Sunday Observer Online


Sunday, 6 February 2011





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Government Gazette

Fever fits

Common condition in young children:

Parents should be cautious and mindful when their children have fever fits because not all are related to epilepsy. More often than not, we tend to worry about it confusing it with epileptic fits but for any problem, a medical consultation is vital to determine what exactly is the cause. President of the College of Paediatricians, Dr. Deepthi Samarage spoke to the Sunday Observer about a particular type of fainting attack called fever fits.

Q: What are febrile convulsions (fever fits) ?

A: Febrile convulsions (also called fever fits, fits with fever or febrile seizures) is a common condition in children, in the age group of six months to about six years. They occur in 3-4% of all children.

The child loses consciousness briefly and may develop jerky movements coupled with a bout of fever.

This is not a prolonged fever because it is nothing to worry about but parents should ensure that the child is safe and not in harm’s way.

Q: Do fever fits need prompt treatment if there are repeated fits?

A: No. Since it is an age-related condition, it will pass when the child becomes older, after six years.

Long-term medications have their own side effects because it can be harmful later on in the individual’s life. As febrile convulsions are self-limiting, ensure that the child is in a safe environment when such a fit occurs.

Q: In what way can parents or the guardians help the child when a fit occurs?

A: Unwanted manoeuvres during the time of the fit can endanger the child’s health and will have dramatic consequences. This can lead to choking and difficulty in breathing so parents/guardians should be educated on what to do. The important thing is not to panic and bring the child to a position lying down (horizontal) in a foetal position.

No external substances should be administered by mouth during the time of the fit as it can have a dangerous impact. If the fit doesn’t subside after about five minutes, the child should be taken to the doctor immediately.

Q: Is there a particular drug which the parents/guardian can administer at home?

A: Yes, if the fit doesn’t resolve spontaneously within five minutes, the parent/guardian can administer a medicine called diazepam which is given through a vial through the rectum.

The child should be kept under observation and consult the doctor on a frequent basis.

Q: Do febrile convulsions develop into epilepsy later in life?

A: This is very rare but if febrile convulsions prolong for more than 20 minutes then the chances of developing epilepsy can be more.

Even though febrile seizures are quite benign, every episode should be fully evaluated by a doctor. A child may have had three febrile seizures from which they recovered quickly and easily, but the fourth episode of convulsions and fever may be a serious illness, not febrile seizures. So it really depends from each child as it can trigger different reactions in children.

Q: Do children with febrile convulsions need EEG (Electroencephalography) and CT (computed axial tomography) scans?

A: Not at all. If the diagnosis of febrile convulsions are very clear these investigations are not really necessary.

Best is to talk to a doctor first before doing any sort of investigations.

Q: Do febrile convulsions affect the development of the child?

A: No. A child will develop normally and achieve their full potential even if they have had febrile convulsions when they were small.

Breast cancer cells outsmart the immune system and thrive

Scientists have discovered a new way breast cancer cells dodge the immune system and promote tumor growth, providing a fresh treatment target in the fight against the disease. While comparable mechanisms to avoid the immune system have been identified in mice with breast and other cancers, the study tested human breast tumor cells, putting researchers closer to understanding how the disease progresses in real patients.

The study, published in the journal Cancer Research, found high levels of the protein Hsp27 (heat shock protein 27) are released from human breast cancer cells and may not only render immune cells unresponsive to the tumor, but increase blood flow to the tumor as well, both of which fuel tumor growth.

“Our study is very unique because we used human breast cancer cells, which are extremely difficult to get,” said Asit De, lead author and research associate professor in the Department of Surgery at the University of Rochester Medical Center, who worked closely with physicians at the Wilmot Cancer Center. “The way tumor cells operate in mice is not identical to humans, so we need to do more of these types of human studies to confirm or reject cancer-related discoveries in mice.”

Past research reports Hsp27 is present in high levels inside breast tumor cells and is associated with resistance to chemo and radiation therapy. De and his team discovered Hsp27 is also released, or pushed out of breast tumor cells, into the area surrounding the tumor, known as the breast tumor microenvironment.


Once outside the cells, Hsp27 may transform circulating white blood cells called monocytes that enter the tumor into cells known as macrophages, which do the opposite of what they are meant to do.

