Monday, 11 December 2017

Height And Weight Evolved At Different Speeds In The Bodies Of Our Ancestors

Bones

Hominin Bodies Developed in `Pulse & Stasis’ Variation

 
An extensive latest research of fossils covering over four million years suggests that physique and body mass advanced at different speeds at the time of evolution of hominins, the ancestral heredity of which Homo sapiens alone still prevails.

As published in the journal Royal Society: Open Science, the research portrayed that instead of progressively growing in size, hominin bodies developed in `pulse and stasis’ variation with some linages that seemed to be shrinking. Discoveries have come from the largest research of hominin body sizes comprising of 311 specimens that date back from earliest upright species of 4.4m years from the modern humans and followed the last ice age.

Though the researchers have defined the physical evolution of assorted hominin species as `long and winding road having several branches and dead ends,’ they have informed that broad patterns in the data recommends bursts of growth at crucial stages together with plateaus with little alteration for several millennia.

The scientist had been amazed to discover `decoupling’ of bulk and stature of about one and a half million years back when hominin grew about 10cm taller though could not consistently gain any weight for a further million years having an average increase of 10-15kgs taking place at about 500,000 years back.
 

Increase in Stature – Increase Slimmer Structure

 
The height and weight in hominin species, before the event seemed to evolve `in concert’ according to the authors of the first study to jointly analyse the aspects equally of body size over millions of years.

Lead author Dr Manuel Will from Cambridge’s Department of Archaeology and Research Colleague at Gonville & Caius College had mentioned that an increase exclusively in stature could have increased a slimmer structure with long legs and narrow hips and shoulder. This could have been a variation to new environments and endurance hunting as early Homo species who had left the forests and progressed to more arid African savannahs.

He further added that the higher surface-to-volume ratio of tall, slender body would be beneficial when stalking animals for hours in dry heat since larger skin area tends to increase the capacity for evaporation of sweat. Besides this he also added that the later addition of body mass tends to coincide with the increasing migrations to higher latitudes wherein a bulkier body would be suited better for thermoregulation in colder Eurasian climates.
 

Body Size Highly Variable

 
But Dr Will points out that though these seem valid theories, vast openings in the fossil record endure to cover the complete truth. Dr Will together with his colleagues in fact had to evaluate body sizes often from highly fragmented remains and in some instances, from only a single toe bone.

From the study it was observed that the body size was highly variable at the time of the earlier hominin history having a range of various shaped species, from broad, gorilla-like Paranthropus to the more gracile Australopithecus afarensis.

 The hominin from four million years back had weighed around an average of 25kg and stood at 125-139cm. Dr Will and his colleagues state that evolutionary pressures which could have made their contribution, comprise of `cladogenesis’ the splitting of a lineage with one line, in this instance, the smaller-bodied one seemed to be extinct, probably as a consequence of inter-species competition.

Friday, 1 December 2017

Revolutionary New Cancer Therapies Come With Big Risks

Cancer Therapies
Drug Makers Must Be Prepared As Revolutionary New Cancer Therapies Come With Big Risks 

Personalised cell therapy may have been established today with the authorization of two novel drugs recently called Kymriah and Yescarta that genetically modify the patient’s own immune cells to combat cancer. Still, pharmaceutical companies face many obstacles, which include many ethical
and social problems, if they want to make these cancer therapies a success.

These recent drugs, first of its type in the latest family CAR-T cell therapies, could transform the face of cancer therapies altogether. They function by separating immune cells called as T cells from a patient’s blood, and genetically engineer these cells to create receptors that identify particular tumor cells, producing many millions of replicas of these cells in a laboratory and then injecting them back into the patient. If everything goes well, these cells will identify and destroy the tumor cells in the patient.

Even though a few exciting clinical successes have been achieved, the companies manufacturing these drugs face a variety of problems. Business-wise, they have to figure out how to go into manufacturing of these drugs consistently and affordably, justifying the research through sufficient maintenance of reimbursements and persuade physicians to adopt this new and effective, yet complex treatment concept.

The need of the hour is to get these treatments perfected for patients who have no other alternative. CAR-T cancer therapies will, in all probability, kill some patients more quickly than their cancers would. So efforts need to be stepped up to reduce considerably the grave and occasionally fatal side effects that come along with these cancer therapies and strategies need to be developed to deal with them when they arise.

