Today is World Leprosy Day:

Early treatment cures leprosy without deformities

Leprosy is a disease that has been known since biblical times. It causes skin sores, nerve damage, and muscle weakness that gets worse over time.

It is said that it would cost a person heavily to de-construct the parts of their body affected by leprosy. People in poverty-stricken countries can hardly afford that. However, one can help change their lives by raising awareness and funds for this cause.

The leprosy awareness day is held on the last Sunday in January each year.

In Sri Lanka, the Health Education Bureau of the Health Ministry is spearheading a program to mark the Day with the slogan 'Leprosy can be cured with no deformities'. There have been 2,225 newly diagnosed leprosy patients in 2011 among whom 45 percent (1,012) were from the Western province. In 2011, the highest number (446) of leprosy cases was reported from the Colombo district.

In 2012, 2,007 new leprosy patients were diagnosed, which means that the disease is still a major public health issue, according to the ministry conclusions.

Medical officers maintain that early detection and treatment can cure leprosy without deformities, but it is of utmost importance that treatment should be carried out to its completion. An alarming issue is that 20 percent of the patients do not complete the course of treatment in full, and defaulters have a higher risk of developing drug resistance and relapses. Leprosy is a chronic disease affecting the nerves and the skin - if not properly treated, sufferers can become blind, lose the sensations in their hands and feet; and become prone to a disability through the threat of injury.

In Sri Lanka, segregation of leprosy patients started in 1700 A.C. For this purpose the first Leprosy hospital in Sri Lanka was established by the Dutch rulers in 1708 at Hendala. The Government passed legislative enactments and issued leprosy ordinances in 1901 for prevention and the care of leprosy sufferers. Dapsone mono-therapy was first used in Sri Lanka in 1940s and in 1954 Anti Leprosy Campaign was established as a vertical program.

In 1983, Multi drug therapy was started in Sri Lanka. In 1989 the most successful social marketing campaign against leprosy began which enhanced self reporting among patients. In 1995, Sri Lanka achieved the elimination target as a country.

Anti-leprosy campaign

The anti leprosy campaign was responsible for diagnosis, management and providing drugs for leprosy until 2001 in which year the leprosy services were integrated in to the general health services.

Following the integration, Consultant Dermatologists are responsible for the diagnosis and management of the disease and follow up should be carried out by the PHI Leprosy attached to the Regional Director of Health Services. Leprosy should be suspected in people with any of the following symptoms:

1.Skin patch - hypo-pigmented or erythematous skin lesions.

Anesthesia or hyperesthesia is a major characteristic of these lesions.

2.Skin nodules and lumps -nodules usually without characteristics sensory loss, earlobe thickening, skin thickening, eyebrow thickening

3.Neurological symptoms - Sensory and motor impairment of the peripheral nerve will lead to Numbness, Clawing of fingers, wrist drop, foot drop and Painless wounds/ ulcers in hands and feet

4.Ocular manifestations- paralysis of the eyelid muscle, inflammation of the tear duct and lacrosse gland will contribute to the development of lesions due to exposure of the eye. It will lead to loss of visual acuity, cataract development, glaucoma and eventually blindness.

Diagnosis

Diagnosis is mainly a clinical one. However, in some instances investigations could be carried out. The total skin area should be examined carefully with the brightest available natural light.

Treatment

•Multi-drug therapy (Combination of antibiotics) is available in all government skin clinics free of charge.

•Depending on the type of disease duration and type of the drugs are different. Paucibacillary cases are treated with two drugs for six months duration whereas multi bacillary cases are treated with three drugs for 12 months duration.

•With early diagnosis and completing treatment regimes on time patients could be cured without any deformity.

Current situation of leprosy

•Around 2,000 new patients reported every year for the past 10 years.

•32,225 new patients were identified in 2011

•32,007 new patients were identified in 2012 up to November

•Patients are reported from all 25 districts in the country

•Around 45 percent of patients are reported from western province 1,012 patients in 2,011

•Highest Number of cases are from Colombo district, 446 cases reported in 2011

•Sri Lanka compared to other South East Asian countries has a high percentage (7 - 8 percent )of patients with visible deformities at the time of diagnosis

•Around 9 percent of new cases are children less than 15 years indicating active transmission of disease from undiagnosed individuals

•Child case rates have remained high in districts such as Puttalam, Batticaloa, Trincomalee, Colombo, Kalutara districts

•Around 20 percent of patients do not complete treatment. These defaulting patients have a higher risk of developing drug resistance and relapses.

