Mutation linked to Alzheimer’s may cause neuron blockages

Mutation linked to Alzheimer’s may cause neuron blockages

Alzheimer’s is a disorder that is known to impact the brain cells progressively towards degeneration. The disease is also known as dementia or amnesia, wherein the person suffers from a progressive decline in memory or thinking abilities over time. The social and behavioral skills are disrupted and the individual faces difficulty functioning independently. To date, many pieces of research have been carried out to understand the reason behind the disease through a focused approach on amyloid aggregates. In Alzheimer’s, the amyloid peptides are known to aggregate leading to memory loss, it is considered to be the hallmark of the disease. Therefore, to find an effective treatment for Alzheimer’s, researchers are focused on these peptide aggregates. However, very little success has been achieved, where the scientist tried to inhibit the protein responsible for the production of amyloid- β (a protein called BACE1). Various failures have been observed by the researchers in the targeting of BACE1 in phase 3 clinical trials.

Recently, a team of researchers targeted another gene variant named GGA3, which is a potential risk factor for Alzheimer’s. The study has been published in Science Translational Medicine in November, highlighting the role of GGA in altering the BACE1 movement across brain cells. It is found that they cause aggregation of BACE1 protein leading to axonal damage as observed in the pre-symptomatic stages. Thus, it lays a path of hope for BACE inhibitors as an effective treatment for Alzheimer’s.

To date, researchers knew the cause of Alzheimer’s as the result of amyloid build-up. But questions like what precedes this build-up? What initiated the amyloid aggregation? What are the initiators of this pathogenic process and more such questions remain to be unknown. However, now the understanding of risk genes can be considered as an addition of a very important piece in the whole puzzle. The research may unravel the cause of neuro-dysfunction in much more detail than ever known.

“I think the core message from this paper is that this could be one additional primary pathogenic development that precedes amyloid plaques buildup,” -Henrik Zetterberg, Neuroscientist at the University of Gothenburg.

The present studies unfold certain genetic mutation in GGA3 gene that increases the risk of Alzheimer’s. The researchers found out that GGA3 protein plays a very important role in the transportation of BACE1 protein across the brain cells. Additionally, BACE1 is a protease that is considered to cleave the APP protein leading to the production of beta-amyloid and thus unwanted aggregation.

Some researchers consider that one of the biggest lacunae in understanding such complex problems is we often don’t merge the different sciences. The present study highlights how taking genetics, biochemistry, pathology, and cell biology together can pose the potential to unravel many difficult problems in science.

In the present research, the scientist learned that any mutation in the GGA gene or deletion of the gene segment can impact the transport of BACE1 protein across the axons. As a result, the protein aggregates in the axon region, leading them to swell. This is one of the reasons where this damage is being recognized among patients with Alzheimer’s. Early-onset of Alzheimer’s can be identified with the help of above mentioned axonal pathology.

“If a patient doesn’t have the GGA3 mutation, it’s still possible that defects in axonal pathology are caused by other genes. It is still valuable to know that once you have axonal pathology early, BACE accumulation could be a factor. So these mechanisms can apply more generally.”

The science of the BACE1 target has been used and reached till the phase 3 trials but failed. Because there were too many side effects observed that impacted the memory and thinking capability among people worse. It is stipulated that the blocking of BACE1 among Alzheimer patients is impacting the other crucial role played by BACE1 protein.

“The clinical trials that have been conducted, they had a pharmacological inhibition of BACE activity, up to ninety percent in some cases. So I think that what we learned is that probably we need to inhibit BACE to a lesser extent,” says Tesco, a researcher.

It is observed that the early damage to brain cells occurs about 20 years before the complete emergence of clinical symptoms. Thus, any treatment prepared to be given over a period of time can be considered as a good alternative. So, in the present case, if weaker inhibition of BACE1 opted for a long period the side effects will be reduced, and the chances of recovering increases.

Learning how SARS-CoV2 hijacks and damages lung cells

Learning how SARS-CoV2 hijacks and damages lung cells

The emergence of the SARS-CoV2 virus has caused turmoil across the globe, forcing the researchers to study it in more detail. However, the behavior of the virus has been quite notorious. The frequent mutations and very less prior knowledge has caused some obstacles. However, scientists were acquainted that if they understand the underlying pathways in lung cells and host protein being impacted during the viral infection then there can be chances of identifying potential solutions. Considering this, scientists have recently found out how SARS-CoV2 hijacks and damages the lung cells.

