks after surgery.
This is the time period that scar tissue takes to form, and as it forms it can cause the nerve root to become adherent within the spinal canal. Keeping the nerve moving through stretching exercises can help prevent this scenario.
Pain that starts years after surgery, or pain that continues after surgery and is never relieved, is not from scar tissue.
After an incorrect preoperative diagnosis and subsequent spine surgery, improper and/or inadequate postoperative rehabilitation is probably the second most common cause of continued back pain after surgery.
It often takes months to a year to heal after many of these back surgeries, and a postoperative rehabilitation program that includes stretching, strengthening and conditioning is an important part of any successful spine surgery.
In general, the bigger the back surgery and the longer a patient has had their preoperative symptoms, the longer and harder the postoperative rehabilitation will be. It is often far more reasonable to continue with rehabilitation after spine surgery than to consider further surgery (with some exceptions, such as if there has been a recurrent disc herniation).
Secondary Problems after Spine Surgery
Often, there are other secondary problems that must be worked out after back surgery. For example, a patient with a pinched L5 nerve root from a disc herniation may still need physical therapy afterward because they may have a secondary piriformis syndrome. Unpinching the L5 nerve root may relieve the radiculopathy (sciatica) but the patient still has pain in the buttocks from continued muscle spasm in the piriformis. Until this is worked out, the patient will not feel like the back surgery is successful.
Many times, spine surgery is necessary to provide enough back pain relief for the patient to start a rehabilitation program, but it should only be one component of the patient’s healing process. Unfortunately, some patients feel that if they have had back surgery they have been “fixed” and no further treatment is necessary. However, this is rarely true, and continued therapies and rehabilitation are usually necessary for a successful outcome.
Rehabilitation Considerations after Back Surgery
After spine surgery, careful follow-up and rehabilitation is very important. If there is continued pain after surgery despite adequate time to heal and rehabilitate, then further workup may be warranted to find if there is a new lesion or a different type of problem that could contribute to the patient’s pain.
Failed back surgery syndrome is really not a syndrome, and there are no typical scenarios. Every patient is different, and a patient’s continued treatment and workup need to be individualized to his or her particular problem and situation.
To watch a video about post-laminectomy syndrome, click below:
At Restore Medical Partners, we will ask patients to describe the location, severity and type of pain, in addition to the history of the pain: when the patient started to feel it, and any activities or positions that make the pain better or worse. We will review your MRI or order imaging if you do not have imaging completed on your first visit. Then, we will explain to you what is causing your neck pain. Our goal is to prevent repeat surgery and use minor interventional techniques to relieve your pain and get you back to doing the things you enjoy. For a residual disc herniation after surgery or inflammation around a nerve root causing foramina stenosis or radiculopathy, we may recommend an epidural steroid injection. For muscle spasm, we may recommend trigger point injections into the muscles. For chronic post laminectomy pain we may recommend spinal cord stimulation. Some patients may require a combination of techniques to completely resolve their pain symptoms.
To learn how we perform a spinal cord stimulation implant, please click here:
Actin Filament – an overview
4 Actin filament capping restricts filament lengths in RBCs
Actin filaments are polarized polymers of actin subunits, with one filament end that polymerizes and depolymerizes at about 10 × the rate of the other; the former is referred to as the fast-growing (barbed) end, while the latter is referred to as the slow-growing (pointed) end. During assembly, actin filaments can elongate up to many microns in length, but the RBC actin filaments are less than 40 nm long (Section 3.2). At steady state, actin monomers continue to associate and dissociate from filament ends, so that over time, purified actin filaments achieve an exponential length distribution with filaments of varying lengths (Littlefield & Fowler, 1998). Thus, the uniform (Gaussian) length distribution of the short RBC actin filaments suggests that they are capped tightly at both ends to prevent subunit loss or gain that would otherwise lead to filament length changes over the RBC lifetime (~ 120 days in humans, ~ 40 days in mice). In the 1990s, I and my colleagues identified RBC Tmod1 and αβ-adducin as the pointed and barbed end actin filament capping proteins, respectively, supporting the idea that actin capping restricts RBC actin filament length (Section 4). This is a nice example of how the unique properties of the RBC membrane (short filaments with abundant numbers of filament ends) enabled discovery of novel actin capping proteins and provided insights into the important problem of actin filament length regulation in all cells.