Companies that commercialise these cancer therapies must be ready for the possibilities of deaths and acute side effects to patients, physicians, regulators and investors. They must also be well prepared in advance to address such events promptly, clearly and realistically, whenever they occur. Also, necessary measures must be taken to create awareness among patients and their advocacy groups and emergency plans and communication strategies need to be developed.

While any demise due to medical reasons is dreadful, for few patients the possible benefit of CAR-T cancer therapies will be an advantage to that risk. This estimate will change quickly, however, as CAR-T cancer therapies will focus on patients with an initial stage cancer who have a wider set of alternatives. It may also be the same case for the society on a broader scale where undesirable events could hamper the development of CAR-T cancer therapies and curb their capabilities.

Despite many requests and pleas from individual patients and patient organisations to swiftly widen the range of use of CAR-T therapy and the huge financial opportunities and the pressures that come along with it, companies need to refuse to give in to the temptation of widening the CAR-T cancer therapies too far and fast. On the contrary, they should tune and tweak these potentially reliable therapies to be useful as a last-option solution for patients, maybe with some support from appropriate government agencies.

Even though it seems like the most common expectation, a slow and cautious approach to this new type of cancer therapies is probably the best shot in transforming personalised cell therapies into a well-known and efficient medical and financial success.

Wednesday, 1 November 2017

Stanford Scientists Seek to Speak the Brain’s Language to Heal Its Disease

A recently conducted research by a flock of scientists, associated with the Stanford University, found that the interface of the Human brain mechanism can treat the neurological troubles as well as bring a change in the ways paralytic patient communicates with the world. The chances to incorporate improvements in the functions of similar devices depend on the efficiency of translating the brain’s language. Thus, the Brain Computer Interface project has triggered interest among the experts from round the globe.

Listening to the brain’s Language


The aspiration of the scientists to establish a correlation between the human brain and the machines started with the onset of 1970’s, with Jacques Vidal embarked on a project that coined the name, Brain Computer Interface project. As his research paper narrates, it includes an EEG mechanism that records electrical signals, originating from the brain and a plethora of computers, processing the information and subsequently, translating the information into a set of action, like playing the video games. Vidal held the notion that in the long run, the interface of brain-machine would control the external mechanism, like the spaceships.

Though, there are lots of actions that can be taken in this regard, experts are of the opinion that there is every reason to reach some significant achievements in the forthcoming time. For instance, this mechanism involved in the Brain Computer Interface project can be employed in treating strokes and epilepsy as well as medical conditions, wherein the human brain starts speaking a language that scientist are yet to get familiar with.

Comprehending the wrong signs


If the interface of brain-machine can comprehend the language that the human brain is trying to speak as well as use such information for moving a cursor on the computer screen, while others can get to hear what the brain is actually trying to speak. This will enable people to comprehend if the human brain is projecting wrong signals.

Neuropace, an identical interface of brain-machine, features similar scope of actions. This mechanism, which is developed by the scientists from the Stanford University, utilizes electrodes that have been implanted under the human brain’s surface. It reads the pattern of the activity of the brain as it happens just before the onset of the epileptic seizures and subsequently, when the mechanism comprehends such patterns, it will stimulate the human brain with pleasant electrical pulses.

Though the Brain Computer Interface project tasted success, a few problems were noted in the method. Just like the 1st generation cardiac pacemakers, these brain stimulators always stay on. Even if the consequences are coming less dire, those pacemakers often trigger more arrhythmias than what it can actually treat.

Experts are reviewing this effort by the Stanford Scientists on very high notes and in their opinion, the efforts of these flocks will pave the ways for more intensive and extensive works in this regard, in the days to come. Should the Brain Computer Interface project taste success, healthcare providers will be able to offer better treatment to the patients, thus, bringing collective advancement in the standard of healthcare services, in the forthcoming days.

