Scientists Begin to Unlock Some of the Keys to Drug Resistance

World Health Organization meeting on Drug Resistance in Leprosy.
Image credit to National Leprosy Eradication Programme

Some time ago I talked about the threat that drug resistance by disease-causing microorganisms poses to mankind if nothing is done now to tackle it. A few days later, the World Health Organisation echoed the same warning and emphasized the need for urgent action in finding new and potent ways to thwart this potential (and what I call) global terrorist attack by these disease-causing microorganisms as they continue to challenge our God-given right to replenish, conquer and dominate the world (for the animal activists out there, don't misunderstand me: I'm not talking about total annihilation of all microorganisms because there are the good guys among them who are minding their own business--the normal flora of our environment--and who are not challenging our God-given rights).

One of the disease-microorganisms that has developed what I call smart resistance to drugs which previously dealt with it is the tuberculosis-causing organism called Mycobacterium tuberculosis. This microorganism has evolved into to variants now known as Multi-Drug Resistant (MDR) and Extensive Drug Resistant TB that is unaffected by most of the first-line and second-line anti-TB drugs, requiring combination of anti-TB drugs from more than one class before the patient's condition can see any improvement. This type of treatment, to be effective, may take up to one year or more, meaning more cost and more side effects of these drugs to the patient (and the patient will have to pay for other drugs needed to counter some of the side effects): this places a big burden on patients in parts of the world where TB is more likely to flourish: the poor populace of the world where access to health care is very limited. In addition to this problem, a case of a variant of a particular disease-causing bacterium resistant to all known potent antibiotics has been documented.

Crystal structure of the LptDE complex.
Image credit to Nature.

But rights (our God-given rights), I believe, come with the necessary provisions and weapons to defend and protect them. According to a research published in the journal Nature, scientists have unraveled the structure and mechanism with which a group of drug-resistant bacteria, termed gram-negative, build their exterior coating wall that, over generations of mutations, has become impermeable to most antibiotics and also able to conceal the bacteria from the attack of its host (human) immune system. Scientists used the Diamond Synchroton facility in Oxfordshire, Oxford, which produces intense X-rays about 10 billion times brighter than that the light from the sun, to study crystalline forms of the isolated protein samples from the exterior of these bacteria at the atomic level. The result was an atomic-scale revelation of the structure of a protein complex called LptDE, in the cell wall of the bacteria. The detailed information gathered was then used to create models to simulate how this protein complex assembles molecules called lipopolysaccharide in the bacteria cell wall from the inside of the organisms; it was also found that the final stages of this assembly could be attacked from the outside using new antibiotics to shatter the whole assembly process and leave the bacteria exposed without a covering and vulnerable to the environment--the host immune system attack. One more good news is that the protein complex LptDE has been found to be almost the same across a broad range of gram-negative bacteria that cause a large number of diseases such as meningitis, meaning that designing a class potent antibiotics against this key structure could be the master key to treating these diseases. The way forward now, according to experts, is to start exploring this great opportunity to design novel drugs that can inhibit the mechanism of the protein complex, LptDE.

Diamond Light Source of the Synchroton Facility in Oxfordshire, Oxford.
Image credit to Diamond UK.

While this is a great basic and fundamental discovery and has brought much to hope for, isn't there a possibility that sustained offense against the LptDE mechanism (when we develop antibiotics against it) can trigger the need for these bacteria to undergo mutations that will alter some parts of the structure of the component proteins involved in the assembly work to render the designed antibiotics useless? There was a time when our current antibiotics were working wonders because they targeted what were found then as structures and mechanisms crucial to these microorganisms' survival; but the same crucial targets have become smart at adapting to our offenses.

Simulated model of the Lipopolysaccharide Assembly.
Image credit to Nature.