Despite the a priori necessity for actin capping proteins to restrict actin filament lengths, the idea that RBC actin filaments were capped at both ends was under dispute for some time before the Tmod1 and αβ-adducin cappers were discovered. For example, under some conditions, exogenous actin was observed to elongate from the ends of the short red cell actin filaments, indicating that filament ends are not always capped (Byers & Branton, 1985; Pinder & Gratzer, 1983; Pinder, Weeds, & Gratzer, 1986; Podolski & Steck, 1988; Tsukita, Tsukita, Tsukita, Hosoya, & Mabuchi, 1985; Tsukita, Tsukita, & Ishikawa, 1984). In some investigators’ experiments, incubation of the exposed cytoplasmic surface of ghosts with actin monomer concentrations above the barbed but below the pointed end critical concentration led to elongation only from barbed ends, while incubation at concentrations above the pointed end critical concentration led to elongation from both ends—results similar to experiments with purified uncapped filaments (Tsukita et al., 1984, 1985). In others, elongation was only observed from barbed, but not pointed ends (Pinder & Gratzer, 1983; Pinder et al., 1986; Podolski & Steck, 1988). Experiments measuring binding of dihydrocytochalasin B (binds specifically to barbed ends) or DNAseI (binds specifically to pointed ends) to ghost membranes were also consistent with the existence of many short, uncapped red cell actin filaments (Lin & Lin, 1978; Podolski & Steck, 1988).
Subsequent investigations revealed that the low ionic strength conditions typically used to purify RBC membranes most likely led to filament uncapping. For pointed ends, low ionic strength conditions without magnesium extract RBC TMs (Fowler & Bennett, 1984a, 1984b), Tmod1’s binding partner, and would be expected to convert Tmod1 to a low-affinity cap (Section 4.1.1), thus allowing actin subunit addition and filament elongation from pointed ends or DNAseI binding by displacement of the weak Tmod1 cap from the pointed ends. For the barbed ends, osmotic lysis and washing of ghosts in low ionic strength buffers without divalent cations leads to extraction or uncapping by αβ-adducin, allowing actin subunit addition and filament elongation, or binding of EcapZ (a barbed end capping protein) to the free barbed ends (DiNubile, 1999; Kuhlman, 2000; Kuhlman & Fowler, 1997; Section 4.3).
Actin filament breakage during osmotic lysis and centrifugal shearing of RBCs to prepare ghosts may also have accounted for the appearance of new filament ends, based on the presence of fewer EcapZ binding sites on membranes when the filament stabilizer, phallacidin, was included in the osmotic lysis buffers (Kuhlman & Fowler, 1997). This raises the possibility that at least some of the short actin filaments observed at nodes of the quasi-hexagonal spectrin–actin lattice prepared by low ionic strength expansion and mechanical stretching may have been created by filament breakage (Byers & Branton, 1985; Liu et al., 1987; Shen et al., 1986). The idea that some RBC actin filaments may be longer than is commonly accepted was originally proposed by Atkinson and colleagues, from observations of ~ 100 nm-long actin filaments in extracts prepared from membranes by phalloidin stabilization, mild proteolysis, and gel filtration (Atkinson, Morrow, & Marchesi, 1982). Long actin filaments have also been observed in spectrin–actin networks prepared by nonionic detergent extraction followed by high salt extraction (Shen et al., 1984). However, proteolysis or extraction of filament caps, followed by end-to-end annealing of the short filaments, cannot be ruled out in these preparations.
90,000 Scientists are investigating a peptide that could block COVID-19 thorns
An international group of scientists, which included researchers from St. the way to create a cure for COVID-19.
The structure of the coronavirus, including SARS-CoV-2, has already been studied by many. To bind to human cells, the coronavirus uses spikes on the surface of which a receptor protein is formed.It binds to a special enzyme.
According to the press service of St. Petersburg State University, about a month ago, Chinese researchers studied the structure of this enzyme and, based on the published data, scientists from the Massachusetts Institute of Technology identified a peptide of 23 amino acid residues. Previously, this peptide can stop the process of binding of the virus to the cell of the body.
Now it is being studied by St. Petersburg and Chinese scientists. The main problem is that when creating peptides, it is far from always possible to predict their physicochemical properties.Therefore, as noted in the release of the St. In such a situation, the peptide, called SBP1, may at best not reach its target and be useless, and at worst, it can harm the body. Therefore, the research group is now studying all possible reactions of the peptide, in particular, tests for non-specific binding with a number of test proteins will be carried out.
– The likelihood that SBP1 specifically, that is, as a key to a lock, will approach some extraneous receptor and be able to start some unforeseen processes in the cell, is very small, but it cannot be completely ruled out either, says Olga Rogacheva.
Meanwhile, if it turns out that the peptide does not bind to any other proteins and has no non-specific properties, then it may be used to create a cure for coronavirus infection.
Scientists from St. Petersburg State University are investigating a peptide potentially capable of blocking coronavirus
The complex of the spike protein and ACE2 according to the data of X-ray structural analysis.The ACE2-binding domain of the spike protein is shown in gray, ACE2 is shown in red, and the ACE2 fragment corresponding to SBP1
is shown in blue. To invade human cells, coronaviruses, including SARS-CoV-2, use the so-called spikes. With the help of these “spikes”, formed on the surface of the virus by a special protein, the virus docks with the human cell. For docking, one of the many types of receptor proteins on the surface of the human cell is used. In the case of SARS-CoV-2, this is angiotensin-converting enzyme 2 (ACE2).
