Category Archives: Cell Biology

Cell Biology

Why coronavirus is so lethal & fast-spreading: Its biology, disease, cure & call for united action – MyNation

1. What is a virus?

We have to first understand the simple structure of a typical cell very briefly. Then, even as laymen, we will be able to understand how the structure of the coronavirus is different from that of a typical cell. A common mans understanding and knowledge of the coronavirus holds the key to implementation of preventive measures and solutions to contain the pandemic.

That "protoplasm is the physical basis of life" is a fundamental concept of cell biology and life science defined by William Huxley, an English biologist and anthropologist. The cell content within the cell membrane is called protoplasm. The matrix residing within the cell membrane and outside the centrally located nucleus is called cytoplasm. So, cytoplasm with organelles and nucleus containing the genetic material (DNA) are the constituents of protoplasm.

2. Virus as a bridge between the living and non-living: A virus is an unusual, very primitive parasitic entity that has both living and non-living characteristics. It is a mysterious invisible, non-living, micro-crystal or dust particle when outside a living host. But it assumes life soon after it enters a living host (ranging from amoeba to man and also plants). Therefore, it is an obligatory parasite. It has neither cytoplasm nor cell organelles. It has only genetic material, either DNA or RNA, surrounded by a protein coat. Therefore, the virus is considered as a bridge between the living and the non-living by those who have studied biology and theories of the origin of life.

3. Understanding the nature of the coronavirus: The coronavirus is a virus belonging to the family Coronaviridae. It is opined that the original reservoir of this virus is a non-human host, the horse-shoe bat (in which it causes no harm), from which it jumped to humans. The immune system of the bat is distinct from the human immune system and allows the virus to rapidly multiply within the bat while also protecting it from the harmful effects. Accordingly, bats have been the source of other recent viral disease outbreaks such as SARS, MERS and Ebola This coronavirus emerged in the Chinese city of Wuhan in November 2019 and spread all over the world in a short period. The epidemic is now known as COVID-19 and the virus is known as SARS-CoV-2. The virus is a mutant variety of the SARS (Severe Acute Respiratory Syndrome) coronavirus. This non-living micro dust-like form of the virus is transmitted between people through respiratory droplets when an infected person sneezes or coughs.

4. Structure of the coronavirus: This coronavirus is a spherical, single-stranded RNA (genetic material) virus with a protein coat. It has corona-like extensions called spike proteins on its surface. Hence the name coronavirus. The spike proteins bind to the receptors on the host cell. It is called novel coronavirus (nCoV) because of these spike proteins, which are different from those of other coronaviruses.

5. Fast replication process once it enters the host: In general, the coronavirus multiplies swiftly once it enters the living host. Its RNA replicates after entering the host and produces multiple copies of itself. The RNA particles get themselves covered by protein coats and then come out of the host cells, only to infect new cells. During infection, they enter through the mouth or nostrils through respiratory droplets, make their way into the bronchial tract and lungs gradually, and then they multiply in the alveoli of the lungs. This reduces the expanding and contracting mechanism of the alveoli, leading to fibrosis of the lung. As a result, the function of our oxygen-supplying organ, the lung, gets badly mutilated and respiration gets hindered, making us unable to breathe. This results in a shortage of oxygen supply to the brain and the entire body and the patient dies within a few days.

6. Why is the coronavirus so lethal and fast- spreading? How to break the protein coat of the virus and paralyze its RNA when it is in the non-living form outside the host and in a living form inside the host is a matter of research. Of course, its duration of life outside the host is very limited, to the extent of 3 or 4 days, especially in a tropical hot climate like in India, where the relative humidity is also relatively high. It is believed that a type of WBCs called the natural killer cells (NK cells), which are a component of our innate immunity and which resist any pathogen as the first line of defence, are not very effective against these viruses. People may be carriers of infection of the virus for 1 to 14 days before developing symptoms. The most common symptoms are fever, dry cough, tiredness, and excessive drowsiness. In severe cases, breathing will be difficult. If not contained, it can be fatal, particularly in individuals with co-morbid health conditions like diabetes, high blood pressure, and chronic diseases of heart, lungs, kidneys and liver, and infants aged 12 months and under. Since the coronavirus is spread through respiratory droplets, it is advised not to touch the nose and mouth as these viruses stay on the surface of the hand in a viable state for quite a long time. Also, it is advised to wash the hands thoroughly for at least 20-25 seconds frequently with soap. Sanitizers can also be used to keep the hands clean.

7. Prevention of COVID-19 -- the scientific and social approach: Our body's immune system is yet to develop a new strategy to counter this novel mutant coronavirus. Presently, our WBCs can kill many other invading pathogenic forms like bacteria and others. But we have not yet developed an immune system that can kill the SARS-CoV-2. So, we are neither able to effectively deal with the coronavirus outside the body nor inside. The greater challenge is to find a way for our defence mechanism to deactivate the RNA of coronavirus when it enters the human body or by antibiotics or in developing a vaccine. Since it is fast-spreading through human agency, the epidemic has now become a pandemic, killing human beings fast without yielding to any known medical system. That is the reason thousands have died in such a short time, in China, Italy, Spain and South Korea. As a result of the deeply inter-connected world we now live in involving convenient air travel and cruises, it has spread to nearly 200 countries now. As of 31st March 2020, there were 750,890 confirmed cases and 36,405 deaths. Realizing the magnitude of the epidemic, the Government of India has decided that the only way to contain the epidemic is by making humans not accessible to it by social distancing. People affected by coronavirus have to be isolated in quarantine. Thus, the virus chain has to be broken by not allowing it to enter the human host, so that it perishes after being deprived of a host for a considerable period.

8. Social distancing and Stay at Home are the only Mantra: That is why we have messages of preventing the coronavirus infection on the telephone ringtone. We should broadcast it in all media and all possible manners. It is with this intention that the Government of India and all the States have announced a strict lockdown. That is why the COVID-19 preventing "mantras" are "stay at home" and maintain social distance everywhere. Even while shopping for essentials, one must maintain a distance of one or two meters from the next person. 'Prevention is better than cure' is the golden proverb we all have heard, but in the context of the coronavirus, prevention is the only cure thus far.

