Cell (biology)

Scientists ‘print’ new eye cells

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human eye
Many teams are researching different ways to repair the sight-giving cells of the retina

Scientists say they have been able to successfully print new eye cells that could be used to treat sight loss.

The proof-of-principle work in the journal Biofabrication was carried out using animal cells.

The Cambridge University team says it paves the way for grow-your-own therapies for people with damage to the light-sensitive layer of tissue at back of the eye – the retina.

More tests are needed before human trials can begin.

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This is a step in the right direction as the retina is often affected in many of the common eye conditions, causing loss of central vision which stops people watching TV and seeing the faces of loved ones”

Clara Eaglen of the RNIB

At the moment the results are preliminary and show that an inkjet printer can be used to print two types of cells from the retina of adult rats―ganglion cells and glial cells.

These are the cells that transmit information from the eye to certain parts of the brain, and provide support and protection for neurons.

The printed cells remained healthy and retained their ability to survive and grow in culture.

Retinal repair

Co-authors of the study Prof Keith Martin and Dr Barbara Lorber, from the John van Geest Centre for Brain Repair at the University of Cambridge, said: “The loss of nerve cells in the retina is a feature of many blinding eye diseases. The retina is an exquisitely organised structure where the precise arrangement of cells in relation to one another is critical for effective visual function.

Human eye
The retina sits at the back of the eye

“Our study has shown, for the first time, that cells derived from the mature central nervous system, the eye, can be printed using a piezoelectric inkjet printer. Although our results are preliminary and much more work is still required, the aim is to develop this technology for use in retinal repair in the future.”

They now plan to attempt to print other types of retinal cells, including the light-sensitive photoreceptors – rods and cones.

Scientists have already been able to reverse blindness in mice using stem cell transplants.

And there is promising work into electronic retina implants implants in patients.

Clara Eaglen, of the RNIB, said: “Clearly it’s still at a very early stage and further research is needed to develop this technology for use in repairing the retina in humans.

“The key to this research, once the technology has moved on, will be how much useful vision is restored.

“Even a small bit of sight can make a real difference, for some people it could be the difference between leaving the house on their own or not.

“It could help boost people’s confidence and in turn their independence.”

Prof Jim Bainbridge of London’s Moorfields Eye Hospital said: “The finding that eye cells can survive the printing process suggests the exciting possibility that this technique could be used in the future to create organised tissues for regeneration of the eye and restoration of sight.

“Blindness is commonly caused by degeneration of nerve cells in the eye. In recent years there has been substantial progress towards the development of new treatments involving cell transplantation.”

Stem Cells Converted Into Lung Tissue.

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Lung transplant recipients have a relatively low 10 year survival rate of about 28%. Cellular rejection of the donor organ occurs about 90% of the time, which brings additional obstacles for the patient and doctors. This might be about to change, as functional lung tissue has been created from human stem cells. The research comes from Hans-Willem Snoeck from the Columbia Center for Translational Immunology and was published in the current edition of Nature Biotechnology.

A couple of years ago, Dr. Snoeck was able to convert stem cells into the precursor endoderm cells that can eventually differentiate into lung cells. This was done with human embryonic stem cells as well as human induced pluripotent stem cells, which involve a bit more work but are easier to come by. Those precursor cells were shown to actually differentiate into six different respiratory tissues, including the coveted type II alveolar cells. which facilitate gas exchange and produce surfactant.

Type 2 alveolar cells, also called pneumocytes, are responsible for producing surfactant, the compound that allows the lungs to remain inflated with air. These type II cells also aid in gas exchange and lung repair.

The lung tissue produced by stem cells could give researchers a unique perspective to study the tissue and learn more about how lung diseases originate. This could lead to better treatment options for lung diseases.

If treatments do not work and transplant becomes inevitable, physicians can use the patient’s own cells to provide a new disease-free organ. This eliminates both the potential for cellular rejection as well as the stress of waiting on the transplant list. To make a replacement lung, researchers would first remove the patient’s lung and decellularize it, leaving only a cartilaginous scaffold. The stem cells would then be used to coat the scaffold and regrow functional tissue to be put back into the patient.