At the end of March, Chinese scientists published the crystal structure of this enzyme in combination with the receptor-binding domain of the viral spike protein, which allowed researchers at the Massachusetts Institute of Technology (USA) to identify the ACE2 fragment with which the virus binds. It is a 23 amino acid peptide (IEEQAKTFLDKFNHEAEDLFYQS). As conceived by the creators of the peptide, it should block the binding site of the “spike” protein, thereby depriving the virus of the ability to “dock” with ACE2 and penetrate the cells of the human body.In accordance with this interpretation, the authors named their peptide spike-binding peptide 1 (SBP1). The study of this peptide was undertaken by the scientists of St. Petersburg State University together with colleagues from Tsinghua and the Institute of Cytology of the Russian Academy of Sciences.
The idea to create such a peptide could have appeared only after the publication of the structure of the ACE2 complex with the coronavirus “spike” protein, because only by seeing the structure of the complex of two proteins, it is possible to identify a small fragment in one protein that could bind to the second protein.
Employee of the Department of Biochemistry of St. Petersburg State University and the Laboratory of Biomolecular NMR of the Institute of Translational Biomedicine of St. Petersburg State University Olga Rogacheva, Ph.D.
When creating peptides, it is not always possible to predict their physicochemical properties, and therefore it often turns out that the proposed peptide can nonspecifically bind with other human proteins or lipids of cell membranes, that is, do not only what it was sent to the body for. “A peptide with such properties is at least useless, since it is unlikely to get to its target. This is usually how hydrophobic peptides behave. SBP1 is not hydrophobic, but we will definitely test it for nonspecific binding to a number of test proteins. The likelihood that SBP1 is specific, that is, as a key to a lock, will approach some extraneous receptor and be able to trigger some unforeseen processes in the cell, is very small, but it cannot be completely ruled out either. Usually these effects are visible already at the stages of cell experiments and experiments on animals, ”said Olga Rogacheva.
Research is carried out by Olga Rogacheva, Dmitry Luzik and Irina Tyuryaeva, researchers at the Biomolecular NMR Laboratory of St. Cellular experiments are supposed to be carried out on the basis of the Institute of Cytology of the Russian Academy of Sciences. Part of the working collaboration is done in Professor Yi Shu’s laboratory at Tsinghua University in China. The project is headed by the head of the bio-NMR laboratory, Professor Nikolai Skrynnikov.
“Our laboratory has already studied protein-peptide complexes, so we have some experience in solving such problems. First, we study the binding of a peptide to a protein “in vitro” by nuclear magnetic resonance and a computer model by molecular dynamics. The main goal of these experiments is to prove that the peptide binds to the site of interest on the surface of the protein and that this binding is strong enough. Also at this stage, we test the peptide for its ability to interact nonspecifically with other proteins.If the peptide passes all of these tests, we begin cell culture studies. Unfortunately, now only computer modeling is available to us from the whole range of methods. Work in the laboratory is currently suspended due to quarantine, ”Olga Rogacheva said.
At this stage, the researchers launched a molecular simulation of the binding of the SBP1 peptide to the ACE2 protein and ordered everything needed for the “in vitro” experiments.
If the blocking properties of SBP1 are confirmed, and it is also possible to prove the absence of non-specific binding of the peptide to other proteins, it can potentially be used to create a drug against COVID-19. Moreover, according to scientists, even possible mutations of the virus should not become an obstacle to further work. “Blocking viral proteins is not the most popular strategy, because viruses are constantly mutating and at some point the created molecule can stop binding to the viral protein. But SBP1 is cut from human ACE2, so if, due to some mutations, the “spike” protein stops binding to SBP1, then such a “spike” will lose its ability to effectively bind to ACE2 and this strain of SARS-CoV-2 will no longer be dangerous for people.On the other hand, if someday a new coronavirus appears that uses ACE2 to enter the cell, then SBP1 will be applicable against it, ”Olga Rogacheva noted.
Most often, coronaviruses enter the human body through the respiratory system. Nevertheless, preliminary data indicate that the ace2 gene is only weakly expressed in the respiratory system. “This is probably related to the immunity of most people to SARS-CoV-2. If we look in more detail on the parts of the respiratory system, then the maximum expression of the ace2 gene is found in the nasal cavity, and the minimum in the alveoli of the lungs. This means that most of the sick will only have a runny nose, and SARS-CoV-2 simply cannot multiply in the lungs of these people. However, severe cases of COVID-19 suggest that, in some conditions, the expression of the ace2 gene in the lungs is increased. Then the multiplication of SARS-CoV-2 in the lungs can lead to pneumonia, and in the case of an inadequate response of the immune system, to acute respiratory distress syndrome. Blocking the interaction of the spike protein SARS-CoV-2 and ACE2 in the early stages of the disease in such people could reduce their vulnerability to the virus and prevent a severe course of the disease, ”Olga Rogacheva said.