Thursday, 26 October 2017

Daydreaming is Good. It Means You’re Smart

Daydreaming is Good. It Means You’re Smart
Image Credit: Georgia Institute of Technology
If you are ‘daydreaming’ then you are ‘smart’

Finally, it’s true you aren’t an idiot. A new study has proven that daydreaming isn’t a bad thing at all rather it suggests that the person is incredible smart and creative. A number of people all around the world are caught daydreaming at their desk, during work, walking around the park, in a meeting, eating, travelling and almost any time. This habit is seen as a bad attention span or inattentiveness or laziness on the part of the person and sometimes it even comes with social stigma. However scientists from the Georgia Institute of Technology has stated that mere reason some people daydream is that their efficient brain has so much brain capacity that it can’t stop their mind from wandering off.

The people behind this awesome discovery


This discovery has been made by Eric Schumacher, associate psychology professor from Georgia Tech, and his team of students and colleagues. They had worked hard to measure the brain patterns of more than 100 people using the MRI machine. While lying down in the MRI machine participants were simply asked to focus their brain on a stationary fixation point for just five minutes. Next the team of researchers used the collected data from the participants in order to identify which of the brain parts worked together in this experiment.

The lead co-author of this research Christine Godwin had clarified that analyzing the correlated brain regions they were able to see which brain areas were utilized during the awake and resting state. During the research scientists found that these brain patterns also brought an astonishing insight into the view. These brain patterns also showed varying cognitive abilities in different participants which was a surprise for everyone.

 

Finding the new things about DayDreaming


At first researchers analyzed the data to understand how brains works in unison during ‘resting’ state. Then this data was used to compare the tests in which participants intellectual and creative ability was measured. Apart from the analysis of the collected data researchers also gave a questionnaire to the participants which mainly focused on how much their mind usually wandered in daily life. After carefully going through all the data researchers found that participants who reported frequent dray dreaming instances usually score higher on the intellectual and creative ability while those with fewer day dreaming instances happened to showcases lesser intellectual and creative ability.

Schumacher has stated that usually people saw the daydreaming habit as a really bad thing which isn’t the case anymore. This research shows that some of the people have highly efficient brain which makes it difficult of the person to pay attention even if they want to and thus their mind goes wandering around. A trick can help in finding whether your brain is highly efficient or not. If any person tend to zone in and out of the conversation or tasks but they have the ability get back to it without missing any important point or steps then such person has a efficient brain.

Friday, 20 October 2017

New Method for Tissue Regeneration, Inspired by Nature

Tissue Regeneration

Tissue Regeneration through Vesicles


Elderly people as well as many others have suffered bone damage, teeth problems and the like at some point in their lives. While in elderly people, the occurrence of such problems may be common place, there is still a percentage of middle age as well youth who go through bone related issues in their lives.

Repairing bones, teeth and cartilage today is not a cheap affair. Methods involving one’s own cells to regenerate tissue or methods involving tissue taken from other patients are all very expensive and have associated problems to the patient like patient morbidity.

Having bone related issues can affect a person’s quality of life detrimentally. Research shows that by the year 2020 bone fractures would have gone up to such an extent that the incoming patients would put a tremendous strain on healthcare facilities. It also shows that fractures caused by osteoporosis alone will cost the NHS a whopping 1.5 billion pounds to handle, not to mention the effect it would have on a person’s quality of life.

Given all of the above, it is time to look at other methods to regenerate tissue growth in an individual and scientists have done just that. Researchers have stimulated cells to make nano- sized particles called vesicles to regenerate tissue. This method of tissue regeneration can be used to repair teeth, cartilage and bone.

In the past researchers have used cell based methods to regenerate tissue but this process involved a lot of costs, regulatory issues and raised ethical objections. But with this new method of tissue regeneration using vesicles, all these issues are overcome. Tissue regeneration using this novel method uses the natural vesicles that are made during bone formation itself and does not take viable cells.

This new method of tissue regeneration using extracellular vesicles is combined with a phosphate. This type of tissue regeneration far out performs the current gold standards of tissue regeneration.
Although science cannot at this stage replicate cells in exactly the natural way it occurs in our bodies, this new approach at tissue regeneration allows researchers to move in the right direction and look to improve on methods to regenerate tissues in bones, teeth and cartilage.

This novel method uses our own body’s healing process to regenerate tissue. Right now current methods are lacking, in the sense that they cause patient morbidity and have other side effects that are all detrimental to a person’s health.