The study was a multi-group collaboration between the Center for Network Systems Biology (CNSB), Center for Regenerative Medicine (CReM), and National Emerging Infectious Disease Laboratory (NEIDL). The researchers have mapped the molecular responses emerging from lung cells infected with the SAR-CoV2 virus. The finding of the study has been published in the Journal of Molecular Cell.

To understand the disease pathology and gain new insights to discover potential therapeutic targets, the researchers bioengineered the human alveolar cells. The cells when combined with high-end mass spectroscopy technology, it helped the researchers to identify potential host proteins and pathways changing during SARS-CoV2 infection. The researchers found out that lung cells infected with SAR-CoV2 have abnormal phosphorylation.

Phosphorylation is a very crucial protein modification process contributing to protein functionality in the cells. The proper phosphorylation process is important for healthy cells. However, it was noticed that the infection alters this process leading to cascading abnormal changes. These changes increase the chances of the virus to thrive within the cells and eventually destroy it.

The study also showed that as soon as the virus encounters the lung cells, it initiates exploiting the resources required for the normal functioning and growth of the cell. The invasion of the virus further disrupts the functioning of the cell and damaging it extensively. The resources used, powers the virus eventually leading to rapid proliferation and expansion in nearby regions. As a result, the exhausted and damaged cells undergo self-destruction and the virus starts infecting the cells in the vicinity while evading the body’s immune system. This cycle repeats continuously leading to the hijacking of lung cells and widespread damage.

The researchers examined lung alveolar cells from one to 24 hours after infection with SARS-CoV-2 to understand what changes occur in lung cells immediately (at one, three, and six hours after infection by SARS-CoV-2) and what changes occur later (at 24 hours after infection). These changes were then compared to uninfected cells. All proteins from infected and uninfected alveolar cells, corresponding to the different time-points were extracted and labeled with unique barcoding tags called “tandem mass tag.” These tags, which can be accurately detected only by a mass spectrometer, permit robust quantification of protein and phosphorylation abundance in cells.

“Our results showed that in comparison to normal/uninfected lung cells, SARS-CoV-2 infected lung cells showed dramatic changes in the abundance of thousands of proteins and phosphorylation events,” said Darrell Kotton, MD, BUSM, CReM.

“Moreover, our data also showed that the SARS-CoV-2 virus induces a significant number of these changes as early as one-hour post-infection and lays the foundation for a complete hijack of the host lung cells,” adds Elke Mehlberger, PhD, NEIDL.

Scientists also tried to examine the data obtained from the study to identify any potential opportunities for COVID-19 treatment. They found that about more than 18 existing drugs that have been already clinically approved can be re-purposed for the treatment. The research team believes that the current findings are very crucial and can contribute a lot to the field, specifically in terms of devising a cost-effective, robust and life-saving treatment to overcome COVID-19.


Five steps to write a paper

Five steps to write a paper: Beginners guide

Don’t you think writing a paper takes a lot of your time? It becomes more tedious if you are a beginner. That stands true because you might not know what to write and in which order. Well, we just want to tell you that you are not alone in this struggle. In this blog, we will be talking about some basic steps that can help you write a paper with great ease.


We have come across some of the clients who had told us about their struggles about writing the paper when told by the advisor. Writing a paper for a newbie means spending weeks on research, then writing and tweaking the work to get it in perfect shape. This may not still lead your work to the final stage, there still be alterations needed across multiple paragraphs, headings, conclusion, and more. The reality behind academicians facing issues in writing paper is that no one teaches them the right and easy way to do it. This often keeps most researchers in dark to figure out how to write a great paper that can be easily published in a high-impact journal.


Let us help you understand this process in detail. To start with, you need a well-defined process that allows you to write papers as per your need. Here are some basic five steps we think can be helpful to kick-start your paper writing experience.


Step 1: Defining the central message

When writing a paper, most people do the mistake of starting with an introduction without much clarity. This often leads to multiple edits at the end. To start, we suggest understanding what your paper wants to tell your audience. You must need to define a central idea/message around which the entire paper will be focused. For this, one must begin by visiting their research data. Pull out all data and inferences of your research. Find out what theory or argument you want to put forth. Create a rough storyboard with all the ideas, figures, and tables.