Since at the initial stages of the disease the virus multiplies in the cells of the respiratory system and does not enter the bloodstream, the optimal methods of SBP1 delivery, according to scientists, may be inhalation and intranasal.
The feasibility of using blockers of the interaction between the protein “spike” and ACE2 at the stage of acute respiratory distress syndrome should be investigated separately. In my opinion, in this case, the regulators of immune responses should be of great benefit.
Employee of the Department of Biochemistry of St. Petersburg State University and the Laboratory of Biomolecular NMR of the Institute of Translational Biomedicine of St. Petersburg State University Olga Rogacheva, Ph.D.
In her opinion, SBP1 has prospects of becoming a medicine, but it is too early to speak with 100% certainty about it as a future medicine. However, the researcher noted, the ongoing clinical studies of a recombinant non-membrane form of ACE2 for the treatment of COVID-19 inspire optimism.“SBP1, according to its creators, is only slightly inferior to ACE2 in binding of the spike protein. At the same time, unlike ACE2, it should not participate in any processes in the human body. Ideally, if all this is confirmed, SBP1 has a chance to make it to clinical trials as an inexpensive and safe drug, active against all coronaviruses that use ACE2 to enter the cell. Unfortunately, in reality, only a few developments manage to go all the way from laboratory experiments to the pharmacy shelf, and this path takes a very long time.The methods that we use will allow us to unambiguously decide whether to start experiments on animals with SBP1 or not. At the moment, the answer to this question is really relevant, ”concluded Olga Rogacheva.
Averaging of Viral Envelope Glycoprotein Spikes from Electron Cryotomography Reconstructions using Jsubtomo
Electron cryo-tomography is an electron cryo-microscopy imaging technique that allows the calculation of three-dimensional (3D) reconstructions of complex biological samples.Suitable samples range from purified macromolecular complexes 1, filaments 2, coated vesicles 3 and pleomorphic membrane viruses 4 to whole prokaryotic cells 5 and even thin regions of whole eukaryotic cells 6. After data collection about series slope, 3D tomographic volumes, or tomograms, can be calculated using several installed software packages, including Bsoft 7 and UPM 8.
Two aspects inherent in the study of biological samples using electronic cryo-tomography limit the biological interpretation of the corresponding tomographic volumes. First of all, due to the limited dose of electrons that can be applied to biological materials before significant radiation damage is introduced, SignaL-to noise in tomographic data is usually very low. Secondly, as a result of the tilt geometry of the limited specimen during data collection, some types of object remain absent, which leads to the so-called missing wedge ‘artifact in the tomographic volume.However, both of these limitations can be overcome if the tomographic volume contains repeating identical structures, such as macromolecular complexes, which can be successfully averaged 9-12.
Prior to the average structure from tomogram reconstructions, objects of interest must be found and aligned with the same orientation. The arrangement of such structures can be achieved using an approach that is often referred to as template matching 13 to cross-correlate the structure of the template in the tomographic volume.The template used in this matching process can be obtained from a cryo-electron microscope or cryo-tomography in combination with 3D reconstruction, or it can be a density map simulated by a satomic structure. Several computational packages have been developed to accomplish these tasks 11.
Averaging the glycoproteins of the spines of membrane viruses such as HIV-1 has been a particularly successful approach for studying their structure 14-16. An understanding of structure is integral to identifying both the molecular basis of virus-host interactions and guiding the development of antiviral and vaccine development.While crystallography of macromolecules is the method of choice for high resolution (usually better than 4 a) structural analysis of individual viral glycoproteins and their complexes, the X-ray structures resulting from this method are proteins isolated from the natural membrane environment on the virion. Thus, important details, such as the higher order architecture of viral glycoproteins, in the context of the virion, are still missing. On the other hand, electron cryo-microscopy and single particle reconstruction of whole enveloped viruses is limited to virions with icosahedral symmetry 17,18. Electron cryotomography combined with sub-volume alignment has thus emerged as a complementary method allowing the study of glycoprotein spines of irregularly shaped, pleomorphic viruses in situ.
We have developed software named Jsubtomo (www.opic.ox.ac.uk/jsubtomo) for detecting, aligning and averaging tomographic subvolumes. Jsubtomo has been used to structure a number of cellular and viral structures 19-26. Here we provide a detailed protocol that allows the detection of viral-surface spike structures. To bypass over-refinement of averaged structures by comparing noise, the gold-standard refinement scheme is adopted at 10.27. Finally, strategies for visualizing and interpreting typical results are discussed.
Dandelion leaf extract blocks spike proteins from binding to the cell surface receptor ACE2 (06/28/2021)
(UfoSpace) The engineered spike proteins of the SARS-CoV-2 virus can be stopped by a common “weed” that is annually destroyed on lawns.A study by a German university showed that common dandelion (Taraxacum officinale) can block spike proteins from binding to the ACE2 cell surface receptors in human lung and kidney cells. Dandelion water extract, obtained from the dried leaves of the plant, was effective against the D614 spike protein and a variety of mutant strains including D614G, N501Y, K417N and E484K.