My point is that we've got to have many potent options (like I said in a similar post) at dealing with these microscopic bad guys. In addition to leveraging on this current discovery, and also embarking on a suggestion I made in a similar post, I believe there may be special areas in these microorganisms that are very vital to their survival and at the same time do not undergo mutations at the genetic level because any alterations in the molecular structure of these vital areas would destabilize the microorganisms. Efforts should be geared towards identifying these areas in the global MutaGenome Project-areas I will want to tag Rigidity Importance Sites in drug-resistant microorganisms because they are very important to their survival but do not undergo mutations no matter the changes in the organisms' environment. This will enable the development of drugs targeted towards the translational outcomes (protein structure) of these Rigidity Importance Sites (RIS) in the DNA of the microorganisms. And one way to do this could be by creating models of the genome of some of these microorganisms and try to simulate their genomic replication, transcription and translation using data gathered from accumulated laboratory investigations and all possible effects of environmental changes on their genome over several generations--this I believe may reveal these areas of the genome that hardly undergo mutations, irrespective of the extent of external threats, but are very very crucial to their survival. Drugs designed against these Rigidity Importance Sites will be extremely potent at eradicating these disease-causing niggers, and any attempt to develop resistance to the drugs by mutations will be fatally detrimental to them; hence, we have a double-edged sword against them.

And we'll keep on exercising our God-given fundamental rights to dominate over disease-causing microorganisms because there is hope and we are smarter than they are.

Drug Resistance: Man's greatest threat in the survival of the fittest.

Drug Resistance. Image credit to ZME Science

The rate at which microorganisms harmful to our health are adapting to the various treatment modalities (drugs) currently available is very alarming and dreading. It is unfortunate to say that it seems that we're not one step ahead of these tiny, invisible-to-the-naked-eye organisms that are behind the various diseases that have affected humans since the beginning of history.

Prof. Randy Schekman, Nobel Medicine Laureate. Image credit to Nobel.org

Why it seems that we in the medical field are not one step ahead of these tiny organisms there can be many reasons. Topmost among them is the lag in basic fundamental research. Late last year, Professors Randy Schekman, James Rothman and Thomas Suedhof who jointly shared  the 2013 Nobel Prize in Medicine lamented over what they termed a neglect on basic research when the the US National Institute of Health created a Centre for Advancing Translational Sciences. In the words of Prof. Suedhof "......we don't have anything to 'translate' because we just don't understand the fundamental diseases of the brain....". His opinion is buttressed by the fact that there have emerged strains of the tuberculosis-causing organism, Mycobacterium tuberculosis, that are resistant to all known anti-TB drugs; the same could be said of some strains of the Staphylococcus species which cause myriads of diseases in humans. The problem here is that even the most recent drugs used in eradicating these organisms have the chemical structural framework and pharmacodynamics (a drug's way of carrying out its work in the body) that was developed in the 1960s and 70s; and there is no enemy being fought by its adversary with the same tactics over 4 to 5 decades, who will not evolve defence mechanisms that will one day confer on it total immunity from such tactics and also allow it to mount fatal attack on the adversary.

Another reason for this lag in our effort to be ahead of these disease-causing organisms is the lack of a large scale, collective and multidisciplinary undertaking to study in minute details the various ways in which these organisms evolve drug-resisting defence mechanisms. And what I mean here is an undertaking similar to the global Human Genome Project that saw to the successful sequencing of the whole human genome.

Having outlined these two reasons, I would now set out suggestions as regards how we can totally be in control of this fight against these human disease-causing organisms.

Prof. Kary Mullis. Image credit to NNDB

While it may seem that basic research in the area of drug development is not blossoming as we expect it, some tiny silver linnings I can fathom from some corners around the world. The one that comes to my mind is the work being done by the Nobel Chemistry laureate, Prof. Kary Mullis (he won the 1993 Nobel Prize in Chemistry for his invention of the Polymerase Chain Reaction, a technique used to create billions of a single DNA segment in a few hours).His concept of Altermune which he explained on the TED talk show conference is something that will give our tiny, microscopic adversaries a surprisingly lethal blow. Prof. Kary Mullis is taking a new, novel and radical approach towards fighting drug resistance in bacteria and other disease-causing microorganisms. The Altermune concept is a technique that uses an artificially synthesized molecule called Alphamer or Altermune linker to re-direct our own immune system to destroy these invading bacteria and other disease-causing microorganisms. An Alphamer or Altermune linker consists of a short sugar chain (an alpha galactose oligosaccharide)---which normally is not attacked by the body's immune system despite the immune system producing antibodies in response to its exposure---linked to a synthetic DNA segment called an aptamer with a specificity for only a particular strain of a virus or bacterium such that once this particular microorganism (which may be resistant to all available antibiotics, antiviral agents and other drugs in this case) invades the body, the aptamer segment of the Altermune linker binds to it and the antibodies produced in response to the galactose oligosaccharide exposure (but which does not harm it) will in the process be exposed to fresh food (the invading disease-causing organism), destroying it, both personally and by inviting other hungry guys of the immune system---the macrophages, the cytotoxic T cells and the complement system. Prof. Mullis has tested  his new work on mice infected with a strain of Staphylococcus aureus resistant to even the most potent antibiotic---this became his enemy because it killed his professor friend---and recorded almost 100% wipe out of this bacterium from the blood of the mice after a set period unlike in the controls which used various antibiotics such as doxycycline; further studies are going on in other animals such as chicken infected with the flu virus, using Altermune linkers designed for such microorganisms. Human trials will likely start soon, especially if there are emergency cases where the patient could be at the point of death because every other available option has been explored with no results. And this will unleash a whole new field of fighting against microorganisms causing disease in humans (if this works out well in human, Professor Mullis may win another Nobel Prize but this time in Medicine in about ten to fifteen years' time).

