Tuesday, 1 November 2011

The magpie-sized Archaeopteryx had bird and dinosaur features and helped show that birds evolved from dinosaurs. However, recent research in the journal Nature questions its position in the dinosaur-bird family tree.

Scientists know birds evolved from dinosaurs because many fossils have been found of ancient animals with both bird and dinosaur features, including the famousArchaeopteryx that lived 147 million years ago.

Painting of how Archaeopteryxmay have looked 147 million years ago © John Sibbick / Natural History Museum

Archaeopteryx had a feathered tail and wings with a flight feather arrangement just like modern birds. But it also had a long bony tail, teeth, and 3 fingers ending in claws, like dinosaurs.

The first Archaeopteryx skeleton fossil was uncovered in 1861 in Solnhofen, Germany, and is looked after at the Natural History Museum. It provided the first evidence that helped demonstrate that modern birds descended from small meat-eating dinosaurs.

Along with researchers from all over the world, Museum scientists have studied the specimen ever since, and they have been able to reveal that it had hearing like an emu and a brain like a chicken.

Still a bird?

Close up of MuseumArchaeopteryx specimen showing the bird characteristic of a reversed perching toe.

No other fossils of bird-like creatures older thanArchaeopteryx were known at the time, or for most of the time since this early discovery. So it became established as the earliest known bird. But is this still so?

Since the discovery of Archaeopteryx, many more fossils with combined dinosaur and bird features have been uncovered, especially in the last 10 years (with only 9 other Archaeopteryxfinds over the last 150 years).

In June, scientists revealed a new species from China that they say shows Archaeopteryx was not a bird at all.

Xing Xu from the Institute of Vertebrate Paleontology and Paleoanthropology, in Beijing, and colleagues, identified the feathered and chicken-sized Xiaotingia zhengi. It was very similar to Archaeopteryx, sharing features such as long and robust forelimbs, which the team says puts them together in the dinosaur group rather than with birds.

Fossil tail of 147-million-year-old Archaeopteryx shows bird-like feather

Museum specimen showing the fossil tail of 147-million-year-oldArchaeopteryx that shows the bird-like feather and dinosaur-like long bony tail.

Dr Paul Barrett, Museum dinosaur expertsays, ‘The June research shows just how fine the line between birds and non-avian dinosaurs really is’.

Species that have a mixture of features, and are hard to place in one group or another, are known as transitional forms, sometimes incorrectly called a ‘missing link’. Their fossils provide a record of significant steps in the evolution of new features.

Although Archaeopteryx and X. zhengi had some bird-like features, the researchers say they had more features that put them in the group Deinonychosauria, which includesMicroraptor and Velociraptor, rather than in the bird group Avialae.

So, does the whole bird family tree need re-arranging?

Not according to Barrett. ‘Xiaotingia does not necessitate a major re-writing of early bird evolution, but shows that the evolution of many of the detailed anatomical features that changed during the origin of birds may have been slightly more complex than previously thought.’

Dr Angela Milner, Museum dinosaur expertcomments. ‘This recent research in no way diminishes the scientific and historical importance of Archaeopteryx.

‘Thomas Henry Huxley [pioneering biologist and educator] pointed out in 1868 that it was the first fossil to provide a snapshot of evolution in action between two major groups, dinosaurs and birds, and a clear demonstration that birds are the descendents of small meat-eating dinosaurs.

Another bird-like branch?

If Archaeopteryx is not a direct ancestor of birds, why does it have bird-like features and where does it sit in relation to the transition of dinosaurs to birds?

Archaeopteryx could be on another branch of the dinosaur family tree with bird-like feathers and skeletal features evolving in another closely related dinosaur group, suggests Barrett.

‘Maybe Archaeopteryx wasn't on the direct ancestral line to birds, but was part of an early experimentation in how to build a bird-like body.’

Overall bird origin picture

The overall picture of birds descending from meat-eating dinosaurs is firmly established. Now scientists need to rearrange the details of the early stages in the bird evolutionary tree.