Dandelion extract blocks SARS CoV-2 spike proteins and their variants
The researchers used macromolecular compounds derived from dandelion water extract and tested them on HEK293-hACE2 human kidney cells and A549-hACE2-TMPRSS2 lung cells.Dandelion blocked protein-protein interactions between the S1 subunit of the spike protein and the human ACE2 cell surface receptor. This effect was also true for mutations in the spike protein from prevalent circulating variants, including the variant from the UK (B.1.1.7), South Africa (B.1.351) and Brazil (P.1).
Dandelion extract stopped the attachment of SARS-CoV-2 spike pseudotyped lentiviral particles to lung cells and stopped an inflammatory process called interleukin-6 secretion.Since the study was conducted in vitro, further clinical studies are needed to understand how dandelion extract is absorbed and used in the biological systems of the human body.
Since vaccines weaken herd immunity, natural herbs promise true prevention, more substantial immunity
While tens of billions of government funds have been poured into experimental vaccine development and advocacy campaigns, the world continues to fight new respiratory infections as SARS-CoV-2 mutates into variants under pressure.There is no reason to believe that coronaviruses can be eradicated on Earth, so human adaptation to new conditions will be extremely necessary. Dandelion extract is one of the many herbs that help support a healthy immune response. Better yet, dandelion extract is able to completely prevent infections by blocking the exact channel through which the spine proteins attach and cause viral replication.
Other natural compounds have been investigated using molecular coupling.Nobiletin is a flavonoid isolated from the peel of citrus fruits. Neohesperidin, a derivative of hesperetin, is a flavanone glycoside also found in citrus fruits. Glycyrrhizin is a molecular compound isolated from licorice root. All three of these natural substances also block the binding of spine proteins to ACE2 receptors. Hydroalcoholic pomegranate peel extract blocks the spike protein on the ACE2 receptor with 74 percent effectiveness. When its major components were tested separately, punicalagin was 64% effective and ellagic acid 36% effective.
These natural compounds (along with dandelion extract) can be easily mass produced, combined and used as a prophylactic agent for all future spike protein variants. These herbs are generally considered safe and there is no known overdose of Dandelion Leaf Extract. According to the European Scientific Cooperative for Herbal Medicine, the recommended dose of dandelion leaves is 4-10 grams, brewed in hot water, up to three times a day.
The study authors warn that relying on vaccines is risky and dangerous not only for individual health, but also for herd immunity. Vaccinations are aimed only at increasing antibody levels and are risky with short-term results. Vaccine-related injuries are frequently reported. Re-infections after vaccination are also common, as the vaccine puts pressure on the original developed spike protein, causing it to mutate.
The authors conclude: “Thus, factors such as low toxicity in humans and effective inhibition of the binding of the five corresponding spine mutations to the human ACE2 receptor, reported here in vitro, prompts a deeper analysis of the efficacy of T.officinales in the prevention of SARS-CoV-2 and now require further supporting clinical evidence. “
Article by Lance D Johnson. The opinions expressed in this article may not coincide with the opinions of the author, site administration or reader.
|Except for a couple of thorns named Dov and Pitz.||Except for a couple of thorns named Dov and Peez.|
|In Norwegian, Swedish and Danish, the holly is known as the thorns of Christ, a legend being that Christ wore the crown of holly thorns before his death.||In Norwegian, Swedish and Danish, holly is known as Christ’s thorns, the legend being that Christ wore a crown of holly thorns before his death.|
|In it, Carson tricks Amber into intercourse, which includes bondage and rough sex.||In that scene, Carson introduces Amber to BDSM by binding her to a bed as they have rough sex.|
|Gaby suffered a lot while she cut it and sewed it with needles from thorns.||It had taken Gaby a lot of hard work to cut it into usable sizes and sew it together with thorn needles.|
|Specially provided stud holes hold the studs securely in the tire.||The preshaped stud holes keep the studs firmly attached to the tire.|
|Bonding the ground by wetting the soil in areas where water is available also minimizes sand movement.||Binding the surface by wetting in areas where water is available also minimizes sand movement.|
|Paste an Excel chart or graph into your presentation and link to data in Excel|
|Import or link data in an Excel workbook||Import or link to data in an Excel workbook|
|Create or link to a collaboration workspace (Sales and marketing) [AX 2012]||Create or link to a collaboration workspace (Sales and marketing) [AX 2012]|
|Details For information on linking a SharePoint list to Access, seeFor more information, see Import data from a list or link data to a SharePoint list.||For help about linking to a SharePoint list from Access, see Import from or link data to a SharePoint list.|
|In the External Data – SharePoint Site dialog box, choose to import or bind data.||Select to import or link to a SharePoint site on the Get External Data – SharePoint Site dialog box.|
|Define the tables or views to link to or to import, and fields with unique values in the linked tables.||Identify the tables or views that you want to link to or import, and uniquely-valued fields for linked tables.|
|3. Find related entities, and associate them with the product change case|
|No roses without thorns.||There is no rose without a thorn.|