9. The absolute need for a strict, nation-wide lockdown: If we see the extent of devastation caused by the coronavirus in developed countries like Italy, China, Spain, UK, and America, India with its less developed medical infrastructure and habitual group-living in cities and slums, especially in villages, needs to be extra vigilant and cautious in preventing the entry and spread of coronavirus. Our national lockdown may have to be inevitably continued for some more reasonable time and all of us have to educate fellow citizens about the preventive measures more aggressively and convincingly.

10. Therapeutic approaches being tested for potential treatment of COVID-19 in the future: Scientists and physicians all around the world are working together to explore potential treatments for coronavirus. Clinical trials are underway to test a number of candidate treatments that are already approved and safely administered to patients for other diseases. These include the anti-malarial agents chloroquine and hydroxychloroquine; HIV treatments lopinavir and ritonavir. An experimental antiviral agent called Remdesivir that was previously developed for treating Ebola is also being explored. Another treatment called convalescent plasma is also under investigation that involves transfusion of critically ill patients with plasma obtained from the blood of patients who have recovered from COVID-19 and built up high levels of antibodies to SARS-CoV-2 to help stimulate a stronger immune response. Several unconventional approaches for rapid vaccine development are being explored that are expected to deliver results in 12-18 months. The first patient was recently dosed in a clinical trial in the USA for a candidate mRNA based vaccine which encodes for a stabilized form of the coronavirus spike protein.

11. Need for a positive attitude at the time of fear and uncertainty: It is very hard to retain positive energy when we are being constantly bombarded with the news of death and economic crisis. However, this time of lockdown is a golden opportunity for reflection, spending quality time with family and exploring hobbies we never had a chance to pursue due to the unending grind of routine life. While social media is a blessing in times of a lockdown to keep in touch with family and friends, it is also a source of rumours and misinformation. We should only rely on government agencies for the most accurate information and guidelines.

12.Need for basic existential solidarity transcending the barriers of caste, creed and religion: It is time that we Indians demonstrate that we are all solidly united, transcending barriers of caste, creed, religious customs and traditions to protect not only our country but the world. Let us pray intensely for the wellbeing of all. Let us invoke the noble and powerful survival instinct and motherly caring instinct hidden in all of us. Let us work together constructively, lovingly, as Indians. This feeling of unity, amity, and love for each other is needed now to keep the COVID-19 pandemic away. This should be our religion, throb of life, the wave of mind, and line of action. So, let us together pray for the protection from this lethal coronavirus and wellbeing of all and take a pledge to stay at home. The famous French surgeon and Nobel laureate, Dr. Alexis Carrel, who was awarded the Nobel Prize in Physiology or Medicine in 1912, has said, "Prayer is the most powerful form of energy one can generate. As a physician, I have seen the patients coming out of melancholy and disease by the serene efforts of prayer."

Our united and the sincere cry of the soul shall be heard by the Almighty, the Omniscient, Spiritual Consciousness, which has created and is sustaining the universe. Let our patriotism, universal brotherhood, and unity find its true expression in this hour of unprecedented crisis. Let the scientific capability of the West and the spiritual capability of the East come together and work reciprocally to fight this terrible pandemic and stave off nemesis. If political and religious leaders, government employees, police, the medical, pharmaceutical and nursing brigades and the business community work with sincerity and honesty as per the scientifically defined line of action, we shall not only conquer the coronavirus pandemic, but also create a new eco-friendly, clean, and spiritually vibrant world of understanding, friendship and love.

More on Swami Muktidananda

He is a post-graduate in science from Institute of Science, Bombay University. He joined the Ramakrishna Order at Sri Ramakrishna Ashrama, Mysore in 1982. He is initiated by Revered Swami Vireswaranandaji Maharaj and had his Sannyasa Diksha from Revered Swami Bhuteshanandaji Maharaj in the year 1993. He served at Sri Ramakrishna Vidyashala, a premier residential Educational Institution of Mysore centre itself for over two decades and as Chief Administrator for 16 years.

He has contributed articles to monthly journals of the Ramakrishna Order like Prabuddha Bharata, Vedanta Kesari and Kannada magazine Viveka Prabha. He has a special grounding in Education, Indian Philosophy, Yoga Psychology, Indian Culture. He has given a series of talks in Chintana Radio Programme Akashavani, Mysore.

He has been also conducting Guided Meditation classes for students and spiritual seekers for years.

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Why coronavirus is so lethal & fast-spreading: Its biology, disease, cure & call for united action - MyNation

Cell Biology

Microbes in your blood could be the tell-tale of cancer | Forge – ForgeToday

Scientists have developed a novel method of cancer detection and diagnosis from a single blood draw, even at early stages.

In 2017, Dr Ravid Straussman of the Weizmann Institute of Sciences Molecular Cell Biology Department and his team found live bacteria within pancreatic tumours. These bacteria metabolised a common chemotherapy drug and rendered it ineffective. This shone light onto the possibility that bacteria and viruses may influence prognosis to a larger extent than previously thought.

Recent investigation into these microbes revealed that they are detectable in the blood, even before symptoms arise. Researchers at the University of California San Diego School of Medicine have exploited this to develop a new method to determine who has cancer, and which type, by a simple analysis of microbial DNA in the patients blood.

The researchers were granted access to The Cancer Genome Atlas, which stores microbial data as well as genetic information from thousands of patients tumours. From this, distinct patterns of microbial DNA were found to be associated with specific types of cancer.

Of course, some of these associations are well-known. For example, human papillomavirus (HPV), has a clear link to cervical cancer. However, the team also found new microbial patterns, or signatures, which were previously unknown and were able to distinguish between specific cancer types. If these were found present in the blood of a patient, this would allow accurate and complete diagnosis.