Barrett adds, ‘As the authors of the June paper note, the evidence suggesting thatArchaeopteryx is not a bird is fairly equivocal and new analyses or new animals could very easily change this picture.

‘In reality what we now have are a set of animals incredibly close to bird origin – unsurprisingly these are very similar to each other, to birds and to other small meat-eating dinosaurs. As they are so similar, it becomes exceptionally difficult to disentangle their relationships accurately.’

Milner concludes, ‘The fact that Archaeopteryx may represent one of many early flying experiments rather than being the direct ancestor of modern birds is no surprise at all.

‘It is only now that Archaeopteryx can be assessed in the context of all the recent discoveries in China which provide so much more information.

Bacterium linked to bowel cancer

A barium X-ray can reveal the site of the tumour

A type of bacterium known to cause dental decay and skin ulcers may also be linked to bowel cancer, scientists suspect.

Two independent research teams have now found the bug Fusobacterium in colon tumours.

It's not yet clear if the pathogen might cause cancerous changes or whether it is an incidental finding, they toldGenome Research journal.

If it is to blame, antibiotics might be able to treat it and prevent cancer.

Bowel cancer is the third most common cancer in the UK after after breast and lung.

Although the exact cause of bowel cancer is unknown, there are certain factors that increase risk, such as a strong family history of the disease and older age.

It may be that Fusobacterium infection can be added to that list, according to the experts, but they say much more work is needed to establish this.

The infection has already been linked with a gut condition called ulcerative colitis which is itself a risk factor for bowel cancer.

Early warning signs and symptoms

A persistent change in normal bowel habit, such as going to the toilet more often and diarrhoea, especially if you are also bleeding from your back passage
Bleeding from the back passage without any reason, particularly over the age of 50
A lump in your tummy or a lump in your back passage felt by your doctor
Unexplained iron deficiency in men or in women after the menopause
Unexplained extreme tiredness

And other cancers are known to be linked with certain bacteria and viruses - for example, HPV and cervical cancer.

The first study, led by Dr Robert Holt from Simon Fraser University in Canada, identified Fusobacterium's hallmark in RNA present in bowel cancer tumours. RNA is genetic material similar to DNA which is involved in transmitting and translating the genetic code.

The other team, led by Dr Matthew Meyerson from the Dana-Farber Cancer Institute in Boston, US, found microbial sequences of DNA indicative of Fusobacterium.

Together, they looked at more than 100 samples of healthy and cancerous bowel tissue.

Sarah Williams, of Cancer Research UK, said the research gave a clue about the environment in which bowel cancer grows, but added: "It's early days and we look forward to the results of more specific, in-depth studies.

"In the meantime, people can reduce their risk of bowel cancer by not smoking, cutting down on alcohol, keeping a healthy weight, being active, reducing the amount of red and processed meat in their diet and eating plenty of fibre."

breakthrough in Alzheimer’s research holds out hope not only of early detection of the crippling brain disease but also potential new treatments

Friday October 28 2011

Deposits of amyloid beta are found in the brains of Alzheimer’s patients

“A major breakthrough in Alzheimer’s research holds out hope not only of early detection of the crippling brain disease but also potential new treatments,” reports the Daily Express.
The headline is based on research into a peptide (small protein) called amyloid beta that is linked to Alzheimer’s disease. This protein is found in plaques (deposits) in the brains of Alzheimer’s patients and, according to one theory, is responsible for the disease. The researchers created a type of genetically modified yeast and used it to identify genes that could alter the toxic effect of amyloid beta. They found that the genes they identified also changed the toxic effect of amyloid beta in worms and rat brain cells. A further experiment in the yeast showed that amyloid beta disrupted a process called endocytosis in yeast cells. In endocytosis, cells take up and transport substances around the cell. This process also occurs in human cells, and genes involved in this process have already been identified as risk factors for Alzheimer’s disease.
This sort of research is important in working towards treatments for Alzheimer’s disease. However, this is early research and although the researchers are confident that these findings apply to humans, we will still need to wait for research using human cells before this can be confirmed. New treatments and diagnostic tools based on these findings are a long way off.