|For help connecting your headset to your Windows Phone, seeSee Pair your phone with a Bluetooth accessory.||For help connecting your headset to a Windows Phone, see Pair my phone with a Bluetooth accessory.|
|For help connecting your headset to your Windows Phone, see Pair your phone with a Bluetooth accessory.||For help connecting your headset to a Windows Phone, please see Pair my phone with a Bluetooth accessory.|
|Access can only link for the first 255 characters, so you should import the data instead of linking.||Access can only link to the first 255 characters, so you should import the data instead of linking to it.|
|Create a document template and associate it with a document type [AX 2012]|
|They are called rough roses because of the thorns.||They’re called rugged roses- full of thorns.|
|The trunk of the palm tree is climbing due to the rough hooked thorns that it sheds.||The palm stem is scandent because of the rugged, hooked prickles that could shed.|
|But seeing Ted and Honey hit it off was more than her gentle heart could bear, so Zoey left early, pricked by love’s fickle thorn.|
|Involuntarily, the cardinal let go of the branches and, not noticing the thorns, stepped straight forward.||Without meaning to, Cardinal Ralph let the roses fall into place and stepped through them, heedless of the thorns.|
|Put on things like headphones, a crown of silver spikes on the graphite-coated temples.||Put on those things like headphones, crown of silver thorns over the graphite at his temples.|
|That night it seemed to me that my bed had no thorns and that there were no fears lurking in my room.||My couch had no thorns in it that night; my solitary room no fears.|
|Needless to say, beautiful, – agreed Semyon Yakovlevich, – but there is no rose without thorns.||I should say it’s fine, agreed Simon Yakovlevich; but there are no roses without thorns.|
|The sharp-tongued Queen of Thorns.||The famously tart-tongued Queen of Thorns.|
|Listen, we wanted to come in and let you know, so we apologize for all this tying-and-keeping-you-here.||Listen, we wanted to come in and just let you know we’re sorry about this whole tie-up-and-hold-you-here thing.|
|This way we can use contention-based binding and find a match.||That way, we can use competitive binding and find a match.|
|Body binding is not required to return.||Binding the body is not required for return.|
|But Henry Poindexter drew the attention of his companions not to the plant itself, but to a small white card impaled on one of its thorns.||It was not to the plant itself that Henry Poindexter directed the attention of his companions; but to a small white disc, of the form of a parallelogram, impaled upon one of its spines.|
|Your champion has more arrows in his throat than a thistle of thorns.||Your champion’ll have more arrows in his gizzard than a thistle has spikes.|
|Jellyfish do not have thorns.||Jellyfish don’t have spines.|
|They rush forward through the bushes and thickets, not afraid of anything, not noticing the thorny thorns of the cactus and the sharp needles of the acacia.||On go they, regardless of bush or brake-fearlessly, buffeted by the sharp spines of the cactus, and the stinging thorns of the mezquites.|
|Workers on Reunion Island had to artificially pollinate it with cactus thorns in order to be competitive in the global market.||workers in Reunion and Madagascar … have to artificially pollinate them with cactus spines, just to have enough for the world market.|
|Abrasions on the wrists indicate tying, possibly handcuffs.||And abrasions on the wrists consistent with ligature restraints, possibly shackles.|
|Kidnapping and tying me up in your cute murder room won’t help.||Kidnapping me and tying me up in your honeycomb kill room is not helping your case.|
|This is the binding of quantum particles.||It’s quantum particle entanglement.|
|A beam, like neon smoke, flies out of the black panel in the room, grabs his forehead with pits from thorns and drags him in like a dog on a leash.||A beam like neon smoke comes out of the black panel in the room, fastens on his cleat-marked forehead and drags him in like a dog on a leash.|
|These cleats have one point always pointing up.||These are roadspikes – always have one point facing up.|
|We can cut inventory, trim dead assets by occupying warehouse space and tying up capital, plus we get a more accurate point of analysis.||We can reduce inventory, cut back on dead assets taking up warehouse space and tying up capital, plus we get a more accurate point-of-sale analysis.|
|If our bed of roses is now full of thorns and your heart is somewhere in the sea, what can I say or suggest?||Well, if our bed of roses ls now just full of thorns, And your heart is now sea-born, What can I say or propose?|
|So what is this, end-to-end bonding?||So what is this, tying up loose ends?|
|Has he ever played bondage with you?||Did he ever role play by tying you up?|
|Rumor has it that Adrian loves bondage.||Rumor has it that Adrian likes to be tied up.|
|Before we talk about the murders of Gray and Stephanie’s husband, I want you to know that linking them to new murders is a prosecutorial nightmare||Before we talk about the murders of D.D.A. Gray and Steph’s husband, I need you to know that connecting them to these new homicides through the murder weapon is a prosecutorial nightmare.|
|I’ve never seen a rose without thorns.||I never met a rose that didn’t.|
|No Janis thorns, do you understand?||No more janis thorns, you understand?|
|We have to remove it from the spikes.||We need to get her off.|
|Brian is moving too fast to avoid all the spikes.||Brian’s going too fast to avoid all the tacks.|
|Your jacket is full of spikes.||Your jacket is full of studs.|
|On a bed of thorns I will wait for her||On a bed of nails she makes me wait|
|These are one of the thorns that dug into the Savior’s head.||This is one of the very thorns that cut our savior’s head.|