Usually, macrophages work to wipe out tumor cells, but in this case they help, rather than hurt, tumor cells.

These particular macrophages may make human T cells - the main immune cells that attack and kill foreign invaders, like tumors - totally indifferent to the tumor and the body’s call to destroy it.

In addition to suppressing the immune response to the tumor, these macrophages encourage rapid formation of extra blood vessels that can help in supplying blood to the tumor - a process known as angiogenesis - essentially feeding the tumor so it can continue to grow.

Elevated levels of Hsp27 have been found in the blood of cancer patients with other solid tumors, such as liver and pancreatic cancer tumors, leading study authors to believe the protein may play a role in tumor progression beyond breast cancer.

“Our finding that Hsp27 aids tumor progression is just the start - we know there are several other molecules that help breast tumor cells suppress the immune system and we hope to identify more of them in future research,” noted De.


A new way to kill cancer - Scientists have discovered a way to kill cancer cells. Hsp27 is a ubiquitous protein that is important in all the body’s cells.

When it remains inside cells at normal levels it acts as a chaperone, protecting cells from stress, such as exposure to high heat or chemicals.

Only when the protein is let loose outside cells does it appear to have a detrimental effect on the immune system.

To carry out the study, De worked closely with clinicians in surgical oncology and plastic surgery at the Medical Center to obtain and analyze tumor-containing breast tissue samples from breast cancer patients undergoing surgery and normal breast tissue samples from healthy volunteers undergoing breast reduction. He also collected and tested blood samples from untreated breast cancer patients and age-matched healthy women.

Besides skin cancer, breast cancer is the most commonly diagnosed cancer among women in the United States.

It is also the second leading cause of cancer-related death in American women, behind lung cancer.

The development of treatment strategies that stop a tumor’s ability to silence or circumvent the immune system require a better understanding of tumors’ various avoidance mechanisms, such as the one identified by De.

De plans to continue research on Hsp27 in breast cancer, studying whether blocking Hsp27 slows tumor growth.

Source: Emily Boynton, University of Rochester Medical Center

Parkinson’s disease

Researchers develop new, working mammalian model to combat genetic causes of Parkinsons:

Evidence is steadily mounting that genetic factors play an important role in many cases of Parkinson’s Disease (PD). In a study published February 2, 2011, online in the Journal of Neuroscience, researchers from the Ecole Polytechnique Federale de Lausanne (EPFL) in Switzerland report a new mammalian model for studying a specific gene mutation commonly found in PD sufferers, opening the door to new drugs to fight the malady.

“This is a great step forward toward a more comprehensive understanding of how the disease works, and how it can be diagnosed and treated,” explains neuroscientist and EPFL President Patrick Aebischer, lead author of the study.

PD is a common neurodegenerative disease that greatly reduces quality of life and costs the United States around 23 billion dollars a year.

Until now, researchers have encountered difficulty in reproducing PD pathology in animals because of an incomplete understanding of the disease.

Recently, a mutation of the gene coding for LRRK2, a large enzyme in the brain, has emerged as the most prevalent genetic cause of PD (genetics are implicated in about 10 percent of all PD cases). When the enzyme is mutated, it becomes hyperactive, causing the death of vulnerable neurons and leading to a reduction in levels of the brain neurotransmistter dopamine. This decrease in dopamine eventually triggers the symptoms characteristic of Parkinsons, such as tremors, instability, impaired movement, and later stage dementia.

Now, with funding from the Michael J. Fox Foundation for Parkinson’s Research, Aebischer and his team in the Neurodegenerative Studies Laboratory at EPFL, have successfully introduced mutant LRRK2 enzyme into one hemisphere of a rat brain, resulting in the same PD manifestations that occur in humans in one side of the rodent’s body.

To do this, the researchers spent two years producing and optimizing a viral vector to deliver mutated, LRRK2 coding DNA into the rat brain.

LRRK2 is a large and complicated enzyme and designing a vector capable of transporting its extremely long genetic code was no small feat.