Where did the story come from?

The study was carried out by researchers from the Whitehead Institute for Biomedical Research, and a number of other American and international universities and research centres. It was funded by an HHMI collaborative Innovation Award, an NRSA fellowship, the Cure Alzheimer’s Fund, the US National Institutes of Health (NIH), the Kempe Foundation and Alzheimerfonden.
The study was published in the peer-reviewed journal Science.
Contrary to the report in the Daily Express, new diagnostic tests for Alzheimer’s and new treatments based on this research are not on the horizon. Instead, this early research investigated the reason for the toxicity of the amyloid beta protein, and whether other genes can influence it. Any practical application is probably years away.

What kind of research was this?

This was a laboratory study that involved experiments in yeast, worms and cultured rat brain cells to try to identify other genes that are involved in amyloid beta toxicity. Amyloid beta is the peptide (small protein) implicated in Alzheimer’s disease as it is found in plaques (deposits) in the brains of Alzheimer’s patients. The researchers aimed to understand further what happens during Alzheimer’s disease, and why the amyloid beta peptide is toxic.
A laboratory-based study is the only way that this type of question can be answered. In this study, the findings in yeast were validated in worms and mammalian cells. Many of the genes identified are present in humans, and mutations in the genes encoding these proteins have been linked to susceptibility to Alzheimer’s disease. The process that amyloid beta was shown to affect (endocytosis) is common to human cells. However, further research will have to be performed to confirm whether the findings hold true in humans.

What did the research involve?

The researchers decided first to test amyloid beta toxicity in modified yeast cells. To do this, they introduced into the yeast cells DNA that encoded amyloid beta. They then forced the cells to overexpress amyloid beta. They added a special targeting sequence to the end of amyloid beta so that it would move through the yeast cell in a similar way to that in which it moves through human cells. The researchers also constructed other control strains that overexpressed other proteins with similar properties. They then looked at the amyloid beta peptide that was produced, to confirm whether it behaved in a similar manner to amyloid beta in mammals.
A genetic screen was then performed using this yeast model. In this screen, strains which overexpressed every gene which codes for a protein were created. The researchers tried to identify two gene types. One, when overexpressed, could reverse the reduction in growth of yeast caused by expression of amyloid beta, so growth was increased (termed suppressors). The second could add to it, so growth of the yeast was further reduced (termed enhancers). The researchers then investigated whether equivalent genes are also present in human DNA, and whether they have been implicated in Alzheimer’s disease susceptibility.
The researchers then determined whether the modifiers of amyloid beta toxicity they identified had an effect on the viability of neurons (brain cells). To do this experiment, they used a type of worm called C. elegans, which they genetically modified so it expressed the amyloid beta peptide only in glutamatergic neurons, a particular type of neuron that is especially vulnerable in Alzheimer’s disease. The researchers chose C. elegans because it has been extensively studied, and the location and number of glutamatergic neurons is known.
The effect of one of the suppressors, PICALM, on the toxicity of amyloid beta aggregates was investigated in more detail in cultured rat neurons.
The researchers then returned to the yeast cells to investigate how PICALM may reduce the toxicity of amyloid beta.

What were the basic results?