Though it is a long way from getting implanted into a human body, these results are exciting. A patent has been filed by Columbia University for their technique of converting induced pluripotent stem cells into the functional tissue.

Scientists generate “mini-kidney” structures from human stem cells.

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Diseases affecting the kidneys represent a major and unsolved health issue worldwide. The kidneys rarely recover function once they are damaged by disease, highlighting the urgent need for better knowledge of kidney development and physiology.

Now, a team of researchers led by scientists at the Salk Institute for Biological Studies has developed a novel platform to study  diseases, opening new avenues for the future application of regenerative medicine strategies to help restore kidney function.

Salk scientists generate “mini-kidney” structures from human stem cells

For the first time, the Salk researchers have generated three-dimensional kidney structures from human stem cells, opening new avenues for studying the development and diseases of the kidneys and to the discovery of new drugs that target human . The findings were reported November 17 in Nature Cell Biology.

Scientists had created precursors of kidney cells using stem cells as recently as this past summer, but the Salk team was the first to coax human stem cells into forming three-dimensional cellular structures similar to those found in our kidneys.

“Attempts to differentiate human stem cells into renal cells have had limited success,” says senior study author Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory and holder of the Roger Guillemin Chair. “We have developed a simple and efficient method that allows for the differentiation of human stem cells into well-organized 3D structures of the ureteric bud (UB), which later develops into the collecting duct system.”

The Salk findings demonstrate for the first time that pluripotent stem cells (PSCs)—cells capable of differentiating into the many cells and tissue types that make up the body—can made to develop into cells similar to those found in the ureteric bud, an early developmental structure of the kidneys, and then be further differentiated into three-dimensional structures in organ cultures. UB cells form the early stages of the human urinary and reproductive organs during development and later develop into a conduit for urine drainage from the kidneys. The scientists accomplished this with both human  and induced  (iPSCs),  from the skin that have been reprogrammed into their pluripotent state.

After generating iPSCs that demonstrated pluripotent properties and were able to differentiate into mesoderm, a germ cell layer from which the kidneys develop, the researchers made use of growth factors known to be essential during the natural development of our kidneys for the culturing of both iPSCs and embryonic stem cells. The combination of signals from these growth factors, molecules that guide the differentiation of stem cells into specific tissues, was sufficient to commit the cells toward progenitors that exhibit clear characteristics of renal cells in only four days.

The researchers then guided these cells to further differentiated into organ structures similar to those found in the ureteric bud by culturing them with kidney cells from mice. This demonstrated that the mouse cells were able to provide the appropriate developmental cues to allow human  to form three-dimensional structures of the kidney.

In addition, Izpisua Belmonte’s team tested their protocol on iPSCs from a patient clinically diagnosed with polycystic  (PKD), a genetic disorder characterized by multiple, fluid-filled cysts that can lead to decreased  and kidney failure. They found that their methodology could produce kidney structures from patient-derived iPSCs.

Because of the many clinical manifestations of the disease, neither gene- nor antibody-based therapies are realistic approaches for treating PKD. The Salk team’s technique might help circumvent this obstacle and provide a reliable platform for pharmaceutical companies and other investigators studying drug-based therapeutics for PKD and other kidney diseases.

“Our differentiation strategies represent the cornerstone of disease modeling and drug discovery studies,” says lead study author Ignacio Sancho-Martinez, a research associate in Izpisua Belmonte’s laboratory. “Our observations will help guide future studies on the precise cellular implications that PKD might play in the context of .”

Depression ‘speeds ageing process’

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Depression can make us physically older by speeding up the ageing process in our cells, according to a study.

Lab tests showed cells looked biologically older in people who were severely depressed or who had been in the past.

These visible differences in a measure of cell ageing called telomere length couldn’t be explained by other factors, such as whether a person smoked.