|This means that the victim tried to loosen the bond, but there was a response.||Which suggests the victim struggled to loosen her ligatures, but was rebound.|
|Block 1 uses canonical digit assignment and is not required for a unique identifier.Identifying and linking equivalence classes uses the smallest identifier within the class.||Block 1 uses a canonical digit assignment and is not needed for a unique ID. Equivalence class identification and linkage uses the lowest ID within the class.|
|However, linking keys together in this way increases the damage that can result from a security breach, since attackers learn something about more than one key.||However, tying keys to each other in this way increases the damage which may result from a security breach as attackers will learn something about more than one key.|
|These mutations impair the binding of the PGE2 substrate to HPGD.||Due to these mutations, the binding of the substrate PGE2 to HPGD is disrupted.|
|Linking this asset to Treskov’s resistance group in Army Group Center created a viable coup apparatus.||Linking this asset to Tresckow’s resistance group in Army Group Center created a viable coup apparatus.|
|The environment plays a vital role in the game as there are several hazards that will instantly kill the enemy, such as holes in the floor or spinning wheels of spikes.||The environment plays a vital role in the game, as there are several hazards that will instantly kill an enemy, such as pits in the floor or rotating wheels of spikes.|
|This correlation, suggesting that receptor binding is causally related to therapeutic efficacy, was reported by two laboratories in 1976.||This correlation, suggesting that receptor binding is causally related to therapeutic potency, was reported by two laboratories in 1976.|
|Binding of benzene rings gives biphenyl, C6H5 – C6H5.||Linking benzene rings gives biphenyl, C6H5 – C6H5.|
targeting the receptor-binding domain of the protein spikes of the SARS-CoV-2 virus
Sudden spread of coronavirus infection (at the time of this writing, more than 42.5 million confirmed cases of infection and more than 1.1 million deaths were detected [1 ] / 90,089 65.9 million cases of infection and more than 1.5 million deaths at the time of translation – approx.per. ) endangered public health. Despite global efforts to control this viral infection, the pandemic is still gaining momentum. Faced with this serious and unprecedented problem, it seems that vaccination alone is the most promising method of controlling the incidence of the new coronavirus infection. A recent study by Yang et al. ( rice.one).
A recombinant vaccine targeting the receptor binding domain (RSD) of the SARS-CoV-2 spike protein may elicit a protective immune response. The recombinant RSD protein is expressed in insect cells using the Bac-to-Bac system and precipitated (precipitated with alum) to form a vaccine. After vaccination of primate monkeys (non-hominid) with RSD vaccine, the formation of serum antibodies was detected, which could bind RSD and neutralize virus infection.This served as material for the development of a vaccine, the action of which is based on the principle of producing antibodies against RSD.
For infection, the coronavirus needs to enter the cell, for which it binds to the receptor for angiotensin converting enzyme II (ACE2) . This process of recognition of the receptor is mediated by spikes, which are embedded in the viral envelope, consisting of protein trimers. Both structural and functional data on the virus indicate that spine RSD specifically interacts with ACE2 .Antibodies targeting RSD interfere with the binding of the virus spines to ACE2 and can block the penetration of the virus into the cell, which neutralizes the infection. Thus, thorn RSD is a good immunogen for vaccine development. Recognizing the irreplaceable role of RSD thorns in the development of SARS-CoV-2 infection, Yang et al. selected the region of the viral spike, covering residues 319-545, as a candidate for immunogens. This area of the thorn, in accordance with the established complex structure of the viral RSD , is an integral structural unit necessary for the interaction of the virus with the ACE2 receptor.
To ensure that the RSD of the spike protein can be efficiently expressed and the expressed protein will maintain its natural spatial configuration, Yang et al. selected for the preparation of the immunogen Baculovirus Expression System Bac-to-Bac. As one of the most powerful and versatile expression systems available, the Baculovirus Vector Expression System (BEVS) is an autonomous viral system that is designed to express heterologous genes in insect cells.The Bac-to-Bac baculovirus expression system is a modified BEVS in which a recombinant baculovirus containing a foreign gene is first generated and then used to infect insect cells for enhanced expression of genes from many different sources. Compared to other heterologous expression systems, Bac-to-Bac has several advantages. It has a good ability to clone foreign genes, provides easy screening for recombinant baculoviruses, has a high degree of protection, has a complete system of post-translational processing and modification, and in most cases can guarantee efficient expression of the gene of interest.Since its inception in the 1980s.  BEVS has been widely used in vaccine development, gene therapy and other fields. As expected, using the Bac-to-Bac system, it was possible to qualitatively express the RSD of the coronavirus thorns. The subsequently isolated RSD protein turned out to be both N- and O-glycosylated, retaining its functional, interacting with ACE2 with nanomolar binding affinity. In addition, the recombinant protein specifically interacted with the sera of patients recovering from coronavirus infection, but not with the sera of healthy people.