Step 2: Structuring your text

Once you know the central message, it is important to share it in a way where readers can easily understand. Many researchers do the mistake of haphazardly representing their ideas, which often reduces the interest of readers leading to low citations. This is where structuring the text comes into the picture, whenever thinking of writing a paper. You need to write your research content in an easy flowing manner. This helps readers to engage more and make the research content interesting and easy to comprehend. For this, you must plan your content in every section beforehand. Chart out how every section should start and end. We have seen many students starting every new section without raising an argument or question in the previous section. This is very important to maintain the flow of text, not only within a particular section but also across various sections. Thus, aligning the overall flow of the research paper.


Step 3: Catching the reader’s attention

The most important part of writing a paper is ‘Introduction’, as it decides the fate of your paper. Why so? Because the introduction is the first thing anyone will read and if you are not able to comprehend your central message of the paper here then your efforts may end in vain. For beginners, we suggest you, write the introduction at last. The introduction of a paper should be started in a way that catches the reader’s attention. You can start by highlighting the problem, stating some stats, taking events of history (relatable to the topic of research) at a glance, and more. An introduction is the section of your research paper where most of the storytelling happens. However, you have to make sure that the right facts and the central message is comprehended efficiently.


Step 4: Figures and the table

Do you know most of the people before actually reading the paper, just scroll through it to see the figures and table! This is why papers with good figures and tables get good citations. One of the important reasons for having figures and tables in your paper is that it adds a visual expect to it. The reader can comprehend the message briefly from the figures and tables. This often catches the interest of the reader at first glance, making them read the entire paper. So, focus on your figures and tables.


Step 5: Summary is the key

Well, most of the important parts of your paper are written. Now it’s time to summarise the entire idea with a take-away message. Writing a summary won’t take much of your efforts as you have already completed the tedious part. In this section, you must focus on your central message/argument and share the prospects of the research work. This is crucial because people will be keen on looking for further developments in your field of research.

These are the most basic five steps you can follow to kick start your research paper writing journey. However, if you still face any difficulty, feel free to connect with our team. We have a team of expert scientific writers helping academicians and corporates to get their finest work out in the high impact factor journal. We will be happy to assist you in writing a paper for you.

Nanopore sequencing enables high-resolution analysis

Nanopore sequencing enables high-resolution analysis of resistance determinants and mobile elements in the human gut microbiome

High-resolution analysis of resistant determinants and mobile elements in the human gut microbiome is quite difficult with the existing technologies. However, in the present research study, the authors highlight the effectiveness of Nanopore sequencing in getting the desired results. The analysis of genomic data derived from mobile elements in the human gut microbiome can often be limited due to the fragmented assembly from short-read sequencing.

One can overcome the limitations of fragmented assembly by using third-generation sequencing technology, which helps in getting long-reads. However, it is noted that third-generation based sequencing technologies give high-error rates and very poor throughput rates. This has resulted in limited use of technology in metagenomic related studies. The researchers in the present study have found a new way to overcome the exiting challenges by developing the first hybrid metagenomic assembler which will combine the properties of both long and short-read technologies. This will surely be considered to give high improvement when compared with the older version of assemblies along with high base par accuracy.

The approach includes a metagenome clustering technique which will be unique. It will include a scaffolding algorithm that can repeat-rich sequences with high accuracy and low error rates. Based on the numerous analysis done, the researchers identified that near-complete genomes from metagenomes can be assembled with as little as 9x long read coverage. This can enable the high-quality assembly of less abundant species. To take this understanding further, the researchers applied the concept of nanopore sequencing to analyze the gut microbiome of patients under antibiotic treatment. It was found in the study that long reads can be obtained from the samples to create accurate and efficient assemblies.

A critical review on quantum dots

A critical review on quantum dots: From synthesis toward applications in electrochemical biosensors for determination of disease-related biomolecules

Nanoscience or nanotechnology is a very fast-growing field of science, which has introduced various new transforming technology in the present era. One such technology is fluorescent quantum dots (QDs), which have been a part of nanotechnology since the very beginning of the field. Fluorescent quantum dots are very small nanocrystals, defines by a diameter of about 2-10 nanometers i.e. around 10-50 atoms. The most unique property of quantum dots is the resultant fluorescence of distinctive colors produced, which is highly dependent on the size of the nanocrystal.