Thursday, 5 October 2017

New Target to Fight Motor Neurone Disease Using Gene Therapy

In the UK, six people die each day from Motor Neurone Disease, which results in paralysis that is progressive as the nerves supplying muscles deteriorate for reasons that are not fully known. At a given time, there are almost half a million people all over the world that have this condition but in most of the cases the reason why the nerves supplying muscles or the motor neurons die is not known. The most common known reason is a gene mutation known as C9ORF72.About 1 out of 10 Motor Neurone Disease cases is related to having an extended repeating region of DND in a portion of the C9ORF72 gene that is uncommonly converted into protein.

Scientists at SITraN have stumbled upon an important trail in the C9ORF72-linked Motor Neurone Disease by probing into the molecular principals of the behaviour pattern of this gene’s products in the cell. Testing patients’ cells and minute models of the Motor Neurone Disease indicatethat focusing on this plan is a unique way to tackle the nerve cells degeneration that takes place in Motor Neurone Disease.

Dr Guillaume Hautbergue from the University of Sheffield, who has spent over 25 years studying the molecular biology of RNA, also studied mechanisms that transfer messenger RNA to the cell cytoplasm from the nucleus through a model of how this functions in humans. Interpreting the findings in vital discovery science into actual profits for patients is the ultimate goal for SITraN and so using Dr Hautbergue’s findings in the RNA biology field has now led to the innovation of a new beneficial approach of neuroprotection in Motor Neurone Disease and possibly other diseases that are neurodegenerative.

While the primary function of DNA is to code for proteins that are to be built in the cell, we are aware that many DNA does not, after all, code for protein, like the region that is repetitive of the C9ORF72 gene. The repeated region is simply left out of the RNA replica of the gene before it is sent out of the nucleus, in its healthier version. Dr Hautbergue and his colleagues have developed their expertise in the field of RNA nuclear export mechanisms.

They have also put in a research in the area of the pathological recurring originator RNA molecules that is generally restrained in the nucleus itself. These may be getting exported out to the cell cytoplasm where the protein is produced, which is toxic in nature. Findings showed that only one component of the nuclear-cytoplasm transport system was the reason for the transportation of the RNA out of the nucleus and into the cytoplasm. This is a protein called SRSF1 and a significant discovery found in this research is that this protein in required only to assist the pathological C9ORF72 RNA to exit the nucleus.

Rest of all the other useful RNAs that code proteins can get to the cytoplasm without this. There were no undesirable effects in the fruitfly models and culture cells from the MND patients once the SRFS1 was partially removed from them using gene therapy and the only result was that the toxic dipeptide replicates were prevented from being formed. This is the first instance where the nuclear export of the RNAs that are pathologically repeated has been made clear in a neurologically degenerative disease and it is revealed for the first time that focusing on this method provides a reliable remedial approach of neuroprotection.

Surprisingly there are a number of other genes that cause diseases that are neurodegenerative such as Huntington’s disease, Myotonic Dystrophy, Fragile-X associated Tremor/Ataxia Syndrome and other disorders that have an effect on muscle dexterity. These include related recurring expansions like those found in the C9ORF72-MND gene.

So observing whether those expansions are transformed into proteins that are toxic and whether this can be avoided by deactivating a particular nuclear exporter also, this might give rise to a whole new avenue of possibilities for research in the field of neurodegenerative disorders treatment. An application with exclusive copyrights was filed for the use of SRSF1 adversary in the treatment of neurological disorders.
 
The Technology Explained
 
The approach of gene therapy used in the research utilised a virus that was engineered therapeutically, to get an RNA molecule inside the cell that would meddle with RNA for the manufacture of SFSR1. Interfering RNA thwarts the production of the targeted protein. Efficiently pulling down the quantity SFSR1 in the cell blocked the toxic C9ORF72 dipeptide repeat protein from being produced and salvaged the cell from neurodegeneration. Using viruses in the gene therapy is exceptionally successful as the virus remains inside the cell and incessantly creates the therapeutic interfering RNA for an extensive duration while the treatment of a genetic disease is going on.

At SITraN, Dr Hautbergue along with colleagues Prof MimounAzzouz and Prof Pamela Shaw are at present making efforts to collaborate with companies such as AveXis Inc. and Pfizer to further develop on a translational gene therapy program.