The findings, in more than 2,000 people, appear in Molecular Psychiatry.

Experts already know that people with major depression are at increased risk of age-related diseases such as cancer, diabetes, obesity and heart disease.

This might be partly down to unhealthy lifestyle behaviours such as alcohol use and physical inactivity.

But scientists suspect depression takes its own toll on our cells.

Telomere shortening

To investigate, Josine Verhoeven from the VU University Medical Centre in the Netherlands, along with colleagues from the US, recruited 2,407 people to take part in the study.

More than one third of the volunteers were currently depressed, a third had experienced major depression in the past and the rest had never been depressed.

The volunteers were asked to give a blood sample for the researchers to analyse in the lab for signs of cellular ageing.

The researchers were looking for changes in structures deep inside cells called telomeres.

Telomeres cap the end of our chromosomes which house our DNA. Their job is to stop any unwanted loss of this vital genetic code. As cells divide, the telomeres get shorter and shorter. Measuring their length is a way of assessing cellular ageing.

People who were or had been depressed had much shorter telomeres than those who had never experienced depression. This difference was apparent even after lifestyle differences, such as heavy drinking and smoking, were taken into account.

Furthermore, the most severely and chronically depressed patients had the shortest telomeres.

Dr Verhoeven and colleagues speculate that shortened telomeres are a consequence of the body’s reaction to the distress depression causes.

telomere at the end of chromosomes

“This large-scale study provides convincing evidence that depression is associated with several years of biological ageing, especially among those with the most severe and chronic symptoms,” they say.

But it is unclear whether this ageing process is harmful and if it can be reversed.

UK expert Dr Anna Phillips, of the University of Birmingham, has researched the effects of stress on telomere length.

She says telomere length does not consistently predict other key outcomes such as death risk.

Further, it is likely that only a major depressive disorder, not experience of or even a lifetime of mild-to-moderate depressive symptoms, relates to telomere length, she said.

starving-cancer-to-death-by-removing-one-food-refined-sugar.

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While all of our cells need glucose (a form of sugar which is turned into energy), cancer thrives on a body full of simple carbohydrates (which become sugar in the body) and refined sugars that come from processed foods and overly sweet goodies. If you or someone you know is suffering from cancer, one of the best things they can do is take away the disease’s favorite food – sugar. 

Starving Cancer to Death by Removing one Food: Refined Sugar

Dr. Otto Wartburg and other health experts have been talking about how cancer loves sugar since the 1920s, but surprisingly many doctors don’t tell their cancer patients that as long as they continue to eat processed foods full of the stuff, they will likely have a more difficult time fighting this disease. The German physiologist, leading biochemist, medical doctor, and Nobel laureate was convinced that you could starve cancer right out of the body. While it may not always be that easy, this is something that could significantly change the game. His theory was that malignant cells and tumor growth was caused by cells that generated energy via adenosine triphosphate (ATP) through a nonoxidative breakdown of glucose (sugar). The recycling of the metabolite from this process called glycolysis and the circulation of adhA back into the body caused anaerobic respiration. This is the reverse of what happens with healthy cells. Healthy, non-cancerous cells generate energy for the body to use through the oxidative breakdown of pyruvate, the end product of glycolysis, which leads to oxidized mitochondria. He therefore concluded that cancer was really a mitochondrial dysfunction. The normal process of respiration of oxygen in the body is changed to the fermentation of sugar. If you remove the sugar, the body should not develop cancer. The connection between sugar and cancer development is certainly not new. 