Alphamer or Altermune Linker. Image credit to Prof. Kary Banks Mullis

While this is ingenious, there is also great wisdom in exploring other ways so as to have several novel strategies for attacking these current-drug-resistant microorganisms. And I think one possible way to do this is to extend the kind of global interdisciplinary collaboration enjoyed by the Human Genome Project to the study of drug resistance in every known disease-causing microorganisms, not just some small scale collaborative studies that are obtainable currently (however, this is not condemning small scale collaborative researches as they form the foundation for large scale collaborations). Drug resistance by microorganisms comes into play when these organisms undergo mutations. Mutation is a change in the framework of some portions of an organism's genetic architecture responsible for encoding proteins that make up the structure and function vital to its existence and continual survival in the face of factors (drugs and other therapeutic strategies) that threaten them. What if we have what I call the global MutaGenome Project in which researchers from all fields will collaborate at a global scale to map all the genetic mutations in all known disease-causing organisms over generations? These mutations will then be graded on a conventional scale, depending on the extent to which their phenotypic manifestations cause diseases in humans and mount resistance to our therapeutic strategies. By engaging in such large scale endeavour, we create what I call a mutagenomic database from which patterns in which these genetic mutations occur both among similar organisms and across different organism can be outlined, hence enabling us to use mathematical tools---such as the Nash Game Theory, Permutation and Combinations and so on already employed in evolutionary biology---to predict possible future genetic mutational patterns, outcomes, and understand clearly the working dynamics between each particular threat at the molecular level (in the form of therapeutic modalities) and mutational response (resistance development) in these organisms. This could then lead to different predictive therapeutic designs for a particular bacterium over time in response to its possible resistance development options. With this approach we can have centres for MutaGenomics and MutaGenomic Therapy (Mutational Genomics) in universities and research institutes around the world designing novel therapies for various diseases.

This is a very daunting and big ambition. But we did it in the Human Genome Project, and we can also do it in the global MutaGenome Project.

Male Oral Contraceptive Pill is on the Way.

Process of fertilization. Image credit to The Telegraph

There are approximately 7 billion people on the planet currently and close to half of this number live in abject poverty. Coupled with this is the fact that these people living in poverty are most likely to give birth to more children, far more than they can train with the little resources at their disposal.

On the other hand, even some fractions of the enlightened segment of the world population in especially developing parts of the world still have mixed reaction towards the need for family planning. There are so many reasons behind this. Among them is the view held by some religious sects concerning the use of contraceptives; there is also the issue of the unwanted side effects of the various oral, injectable and implantable contraceptives used by married women, one of which is excessive weight gain (women are very concerned when it comes to their weight and I fully support them in that); some married men are not willing to use the Durex as they believe it reduces the pleasure that is derived from sex; and when it comes to the permanent contraceptive option, bilateral tubal ligation (the two Fallopian tubes of the uterus are surgically sectioned in the woman) and vasectomy (the man's vas deferens which transport sperm from the testes to the prostate gland is sectioned surgically), it has been shown that the married woman is more likely to go for it, the bilateral tubal ligation.

This is very unlike the man, especially here in Africa, who believes that one of the major attributes of a man is his ability to impregnate a woman-and hence that special characteristic must not be taken away (this is somehow selfish but I'm indifferent on it anyway).

Since there are very few contraceptive options outside this for men--condoms, withdrawal and the rhythm method-- all of which are most likely to be unpalatable to a greater percentage of married men, people in the medical field have been musing over the possibility of a method that will not take away permanently the man's ability to impregnate a woman; that will still allow him to get the full pleasure of sex; but which will prevent him for that moment from getting his wife pregnant.