Quantum dots are known to be consisting of a variety of structural, photochemical, and electrochemical properties also, which can be exploited to use them as a very promising technology in the field of sensing applications. The use of quantum dots as a nanomaterial in these sensing applications can increase the performance of biosensors in the market, specifically in terms of overcoming the existing issues such as detection limit, selectivity, and sensor sensitivity. The applications of quantum dots is not only limited to this, instead, it also expands to their high-level functionalization with bioreceptors. In this review article, the authors highlight how fluorescent quantum dots function and their core knowledge along with a detailed explanation of their applications in sensors to receptors.

The potential of quantum dots is immense, one of the reason is their enhanced capability to associate nanotechnology and biotechnology together. They indeed possess a huge potential to set a new paradigm in the research field to give a comprehensive view of zero-dimensional nanoparticles. These nanoparticles can be effectively used in the designing of electrochemical sensors which can be used in the diagnosis of diseases. This can specifically include identifying biomolecules such as tumor markers, depression markers, inflammatory markers, and more. Considering the huge application of quantum dots, the researcher highlights more in-depth research in the field. Detailed insight about quantum dots can help in understanding their electronic and magnetic properties in more detail. One can understand how they can be synthesized in labs efficiently for further large scale production to be used effectively at the industrial scale for biomolecule diagnosis and other related applications.

Silent Mutations and RNA folding can give answer, Why COVID became Unstoppable?

Silent Mutations and RNA folding can give answer, Why COVID-19 became Unstoppable?

Till now, it’s very evident that almost every person must be knowing about the lethal impact of COVID-19 across the globe. But hardly, anyone knows the reason that how COVID-19, which was once living harmlessly in wildlife crossed the species barrier, giving it an evolutionary edge.

Recently, scientists at Duke University have found out that there have been numerous silent mutations in the genetic code of the coronavirus which helped it get the evolutionary edge and made it thrive beyond wildlife, leading to a global pandemic. These silent mutations guided the folding of RNA molecules in a unique way when present in human cells, setting the stage for the global crisis. The study has been published in the journal Peer. J.

The study involved various statistical methods that help in identifying various adaptations that the virus underwent. Researchers analyzed the genome sequence of the SARS-CoV-2 virus and other related coronaviruses often found in bats and pangolins to find out the adaptive changes in SARS-CoV2. “We’re trying to figure out what made this virus so unique,” said Alejandro Berrio, lead author of the paper and researcher at Duke University.

The earlier research highlighted the presence of positive selection within a gene that is responsible for encoding “Spike protein” on the surface of SARS-CoV2 surface. This increases the ability of the virus to infect the new cells in humans more outrageously. The study also indicated the presence of certain mutations in the viral genome that must have altered the spike protein, which made it thrive more easily among humans leading to a global pandemic. But this is not enough, the researchers also found out various other aspects which were not studies in previous researches, highlighting the reason that COVID has become so lethal and infectious. One of the critical reasons was a silent mutation in the two very important regions of the SARS-CoV2 genome, also referred to as Nsp4 and Nsp16. These mutations have been considered to give COVID-19 an evolutionary edge when compared with other similar strains, without impacting the proteins they naturally encode.

The study helped in understanding that the silent mutation instead of affecting the resultant protein affected how the RNA folds up in 3D shape, which eventually affects its functions in human cells. The deeper insights about how exactly these mutations govern the changes I RNA structure is yet to be elucidated in more detail. But never the less, the present study has very well contributed to understanding the viral leap from wildlife to humans.

“Nsp4 and Nsp16 are among the first RNA molecules that are produced when the virus infects a new person,” Berrio said. “The spike protein doesn’t get expressed until later. So they could make a better therapeutic target because they appear earlier in the viral life cycle.”

“Viruses are constantly mutating and evolving,” Berrio said. “So it’s possible that a new strain of coronavirus capable of infecting other animals may come along that also has the potential to spread to people as SARS-CoV-2 did. We’ll need to be able to recognize it and make efforts to contain it early.”

Artificial Intelligence on its way to help to predict drug resistant bacteria

Artificial Intelligence on its way to help to predict drug resistant bacteria

Researchers of Washington state university have developed a feasible software in their lab which helps to identify drug-resistant contributing genes in bacteria.