The team tested thousands of cancer samples on computer-based models which were trained to associate the presence of certain microbial DNA with specific cancer types. They found that the computer was able to recognise a patients cancer type, even at early stages, using only a small blood sample.

Gregory Poore, MD/PhD, his supervisor Professor Rob Knight and their team have undertaken the largest-ever attempt (to their knowledge) to identify specific microbial DNA in human blood. They have successfully produced a technique to exploit non-human molecules in the diagnosis of a major human disease. The ability of this technique to detect traces of microbes at the earliest stage of disease progression gives it great therapeutic potential it is no secret that earlier diagnosis produces a better prognosis.

The team is now looking to introduce their method into the clinical setting and are encouraging other cancer researchers to invest their efforts into the study of microbes in the disease.

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Microbes in your blood could be the tell-tale of cancer | Forge - ForgeToday

Cell Biology

Meet Ghanaian scientist Professor Awandare helping us understand the coronavirus – GhanaWeb

General News of Monday, 13 April 2020

Source: mynewsgh.com

Professor Gordon Akanzuwine Awandare

One of the leading Ghanaian scientists helping us understand the novel coronavirus disease is Professor Gordon Akanzuwine Awandare of the School of Biochemistry and the West African Centre for Cell Biology of Infectious Pathogens (WACCBIP) at the University of Ghana.

He, together with other leading scientists at the University of Ghana, has successfully sequenced the genome of the novel coronavirus disease by examining some 15 confirmed cases of the disease in the country.

Prof Awandare has been a leading light in research on many diseases in the country, especially the malaria parasite.

Born in Kandiga in the Kassena Nankana West District of the Upper East Region, Prof Awandare battled with recurring malaria as a child.

Defying all odds to have a good education, he obtained an a Bsc in Biochemistry from the University of Ghana in 1998 and an MSc in the same field in 2002 before obtaining his PhD in the area in 2007 from the University of Pittsburgh in the United States of America. His area of interest was the malaria parasite, inspired partly by his battle with the disease as a child.

Driven by patriotism, he returned to Ghana after spending three years in America contributing to knowledge there.

Prof Awandare took extraordinary steps to set up his own research group notwithstanding the lack of funds and other bottlenecks.

His major breakthrough came in 2013 when he led a consortium that secured funds to set up a new state of the art centre in the country to research into infectious pathogens. The consortium secured some $8 million from the World Bank, and Prof Awandare became the founding director of the West African Centre for Cell Biology of Infectious Pathogens (WACCBIP) in 2013.

The Centre cutting edge research has ensured that it has secured several other funding to undertake research into many diseases.

He has received many awards for his excellence on research.

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Meet Ghanaian scientist Professor Awandare helping us understand the coronavirus - GhanaWeb

Cell Biology

Dr. Kevin Dalby on How to Decrease Your Risk of Developing Cancer – Thrive Global

Life expectancy in the United States is about 78 years, though longevity is not without medical concerns. As many as one in three Americans will develop malignant cells in their lifetime. While the scientific community has significantly increased their understanding of cancer in recent years and applied that knowledge to treatment, prevention research remains a top priority; however, since cancer is a series of diseases, the exact cause is not always known. Genetics plays an important role, yet so does diet and lifestyle.

Dr. Kevin Dalby, professor of chemical biology and medicinal chemistry, is studying the mechanisms of cancer cells and currently working on cancer drug discovery. His research primarily focuses on developing targeted therapeutics, but he does acknowledge that specific behavioral changes can help lower a persons risk for cancer. The Harvard School of Public Health estimates that 75% of American cancer deaths could be prevented if tactics are adopted on a mass scale.

Below, Dr. Kevin Dalby reviews practical behavioral choices that anyone can take up to help prevent cancer, thus reducing the risk of the emotional and the financial burden inflicted by this crippling disease.

Avoid Tobacco

The correlation between tobacco use and cancer is staggering. In the United States, one out of every five deaths is related to tobacco. Moreover, cigarette smoking accounts for 85-90% of lung cancer deaths and 70% of oral and laryngeal cancer deaths.

Tobacco use (smoking or chewing) is a difficult habit to quit. Still, it could help you as well as those around you (secondhand smoke kills) avoid a future collision with the following cancers: lung, mouth, throat, larynx, pancreas, bladder, cervix, and kidney.

Limit Alcohol

Research has yet to pinpoint exactly how alcohol influences your susceptibility for cancer, but excess use does increase the risk for mouth, throat, liver, colon, rectal, and breast cancer. Men should limit their acholic beverages to two a day and women to one. For context, one drink equates to approximately twelve ounces of beer, five ounces of wine, or one and a half ounces of liquor.

Eat A Healthy Diet

40% of cancers are associated with dietary factors: habits, foods, and nutrients all play a role. The American Cancer Society suggests a daily nutritional regimen consisting of whole grains, fish or poultry, and a variety of vegetables and fruits to lower your risk for cancer. Try to limit red and processed meats, eat fewer sweets, and reduce your intake of saturated fats.

Exercise

Regular physical activity helps you maintain a healthy weight, control blood pressure, and may lower the risk for several types of cancer such as colon, prostate, and even breast cancer. Obesity is especially of paramount importance since it has been linked to 20% of all cancer-related deaths.

Adults should strive to exercise moderately for 150 minutes each week. Alternatively, you can aim for 75 minutes of vigorous activity if that suits your lifestyle better.

Sun Protection

Skin cancer is common but also preventable. To reduce your risk, proportionately apply sunscreen, avoid the sun at midday if possible when its rays are most reliable, cover exposed skin and forgo tanning beds and sunlamps, which are just as dangerous as actual sunlight.

Regular Medical Care

Cancer may not be entirely preventable, but if caught early, your chances of survival improve drastically. Schedule regular checkups with your doctor, be transparent, and ask what tests make sense for you. Depending on your sex, age, and medical history, your doctor may recommend screenings for breast, cervical, colon, lung, or prostate cancer.