The researchers found that overexpression of amyloid beta decreased cell growth. The overexpression of other similar proteins was less toxic, demonstrating that the amyloid beta peptide itself was responsible for the toxicity. The amyloid beta peptide that was produced was of the correct size and was localised correctly in the cell. It could also aggregate, or stick together. These amyloid beta aggregates form the amyloid plaques seen in Alzheimer’s disease.
Twenty-three suppressors, which reversed the reduced growth seen when amyloid beta was overexpressed, and 17 enhancers, which reduced growth further, were identified. Twelve of the modifiers of the effect of amyloid beta had clear human equivalents (homologues), and the researchers concentrated on these. Many of the modifiers are associated with Alzheimer’s disease susceptibility, for example the human homologue of yeast YAP1802 is PICALM, which research indicates is a risk factor for sporadic Alzheimer’s disease.
Expression of amyloid beta caused the age-dependent loss of glutamatergic neurons in C. elegans. The researchers tested the effect of overexpressing the modifiers they identified in yeast. Overexpression of C. elegans homologues of every gene they tested had a similar effect: either decreasing or increasing the loss of neurons. PICALM was found to suppress the toxicity of amyloid beta aggregates on cultured rat neurons.
Using the yeast system they created, they found that amyloid beta affects a process termed endocytosis. Endocytosis is a process by which the cell brings substances into the cell. Amyloid beta also affects how these substances are then moved around once in the cell (termed trafficking). Yeast YAP1802 and its human homologue PICALM has already been shown to be involved in endocytosis and trafficking, and overexpression of YAP1802 compensates for the effects amyloid beta has on these processes.

How did the researchers interpret the results?

The researchers conclude that throughout the diverse organisms examined in this study, “endocytosis is a critical point of vulnerability to [amyloid beta]”. They also say that the yeast model that they have created “provides a tool for identifying genetic leads, investigating their mechanisms of action, and screening for genetic and small molecule modifiers” of Alzheimer’s disease.

Conclusion

In this study, the researchers used yeast, worms and cultured rat brain cells to model the effect of amyloid beta, the peptide (small protein) implicated in Alzheimer’s disease. The researchers aimed to understand further what happens during Alzheimer’s disease, and why the amyloid beta peptide is toxic.
They created a yeast model of amyloid beta toxicity. Using this model, they identified genes that altered the effect of the amyloid beta peptide. Many of these genes had clear human equivalents, which have already been linked to Alzheimer’s disease susceptibility. The researchers then confirmed their findings by investigating the effect of amyloid beta and the modifier genes on worm neurons. They further investigated PICALM, a highly probable human Alzheimer’s disease risk factor, which had been identified during the study. They found that overexpression increased survival of rat neurons treated with amyloid beta aggregates.
Returning to the yeast model, the researchers investigated why the amyloid beta peptide was toxic, and how some of the modifiers could be changing the toxicity of amyloid beta. As several genes are involved in the update of substances from outside the cell and the movement of these substances inside the cell (processes called endocytosis and trafficking), they examined whether amyloid beta was affecting these processes, and found that it was.
This research has demonstrated that a variety of model systems can be used to explore the causes of Alzheimer’s disease. It has also provided reasons why certain genes might be genetic risk factors. Further research could help understand the process behind Alzheimer’s disease.
This sort of research is important and vital to working towards treatments for Alzheimer’s disease. However, this is early research and although the researchers are confident that these findings apply to humans, we will still need to wait for research using human cells. New treatments and diagnostic tools based on these findings are a long way off.

Links to the headlines

Genes research breakthrough on Alzheimer's. Daily Express, October 28 2011

“Sunbeds may be even more dangerous than previously feared

Friday, 14 October 2011

“Sunbeds may be even more dangerous than previously feared

“Sunbeds may be even more dangerous than previously feared,” the Daily Mail has today reported. The newspaper said UVA rays, the main type of ultraviolet light emitted by tanning devices, has been found to cause the type of DNA damage that can lead to cancer.

The news is based on laboratory research that compared the DNA damage caused by UVA rays to that from UVB rays, which are already known to cause skin cancer. While UVB has long been linked to burning and skin cancer, UVA has previously been considered to be relatively harmless. However, this research builds on other studies that have suggested that UVA is not harmless and, like UVB, can lead to changes in the cell that increase the risk of skin cancer.
By exposing different areas of volunteers’ skin to UVA and UVB and examining skin tissue samples, the experimental study found that both could cause similar types of DNA damage, but that UVA tended to affect cells deeper in the skin. However, UVB affected cells at the surface of the skin more.
This research emphasises the need to use an appropriate-strength sunscreen that protects against both UVA and UVB. These sunscreens may be labelled as offering “broad spectrum” protection, and rated according to a five-star system in the UK. Cancer Research UK recommends that people use sunscreen of at least SPF 15 and with at least four stars to get good balanced protection across the UV spectrum.