The software developed makes it feasible to use and easily identify the fatal anti-microbial resistant bacteria existing with us in nature. Figures show that anti-microbial resistance bacteria alone cause more than 2.8 million cases of deadly pneumonia, blood infection, and 35000 deaths annually. Researcher Abu Sayed- Doctoral graduate in computer science, Shira Broschat from School of Electrical Engineering and computer science, and Douglas Call from Paul G. Allen School for Global Animal Health have shared the insight of their work with the Scientific Reports journal.

Antimicrobial resistance is a process that is observed when a microbe acquires or evolves with a drug resistance gene thus further causing AMR. Bacteria responsible for staphylococcus or streptococcus infection or in that manner tuberculosis and pneumonia, all these infectious diseases have developed due to the occurrence of drug resistance strains thus causing hindrance in the treatment regime. The AMR issue is estimated to worsen more in the coming decades in terms of AMR-related infection, deaths, and an increase in health costs as the bacteria is evolving in a way where there is a limited option of antibiotic treatment against it.

“We need to develop tools to easily and efficiently predict antimicrobial resistance that increasingly threatens health and livelihoods around the world,” said Chowdhury, lead author of the paper.

With the ease of large-scale genetic sequencing, scientists are looking in the environment for the presence of AMR genes. They are interested to know the habitat of such genes and how potentially such AMR microbes can spread and affect human health. While they can identify genes that are similar to known AMR-resistant genes, they are probably missing genes for resistance that look very unique from a protein sequence perspective.

The team at WSU developed a machine learning algorithm that has a unique feature of having data of AMR proteins instead of using gene sequences to find a similarity and identify AMR genes. The above algorithm was developed with the help of a theory known as Game theory. Game theory is a tool used in various fields more precisely in economics, to model strategic interactions between game players, here, in this case, helps to identity AMR genes. Using algorithm and theory together, the researcher looked at the interaction of various aspects such as genetic material, structure and physicochemical properties, and properties of protein sequences rather than simply looking at sequence similarity.

“Our software can be employed to analyze metagenomic data in greater depth than would be achieved by simple sequence matching algorithms,” Chowdhury said. He further added, “This can be an important tool to identify novel antimicrobial resistance genes that eventually could become clinically important.”

“The virtue of this program is that we can actually detect AMR in newly sequenced genomes,” Broschat said. “It’s a way of identifying AMR genes and their prevalence that might not otherwise have been found. That’s really important.”

The pioneer research team at WSU took Clostridium, Enterococcus, Staphylococcus, Streptococcus, and Listeria species where resistance genes are found. The above-mentioned bacteria are one of the major causes of infections such as staph infection, food poising, life-threatening pneumonia, and colitis. The algorithm developed by the team was able to categories the resistance genes accurately up to 90 percent.

The algorithm is embedded as a software package that is downloadable easily and can also be used by the scientific fraternity to look into AMR in a large pool of genetic material. The software can be updated timely. As more sequences and data become available, researchers will be able to continue with the algorithm without any hassle. “You can bootstrap and improve the software as more positive data becomes available,” Broschat said.

Antibiotic Resistance- An ongoing crisis

Antibiotic resistance is an ancient and mounting problem. Common causes are overpopulation, increased use of antibiotics, and even due to enhanced global migration.  For a long time, antibiotic treatment has been the main approach of treatment in modern medicine to combat infections. The golden era of antibiotics was between the 1930s to 1960s, giving rise to many antibiotics. Antibiotic resistance poses a very serious global threat due to the growing concern of human and animal health. This is due to multidrug-resistant bacteria or popularly known as “superbugs”.

The plausible causes of global microbial resistance include overuse of antibiotics in animals consumed as food by humans. Other superficial causes include, increase in international travel and poor hygiene. These factors mainly play a role in the genetic selection in a community of resisting antibiotics. 

History and Benefits of Antibiotics:

The first documented use of antibiotics was with the discovery of penicillin by Alexander Fleming during the world war. Penciliine was successful in controlling the bacteria and was said to have saved millions of lives. Shortly after the boom in usage, the penicillin resistance was a major problem, threatening many of the advances in the medical field at that time. What was thought as just penicillin resistance later proved to be a multidrug resistance. Microorganisms under Darwinian natural selection to develop the resistance. Naturally, most antibiotics are produced using bacteria or environmental fungi, and few are completely synthetic using sulphonamides and fluoroquinolones. 