About Dr. Kevin Dalby:

Dr. Kevin Dalby has been interested in the why of chemical reactions since he was a student at the University of Cambridge, where he graduated with a Doctor of Philosophy degree in Organic Chemistry. This curiosity has led to his interest in the processes of cell signaling, and ultimately to cancer research. Dr. Dalbys research areas include biochemistry, cancer, cell biology, chemical biology, drug discovery & diagnostics, and enzymology.

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Dr. Kevin Dalby on How to Decrease Your Risk of Developing Cancer - Thrive Global

Cell Biology

Omeprazole As An Additive For Coronavirus Therapy – Science Magazine

One of the notable things about the current pandemic is the way that all our modern biology and analytical techniques are on display. Molecular biology, structural biology, bioinformatics, technologies like cryo-EM structure determination, fast sequencing, protein interaction screening and more this is a real-time look at how basic biomedical research gets done. Ive been reading a new preprint that starts off with protein sequence analysis and ends up with an actionable clinical recommendation (skip to the end for that one!), and I think its a good illustration.

This team from Germany and the UK has been analyzing the new pathogen with a technique theyd already developed to look at differentially conserved amino acids among related strains. Comparing the current SARS-CoV-2 and the earlier SARS-CoV, they find that most of the amino acid changes are conservative (one hydrophobic residue swapped for another), with some polar/nonpolar swaps and very few instances of swapping charged residues. Thats about what youd expect, of course, but the question is whether any of these are functionally relevant. A closer look shows that these differentially conserved positions are found much more in the notorious spike protein region than (say) in the envelope proteins, and that overall 92% of these changes are on protein surfaces rather than buried residues, which makes you think that they are indeed important.

Its already been noted that several residues involved with the spike (S) proteins interaction with the human ACE2 protein vary between the older SARS virus and the new one. This group went on to look at various human cell lines and their susceptibility to viral infection, and found that while the presence of the ACE2 protein in general is important, there are more things at work. For example, 293 cells (kidney-derived) dont express ACE2 at all, and had been shown during earlier work on SARS to be resistant to infection. The new coronavirus doesnt infect them either but if you engineer the cells to express ACE2, original SARS will then infect them, but the new virus doesnt do so nearly as well. Across several other cell lines, there is no good correlation between the amount of ACE2 present (as long as its there in some amount) and the ability of SARS-CoV2 to infect them, so its not just a simple the more ACE2 the worse situation. We dont know what the other factors are, but there clearly are more than just ACE2 levels.

They also looked attransmembrane serine protease 2 (TMPRSS2), another human enzyme that is hijacked to allow viral entry (and which is a target of the serine protease inhibitor camostat, a drug that many readers will have heard of by now and which is in clinical trials against the current virus). As with ACE2, susceptibility to SARS-CoV2 didnt correlate with TMPRSS2 levels, either, though more evidence that things arent as simple as you might hope. The paper goes on to look at camostat itself and another similar protease inhibitor, nafamostat, which is also approved in Japan for pancreatitis. Both drugs are more active against SARS-CoV2 infection in cell culture than they are against the first SARS virus, and nafamosat is more active than camostat. Unfortunately, the concentrations that are needed in the cell assay (0.5 and 1.2 micromolar respectively) are still above what these drugs appear to achieve in vivo (reported plasma concentrations of 0.2 micromolar), so well have to see from the human trial data if thats enough to show efficacy. Its not wildly far off, particularly for nafamostat, but youd still rather have it the other way around, for sure.

But theres some possible good news as well. The team also looked at the serine protease inhibitor aprotinin, a small protein inhibitor of serine proteases that has had an up-and-down history in human therapy and has been looked at as an antiviral as well (via its TMPRSS2 inhibition). As Trasylol, it was used to slow down bleeding during surgical procedures (by inhibiting several proteases in the fibrinolysis pathway), but as with all drugs that either enhance or reduce blood clotting, youre walking a fine line between benefit and trouble. Apronitin was temporarily taken off the market in 2007 because of possible association with clotting events, but this suspension was lifted by the EMA in 2012 after further review of the data. In this work, though, apronitin was not only more potent in the cell assays, it displayed much stronger effects on the formation of double-stranded RNA (a marker of viral infection), and did so at levels below the known blood levels on human administration. Its more effective on the new coronavirus than it is on SARS, which seems to be partly explained by the sequence differences noted above. The authors say:

Since aprotinin interferes with SARS-CoV-2 in therapeutic concentrations and displays more pronounced direct antiviral effects than camostat and nafamostat, it seems to have a greater potential for the treatment of SARS-CoV-2-infected individuals based on our data.

Youd want to be careful with this drug because of its past history, but the authors note that there is actually an aerosol formulation of apronitin thats been approved in Russia, so that mode of administration looks feasible and might have less systematic risk.

The paper goes on to look at another approved drug that I havent seen getting as much attention: omeprazole, the well-known proton pump inhibitor for acid reflux. It has been reported as having some antiviral activity in the past, possibly by increasing the pH in lysosomal compartments. In their assays, it did interfere with viral infection, but at levels too high for realistic human dosing. But heres the interesting part: they found that simultaneous treatment with omeprazole (at human therapeutic concentrations) increased the activity of apronitin by 2.7 fold and increased the activity of remdesivir by 10-fold. That seems like a very useful observation! As far as I can see, the paper did not check for an interaction of omeprazole and camostat/nafamostat, which would be interesting to know as well. The same group had noted in 2019 that the drug increased the activity of acyclovir against the herpes virus.

So while were still figuring out if remdesivir has efficacy by itself, theres an opportunity to administer a widely used, well-tolerated drug to give it a better chance. And both the beneficial interaction of omeprazole with apronitin and the earlier acyclovir/herpes result suggests that this could be a more general effect with many other drug candidates, which seems well worth investigating.