Where did the story come from?

The study was carried out by researchers from King’s College London. It was funded by The National Institute for Health Research, the UK Medical Research Council, British Skin Foundation and the British Association for Dermatology.
It was published in the peer-reviewed, Journal of Investigative Dermatology.
The Daily Telegraph and the Daily Mail both appropriately advised that people should consider UVA protection as well as UVB when choosing a sunscreen.

What kind of research was this?

This laboratory-based research looked at how UVA rays affected skin cells. Light from the sun contains two types of ultraviolet (UV) rays, UVA and UVB. UVB has a shorter wavelength and has generally been thought of as the major carcinogen in sunlight. However, the researchers say that the action of UVA needs further consideration as there are more UVA than UVB rays in sunlight. UVA is also the predominant wavelength generated by sunbeds, and has now been classified as a carcinogen.
UVB is known to causes chemical changes to our DNA. In some cases the body’s natural DNA repair mechanisms can repair the damaged DNA, but in skin cancers these chemical changes have not been fixed and lead to harmful mutations in the DNA sequence. In skin cancers caused by UVB, there is a characteristic pattern of DNA damage that the researchers term a “UVB signature”.
UVA is also known to cause mutations, but this was previously thought to be by an indirect mechanism (i.e. causing chemical changes to other molecules in the cell that may have a knock-on effect on the DNA). However, recent experiments on cells in a lab have shown that UVA may also cause a “UVB signature” in the DNA sequence.
As recent evidence suggests that UVA may cause mutations in a similar way to UVB, this has raised doubts over the belief that UVA may be “safer” than UVB. Given this uncertainty, the researchers devised a series of experiments to see what effect comparable doses of UVA and UVB had on skin cells.

What did the research involve?

The researchers recruited 12 volunteers with healthy skin. The participants had fair, white skin that either always burns and never tans, or usually burns and tans with difficulty.
The participants were exposed to each wavelength of UV on 1 cm2 areas of previously-exposed skin on their buttocks.
Twenty-four hours later, the researchers used three participants to find the minimum doses of UVA and UVB needed to produce just-detectable redness of the skin. The participants were then given doses of UVA and UVB, which were multiples of this minimum dose (half the minimum dose, 1.5 times and 3 times). The degree of skin redness was assessed using a red skin scale.
The researchers took punch biopsies, which involved using a small tube-like device to extract a 4mm plug of skin from the exposed site. They used the biopsies to look at chemical changes to the DNA. To see how well the body could repair and reverse the DNA damage, they performed another set of biopsies on the exposure sites 3, 6, 24 and 48 hours after the UV exposure and examined the changes seen.

What were the basic results?

The researchers found that the skin became redder with increasing doses of either UVA or UVB. However, when they applied increasing multiples of the minimum dose required to cause redness, UVB caused more redness than UVA.
When the researchers looked for DNA chemical changes in skin cells immediately after exposure, they found that UVB led to more of these changes in the top layer of skin, whereas UVA led to more changes in the deeper layers of skin. They also found that as doses increased beyond the minimum dose, UVB caused more detectable chemical changes to the DNA than UVA. Although both UVA and UVB produced one particular type of DNA change, UVB caused additional chemical changes that were not found in UVA-treated cells.
The researchers then attempted to see how well the cells could repair the DNA damage caused by UV exposure. They found that the rate at which the body could repair the DNA damage was similar for damage caused by UVA and UVB. They said that by 48 hours the majority of DNA changes caused by UVA had disappeared but that there was still some DNA damage with UVB. The researchers said that this was because a higher proportion of DNA had been damaged with the UVB dose.