Not only saving lives, but antibiotics have also played a vital role in advancing major breakthroughs in the field of surgery and medicine. They have successfully prevented and treated infections that commonly occur in patients undergoing chemotherapy, who are also suffering from chronic diabetes or rheumatoid arthritis. 


Even as early as 1945, Alexander Fleming with the discovery of penicillin, also warned the public that the era of antibiotics will also lead to the era of misuse and resistance. Epidemiological studies depict a direct relationship between the consumption of antibiotics and the rise in bacterial resistant diseases. These bacteria can be transmitted or inherited between relatives and friends. Resistance can also occur due to spontaneous mutation. Antibiotics remove the sensitive competitors and leave the resistance bacteria by natural selection to reproduce and multiply more. Despite these warnings, antibiotics are overprescribed throughout the world. 

Agricultural use:

In both developing and developed worlds, antibiotics are seen to be used very frequently as growth supplements in livestock. According to a census, almost 80% of the antibiotics sold throughout the world are used in animals to prevent infection and promote growth. Treating livestock with antimicrobials can improve overall health, produce larger yields, and an overall high-quality product.  

The antibiotics used in treating livestock is in turn consumed by the top of the food chain- humans. This transfer of resistant bacteria to humans was first noticed 35 years ago when the antibiotic rates were found high in the intestines of both farm animals and farmers. Recently molecular detection methods prove that resistant bacteria from farm animals reach humans through consumption. 

It should also be noted that the agricultural use of antibiotics also thrive in urine and stool. These are widely dispersed through fertilizers affecting the groundwater and surface. While this may account for a small fraction of overall antibiotic use, the end geographical spread can be a considerable size. This practice also affects the micro

The emergence of resistance:

Organisms develop resistance by several techniques including altering the target site of binding, inhibiting the drug entry, and enzyme production that leads to the degradation of antimicrobials.Various antimicrobial drugs like antibiotics produced by saprophytic bacteria tend to develop mutual benefits with the other organisms surrounding it and sometimes even inhibit growth. Available data suggest that the sublethal concentration is the antibiotics have a significant impact on the microbial flora, and may even be effective in signalling molecules which may induce a microbial and host gene expression. 

Another important finding reveals that few saprophytic bacteria is capable of producing a broad-spectrum antibiotic known as carbapenems. Various genes involved in constructing this antibiotic may also play an important role in biofilm formation. These findings reveal more unexpected impacts of the antibiotics.

More knowledge is needed to the extent of the broad-spectrum antimicrobial resistance. Current panic is due to the inadequate information. The future cannot be predicted with surety at the stage with regards to the resistance with the unavailability of novel antibiotics. Multiple well thought strategies need to be in place to confront this particular issue. Regulations should be implemented by every country to monitor prescriptions and the use of antibiotics. Environmental and ecological issues should not be ignored and all elements should be part of the control policy. Alternatives to antibiotics such as lytic bacteriophages vectors and probiotics can potentially help to decrease the use of antibiotics. 


COVID-19: Ridgeback working on anti-viral tests for patients in the hospital and at home

With efforts underway to find treatments for COVID-19 patients at the hospital, Ridgeback therapeutics are doing things differently.

By the looks of it, COVID-19 does not seem to slow down anytime soon. Thousands of fresh cases are being reported every day, and hospitals are flooded around the world. Most of the pharmaceutical companies are right now focused on finding a treatment for hospitalized patients, in a way that makes sense. After all, they are the most severely affected patients. But Miami based Ridgeback biotherapeutics are currently working differently. 

Currently, the company is kicking off its phase 2 trial for an antiviral that can serve as a treatment for both hospitalized patients and freshly diagnosed patients who are staying at home. The underway antiviral- EIDD-2801 is first being tested on hospitalized COVID-19 patients and the second with cases at home. 

What is EIDD-2801?

Although doctors and scientists around the world are testing out a variety of existing drugs to fight COVID-19, EIDD-2801, an oral antiviral drug stands apart. 

The drug can be used as both prophylactic and a therapeutic against the COVID-19 virus. It is a nucleoside analog that shows broad spectrum activity against RNA viruses, which includes the current coronavirus, COVID-19 and previous virus MERS and SARS. 