Most people can easily remove the obvious culprits that are full of refined sugar – cakes, candies, cookies, etc. The problem is that many foods which are packaged and sold in the US and in other countries are full of refined sugar, but just very sneakily hidden in the packaging labels. Things like ‘healthy’ yogurt, cereals, whole wheat or whole grain breads, and even ‘low-calorie’ items can be full of sugar. Related Read: Kid Drinking 7 Trillion Calories of Sugar from Beverages The easiest way to eliminate unwanted refined sugars is to stop buying ‘convenience’ or pre-packaged foods, and at least temporarily, don’t eat out at restaurants – many dining establishments source their food from big companies that ‘season’ their food with lots of sugar and salt to make it more palatable after being frozen and shipped across the country in trucks. Even salad dressings can be loaded with sugar. To deal with cravings for sugary foods, increase your plant-based and healthy animal based proteins (no red meat) and eat more nutrition-packed foods. 

A Bio-Patch Regrows Bone Inside the Body.

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Researchers from the University of Iowa have developed a remarkable new procedure for regenerating missing or damaged bone. It’s called a “bio patch” — and it works by sending bone-producing instructions directly into cells using microscopic particles embedded with DNA.

In experiments, the gene-encoding patch has already regrown bone fully enough to cover skull wounds in test animals. It has also stimulated new growth in human bone marrow stromal cells. Eventually, the patch could be used to repair birth defects involving missing bone around the head or face. It could also help dentists rebuild bone in areas which provides a concrete-like foundation for implants.

To create the bio patch, a research team led by Satheesh Elangovan delivered bone-producing instructions to existing bone cells inside a living body, which allowed those cell to produce the required proteins for more bone production. This was accomplished by using a piece of DNA that encodes for a platelet-derived growth factor called PDGF-B. Previous research relied on repeated applications from the outside, but they proved costly, intensive, and more difficult to replicate with any kind of consistency.

“We delivered the DNA to the cells, so that the cells produce the protein and that’s how the protein is generated to enhance bone regeneration,” explained Aliasger Salem in a statement. “If you deliver just the protein, you have keep delivering it with continuous injections to maintain the dose. With our method, you get local, sustained expression over a prolonged period of time without having to give continued doses of protein.” Salem is a professor in the College of Pharmacy and a co-corresponding author on the paper.

While performing the procedure, the researchers made a collagen scaffold in the actual shape and size of the bone defect. The patch, which was loaded with synthetically created plasmids and outfitted with the genetic instructions for building bone did the rest, achieving complete regeneration that matched the shape of what should have been there. This was followed by inserting the scaffold onto the missing area. Four weeks is usually all that it took — growing 44-times more bone and soft tissue in the affected areas compared to just the scaffold alone.

“The delivery mechanism is the scaffold loaded with the plasmid,” Salem says. “When cells migrate into the scaffold, they meet with the plasmid, they take up the plasmid, and they get the encoding to start producing PDGF-B, which enhances bone regeneration.”

‘Primitive’ brain recognises edges.

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Scientists at Australia’s Vision Centre (VC) have found a group of rare cells in the human brain that recognise edges – helping us to avoid accidents and recognise everything we use or see in daily life.

BruceRolff_brain_shutterstock

To their surprise, they located the cells in the ‘primitive’ brain – the part of our brain that was previously just thought to pass information from the eye to the higher brain, or cortex, to interpret it.

Their discovery has thrown new light on how the vision system of humans and other primates operates – and how we use vision to move around, find food, read, recognise faces and function day-to-day.

Importantly, the knowledge could help develop medical devices for reversing blindness such as the bionic eye, says Professor Paul Martin of The VC and The University of Sydney (USyd).

“Our eyes and brain work together to give us a recognisable world,” Prof. Martin explains. “The eyes send the light signals they detect to the cortex or ‘modern’ brain which is responsible for higher functions like memory, thought and language.”

“Our vision cells respond to different information – some to colour, some to brightness, and now we’ve found the ones that respond to patterns,” Dr Kenny Cheong of The VC and USyd adds. “If you look at your computer screen, you’ll see it has four sides, and each side has an orientation – horizontal or vertical. The cells are sensitive to these ‘sides’.”

What most surprised the researchers was the location of these cells. “We found these cells in the thalamus, which previously was only thought to pass information from the eyes to the cortex,” Dr Cheong says.