Feasibility of a male contraceptive pill. Image credit to The Royal Society of Chemistry.

And it looks like this particular idea may be brought to reality in the foreseeable future. A new study by researchers in Australia and published on the 4th of November, 2013 in the Proceedings of the National Academy of Sciences of the United States of America shows that it is possible to reversibly prevent sperm from getting into the ejaculate during sex. Though the research was carried out using animals, mice, the prospect of reproducing such in humans is very high. In the study, the scientist used a technique called gene knockout to delete the two genes in mice that encode two proteins responsible for the transport of sperm from the vas deferens to the prostate gland during the emission phase of ejaculation so that the ejaculate produced by these mice contained no spermatozoa, and hence could not fertilize the females. Also, the researchers checked for side effects of this method and found there was mild reduction in blood pressure and heart rate because the two proteins have roles in blood pressure control through the sympathetic part of the autonomic nervous system.

The researchers are now shifting their attention towards achieving that in humans, not by gene knockout anyway, but through the development of drugs that can reversibly bind on the active sites of the human version of these two sperm-transporting proteins; however, this is going take some time according to the researchers. Nevertheless, what matters most is that a safe, viable target for contraceptive pill development has been found; safe and viable in the sense that, unlike other previous attempts at developing drugs to prevent a man from temporarily producing sperm and in the pills for women, this particular modality does not target spermatogenesis (sperm development) and the hormonal regulations guiding it which could lead to untold mutations that can have future impact if the man decides to have more children. And one more good thing about this research is that when the drugs are finally developed they will likely be in form of tablets that can be taken with a glass of water. It would work as long as it is being taken; once the man stops taking it, he can reverse to being able to get his wife pregnant.

Family planning and birth control, to me and how it should be viewed, is giving birth to the number of children a couple can comfortably raise with the resources available to them; spacing the birth of these children to allow for the full recuperation of the mother after each child--and this is extremely important for the health of both the nursing mother and the child being nursed.

Flexible Screens and Bendable Smartphones: the Science behind this Emerging Technology

Bendable Smartphone of the future. Image credit to Smarttechnology

Bendable Iphone of the future. Image credit to Prowl Newspaper

I had my first mobile phone in 2007-one Nokia 2310. Then it was like one precious jewel-honestly if you give me that phone now, I'll throw it into the closet and flush it away-and I could remember that I played all the ring tunes on it over and over again, and also listened to news and jamz on radio stations with it. It was just so sweet. I used to admire the screen and always changed the theme colour-from blue to other colour mixtures I can't remember. But looking back and making comparison with the type of screens we have on phones now, I made a joke that the display of those old mobile phones and that of the current day call-only dumbphones are just films of groundnut oil on water; but that's a joke anyway.

There has been rapid transformation in phones display and hardware from what was obtained back then to things like LCD (liquid crystal display), AMOLED (Active Matrix Organic Light-Emitting Diode); and now the current buzz: flexible display, bendable screens and bendable phones. These new trending buzzwords in the smartphone tech world are not really new ( I mean in terms of the basic, fundamental scientific principles behind them).

Back in secondary school (high school) and in the first year of university when we did the basic sciences, we were taught that metals and semiconductors like silicon are electrical conductors while non metals like plastic and rubber are electrical insulators, meaning that plastics and the likes do not allow current to flow

Flexible Display. Image credit to Treehugger

through them. However, I would say that information was limited in scope maybe to accommodate the curriculum meant for such level. But as far back as the 1970s, three scientists, devised ways through which non metals like rubber and plastics when subjected to certain conditions conducted electricity like metals; this work led to the concept of polymeric conductivity (polymers-composed of thousands of monomers, if you remember your secondary school Chemistry-conducting electricity). The research was so phenomenal and filled with endless prospects for the field of material science and engineering that the three scientists, Professors Alan J Heeger, Alan G. MacDiarmid and Hideki Shirakawa behind it were awarded the 2000 Nobel Prize for Chemistry for it. 

The area of polymeric conductivity in material science has so much expanded since 1970s, giving rise to possible applications in the future such as flexible electronics (electronic devises whose electricity conducting parts are made of polymeric conductors and hence allowing you to bend them, unlike metals used in current devices).

