New sculpture to commemorate Tasmania’s convict women

A major new artwork has been commissioned to honour convict women at the Hobart Female Factory.

Shirley McCarron from the Female Factory Historic Site says $160,000 is needed for the sculpture, which is the first of three pieces planned for the former prison.

Ms McCarron says the artwork will stand in the grounds of the Female Factory, in South Hobart, representing the spirit of convict women.

“[It will be a] larger-than-life-sized bronze scultpture of a convict woman with a child clinging to her skirts, and she’s standing at a glass door that represents her leaving her normal life and going into the life of a convict.”

The second artwork will depict women arriving on Hobart’s waterfront, and the third will comprise a series of plaques featuring convict women’s names, to be placed throughout the city.

Ms McCarron says there is growing acceptance of convict heritage.

“There’s been very little written about the women and not a great deal of interest, and indeed many families didn’t want to acknowledge that they had a woman convict.

“That’s changed dramatically, and people are very interested and wanting to research their history,” she said.

The Female Factory Historic Site Foundation anticipates the first sculpture will be installed late next year.

Network problem harms brain in Alzheimer’s disease!

Mon, Mar 29 12:02 PM

In what could pave the way for new strategies for early diagnosis and effective treatment of Alzheimer’s, scientists have found that the disease makes parts of the brain shrink “as messages fail to get through”.

The findings, published in the ‘Neurology’ journal, suggest a build-up of deposits of the protein amyloid-beta in a region of the brain known as temporal inferior cortex which is connected to the hippocampus involved in memory.

Alzheimer’s disease is characterised by two factors –a build-up of amyloid-beta plaques in the brain, and a loss of neurons.

Lead scientist Dr Cassandra Szoeke of CSIRO said the puzzle for them was that the parts of the brain that had shrunk (atrophied) due to neuron loss were not the same as those showing increased deposits of amyloid-beta.

Using MRI scans to study Alzheimer’s disease affected brain tissue, the scientists found that shrinking (atrophy) of the hippocampus was associated with plaque deposits in the temporal inferior cortex.

The results indicate that the increased accumulation of amyloid in temporal inferior cortex disrupts connections with the hippocampus, causing the neurons to die, say the scientists.

“By helping to better understand the mechanisms involved in the progression of the disease, the study may guide the development of new strategies for early diagnosis,” Dr Szoeke said.
Agencies

‘Thick’ blood causes as well as protects from heart attack, stroke

Washington, Aug 25 (ANI): Animal studies carried out by researchers at Heidelberg University Hospital have shown that “thick” blood can not only cause heart attack and stroke, but also prevent them.

In their study report, the scientists say that mice with a greater tendency to form blood clots have larger plaques in their vessels, but they are more stable.

Thus, there is less risk that these plaques will rupture and obstruct circulation.

Usually, the more blood coagulates, the greater is the risk of vascular obstruction, and anticoagulants are used to protect against these complications.

However, clinical studies have thus far not proven that an increased clotting tendency also has a detrimental effect for plaque development.

Led by Dr. Berend Isermann, the researchers examined mice with elevated blood fat levels, and a genetic defect that leads to an increase in blood clotting.

They found that the mice developed larger plaques than those without the genetic defect, but the plaques were more stable.

In addition, no vascular obstruction was observed, as the vascular wall expanded to adapt to the new situation.

The negative effect of larger plaques on circulation was compensated by the positive effect of stability and a greater vessel diameter.

However,the long-term use of anticoagulants (in this case, low molecular weight heparin) reversed these advantages- the size of the plaques was reduced, but stability was lost, increasing the risk of complications.

“Our findings were made on mice, but they confirm the results of clinical studies on humans. In addition, in vitro studies show that human cells react similarly to mouse cells,” said Isermann.

The team assumed that the results could be transferred to humans and recommends weighing the advantages and disadvantages of anticoagulants carefully before administering them to a patient.

“Currently, there is no indication that these new observations also apply to drugs that inhibit the function of platelets,” said Isermann.

When deciding on therapy, the cause of the coagulation disorder and the degree of already existing atherosclerosis should be taken into consideration.

Additionally, the researchers recommended using anticoagulants that inhibit specific coagulation factors in order to preserve the positive effects on plaque stability.

Various new drugs that inhibit specific coagulation factors are currently being studied in clinical trials.

“It is important that plaque stability and the influence on atherogenesis are also studied in these trials,” said Isermann.

The study has been published in the journal Circulation. (ANI)

Becks, Zidane have their feet cast in concrete in L.A.

Los Angeles (US), July 13 (ANI): England football star David Beckham has got his feet cast in concrete.

Becks, 34, and former French football captain Zinedine Zidane had their respective feet shaped on plaques to kick off a local soccer scheme in Los Angeles.