“This means that the cortex, or the ‘new’ brain, isn’t the only place that forms an image for us,” says Prof. Martin. “Even in the early stages, there are multiple pathways and signals going into the brain, so it isn’t simply doing a step by step construction of the world.

“While other animals including cats, rabbits, bees and chickens also have edge detecting cells, this is the first study to indicate that primate vision – including human vision – does not all happen in the cortex.”

These cells are also exceedingly rare, Prof. Martin says. “We actually saw them ten years ago, but these were a few cells out of thousands, so we thought that it was a mistake and discarded the data.

“But they cropped up every once in a while, and when we finally put them together, they look much more like cells in the cortex than in the thalamus.”

Dr Cheong says the study provides a better understanding of the visual system, which is crucial for the development of devices or treatments to restore vision.

“People who lose their vision lack the nerve cells that respond to light, which contains information such as colour, brightness and patterns,” he says. “So to develop a device like the bionic eye, we have to replicate the visual system, including these cells, using electronics. This means we must know what cells are present, how they work and what information they send to the brain.”

Everything in moderation: excessive nerve cell pruning leads to disease.

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Mechanism meant to maintain efficiency of brain network involved in neurodegenerative disease

Scientists at the Montreal Neurological Institute and Hospital-The Neuro, McGill University, have made important discoveries about a cellular process that occurs during normal brain development and may play an important role in neurodegenerative diseases. The study’s findings, published in Cell Reports, a leading scientific journal, point to new pathways and targets for novel therapies for Alzheimer’s, Parkinson’s, ALS and other neurodegenerative diseases that affect millions of people world-wide.

Research into neurodegenerative disease has traditionally concentrated on the death of nerve cell bodies. However, it is now certain that in most cases that nerve cell body death represents the final event of an extended disease process. Studies have shown that protecting cell bodies from death has no impact on disease progression whereas blocking preceding axon breakdown has a significant benefit.  The new study by researchers at The Neuro shifts the focus to the loss or degeneration of axons, the nerve-cell ‘branches’ that receive and distribute neurochemical signals among neurons.

During early development, axons are pruned to ensure normal growth of the nervous system. Emerging evidence suggests that this pruning process becomes reactivated in neurodegenerative disease, leading to the aberrant loss of axons and dendrites. Axonal pruning in development is significantly influenced by proteins called caspases. “The idea that caspases are even involved in axonal degeneration during development is very recent” said Dr. Philip Barker, a principal investigator at The Neuro and senior author of the study.

Dr. Barker and his colleagues show that the activity of certain ’executioner’ caspases (caspase-3 and caspase-9) induce axonal degeneration and that their action is suppressed by a protein termed XIAP (X-linked inhibitor of apoptosis). “We found that caspase-3- and -9 play crucial roles in axonal degeneration and that their activities are regulated by XIAP. XIAP acts as a brake on caspase activity and must be removed for degeneration to proceed” added Dr. Barker.

This balancing act between caspases and XIAP ensure that caspases do not cause unnecessary or excessive destruction. However, this balance may shift during neurodegenerative disease. “If we understand the pathways that regulate XIAP levels, we may be able to develop therapies that reduce caspase-dependent degeneration during neurodegenerative disease”.

NOBEL PRIZE IN PHYSIOLOGY AND MEDICINE 2013.

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The Nobel Assembly at Karolinska Institutet has today decided to award

The 2013 Nobel Prize in Physiology or Medicine

jointly to

James E. Rothman, Randy W. Schekman
and Thomas C. Südhof

for their discoveries of machinery regulating vesicle traffic,
a major transport system in our cells

Summary

The 2013 Nobel Prize honours three scientists who have solved the mystery of how the cell organizes its transport system. Each cell is a factory that produces and exports molecules. For instance, insulin is manufactured and released into the blood and chemical signals called neurotransmitters are sent from one nerve cell to another. These molecules are transported around the cell in small packages called vesicles. The three Nobel Laureates have discovered the molecular principles that govern how this cargo is delivered to the right place at the right time in the cell.