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Omeprazole As An Additive For Coronavirus Therapy - Science Magazine

Cell Biology

Cardiovascular Repair And Reconstruction Devices Market Is Projected To Expand At A Robust CAGR Of +5.2% By 2026 Analysis by Industry Outlook,…

Global Cardiovascular Repair And Reconstruction Devices market from the in depth perspective of all the ongoing trends that are affecting the market and are important to be understood are studied. These trends are geographical, economic, socioeconomic, political, cultural, political, and many other are studied. The overall effect on the consumer preferences will have a major say on the market working in the years to come. The dynamics which affect the Cardiovascular Repair And Reconstruction Devices market have been studied meticulously.

The global cardiovascular repair and reconstruction devices market size was valued at USD 2,831.1 million in 2018 and is expected to grow at a CAGR of 5.2% over the forecast period. Key factors contributing to market growth are increase in prevalence of Congenital Heart Defects (CHDs) and technological advancements in molecular chemistry, clinical pharmacology, cell biology, and vascular surgery.

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Key players profiled in the report include Medtronic; Bard Peripheral Vascular; Terumo Cardiovascular Systems Corporation; W. L. Gore & Associates, Inc.; Getinge AB; CryoLife, Inc.; Edwards Lifesciences Corporation; Baxter; and Admedus.

The main goal for the dissemination of this information is to give a descriptive analysis of how the trends could potentially affect the upcoming future of Cardiovascular Repair And Reconstruction Devices market during the forecast period. This markets competitive manufactures and the upcoming manufactures are studied with their detailed research. Revenue, production, price, market share of these players is mentioned with precise information.

In the geographic segmentation, the regions such as North America, Middle East & Africa, Asia Pacific, Europe and Latin America are given major importance. The top key driving forces of Cardiovascular Repair And Reconstruction Devices market in every particular market is mentioned with restraints and opportunities. The restraints are also given a counter act which prove to be an opportunity for this market during the forecast period of 2020 to 2026 respectively.

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Cardiovascular Repair And Reconstruction Devices market is also explained to the clients as a holistic snapshot of a competitive landscape within the given competitive forecast period. A comparative analysis of regional players and segmentations, which helps readers get a better understanding of the areas and resources with better understanding.

This report provides:

1) An overview of the global market for Cardiovascular Repair And Reconstruction Devices Market and related technologies.

2) Analyses of global market trends, with data from 2017, estimates for 2018 and 2019, and projections of compound annual growth rates (CAGRs) through 2026.

3) Identifications of new market opportunities and targeted promotional plans for Global Cardiovascular Repair And Reconstruction Devices Market.

4) Discussion of research and development, and the demand for new products and new applications.

5) Comprehensive company profiles of major players in the industry.

Table of Content

1 Introduction

2 Market Research Tactics

3 Market Summary

4 Quality Market Insights

5 Cardiovascular Repair And Reconstruction Devices Market Overview

6 Regulatory Market Synopsis

7 Cardiovascular Repair And Reconstruction Devices Market, By Application Analysis:

8 Cardiovascular Repair And Reconstruction Devices Market, By product Analysis:

9 Cardiovascular Repair And Reconstruction Devices Market, By End User Analysis:

10 Cardiovascular Repair And Reconstruction Devices Market, By Geographic Region

11 Competitive Landscape

12 Company Profiles

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Cardiovascular Repair And Reconstruction Devices Market Is Projected To Expand At A Robust CAGR Of +5.2% By 2026 Analysis by Industry Outlook,...

Cell Biology

Conspiracy theorists claim that 5G increases vulnerability to COVID-19 with baseless theory that it affects hemoglobin – Health Feedback

CLAIM

"Coronavirus pandemic would likely not be nearly as bad if 5G exposure/radiation pollution wasnt already compromising the structure and function of hemoglobin cells."

DETAILS

Flawed reasoning: The argument that 5G increases vulnerability to COVID-19 is inconsistent with the fact that 5G coverage is geographically quite limited and many of the hardest-hit regions do not have 5G.Inadequate support: No scientific studies support the claim that non-ionizing radiation alters the structure of hemoglobin.

KEY TAKE AWAY

Wireless communications use electromagnetic waves to transfer data. Electromagnetic waves carry energy that is proportional to their frequency and can interact with biological tissues. However, the energy level and the penetration depth of the type of waves used for 5G do not allow them to alter the structure and function of important biological macromolecules such as hemoglobin. In addition, there is no correlation between the very limited 5G coverage in the world and the progression of the COVID-19 pandemic.

The claim that 5G technology makes us more vulnerable to COVID-19 appeared in several media outlets, including Natural News on 6 April 2020. The purported reason would be that electromagnetic fields (EMF) from 5G devices decrease the ability of hemoglobin molecules in our red blood cells to bind oxygen and carry it to our organs. This claim is unsupported by current scientific data. In fact, Mats-Olof Mattson, professor of cell biology at Strmstad Academy in Sweden, told Health Feedback that he found it unrealistic, firstly because non-ionizing EMF used in 5G does not carry sufficient energy to alter the structure of biomolecules, and secondly because 5G rollout is very limited and is absent from many regions heavily impacted by COVID-19.

The capacity of the hemoglobin protein to bind and release oxygen is tightly associated with its structure and to the conformational changes it undergoes when bound. According to Mike Adams, the author of the Natural News article, 5G radiation exposure occupies the hemoglobin molecule with other elements that alter its structure and therefore its function, inhibiting its ability to bind with oxygen. The author further states that this binding deficiency is what makes people vulnerable to COVID-19: This is very likely happening all across the world wherever 5G is currently functioning, its just that the coronavirus is now exacerbating the symptoms and conditions to the point where mass death is occurring.

However, the author does not provide any research or scientific data to support his [emailprotected] Mattson says that There is not a single experimental study that has investigated if the radio waves relevant for wireless communication change hemoglobins O2 affinity. More research is needed on the effects of non-ionizing EMF on biological systems, especially on the types of EMF specific to 5G, for which very few studies have been published[1,2]. However, the overall consensus from health agencies such as the World Health Organization (WHO) or Public Health England is that the non-ionizing EMF used for telecommunications are safe. The independent International Commission on Non-Ionizing Radiation Protection (ICNIRP), published updated safety guidelines in 2020 to ensure the protection of the public.