The Footprint Fields Community Programme aims to build football pitches in urban locations and needy places across America.

Afterwards, the two superstars had a kickabout with kids before LA Galaxy ace Becks led a group of local youngsters in a training session. (ANI)

Superior language skills in 20s may protect against Alzheimer’s

Washington, July 9 (ANI): People with greater language abilities in early adulthood may be less likely to develop Alzheimer’s disease later in life, according to a new research.

A team from Johns Hopkins University studied the brains of 38 Catholic nuns after death and found that those with good language skills early in life were less likely to have memory problems – even if their brains showed signs of dementia damage.

“A puzzling feature of Alzheimer’s disease is how it affects people differently,” said study author Juan C. Troncoso, MD, with Johns Hopkins University in Baltimore.

“One person who has severe plaques and tangles, the telling signs of Alzheimer’s disease in their brains, may show no symptoms affecting their memory. Another person with those same types of plaques and tangles in the same areas of the brain might end up with a full-blown case of Alzheimer’s disease. We looked at how language ability might affect the onset of symptoms,” Troncoso added.

In the study, scientists determined two groups: women with memory problems and Alzheimer’s disease hallmarks in the brain and women with normal memory with or without signs of Alzheimer’s disease in the brain.

The researchers analyzed essays that 14 participants wrote as they entered the convent in their late teens or early 20′s.

They studied the average number of ideas expressed for every 10 words. The analysis also measured how complex the grammar was in each essay.

The study found that language scores were 20 percent higher in the women without memory problems compared to those with memory problems. The grammar score, however, did not show any difference between the two groups.

“Despite the small number of participants in this portion of the study, the finding is a fascinating one.

Our results show that an intellectual ability test in the early 20s may predict the likelihood of remaining cognitively normal five or six decades later, even in the presence of a large amount of Alzheimer’s disease pathology,” Troncoso said.

The study has been published in the July 9, 2009, online issue of Neurology. (ANI)

Pet lovers happy with dignified burials of their loved ones

Bangalore, May 15 ANI): Pet lovers are happy as their loved ones get a dignified burial at a cemetery in Bangalore.

A non-governmental organization – People for Animals (PFA) – has made a graveyard for pets giving a sigh of relief to all those pet lovers who cannot bear the pain of dumping their loved ones into garbage.

Several people flock the cemetery everyday to either give a dignified burial to their pets or remember the ones who left them years ago. They also planted trees on the cemetery.

Each tombstone explains a different emotion and abundant love. While some of the graves in the cemetery are simple plaques, others are marble epitaphs where the owners have poured their hearts out.

Some pet lovers claim that they feel comfortable in the cemetery as they can remain close to their loved ones.

“Till they are alive we love them a lot but at the end we usually cant give them a place like this. But now we found a place and it’s really nice. I think every person who has a pet should come here,” said Sahana, a pet lover.

S.V Prasad, manager of People for Animals said that many pet lovers appreciate the place.

“This has been well appreciated in the city by many pet owners. And we continue to improve upon this service so that a large number of people do come and have the facility,” said Prasad.

‘People For Animals’ organization also offers service to bring the dead pet to the burial ground and after doing all the ceremonies they are buried scientifically. By Jaipal Sharma (ANI)

Why certain arterial plaques result in deadly heart attack, stroke

Washington, May 6 (ANI): Scientists at Columbia University Medical Center say that they have gained significant insights into why certain arterial plaques in any given individual eventually lead to an acute blood clot, a heart attack, a stroke, or even sudden death.

The researchers also claim to have identified a key protein that may promote the conversion from benign to dangerous plaques.

While a vast majority of atherosclerotic lesions are relatively harmless, some two percent of all plaques turn out to be problematic.

What separates the average blood vessel plaque from those that are at high risk for triggering the development of dangerous – even fatal – blood clots, is the “billion dollar question,” says lead researcher Dr. Ira Tabas.

Dr. Tabas believes that the real danger from the fatty deposits lies not with their size, but with what lies underneath the surface of the deposit. The researcher says that rumblings in the core of a deposit, which contains dead cells, can break open the plaques.

Once the plaque ruptures, a blood clot in the lumen of the artery can form.

“It is this sudden clotting that restricts blood flow and can cause a heart attack, stroke, or sudden cardiac death,” Dr. Tabas says.

“Just about everybody in our society has atherosclerosis by the time we reach 20. So the wave of the future in treating atherosclerosis will be in preventing harmless lesions in young people from becoming dangerous ones, or soothing dangerous plaques so they don’t rupture as we age,” Dr. Tabas adds.

During the study, the research team found that when a specific gene was deleted in two separate strains of atherosclerosis-prone mice, the dangerous plaques were much smaller.