Randy Schekman discovered a set of genes that were required for vesicle traffic. James Rothman  unravelled protein machinery that allows vesicles to fuse with their targets to permit transfer of cargo. Thomas Südhof revealed how signals instruct vesicles to release their cargo with precision.

Through their discoveries, Rothman, Schekman and Südhof have revealed the exquisitely precise control system for the transport and delivery of cellular cargo. Disturbances in this system have deleterious effects and contribute to conditions such as neurological diseases, diabetes, and immunological disorders.

How cargo is transported in the cell

In a large and busy port, systems are required to ensure that the correct cargo is shipped to the correct destination at the right time. The cell, with its different compartments called organelles, faces a similar problem: cells produce molecules such as hormones, neurotransmitters, cytokines and enzymes that have to be delivered to other places inside the cell, or exported out of the cell, at exactly the right moment. Timing and location are everything. Miniature bubble-like vesicles, surrounded by membranes, shuttle the cargo between organelles or fuse with the outer membrane of the cell and release their cargo to the outside. This is of major importance, as it triggers nerve activation in the case of transmitter substances, or controls metabolism in the case of hormones. How do these vesicles know where and when to deliver their cargo?

Traffic congestion reveals genetic controllers

Randy Schekman was fascinated by how the cell organizes its transport system and in the 1970s decided to study its genetic basis by using yeast as a model system. In a genetic screen, he identified yeast cells with defective transport machinery, giving rise to a situation resembling a poorly planned public transport system. Vesicles piled up in certain parts of the cell. He found that the cause of this congestion was genetic and went on to identify the mutated genes. Schekman identified three classes of genes that control different facets of the cell´s transport system, thereby providing new insights into the tightly regulated machinery that mediates vesicle transport in the cell.

Docking with precision

James Rothman was also intrigued by the nature of the cell´s transport system. When studying vesicle transport in mammalian cells in the 1980s and 1990s, Rothman discovered that a protein complex enables vesicles to dock and fuse with their target membranes. In the fusion process, proteins on the vesicles and target membranes bind to each other like the two sides of a zipper. The fact that there are many such proteins and that they bind only in specific combinations ensures that cargo is delivered to a precise location. The same principle operates inside the cell and when a vesicle binds to the cell´s outer membrane to release its contents.

It turned out that some of the genes Schekman had discovered in yeast coded for proteins corresponding to those Rothman identified in mammals, revealing an ancient evolutionary origin of the transport system. Collectively, they mapped critical components of the cell´s transport machinery.

Timing is everything

Thomas Südhof was interested in how nerve cells communicate with one another in the brain. The signalling molecules, neurotransmitters, are released from vesicles that fuse with the outer membrane of nerve cells by using the machinery discovered by Rothman and Schekman. But these vesicles are only allowed to release their contents when the nerve cell signals to its neighbours. How is this release controlled in such a precise manner? Calcium ions were known to be involved in this process and in the 1990s, Südhof searched for calcium sensitive proteins in nerve cells. He identified molecular machinery that responds to an influx of calcium ions and directs neighbour proteins rapidly to bind vesicles to the outer membrane of the nerve cell. The zipper opens up and signal substances are released. Südhof´s discovery explained how temporal precision is achieved and how vesicles´ contents can be released on command.

Vesicle transport gives insight into disease processes

The three Nobel Laureates have discovered a fundamental process in cell physiology. These discoveries have had a major impact on our understanding of how cargo is delivered with timing and precision within and outside the cell.  Vesicle transport and fusion operate, with the same general principles, in organisms as different as yeast and man. The system is critical for a variety of physiological processes in which vesicle fusion must be controlled, ranging from signalling in the brain to release of hormones and immune cytokines. Defective vesicle transport occurs in a variety of diseases including a number of neurological and immunological disorders, as well as in diabetes. Without this wonderfully precise organization, the cell would lapse into chaos.