Aside from the question of the overall health impacts of EMF, the idea that such non-ionizing radiation would alter the structure of macromolecules is unrealistic. The EMF would have to be produced at energy levels (power density, W/m2) that are many orders of magnitude higher than those used for communication purposes, Mattsson says. In addition, the penetration depth of electromagnetic waves diminishes in proportion to their frequencies[3]. At the frequencies used by the millimetric waves that will be part of 5G (dozens of GHz), this depth is less than 1 mm, and thus practically do not even go beyond the epidermis of the skin. The penetration to blood, and thus a direct interaction with hemoglobin within the red blood cells, is unrealistic.

Finally, the claim that a 5G-driven effect is causing the high death toll from the COVID-19 pandemic is illogical. If it were true, one would expect to see higher rates of death in regions that have 5G. However, a comparison of 5G availability and COVID-19 cases shows no correlation. For example, Italy has 5G in only a few cities, including Bologna, Milan, and Rome, yet the cities that have been hardest-hit by COVID-19 are Bergamo and Brescia, where there is no 5G coverage. In Spain, the hardest-hit Castilla-La Mancha region also has no 5G. The same goes for France where 5G is available in major cities such as Paris, Lyon, Nantes, Montpellier, Marseille, and Lille, but the region with the most COVID-19 cases and deaths is the north-east region of Alsace. The number of new cases in Brazil is currently accelerating even though 5G is not available anywhere in the country.

In summary, the article does not provide adequate scientific evidence to support its claim that 5G increases vulnerability to COVID-19. In addition, no scientific studies have established an impact of 5G electromagnetic radiation on hemoglobin structure. Although research on the potential health impacts of EMF remains relevant, the characteristics of the EMF used in 5G suggest that it is unlikely it would cross the thickness of the skin and reach the blood, nor that it could alter the structure of biomolecules in vivo. The strength of radiation required to alter the structure of biological macromolecules is far higher than that used in telecommunications. Finally, 5G is not available in most parts of the world and the regions that do have it are not hotspots for COVID-19.

SCIENTISTS FEEDBACK Mats-Olof Mattsson, Professor, Strmstad Academy:

In short, there is no evidence available that radio waves used for wireless communication, and at such relevant energy levels, have any effects on biomolecule structures in vitro. That such an effect would occur in vivo under such conditions is extremely unlikely. Furthermore, and specifically regarding 5G, any claim that this protocol would have any health impact on COVID-19 patients at present is unrealistic, since the general roll-out of 5G is very modest and actually absent in most countries.

@: The article only mentions one review article in the journal Environmental Research[4], which scientists studying the biological effects of electromagnetic radiation have identified as extremely biased. This article does not mention non-ionizing EMF-related effects on hemoglobin structure or function. In his comments on the article, Alberto Najera, a professor at the University of Castilla-La Mancha who studies the possible health effects of radiofrequency electromagnetic fields, said that: The author of this work provides a series of evidences to demonstrate the threat that Wi-Fi networks pose to human health. For this purpose, it carries out a review of articles without a detailed methodology, inclusion or exclusion criteria, neither temporary, search keywords, etc., which results in the inclusion of a biased and interested series of inadequate articles to prove his thesis.

In addition, Kenneth Foster, professor of bioengineering at the University of Pennsylvania, and John Moulder, professor emeritus of radiation oncology at the Medical College of Wisconsin, wrote that the author appears to accept experimental findings without critical review for statistical and methodological quality.

Health Feedback covered a similar viral claim that falsely asserts that COVID-19 is due to 5G technology rollout, not a virus.

Health Feedback is working with the CoronaVirusFacts Alliance, a coalition of more than 100 fact-checkers who are fighting misinformation related to the COVID-19 pandemic. Learn more about the alliance here.

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Conspiracy theorists claim that 5G increases vulnerability to COVID-19 with baseless theory that it affects hemoglobin - Health Feedback

Cell Biology

Stem Cell Characterization Kits Market Prospects & Upcoming Trends and Opportunities Analyzed for Coming Years – The Cloud Tribune

Stem cells are biological cells that can be converted into specific type of cells as per the bodys requirement. Stem cells are of two types, i.e., adult stem cells and embryonic stem cells. Stem cells can be used to treat various diseases such as cancer, neurodegenerative disorder, cardiovascular disorder and tissue regeneration. Stem cell characterization is the initial step for stem cell research. Stem cell characterization is a challenging and also an evolving process. Stem cell characterization kits are used for identification of stem cell biology markers. In stem cell characterization, stem cell biology marker profiles differ based on their species, maturity and site of origin. Stem cell characterization kit is required to understand the utility of the stem cells in downstream experiments and to confirm the pluripotency of the stem cell.Request Free Sample Report-https://www.factmr.com/connectus/sample?flag=S&rep_id=2691

Based on type of stem cell, the stem cell characterization kits market is segmented into:Stem Cell Characterization Kits for Adult Stem CellsStem Cell Characterization Kits for Induced Pluripotent Stem CellsStem Cell Characterization Kits for Mesenchymal Stem CellsStem Cell Characterization Kits for Neural Stem CellsStem Cell Characterization Kits for Hematopoietic Stem CellsStem Cell Characterization Kits for Umbilical Cord Stem CellsStem Cell Characterization Kits for Human Embryonic Stem CellsBased on application, the stem cell characterization kits market is segmented into:ResearchDrug Discovery & DevelopmentRegenerative Medicine

Based on end user, the stem cell characterization kits market is segmented into:Biopharmaceutical CompaniesContract Research OrganizationsAcademics and Research InstitutesBiotechnology CompaniesHave Any Query? Ask our Industry Experts-https://www.factmr.com/connectus/sample?flag=AE&rep_id=2691