Can RSD protein trigger an effective immune response? To address this issue, Yang et al. mice and rabbits were immunized with recombinant RSD protein using aluminum hydroxide as an adjuvant. It has been shown that protein precipitate (protein precipitate was formed with the help of alum) induces a stable humoral immune response. Antibodies specific to RSD were obtained from both animals. In addition, it was found that the sera of these immunized animals block the binding of RSD to ACE2 expressed on the cell surface and neutralize infection with both pseudotyped and live SARS-CoV-2 in vitro .More importantly, a functional antibody response was observed as early as seven days after single dose injection; this suggests that the recombinant RSD protein has high antigenic properties.
As a key step in the vaccine development process, Yang et al. tested the immunogenic effect of the spike protein RSD vaccine on non-hominid primates (Macaca mulatta). The immune serum, taken seven days after the first vaccination, effectively blocked infection with a pseudovirus (pseudotyped SARS-CoV-2).In all vaccinated monkeys, neutralizing antibodies against the live virus were detected after two intramuscular injections of the RSD vaccine. During the study of the effect of a live virus preparation in the lung tissues of representatives of the vaccinated groups, it was not possible to detect viral genomic RNA (gRNA) or subgenomic RNA (sRNA), indicating viral replication. In addition, significant histopathological differences were found in lung tissue in the control group and the group of vaccinated non-hominid primates.All unvaccinated animals showed typical histopathological changes characteristic of viral interstitial pneumonia (for example, thickening of the alveolar walls, a large number of infiltrates of interstitial inflammatory mononuclear cells, the disappearance of a well-defined structure of the lung tissue). In monkeys vaccinated with the RSD protein vaccine, no significant histopathological changes were revealed, but mainly the normal structure of the lung tissue prevailed.
Overall, the data reported by Yang et al.clearly demonstrate that the recombinant RSD of the SARS-CoV-2 coronavirus thorn protein could potentially induce a protective immune response in mice, rabbits and non-hominid primates. This requires further research to conduct human clinical trials. Yang’s results also highlight the importance of the spike protein RSD in the development of a SARS-CoV-2 vaccine and provide the basis for this potential vaccine.
Scientists from St. Petersburg are investigating a peptide with potential for treating coronavirus – Science
SAINT PETERSBURG, April 20./ TASS /. An international team of scientists, including researchers from St. Petersburg University (St. Petersburg State University), will test the ability of a peptide located on the surface of a human cell, recently isolated by US scientists, to block the spread of coronavirus. This is stated in a message released by the press service of the university on Monday.
As noted in the press service, at the end of March, Chinese scientists published the crystal structure of a protein called ACE2 from the surface of a human cell, with which the coronavirus “spike” protein binds to enter the cell.This allowed researchers from the Massachusetts Institute of Technology (USA) to identify and isolate the fragment of ACE2, with which the “spike” binds directly. It is a 23 amino acid peptide (IEEQAKTFLDKFNHEAEDLFYQS). As conceived by the creators of the peptide, it should block the binding site of the “spike” protein, thereby depriving the virus of the ability to “dock” with ACE2 and penetrate the cells of the human body. In accordance with this interpretation, the authors named their peptide spike-binding peptide 1 (SBP1).
“The idea to create such a peptide could have appeared only after the publication of the structure of the ACE2 complex with the coronavirus” spike “protein, because only by seeing the structure of the complex of two proteins, it is possible to identify a small fragment in one protein that could bind to the second protein”, – Olga Rogacheva, an employee of the Department of Biochemistry of St. Petersburg State University and the Laboratory of Biomolecular NMR of the Institute of Translational Biomedicine of St.
According to the press service, the scientists will first study the binding of the peptide to the “spike” protein by nuclear magnetic resonance, and computer modeling will also be used.The main goal of the experiments is to prove that the peptide binds to the desired site on the surface of the protein and that this binding is strong enough.
If the blocking properties of SBP1 are confirmed, and it is also possible to prove the absence of non-specific binding of the peptide to other proteins, it could potentially be used to create a cure for coronavirus, the press service noted. Moreover, according to scientists, even possible mutations of the virus should not interfere with further work.
“Blocking viral proteins is not the most popular strategy, because viruses are constantly mutating, and at some point the created molecule can stop binding to the viral protein. But SBP1 is cut from human ACE2, so if due to some mutations the protein the “spike” will no longer bind to SBP1, then such a “spike” will lose the ability to effectively bind to ACE2 and this strain of SARS-CoV-2 will no longer be dangerous to humans.