•356 percent of new patients are diagnosed late more than 6 months after appearance of symptoms indicating lack of awareness among the public.

RG

The skin's response to UVA light

Last year, a team of researchers at Brown University discovered that certain skin cells use a light-sensitive receptor found outside of the eye to sense ultraviolet light and quickly begin pumping out melanin to protect against DNA damage. In a new study, lab members identify a key player in that biomolecular chain of events that could some day become a pharmacological target for improving this protective response.

The new discovery, published in the Proceedings of the National Academy of Sciences, is that human melaoncyte skin cells rely on an ion channel called TRPA1 to allow a flood of calcium ions into the cells when they are exposed to UVA light.

The resulting abundance of calcium ions signals the cell to begin making melanin, the pigment responsible for the tanning response in people.

Several experiments described in the paper show that TRPA1, which is known from a number of other appearances elsewhere in the body, is an essential step in the skin's response to UVA light, said senior author Elena Oancea, assistant professor of medical science in the Department of Molecular Pharmacology, Physiology, and Biotechnology at Brown.

As a matter of basic science, the finding strengthens the evidence of a striking parallel between the skin's response to UVA light and the way the eye detects light."It's exciting because it confirms this phototransduction pathway is similar to those found in the eye. It consists of a light sensitive receptor, molecular signaling cascade, and an ion channel," Oancea said.

"The involvement of an ion channel makes this pathway a lot more like other photo-transduction pathways."

In other parts of the body, TRPA1 has been shown to help detect pungent but benign chemicals, such as those in intensely flavorful foods. Oancea and lead author Nicholas Bellono said the chemical sensitivity of TRPA1 offers the intriguing possibility that it could become a target for experiments to boost melanin production.

"TRPA1 ion channels are involved in the detection of pungent chemicals such as cinnamaldehyde, wasabi, and mustard oil, and we've now found it's important for this melanin response," Bellono said. "There is a possibility that we can pharmacologically alter pigmentation through regulation of this ion channel."Oancea and Bellono emphasised, however, that people who go out in the sun should always take widely recommended precautions to protect their skin, such as using high-SPF commercial sunscreens or wearing protective hats and clothing.

Finding the channel

From the prior research in Oancea's lab, Bellono knew he was looking for some kind of molecular pathway that would start with a light sensitive receptor and trigger an elevated level of calcium ions in the melanocytes.

It seemed possible that a TRP ion channel would be involved because TRPs are involved in photo-transduction elsewhere in the body that lead to an increase in intracellular calcium.

There are, however, many types of TRP channels, and the molecular identity of the UVA-activated channel in melanocytes was not apparent. Oancea confessed that she even suspected another as the culprit. But many experiments later, the team hit on TRPA1 and amassed considerable evidence to confirm its vital role. In one experiment, for example, they treated melanocytes with "antagonist" chemicals known to block TRPA1 activity.

They then exposed the cells to UVA light and measured the resulting electrical response. The cells blocked with the antagonists had 80 to 90 percent reduction in current compared to the unhindered cells.

They used a similar technique of specifically blocking TRPA1 activity to show that the ion channel contributes greatly to the presence of calcium ions after UVA exposure compared to unhindered melanocyte cells. They also found melanocytes produce little or no melanin following exposure to UVA when TRPA1 is blocked. -medicalxpress

Perfectionism and eating disorders

Two aspects of perfectionism are involved in body dissatisfaction and the development of eating disorders, according to a study of over a thousand women published in Journal of Eating Disorders.

Adaptive perfectionism is high standards driving a person towards achieving a goal body image, and maladaptive perfectionism is concerned with mistakes and other people's opinions.

The finding indicates that both are involved in heightened concerns about body image, which in turn places people at risk of developing an eating disorder.