Examples of some of the key participants in the stem cell characterization kits market identified across the value chain include Merck KGaA, Celprogen, Inc., Creative Bioarray, Thermo Fisher Scientific Inc., BD Biosciences, R&D Systems, Inc., System Biosciences, Cosmo Bio USA, BioCat GmbH, and DS Pharma Biomedical Co., Ltd.Pertinent aspects this study on the Stem Cell Characterization Kits market tries to answer exhaustively are:

What is the forecast size (revenue/volumes) of the most lucrative regional market? What is the share of the dominant product/technology segment in the Stem Cell Characterization Kits market? What regions are likely to witness sizable investments in research and development funding? What are Covid 19 implication on Stem Cell Characterization Kits market and learn how businesses can respond, manage and mitigate the risks? Which countries will be the next destination for industry leaders in order to tap new revenue streams? Which new regulations might cause disruption in industry sentiments in near future? Which is the share of the dominant end user? Which region is expected to rise at the most dominant growth rate? Which technologies will have massive impact of new avenues in the Stem Cell Characterization Kits market? Which key end-use industry trends are expected to shape the growth prospects of the Stem Cell Characterization Kits market? What factors will promote new entrants in the Stem Cell Characterization Kits market? What is the degree of fragmentation in the Stem Cell Characterization Kits market, and will it increase in coming years?

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Stem Cell Characterization Kits Market Prospects & Upcoming Trends and Opportunities Analyzed for Coming Years - The Cloud Tribune

Cell Biology

University of California On What Do Soap Bubbles and Butterflies Have In Common? – Sierra Sun Times

The butterflies that Edith Smith selectively bred are much bluer and more iridescent than the wild Common Buckeye, which is mostly brown (see below). The breeding, UC Berkeley researchers discovered, changed the structure of the wing scales to produce a blue rather than golden structural color. (Photo courtesy of Edith Smith)

April 12, 2020 - ByRobert Sanders- Edith Smith bred a bluer and shinier Common Buckeye at her butterfly farm in Florida, but it took University of California, Berkeley, graduate student Rachel Thayer to explain the physical and genetic changes underlying the butterflys newly acquired iridescence.

In the process, Thayer discovered how relatively easy it is for butterflies to change their wing colors over just a few generations and found the first gene proven to influence the so-called structural color that underlies the iridescent purple, blue, green and golden hues of many butterflies.

Her findings are a starting point for new genetic approaches to investigate how butterflies produce intricate nanostructures with optical properties, which ultimately could help engineers develop new ways to produce photonic nanostructures for solar panels or iridescent colors for paints, clothing and cosmetics.

Structural color is different from pigment color, like that in your skin or on a canvas, which absorbs or reflects different colors of light. Instead, it comes from lights interaction with a solid material in the same way that a transparent bubble develops a colorful sheen. The light penetrates it and bounces back out, interfering with light reflected from the surface in a way that cancels out all but one color.

At theShady Oak Butterfly Farmin Brooker, Florida, Smiths breeding experiments with the Common Buckeye (Junonia coenia) a mostly brown butterfly with showy, colorful spots, found throughout the United States and often raised by butterfly farmers for butterfly gardens or wedding ceremonies were ideal for Thayers study of structural color.

A typical Common Buckeye butterfly, Junonia coenia, is brown because of brown pigment and golden structural color in the wing scales. (Photo by Nipam Patel)

Edith noticed that sometimes these butterflies have just a few blue scales on the very front part of the forewing and started breeding the blue animals together, said Thayer, who is in UC Berkeleys Department of Integrative Biology. So, effectively, she was doing an artificial selection experiment, guided by her own curiosity and intuition about what would be interesting.

In a paper appearing online this week in the journaleLife, Thayer and Nipam Patel, a UC Berkeley professor of molecular and cell biology who is on leave as director of the Marine Biological Laboratory in Woods Hole, Massachusetts, describe the physical changes in wing scales associated with Smiths experiment on the Common Buckeye, and report one genetic regulator of blue iridescence.

I especially loved the clear evolutionary context: being able to directly compare the before and after and piece together the whole story, Thayer said. We know that blueness inJ. coeniais a recent change, we know explicitly what the force of selection was, we know the time frame of the change. That doesnt happen every day for evolutionary biologists.

According to Thayer, hundreds of butterflies have been studied because of the showy structural color in their wing scales. The showiest is the blue morpho, with 5-inch wings of iridescent blue edged with black. Her study, however, focused on a less showy genus,Junonia, and found that iridescent color is common throughout the 10 species, even the drab ones. One unremarkable light gray butterfly, the pansyJ. atlites, proved under a microscope to have iridescent rainbow-colored scales whose colors blend together into gray when viewed with the naked eye.

The 75% greater thickness of the scale lamina from the wing of a bred blue buckeye (red bar, top row, right) compared to the thickness of a scale from the brown wing of a typical buckeye (lower panel) is responsible for the blue color. Red arrows show wing area from which scales were obtained. (UC Berkeley images by Rachel Thayer)

One major lesson from the study, she said, is that most butterfly patterns probably have a mix of pigment color and structural color, and which one has the strongest impact on wing color depends on how much pigment is there.

Thayer raised both the wild, brownish Common Buckeye and the cross-bred, bluer variety obtained from Smith. Using a state-of-the-art helium ion microscope, she imaged scales from the wings to see which scale structures are responsible for the color and to determine whether the color change was due to a change in structural color, or just a loss of brown pigment that allowed the blue color to stand out.

She found no difference in the amount of brown pigment on the scales, but a significant difference in the thickness of chitin, the strong polymer from which the scale is built and that also generates the structural color. In the wild buckeye, the thickness of the chitin layer was about 100 nanometers, yielding a golden hue that blended with the brown pigment. The bluer buckeye had chitin about 190 nanometers thick about the thickness of a soap bubble that produced a blue iridescence that outshined the brown pigment.