Sunday, 1 October 2017

Light-Dependent Regulation of Sleep and Wake States

Lights Out: The Neural Association between Sleep and Light

Humans are animals that are diurnal in nature, that is, we sleep during the night time and are awake and active during the day, as a result of light partly available or completely absent. It has been observed that light indirectly affects sleep by altering the length of our circadian rhythms a bit, quickly and directly due to an occurrence called as masking. But while a lot of information is available about how the circadian rhythms are affected by light, there is very little knowledge about the how light affects sleep directly: Why does one’s sleep gets disturbed if the lights are switched on in the middle of the night? Why does being in d dark enable us to sleep better?

Caltech researchers in Professor of Biology David Prober’s laboratory said that they have discovered the answer partly: a particular protein in the brain that is responsive to light and its absence sets and maintains the accurate balance between sleep and alertness. Prober also added that earlier, researchers had recognized the photoreceptors present in the eye to be essential for the direct outcome of light on sleep and wakefulness but how the brain uses this ocular data to induce and control sleep was unknown.

Zebrafish was used as a model organism for observing the sleeping pattern at the Prober laboratory. These organisms are visually transparent, which allows for non-invasive recording of their neurons through images. They also have diurnal sleep and wake patterns similar to like that of humans.

To study and observe in their experiment, how their sleep is responsive to the availability or absence of light, a former graduate in Prober's lab, Wendy Chen, directed the studies where they examined a specific protein present in the zebrafish brain called prokineticin 2 (Prok2).

Chen genetically engineered zebrafish to excessively produce Prok2, which resulted in the availability of the protein in a large quantity. She observed that in comparison to normal zebrafish, these animals were more liable to fall asleep during the day and stay awake at night.

Amazingly, the effects did not rely on the engineered fish's typical circadian sleep/wake cycle but to a certain extent depended only on whether the lights were switched on or off in their surroundings. These studies put forward that a surplus of Prok2 restrains both the natural awakening result of light and the sedating outcome of darkness.

Chen then produced zebrafish with metamorphosed structures of Prok2 and its receptor, and studied the sleep defects in these animals that were dependent on light. For instance, Chen found that a zebrafish with an altered Prok2 receptor were more alert and active in the presence of light and less active in the absence of it, which was quite the contrary of what she had noticed in the animals that over expressed Prok2 and had Prok2 receptors that were functional.

Prober stated his observations saying that although diurnal animals like zebrafish for example, spend their nights sleeping and are awake during the day, they also take small naps during the course of the day and sometimes wake up at night which is very similar to what humans do.

He also added that their experiment’s results put forward that levels of Prok2 play a very vital role in maintaining the accurate balance between wakefulness and sleep during both the course of the day and night.

In their next step, the researchers wanted to observe and study how Prok2 was adapting the effect of light on sleep. To find out the answer to this question, they decided to observe whether other proteins present in the brain that affect sleep, were needed for of Prok2 to have an effect on sleep behaviour.

They found that that the sleep-inducing effect of Prok2 over expression in light requires galanin, which is a protein that promotes sleep. They also observed that Prok2 over expression enhanced the level of galanin expression in the key sleep-promoting centre of the brain, the anterior hypothalamus. But in the animals that were engineered to be deficient in galanin, over expression of Prok2 did not enhance sleep.

These conclusions offer the foremost insights into how light interrelates with the brain to affect sleep and provide a foundation for scientists to start discovering the genes and neurons that trigger the occurrence. However, additional work is required to understand fully describe how light and dark directly impact sleeping and waking, and to establish whether Prok2 has a function akin to humans. If it does, these studies will ultimately result in new drugs that promote sleep and wake.

The title of this paper is based on regulation of sleep/wake states dependent on light with the help of prokineticin 2 in zebrafish. Postdoctoral scholars Chanpreet Singh and Grigorios Oikonomou are other Caltech co-authors.

Sabine Reichert and Jason Rihel of University College London also made contributions to this study. The National Institutes of Health; the Edward Mallinckrodt, Jr. Foundation; the Rita Allen Foundation; and the Brain & Behavior Research Foundation funded the work.