 

James E. Rothman was born 1950 in Haverhill, Massachusetts, USA. He received his PhD from Harvard Medical School in 1976, was a postdoctoral fellow at Massachusetts Institute of Technology, and moved in 1978 to Stanford University in California, where he started his research on the vesicles of the cell. Rothman has also worked at Princeton University, Memorial Sloan-Kettering Cancer Institute and Columbia University. In 2008, he joined the faculty of Yale University in New Haven, Connecticut, USA, where he is currently Professor and Chairman in the Department of Cell Biology.

Randy W. Schekman was born 1948 in St Paul, Minnesota, USA, studied at the University of California in Los Angeles and at Stanford University, where he obtained his PhD in 1974 under the supervision of Arthur Kornberg (Nobel Prize 1959) and in the same department that Rothman joined a few years later. In 1976, Schekman joined the faculty of the University of California at Berkeley, where he is currently Professor in the Department of Molecular and Cell biology. Schekman is also an investigator of Howard Hughes Medical Institute.

Thomas C. Südhof was born in 1955 in Göttingen, Germany. He studied at the Georg-August-Universität in Göttingen, where he received an MD in 1982 and a Doctorate in neurochemistry the same year. In 1983, he moved to the University of Texas Southwestern Medical Center in Dallas, Texas, USA, as a postdoctoral fellow with Michael Brown and Joseph Goldstein (who shared the 1985 Nobel Prize in Physiology or Medicine). Südhof became an investigator of Howard Hughes Medical Institute in 1991 and was appointed Professor of Molecular and Cellular Physiology at Stanford University in 2008.

 

Key publications:
Novick P, Schekman R: Secretion and cell-surface growth are blocked in a temperature-sensitive mutant of Saccharomyces cerevisiae. Proc Natl Acad Sci USA 1979; 76:1858-1862.
Balch WE, Dunphy WG, Braell WA, Rothman JE: Reconstitution of the transport of protein between successive compartments of the Golgi measured by the coupled incorporation of N-acetylglucosamine. Cell 1984; 39:405-416.
Kaiser CA, Schekman R: Distinct sets of SEC genes govern transport vesicle formation and fusion early in the secretory pathway. Cell 1990; 61:723-733.
Perin MS, Fried VA, Mignery GA, Jahn R, Südhof TC: Phospholipid binding by a synaptic vesicle protein homologous to the regulatory region of protein kinase C. Nature 1990; 345:260-263.
Sollner T, Whiteheart W, Brunner M, Erdjument-Bromage H, Geromanos S, Tempst P, Rothman JE: SNAP receptor implicated in vesicle targeting and fusion. Nature 1993;
362:318-324.
Hata Y, Slaughter CA, Südhof TC: Synaptic vesicle fusion complex contains unc-18 homologue bound to syntaxin. Nature 1993; 366:347-351.

What Most Doctors Won’t Tell You About Colds and Flus.

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The next time you experience a cold or the flu, remember this: rather than take conventional drugs to suppress uncomfortable symptoms, it’s better for your health to allow the cold or flu to run its course while you get plenty of physical and emotional rest.

Conventional medicine and the pharmaceutical industry would have you believe that there is no “cure” for the common cold, that you should protect yourself against the flu with a vaccine that is laden with toxic chemicals, and that during the midst of a cold or flu, it is favorable to ease your discomfort with a variety of medications that can suppress your symptoms.

Unfortunately, all three of these positions indicate a lack of understanding of what colds and flus really are, and what they do for your body.

Colds and flus are caused by viruses. So to understand what colds and flus do at a cellular level, you have to understand what viruses do at a cellular level.

Do you remember learning about cellular division in grade seven science class? Each of your cells are called parent cells, and through processes of genetic duplication (mitosis) and cellular division (cytokinesis), each of your parent cells divides into two daughter cells. Each daughter cell is then considered a parent cell that will divide into two more daughter cells, and so on.