In fact, one of the expectations I had for the Samsung Galaxy S5 before its launch was it was going to come with a flexible screen display, and I was mildly disappointed initially because it fell short of that expectation despite all the rumours. But that expectation was not met because of one of the biggest challenges facing the industrial application of polymeric conductivity; and that was what took away that mild disappointment (though some other expectations I had for the smartphone, and which are extremely feasible, were not met with, but their analysis is not the focus of this blog).

According to a new research published in the Proceedings of the National Academy of Sciences by scientists from Stanford Univetsity and the University of California Berkeley and led by Professor Andrew Spakowitz, these conductive polymers at the molecular level exhibit what they termed structural inhomogeneity. In other words, plastic conductors conduct electricity at different rates in their various parts at the molecular level such that bending or flexing them significantly alters the rate of current flow, reducing the electrical conductivity (and I now understood why the Galaxy S5 probably fell short of my flexible screen expectation--some work still needs to be done). Professor Andrew Spakowitz and his team I guess are working to find solutions to this current flow-impeding structural inhomogeneity; and their success, which is on the high side of prospects, will definitely make our dreams of having bending smartphones and tablets and other electronic devices in our hands come true because, for one thing among so many things,
I will no longer panic if my bendable smartphone falls from my hand.

5% of Hypertension Cases can be Prevented

Checking Blood Pressure. Image credit to Shogo Green

We discussed hypertension in one of our tutorials in Internal Medicine II clinical posting this week, probably on Monday, and this was where I first brought up the news--even the resident doctor taking us was a bit surprised not because a medical student said something he has not heard before, but because of the very complex nature of hypertension in terms of its management based on multiple published studies he must have read about.

Back to the tutorial discussion. We discussed the various guidelines for the the definition and classification of hypertension; the various proposed mechanisms underlying its occurrence, and the documented fact that as much as between 90 and 95% of all hypertension cases have not been found (with current research--I say so because I believe with further sophistication in technologies geared towards scientific research in this area and much deeper foresight and insight coming to researchers, we may just begin to get fortunate) to have a specific known cause: that is one single definable underlying structural and functional error. This means that most people diagnosed with hypertension (consistent blood pressure at or greater than 140/90mmHg measured at two or more separate occasions, preferably weeks apart) will be on lifestyle modification and antihypertensive drug treatment probably for the rest of their lives. That's so unfortunate.

Hypertension. Image credit to Medicine Net

But I think some people, let me say some families with an established history of hypertension could actually prevent their kids from having this clinical condition in later life; however, it is if such a family is lucky to fall within the small percentage under the 90-95% class of hypertension of unknown cause that research is bringing a ray of hope to.

In a research published on 4th August 2013 in the journal Nature Genetics and headed by clinical pharmacologists from University of Cambridge and Addenbrooke's Hospital, it is shown that 5% of hypertension cases can prevented. Scientists from laboratories in four European countries collaborated in the study in which the Cambridge University team developed a newer and more powerful PET-CT scan (Positron Emission Tomography-Computed Tomography--they use radiations like x-rays and positron, a subatomic particle to produce functional images of the body's internal structures) that was used to image the adrenal glands (two small structures on top of the kidney which produce adrenalin, cortisol and aldosterone--aldosterone is involved in blood pressure regulation) for benign tumours. These benign adrenal tumours were found to have mutations--which the researchers sequenced using the latest gene sequencing technology--that cause hypertension through a direct mechanism also revealed by the study. The researchers predict that this benign tumour is the likely cause of hypertension for 1 in 20 patients with hypertension, and they affirm that this group of people if diagnosed with this benign adrenal tumour at a young age can have them removed, hence averting the development of hypertension in these people later in life.

I guess we are already beginning to get fortunate.

Google launches smart contact lens

The year 2014 will be the opening door for wearable smart devices, many tech analysts and experts say. Prequel to this, tech giants like Samsung and Sony launched their smartwatches last year. Samsung before that, introduced some compatible wearable accessories such as the S Band and Heart Rate Monitor for their galaxy S4 last year June.

Google Smart contact lens. Image credited to Muktware

Google has not been left out in this elite group as they released the beta version of their Google Glass, a smart eye glass that functions by responding to vocal commands and which will be out in the market probably before this year runs out. And now it has taken its prowess in the wearable technology sector to another level when it announced a few days ago that it was testing a prototype smart contact lens.