Breeding turned a brown area of the buckeyes wing (left) much bluer (right) as the individual scale lamina thickened, replacing a golden structural color with blue. (UC Berkeley images by Rachel Thayer)

They are actually creating the color the same way a soap bubble iridescence works; its the same phenomenon physically, Thayer said.

She also found that, though the scales from theJunoniabutterflies have an elaborate microscopic structure, structural color comes from the bottom, or base, of the scale.

That is not intuitive, because the top part of the scale has all of these curves and grooves and details that really catch your eye, and the most famous structural colors are elaborate structures, often in the top part of the scale, she said. But the simple, flat layer at the bottom of the scale controls structural coloration in each species we checked.

The color comes down to a relatively simple change in the scale: the thickness of the lamina, said Patel. We believe that this will be a genetically tractable system that can allow us to identify the genes and developmental mechanisms that can control structural coloration.

Thayer also investigated the scales of mutant buckeyes created by Cornell University researchers that lacked a key gene, calledoptix, that controls color. The micrograph images demonstrated that lack of the gene also increased the thickness of the thin film of chitin in the scales, creating a blue color.Optixis a regulatory gene that controls many other butterfly genes, which Thayer will be looking at next.

This video produced by the Marine Biological Laboratory explains how a selective mating experiment by a curious butterfly farmer led scientists to a deeper understanding of how butterfly wing color is created and evolves. (Video by Emily Greenhalgh, MBL)

One thing that I thought was cool about our findings was seeing that the same mechanism that has recurred over millions of years of butterfly evolution could be reproduced really rapidly in (Smiths) artificial section experiment, she said. That says that color evolving by changes in lamina thickness is a repeatable, important phenomenon.

Frances Allen, a research scientist in UC Berkeleys Department of Materials Science and Engineering, is also a co-author of the paper. The work was supported by the National Science Foundation (DEB-1601815, DGE-1106400).

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University of California On What Do Soap Bubbles and Butterflies Have In Common? - Sierra Sun Times

Cell Biology

Total-body PET Imaging Successfully Identifies Antibodies up to 30 Days After Injection – Imaging Technology News

April 10, 2020Combining 89Zr-labeled antibodies with total-body positron emission tomography (PET) has extended the utility of novel total-body PET scanners, providing suitable images up to 30 days after the initial injection. A new study, published in the March issue of theJournal of Nuclear Medicine, compared four different types of 89Zr-labeled antibodies in preclinical trials, noting excellent consistency for each radiotracer even at very late time points, as well as differences in antibody behavior that are critical to understanding future outcomes of total-body PET in humans.

Monoclonal antibodies laboratory-developed proteins designed to recognize specific targets have been used in medicine for decades to treat various diseases, such as cancer, rheumatoid arthritis, multiple sclerosis and cardiovascular disease. Many new engineered monoclonal antibodies have been developed with specific molecular functions in order to achieve a balance between potency and safety in patient treatment.

"The tissue biodistribution of these newly engineered antibodies must be measured in vivo over the course of weeks to select the most appropriate candidates for novel therapeutics and understand how to use them in humans to best effect," said Simon Williams, Ph.D., principal scientist, molecular imaging at Genentech, Inc. "In our study, we assessed the feasibility of using a novel total-body PET scanner to image 89Zr-labeled antibodies up to 30 days after injection, allowing for the measurement of tissue biodistribution over a long period of time."

Researchers prepared four types of 89Zr-labeled antibodies, each with a different chelator-linker, to be compared across 12 young rhesus monkeys (three animals for each chelator-linker combination). Each group of animals received an intravenous injection of one of the four 89Zr-labeled antibodies in the left arm, along with an additional mass dose of unlabeled antibodies in the right arm. The animals were imaged on the day of injection, as well as three, seven, 14, 21 and 30 days after the injection.

Excellent image quality was obtained on the initial total-body PET scans for all four types of 89Zr-labeled antibodies. Results from the 30-day scans showed image quality across the four antibody types sufficient to readily identify activity in the liver, kidneys and upper and lower limb joints. However, significant differences in uptake between the various chelator-linker combinations were noted in the late time point liver, bone, and in whole-body clearance. These differences were determined to be partly related to the stability of the radiolabeled compounds prior to injection.

"The results of this study have two key implications for the field of molecular imaging," said Simon R. Cherry, Ph.D., distinguished professor at the University of California, Davis. "First, and most obvious, is that the increase in sensitivity of total-body PET, when compared to conventional PET, enables radiotracers to be followed for a longer period of time thus extending the imaging window. Using 89Zr as the radiolabel, this allows the assessment of slow biological processes and the ability to determine the ultimate fate of agents introduced into the body over a one-month timeframe."

He continued, "Second, studies with 89Zr can be conducted with much lower injected doses of radioactivity. The late time point total-body imaging conducted in this study clearly demonstrates that acceptable quality imaging with 89Zr can be accomplished when there is as little as 1/100th of the activity remaining in the subject. This paves the way for broad and repeat use of 89Zr-radiolabeled tracers in patients with extremely low effective doses."

The authors of "Total-Body PET and Highly Stable Chelators Together Enable Meaningful 89Zr-Antibody PET Studies up to 30 Days After Injection" include Eric Berg, Department of Biomedical Engineering, University of California-Davis, Davis, California; Herman Gill, Jan Marik, Annie Ogasawara and Simon Williams, Department of Biomedical Imaging, Genentech Inc., South San Francisco, California; Guus van Dongen and Danille Vugts, Department of Radiology and Nuclear Medicine, Amsterdam UMC, VU University, Amsterdam, The Netherlands; Simon R. Cherry, Department of Biomedical Engineering, University of California-Davis, Davis, California, and Department of Radiology, School of Medicine, University of California-Davis, Davis, California; and Alice F. Tarantal, Department of Pediatrics and Department of Cell Biology and Human Anatomy, School of Medicine, and California National Primate Research Center, University of California-Davis, Davis, California.

For more information: http://www.snmmi.org

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Total-body PET Imaging Successfully Identifies Antibodies up to 30 Days After Injection - Imaging Technology News