Over a thousand women representing a cross section of the population (aged 28-40) were involved in this study.

They ranged from underweight to morbidly obese, with a BMI of 14 to 64, and overall, the further these women were away from a healthy BMI, the bigger the difference between their current and ideal body images. While perfectionism is recognised as an important factor in eating disorders, the exact role of perfectionism in perceived body image has been difficult to pin down.

Tracey Wade and Marika Tiggemann, from Flinders University, found that women who desired the lowest BMI and the smallest body size tended to be more concerned about making mistakes, and more worried about organisation and higher self doubt than everyone else.

Prof Tracey Wade explained, "While some perfectionism is normal and necessary there becomes a point at which it becomes and unhelpful and vicious cycle.

Knowing that perfectionism of any sort is a risk factor for eating disorders suggests we should tackle 'all or nothing' attitudes with clients, as well as helping them to become less invested in defining their self worth in terms of their ability to achieve high standards."

- MNT

Evolutionary explanations for why we get cancer

Over 500 billion cells in our bodies will be replaced daily, yet natural selection has enabled us to develop defenses against the cellular mutations which could cause cancer.

It is this relationship between evolution and the body's fight against cancer which is explored in a new special issue of the journal Evolutionary Applications.

"Cancer is far from a single well-defined disease which we can identify and eradicate," said Dr Athena Aktipis, Director, Human and Social Evolution, Center for Evolution and Cancer at the University of California, San Francisco. "It is highly diverse and evolutionary theory allows us to consider cancer as a highly complex and evolving ecosystem.

This approach can improve the understanding, treatment and prevention of a number of different cancer types."By applying the principles of evolutionary biology papers in the special issue ask: Why do we get cancer, despite the body's powerful cancer suppression mechanisms? How do evolutionary principles like natural selection, mutation, and genetic drift, work in a cancer ecosystem? How can we use evolutionary theory to minimise the rate of cancers worldwide?

"Nowhere is the diversity of cancer better revealed than the many reasons why we remain vulnerable to it," said Dr Aktipis.

"Evolutionary medicine allows us to see explanations for traits that leave organisms vulnerable to disease."These evolutionary explanations include the role of environmental factors, such as the relationship between tobacco availability and lung cancer; co-evolution with fast evolving pathogens; constraints on what selection can do; trade-offs, such as the capacity for tissue repair vs. risk of cancer; reproductive success at the expense of health; defenses with costs as well as benefits, such asinflammation. - MNT

Safeguarding eye cells could help prevent blindness

Light-sensing cells in the eye rely on their outer segment to convert light into neural signals that allow us to see. But because of its unique cylindrical shape, the outer segment is prone to breakage, which can cause blindness in humans.

A study published by Cell Press in the Biophysical Journal provides new insight into the mechanical properties that cause the outer segment to snap under pressure.

The new experimental and theoretical findings help to explain the origin of severe eye diseases and could lead to new ways of preventing blindness.

"To our knowledge, this is the first theory that explains how the structural rigidity of the outer segment can make it prone to damage," says author Aphrodite Ahmadi of the State University of New York Cortland. "Our theory represents a significant advance in our understanding of retinal degenerative diseases."

The outer segment of photo-receptors consists of discs packed with a light-sensitive protein called rhodopsin. Discs made at nighttime are different from those produced during the day, generating a banding pattern that was first observed in frogs but is common across species.

Mutations that affect photo-receptors often destabilise the outer segment and may damage its discs, leading to cell death, retinal degeneration, and blindness in humans. But until now, it was unclear which structural properties of the outer segment determine its susceptibility to damage.To address this question, Ahmadi and her team examined tadpole photo-receptors under the microscope while subjecting them to fluid forces.

They found that high-density bands packed with a high concentration of rhodopsin were very rigid, which made them more susceptible to breakage than low-density bands consisting of less rhodopsin.

Their model confirmed their experimental results and revealed factors that determine the critical force needed to break the outer segment.The findings support the idea that mutations causing rhodopsin to aggregate can destabilise the outer segment, eventually causing blindness.

"Further refinement of the model could lead to novel ways to stabilise the outer segment and could delay the onset of blindness," says Ahmadi.

- MNT