The smart contact lens has the healthcare sector as its main focus of application according to the BBC. The smart contact lens will use a tiny wireless chip and glucose sensor embedded in two layers of lens materials to measure and record per second glucose levels in tears; and an integrated tiny LED (light emitting diode) light would signal to indicate when glucose levels have passed certain healthy benchmarks, especially in diabetic individuals.

Google Glass. Image credited to Wikimedia

One in ten people of the world's population will have diabetes by 2035 according to the estimates from the International Diabetes Federation. And with this potential technology many catastrophic incidents from sudden rise or drops in glucose levels will be averted as the suffering individuals would have a portable real-time per second reading of their glucose level because this smart contact lens will work with an application on smartphones and tablets; this also means that these individuals' physicians will constantly monitor their patients via smartphones and tablets.

Though this project is still in the experimental stages, Google said its working with the US Food and Drug Administration and other partners (to develop apps) to make it available in the market.

IBM Set to Take Humanoid Computing to the next Level

IBM Watson Supercomputer.

IBM BlueGeneP Supercomputer.

IBM Watson Supercomputer.

 Computing technology firm, IBM are making plans to explore the virtually limitless potential of its supercomputer named Watson after its former president Thomas Watson and which was built in 2005 by the firm's DeepQA project. The supercomputer defeated its human rivals in the America's Favorite Quiz Show, Jeopardy TV game show; and the supercomputer has been shown to compute substantial chunks of information at a rate faster than the human brain.

According to a report on the BBC news site, IBM has earmarked about $1 billion to create a new division solely for the supercomputer. The company aims to harness the supercomputer's capabilities in mimicking how people think (using natural language and analytics) and understanding language complexities and learning from  experience, to develop faster and smarter software solutions for businesses and individuals.

Emerging area of immediate application, according to expert opinion, is healthcare where medical professionals will likely access the supercomputer's gigantic cloud computing database, Softlayer, using smartphones that are linked wirelessly to their diagnostic equipment.

A non-invasive, bloodless malaria test developed.

Researchers at the Rice University, Texas USA, led by Dmitri O. Lapotko, have designed a rapid non-invasive test for malaria, which uses harmless laser pulses, and neither requires drawing blood sample with a needle and syringe nor any reagent. Studies were first carried out on mice; and clinical trials on humans would likely have started .

The research work published on 27th November, 2013 in Proceedings of the National Academy of Sciences, detailed how the scientists harnessed the high optical absorbance of hemozoin, the breakdown product of haemoglobin digestion by the malaria parasite, Plasmodium falciparum in red blood cells, to safe laser beams to generate a picosecond-long localized vapour nanobubble around the hemozoin nanoparticles. These vapour nanobubbles called Hemozoin-generated Vapour Nanobubbles carry an acoustic (sound) signature that can be detected by a nanosensor called optical detector. The overall procedure involved attaching a fibre optic probe to the earlobe of a mouse; this probe sent laser pulses through the skin of the earlobe, and in 20 seconds the nanosensor recorded the acoustic signature obtained, detecting the presence of malaria parasite even when only one red blood cell in a million was infected, with no false positives according to the technology's inventor, Dmitri O. Lapotko.

And according to a report on the New York Times, the technology can be powered by a car battery through a device that is tough enough to work in hot and dusty rural areas , which could transform malaria diagnosis especially in endemic areas of the world by effortlessly screening one person every 20 seconds for less than half a dollar ( N75.00 in Nigeria) down from the current finger-pricking 15 minute-long test which costs more than a dollar.

Cambridge University scientists print new retinal cells

A group of scientists from University of Cambridge John van Geest Centre for Brain Repair, the Institute for Manufacturing, Department of Engineering, Cambridge NIHR Biomedical Research Centre, and the Eye Department, Addenbrooke’s Hospital, Cambridge, has, for the first time, successfully printed two types of retinal cells from adult rats--ganglion cells and glial cells--using a piezoelectric inkjet printer, a type 3-D printing technique known as bioprinting. These two cells, while functioning to relay information from the eye to certain areas of the brain, support and protect the retinal neurons, the cones and rods. The research published on 17th December, 2013 in the journal Biofabrication showed that the printed retinal cells were able to retain their healthy growth and survival in culture

. The scientists who stated that the work was still preliminary hope to carry out more extensive research to perfect their findings, including extending the inkjet bioprinting technology to the light-sensitive photoreceptor cells of the retina responsible for sight, before beginning any human clinical trials that will aim to treat blindness resulting from damage to the nerve cells of the retina.