How did the researchers interpret the results?

The researchers say that they had demonstrated for the first time that UVA can cause DNA changes similar to some of those caused by UVB, although UVB also causes additional chemical changes not seen with UVA exposure. They said that deeper layers of skin are particularly vulnerable to UVA-induced damage and that this has implications for public health policies, particularly the need for developing measures that protect against UV light at a broader range of wavelengths.

Conclusion

This research has shown that UVA can produce some similar damage to the DNA when the skin becomes red as UVB. The research also showed that these changes may increase the risk of developing skin cancer if not repaired by the body. Previously, it was thought that UVB caused burning and was the major carcinogenic component of sunlight, while UVA was considered to be relatively harmless apart from ageing the skin.
In recent times studies, including this one, have suggested that UVA may directly cause the type of DNA damage that can lead to skin cancer. This study emphasises the importance of choosing a sunscreen that protects against both UVA and UVB (often labelled as offering ‘broad spectrum’ protection).
The charity Cancer Research UK has highlighted that there is no international measurement of UVA production, although in the UK there is a five-star system to measure UVA protection (the higher number of stars indicates a more balanced protection against UVA). Sunscreens will also contain a (sun protection factor) SPF rating. Cancer Research UK recommends that people use a sunscreen of SPF 15 or higher, with at least four stars to provide good protection against UVA and UVB. The charity also says consumers should not use sunscreen that has been open for over 12 to 18 months, but should instead buy fresh sunscreen offering appropriate protection.
Newspapers covering this research have also correctly highlighted that sunbeds may have a particularly high UVA output. The Daily Mail includes a quote that the strength of these rays can be 10 to 15 times higher than the midday sun. People using sunbeds and tanning booths should be aware that there is currently no regulation to govern the type or strength of UV rays that sunbeds give out. Even brief use may carry some risk, particularly for people who have fair features, freckles, lots of moles or damaged areas of skin. Read Are sunbeds safe? for more information.

Links To The Headlines

Tanning salons more dangerous than previously thought. The Daily Telegraph, October 7 2011
New sunbed alert: UV rays penetrate far deep into the skin than previously thought. Daily Mail, October 7 2011

Links To Science

Tewari A, Sarkany RP and Young AR. UVA1 Induces Cyclobutane Pyrimidine Dimers but Not 6-4 Photoproducts in Human Skin In Vivo. Journal of Investigative Dermatology, October 6 2011

'Fatty apron' fuels ovary cancer

Ovarian cancer

A "fatty apron" in the abdomen helps fuel the spread of ovarian cancer, research suggests.

In 80% of cases, it has spread to this apron, called the omentum, by the time it is diagnosed.

The Nature Medicine research found once ovarian cancer cells reach the omentum, they take it over.

UK experts said the study was important in aiding understanding of ovarian cancer, the fifth most common cancer in women in the UK.

The omentum lies in the upper abdomen near the stomach. It helps support the organs nearby, but it is not essential.

Often, cancer growth in the omentum exceeds the growth of the original ovarian tumour.

The University of Chicago team injected ovarian cancer cells into the abdomen of healthy mice. They reached the omentum within 20 minutes.

They found that protein signals emitted by the omentum attracted the tumour cells. Disturbing these signals reduced this attraction by at least 50%.

Once ovarian cancer cells reach the omentum, they were found to change so they could feed off the fat cells.

Feeding cancer spread

The researchers suggest that a protein known as fatty acid binding protein (FABP4), a fat carrier, could be key to the process and could be a target for treatment.

Tumour cells next to fat cells in the omentum were found to produce high levels of FABP4, while cancer cells far away from fat cells did not.

“Start Quote

The cells that make up the omentum contain the biological equivalent of jet fuel. ”

Prof Ernst Lengyel,Lead author

When the action of FABP4 was blocked, the transfer of nutrients from fat cells to cancer cells was drastically reduced. It also reduced tumour growth and the ability of tumours to generate new blood vessels.