Viruses are different from your cells in that they cannot duplicate themselves through mitosis and cytokinesis. Viruses are nothing but microscopic particles of genetic material, each coated by a thin layer of protein.

Due to their design, viruses are not able to reproduce on their own. The only way that viruses can flourish in your body is by using the machinery and metabolism of your cells to produce multiple copies of themselves.

Once a virus has gained access into one of your cells, depending on the type of virus involved, one of two things can happen:
The virus uses your cell’s resources to replicate itself many times over and then breaks open (lyses) the cell so that the newly replicated viruses can leave in search of new cells to infect. Lysis effectively kills your cell.

The virus incorporates itself into the DNA of your cell, which allows the virus to be passed on to each daughter cell that stems from this cell. Later on, the virus in each daughter cell can begin replicating itself as described above. Once multiple copies of the virus have been produced, the cell is lysed.

Both possibilities lead to the same result: eventually, the infected cell can die due to lysis.

Here is the key to understanding why colds and flus, when allowed to run their course while you rest, can be good for you:

By and large, the viruses that cause the common cold and the flu infect mainly your weakest cells; cells that are already burdened with excessive waste products and toxins are most likely to allow viruses to infect them. These are cells that you want to get rid of anyway, to be replaced by new, healthy cells.

So in the big scheme of things, a cold or flu is a natural event that can allow your body to purge itself of old and damaged cells that, in the absence of viral infection, would normally take much longer to identify, destroy, and eliminate.

Have you ever been amazed by how much “stuff” you could blow out of your nose while you had a cold or the flu? Embedded within all of that mucous are countless dead cells that your body is saying good bye to, largely due to the lytic effect of viruses.

So you see, there never needs to be a cure for the common cold, since the common cold is nature’s way of keeping you healthy over the long term. And so long as you get plenty of rest and strive to stay hydrated and properly nourished during a cold or flu, there is no need to get vaccinated or to take medications that suppress congested sinuses, a fever, or coughing. All of these uncomfortable symptoms are actually ways in which your body works to eliminate waste products and/or help your body get through a cold or flu. It’s fine to use over-the-counter pain medication like acetaminophen if your discomfort becomes intolerable or if such meds can help you get a good night’s rest. But it’s best to avoid medications that aim to suppress helpful processes such as fever, coughing, and a runny nose.

It’s important to note that just because colds and flus can be helpful to your body doesn’t mean that you need to experience them to be at your best. If you take good care of your health and immune system by getting plenty of rest and consistently making health-promoting dietary and lifestyle choices, your cells may stay strong enough to avoid getting infected by viruses that come knocking on their membranes. In this scenario, you won’t have enough weak and extraneous cells to require a cold or the flu to work its way through your body to identify and lyse them.

Curious about how to differentiate the common cold and the flu? Here is an excellent summary of the differences from cbc.ca:
A cold usually comes on gradually — over the course of a day or two. Generally, it leaves you feeling tired, sneezing, coughing and plagued by a running nose. You often don’t have a fever, but when you do, it’s only slightly higher than normal. Colds usually last three to four days, but can hang around for 10 days to two weeks.

Flu, on the other hand, comes on suddenly and hits hard. You will feel weak and tired and you could run a fever as high as 40 C. Your muscles and joints will probably ache, you will feel chilled and could have a severe headache and sore throat. Getting off the couch or out of bed will be a chore. The fever may last three to five days, but you could feel weak and tired for two to three weeks.

One final note on this topic: because the common cold and the flu are both caused by viruses, antibiotics are not necessary. People who take antibiotics while suffering with a cold or flu often feel slightly better because antibiotics have a mild anti-inflammatory effect. But this benefit is far outweighed by the negative impact that antibiotics have on friendly bacteria that live throughout your digestive tract. In this light, if you really need help with pain management during a cold or flu, it is usually better to take a small dose of acetaminophen than it is to take antibiotics.

Sources: drbenkim.com & realfarmacy.com