EIDD-2801 attacks RNA dependent RNA polymerase the same way as Gilead Sciences’ Remdesivir, a previously FDA-appointed drug for emergency use. But unlike remdesivir which is administered intravenously, EIDD-2801 can be taken orally. 

Why EIDD-2801?

Since the convenience of taking EIDD-2801 orally, patients could take it at home rather than  risking themselves and others by coming to the hospital. By this, the drug is taken at the earlier stages of the infection, potentially killing the virus before it causes havoc on the body. 

EIDD-2801 is completely safe and effective and has a rather intriguing feature of being highly resistant. Usually drugs alert the viruses to quickly mutate that aren’t affected by the drug, making it incompetent. But EID-2801 when tested hasn’t prompted any such resistance.

“We always worry about resistance,” says Andy Mehle, a virologist at the University of Wisconsin–Madison. Though drug resistance is inevitable, sometimes the viruses work on changing so much to overcome a drug’s effects that they cripple. Alternatively, resistance may seem as a simple change, the changes occur with a difficulty of the virus’s ability to multiply. Experts speculate this might be the case with EIDD-2801.

What’s next for Ridgeback?

Though the first set of clinical studies are just beginning, Ridgeback is confident about the drug and is currently gearing up to manufacture hundreds of thousands of doses of the drug. In the near future the company is planning to ramp up the production to millions. 

“While we still need to wait and see the intended efficacy of the drug as ridgeback believes it to be, it is imperative to have a backup of immediate and ample supply to the world, once the clinical trials are successful” stated Wendy Holman, CEO and co-founder of Ridgeback.

Good news as researchers find a key to cystic fibrosis detection and treatment

Good news as researchers find a key to cystic fibrosis detection and treatment

Groundbreaking research by Monash University paves the way to a possibility of better monitoring and treatment of the cystic fibrosis lung disease

For years, cystic fibrosis (CF) has known to be a serious hereditary condition that causes severe damage to the respiratory and digestive systems. The damage starts with a build-up of thick mucosal kind of fluid in the organs especially lungs. 

In particular cystic fibrosis affects the cells that produce digestive enzymes, sweat, and mucus. Usually, these secretions are thin and watery, which function as lubrication for various organs and tissues. However, when affected with CF, due to faulty genes the person experiences thick fluid build-up, clogging up the passages and ducts.  

Early diagnosis and treatment are important for improving the quality and the length of the affected life. Currently available lung assessment tools have many drawbacks, especially the inability to accurately identify the origin of the changes seen in lung health. 

Monash University research team announced the results of the World’s first research promising a possibility of better diagnosis and treatment of cystic fibrosis using X-ray velocimetry. 

What is X-ray velocimetry?

A phase-contrast X-ray imaging makes use of the refractive properties of materials to produce high definition soft tissue images. Recently X-ray velocimetry (XV) has caught the eye of researchers. In particular, XV is used to study the airflow through the lungs and the technique is based on particle image velocimetry. Particle image velocimetry (PIV) is a well-established technique known for years. 

XV is known to provide high quality, non-invasive, real-time images of the airflow through the lungs. The X-ray was first designed and developed by 4DMedical, in hope for clinical use. The technology has also recently been approved by the FDA for its all respiratory indications in adults. 

All about the study:

An effective assessment of the lung cystic fibrosis should be capable of capturing its patchy nature and fluid buildup. This is in particular important for detecting the disease at early stages. 

With the help of XV, a multidisciplinary collaboration of engineers, physicists, and clinicians were able to measure real-time airflow through the lungs. 

The research was led by one of the University’s leading scientists Dr. Freda Werdiger. The study revealed that by using XV, it was possible to pinpoint the precise locations where there was an obstruction of airflow in the lung of a cystic fibrosis patient.  

“In this study, we present two developments in XV analysis. Firstly, we show the ability of laboratory-based XV to detect the patchy nature of CF-like disease in affected mice. Secondly, we present a technique for numerical quantification of that disease, which can delineate between two major modes of disease symptoms,” Dr. Werdiger said.

This particular model provides a very simple, easy top interpret approach, which in the future can be readily applied to large quantities of data generated in XV imaging. 

What does the future hold?

The success of XV lies in its capability of drawing reliable and quantitative measures, and the above study shows how that can be accomplished. 

The researchers of the study recommend that this promising technique should be applied to the numerical characterization of CF lung disease. The analysis can be applied in a straight forward fashion with minimal manual labour required.