Lead author Ernst Lengyel, professor of obstetrics and gynaecology at the University of Chicago, said: "The cells that make up the omentum contain the biological equivalent of jet fuel.

"They feed the cancer cells, enabling them to multiply rapidly. Gaining a better understanding of this process could help us learn how to disrupt it."

The researchers suggest fat metabolism may also contribute to other cancers, such as breast, gastric and colon.

Dr Kat Arney, of Cancer Research UK, said: "These are important results because they suggest that fat cells in the stomach can fuel the spread of ovarian cancer, and point towards potential targets for the development of new treatments for the disease.

"But at the moment these are still early experiments using mice and cells grown in the lab, so there's still a lot of work to be done to turn this knowledge into a treatment that could help women with ovarian cancer."

Monday, 31 October 2011

'Shame on us nurses'

By Prof Ian Peate Consultant editor, British Journal of Nursing

Following the Care Quality Commission's recent report on what it called "alarmingly" poor care for elderly hospital patients, leading nurse Prof Ian Peate says in this week's Scrubbing Up that the profession should look again at how it trains people to look after older people.

Once again we read about the disgraceful care of our elderly and frail population and once again I cringe with embarrassment as I read how we abuse the people who we have the privilege to care for.
Yes I know there are some excellent examples of high quality outstanding care provided to people. But there is something seriously wrong here.
Nursing is well on its way to setting minimum standards for a degree level nursing programme and justifiably so, given the complexities of care and the demands the public rightly make in insisting on high quality, safe and effective care.
The Nursing and Midwifery Council (NMC) regulates nurses and midwives in the UK.
It sets standards for education, attempting to ensure that nurses possess the right skills and qualities when they start work as a qualified nurse.
What the NMC does not do is stipulate any mandatory requirements for elderly care. They leave this up to the individual educational institutions, so each will approach the teaching of elderly care in a variety of ways.
The time has come for the NMC to compel those running courses to stipulate how much time should be dedicated to the care of the elderly, in practice and theory.
There is a need to ensure that students of nursing - our future staff nurses who will be looking after me when I am older - are able to care confidently and competently for older people - geriatrics.
'High touch' - not high-tech
The art and science of gerontology has all but gone and this is a pity.
As a nursing student I was privileged to take a course that instilled in me the skills required to care for geriatrics patients, responding to their unique needs as people who have a number of concurrent illnesses and take a variety of medications.
If nurses get the care of older people right by applying the theory to practice, paying attention to feeding them and providing them with fluids, washing and cleaning them when they are unable to wash themselves, communicating with them and encouraging them through caring, kindness and compassion then caring for other patients will come naturally.

“Start Quote

We need to say sorry to our patients and to tell them what we are going to do to get it right”

End Quote Prof Ian Peate

These are high level skills that require the nurse to apply scientific principles to the art of caring.

As a student I was assessed, on the job - by an experienced nurse - in caring for geriatric patients. But that specific check is no longer required.
We should not be ashamed, embarrassed or made to feel politically incorrect when using the term geriatric.
It is a speciality, with care provided by skilled practitioners, on the geriatric ward as opposed to a busy acute medical ward where high-tech is favoured and preferred over "high-touch".
We have witnessed our medical colleagues embrace so-called "soft skills" (communication skills, a good bedside manner) through their improved undergraduate education.
NMC take heed.
Demand the curriculum you validate has explicit elements of geriatric care in them, in the classroom and on the ward; direct that no student will progress if they do not pass the an elderly care part of their course; continue to reinforce the need for all staff to speak out when they witness substandard or abusive care but also insist that those who speak out are supported.
Shame on us nurses.
We need to say sorry to our patients and to tell them what we are going to do to get it right, and we need to be brought to account each time we fail to provide care that is compassionate, kind and humane.

mengele plus

Tuesday, 1 November 2011

Archaeopteryx and the dinosaur-bird family tree 14 September 2011

Archaeopteryx and the dinosaur-bird family tree