Dr. Tabas has revealed that the gene encodes a protein that is part of a cell stress reaction that can lead to cell death.

The researcher says that the findings of this study raise the possibility that drugs designed to quiet this form of cellular stress might be useful in treating heart disease.

Dr. Tabas, however, concedes that it may take years before such a therapy is available.

The study has been published in the journal Cell Metabolism. (ANI)

Computational model to examine Alzheimer’s pathways in young adults created

Washington, Apr 19 (ANI): Scientists at University of Virginia have developed a computational model to examine the role of certain proteins in the development of Familial Alzheimer’s disease (FAD), which affects people as young as 30.

Biomedical engineers Lydia S. Glaw and Thomas C. Skalak, Ph.D., of the Department of Biomedical Engineering, University of Virginia, Charlottesville, constructed the model to measure plaques and tangles and their influence in causing FAD.

The model tested the hypothesis that certain variables-genetic mutations in proteins and “tau” tangles-might be predicative of the development of the disease.

The model is a first-of-its-kind approach to modelling, understanding and predicting Alzheimer’s pathways.

One of the biggest hypotheses tested by the model was the idea that GSK3 is a link between amyloid beta buildup and tau tangle development.

The researchers studied the proteins presenilin-1 (PS1) (a mutated gene found in familial AD) and glycogen synthase kinase (GSK-3) and amyloid beta (AĆ”) plaque, to quantitatively examine their roles in the development of Alzheimer’s pathology.

The elements were applied to the model, which was constructed of kinetic equations developed from literature searches, and analysed the interactions of the proteins and complexes under various scenarios.

The researchers found that GSK3 had a large effect on tangle formation, but very little on the plaques.

Also, activating GSK3 was not found to be sufficient to cause changes in the brain to the extent seen in Alzheimer’s patients.

However, overproduction of GSK3 as opposed to activation could lead to those changes.

Besides there was no link found between amyloid beta plaque and tau tangles.

They concluded that no single change to the system could cause Alzheimer’s disease; instead it was caused by multiple changes, such as a PS1 mutation combined with GSK3 over-activation.

They suggested that a multi-pronged approach to treating the disease may be best.

The findings will be presented at the 122nd Annual Meeting of the American Physiological Society. (ANI)

Why Alzheimer’s patients tend to develop epilepsy

London, Mar 19 (ANI): An international team of scientists have found out why Alzheimer’s disease sufferers go on to develop epilepsy.

Led by scientists at Aberdeen University in Scotland, the research team have discovered that a protein in the brain accumulates in clumps in the brains of people suffering from dementia.

The clumps of proteins make the nerve cells too sensitive, which in turn lose their ability to communicate coherently with other nerve cells.

The researchers say that this makes Alzheimer’s patients more susceptible to seizures, reports the Scotsman.

While official figures show that nearly one third of Alzheimer’s patients suffer from some degree of epilepsy, this is for the time that a link has been established between the two conditions.

Professor Tibor Harkany, the Aberdeen neurobiologist who led the research, said that the findings could lead to changes in the drugs used to treat Alzheimer’s disease.

He said that the research team had discovered that the “beta-amyloid protein”, a key component of the plaques that clog the brain of an Alzheimer’s patient, was causing cells to short-circuit and fire too many electrical signals. (ANI)

Mechanism that protects against development of Alzheimer’s identified

Washington, Feb 28 (ANI): Researchers from Johannes Gutenberg University Mainz have identified the mechanism that protects against the development of Alzheimer’s disease.

They found that the activity of the enzyme a-secretase is mainly responsible for the protective effect.

“In the past, we postulated that the enzyme a-secretase was involved in preventing the formation of cerebral plaques characteristic of Alzheimer’s disease and also enhanced cerebral functions, such as learning and memory,” said Professor Falk Fahrenholz of the Institute of Biochemistry.

“The a-secretase enzyme is a highly complex one, with many other functions. For example, it also relays signals from the intercellular space into cells and interacts with molecules on other cells,” he added.

In the study involving transgenic mice, the researchers found that is the enzymatic activity alone that guarantees the protective effects.

If this activity is neutralised, the laboratory mice exhibit the symptoms that are characteristic of Alzheimer’s disease: impaired learning ability, poor memory capacity and the build-up of plaques.

It is thus possible that the enzymatic activity of a-secretase could represent the starting point for the development of future treatments.

The researchers suggest that it is not the plaque build-up itself that is responsible for the loss of memory capacity.

Prof. Fahrenholz said, “It is important to consider other aspects in addition to the plaques themselves, particularly their precursors, which are a real cause of the disease.”

The study appears in the Journal of Alzheimer’s Disease (JAD). (ANI)