The new animal model developed by EPFL is sure to benefit future Parkinson’s research. The fact that LRRK2 is an enzyme - a catalyzing protein involved in chemical reactions - makes it drug accessible and therefore of specific interest to researchers looking for neuroprotective strategies, or pharmaceutical treatments that halt or slow disease progression by protecting vulnerable neurons. Armed with the LRRK2 model, new pharmaceuticals that inhibit the hyper-activity of the enzyme could one day prevent the destructive chain of events that leads to neurodegeneration and devastation in many with PD.


Michael Mitchell, Ecole Polytechnique Federale de Lausanne

Arthritis: A degenerative condition

Arthritis is a degenerative condition causing wear of the articulating surfaces, resulting in pain at rest, pain with movements, restriction of movements and in severe cases, deformity.

Arthritis and its types

The most common type is osteoarthritis, which is wear and tear associated with ageing.

It can be accelerated, or aggravated, or even caused by trauma, excess body weight, obesity, mal-alignment of the joints or congenital joint deformities (dysplasia).

The other common type of arthritis is called rheumatoid arthritis. In this disease, the immune system of the body reacts against the joints and musculoskeletal tissues. This causes inflammation of joints, and leads to wear and tear.

The other types of inflammatory arthritis are: aukylosing spondylarthropathy, Lyme disease, gouty arthritis, arthritis associated with connective tissue disease, psoriasis, inflammatory bowel disease, etc.

Can arthritis be stopped or reversed?

Once wear and tear has been established, arthritis progresses relentlessly.

There is no way to stop or reverse arthritis. Certain factors like weight reduction, activity modification, correcting mal-alignment, control of inflammation by anti-inflammatory or disease modifying anti-rheumatic drugs etc. may control wear and tear, but cannot reverse it.

Certain nutritional supplements like chondroitin sulphate and glucosamine and other medications like methyl-sulphonyl methane, esterified fatty acids and diacerin have been shown to have some beneficial effect on arthritis, but cannot completely cure arthritis, or reverse the wear and tear process. These are beneficial in early stages of arthritis, and need to be taken for 3-12 months. They are not beneficial in advanced arthritis, and neither have they any role in inflammatory arthritis.

Currently, tissue culture and genetic engineering are being applied to find a cure for arthritis, but till date, there is no universally successful technique that has effective clinical applicability. Dr Jayateerth W Kulkarni is Senior Consultant Orthopedic Surgeon, Apollo Hospitals, Bangalore.

Courtesy: BPositive

Intermittent drug treatment can curb malaria

WHO estimates that about six billion dollars a year are needed to wipe out malaria.

The intermittent use of preventive antimalarial drugs can be beneficial in curbing the spread of the disease in children, according to the results of a study released Tuesday.

Trials conducted in Mali and Burkina Faso showed that this type of treatment during the malaria transmission season could reduce infection rates by between 70 and 85 percent.

The two randomized controlled trials each involved more than 3,000 children who were treated with intermittently with the antimalarial drugs sulphadoxine pyrimethamine and amodiaquine.

The treatment “provided substantial additional protection against episodes of clinical malaria, severe malaria, and all-cause hospital admissions,” said the study reported in the Public Library of Science journal.

The drug treatment “adds to the benefit of sleeping under bednets” the report said, adding that “that this public health intervention is best delivered by community-based, volunteer village health workers.”

The authors of the Burkina Faso study wrote that the results offer “strong evidence to support the integration of (intermittent preventive treatment for children) into malaria control strategies in areas of seasonal malaria transmission.”

The authors of the study in Mali arrived at a similar conclusion, saying: “These findings indicate that (the drugs) could make a valuable contribution to malaria control in areas of seasonal malaria transmission alongside other interventions.”

The research was led by Diadier Diallo from the London School of Hygiene & Tropical Medicine; Amadou Konate from the Centre National de Recherche et de Formation sur le Paludisme in Ouagadougou; and Alassane Dicko from the Malaria Research and Training Centre in Mali.

A third study in Gambia, also noted in the journal, indicated administering the drugs by community-based, volunteer village health workers was more effective and less costly than delivery by reproductive and child health teams run by the Ministry of Health.

The disease killed an estimated 781,000 people in 2009 - including about 650,000 children aged under five - but that figure has been reduced from 985,000 in 2000, the World Health Organization said recently.

International spending in the war on malaria is predicted to peak at 1.8 billion dollars in 2010, but WHO estimates that about six billion dollars a year is needed to wipe out the disease.




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