In a research of how HIV mutates in response to immune system, scientists claim to have found evidence that the virus can take several escape routes, not one preferred route.

The human immune system has the ability to temporarily overpower HIV in early infection. Recent studies showed that most newly infected patients develop neutralising antibodies.

But, the problem is HIV’s ability to mutate, disguising itself enough to get away from the antibodies.

Now, a team has claimed that if a vaccine component is identified which can stimulate neutralising antibodies, HIV’s capacity for rapid mutation can still be a confounding factor.

“A single type of neutralising antibody may not be enough to contain HIV. These neutralising antibodies work really well — they hit the virus fast and hard. But so far, every time we look, the virus escapes,” lead researcher Prof. Cynthia Derdeyn of Emory University School of Medicine said.

Prof. Derdeyn and her colleagues collaborated with a public health programme which provides thousands of couples counselling and condom supplies every three months. Despite these measures, a low level of HIV transmission still occurs.

The collaboration allowed the team to take blood samples a few weeks after infection occurred and then later as two participants’ immune responses continued.

The scientists isolated individual viruses over the first two years of HIV infection and tested how well the patients’ own antibodies could neutralise them.

“In one patient where we had very early samples, there was evidence that neutralising antibody came up within weeks, and that’s earlier than what was previously thought,” Prof. Derdeyn said.

In both patients, some viruses mutated part of their outer proteins so that after the mutation, an enzyme would be likely to attach a sugar molecule to it. The sugar interferes with antibody attack.

However this tactic, known as the “glycan shield,” was not observed in all cases. Other viruses mutated the part of the outer protein that the neutralising antibodies stick to directly. In both patients, many changes in the virus’ genetic code were necessary for escape.

“We need to understand early events in the immune response if we are going to figure out what a potential vaccine should have in it. What we can show is that even in one patient, several escape strategies are going on.

“That means that in order to be immune to HIV infection, someone may need to have several types of neutralising antibodies ready to go. Seeing how the virus mutates will allow researchers to choose the best parts to put in a vaccine,” Prof. Derdeyn said.

For the first time in the US surgeons used a rare procedure to help a blind woman regain her sight: they implanted her own tooth in her eye to hold a prosthetic lens in place.

60-year old Sharron "Kay" Thornton, of Smithdale, Mississippi, who had been blind for nine years, underwent the sight-restoring procedure, known as modified osteo-odonto-keratoprosthesis (MOOKP), at the Bascom Palmer Eye Institute at the University of Miami Miller School of Medicine earlier this month.

The Institute's chairman, Dr Eduardo C Alfonso, told the press that this was the first time MOOKP, which has been available only in a limited number of eye centres in Europe and Asia, has been used in the US.

Thornton said she was looking forward to seeing her seven youngest grandchildren for the first time. She lost her sight in 2000 as a result of a rare skin condition called Stevens-Johnson syndrome that destroys the cells on the surface of the eye causing severe scarring of the cornea.

"We take sight for granted, not realizing that it can be lost at any moment," said Thornton, "This truly is a miracle."

Corneal specialist Dr Victor L Perez performed a series of surgeries that involved implanting one of Thornton's teeth in her eye:

"For certain patients whose bodies reject a transplanted or artificial cornea, this procedure 'of last resort' implants the patient's tooth in the eye to anchor a prosthetic lens and restore vision," explained Perez.

"In Sharron's case, we implanted her canine tooth, her eyetooth," he added.

Hours following the last surgery on Labor Day, Thornton said she was able to recognize faces, and two weeks later, she was reading newsprint with a visual acuity of 20/70. Her sight is expected to improve further as the scars heal.

MOOKP was first developed in Italy and is used to help patients with end-stage corneal disease or who have suffered damage to the cornea where severe scarring blocks vision and corneal transplants are no longer an option yet inside the eye everything is healthy and working properly, including the optic nerve.

Severe scarring on the cornea, which is the transparent layer of skin on the outside surface of the eye where a contact lens would sit, can come from accidents like chemical injuries and thermal burns, or as a result of disease such as inflammatory and autoimmune disorders like Stevens-Johnson syndrome.

In MOOKP, which comprises a series of lengthy procedures, the surgeons first remove, shave and sculpt a tooth and surrounding bone, and then drill a hole through which to insert an an optical cylinder lens.

They bond the tooth and lens to make one "bio-integrated" prosthetic unit and then implant it under the patient's skin, either in the cheek or the shoulder.

In the meantime, an opthalmologist gets the surface of the eye ready to receive the implanted prosthesis by removing scar tissue in and around the damaged cornea.

About a month later, the surgeons take mucous material from inside the patient's cheek and use it to cover and rehabilitate the surface of the damaged eye.

Then, about two months after this, the surgeons conduct the final stage of the procedure: they remove the bio-integrated prosthetic unit (the bonded tooth and lens) from the patient's cheek or shoulder and implant it in the eye, carefully alinging the unit to the centre of the eye. They make a hole in the mucosa for the prosthetic lens, which protrudes from the eye slightly so that light can enter and the patient can see again.

When Thornton first approached Bascom Palmer six years ago, she underwent an ophthalmic evaluation where they conducted a stem cell procedure but that was unsuccessful. As she was not a candidate for corneal transplant, they referred her to Perez who was thinking about doing MOOKP.

Last year Perez underwent training in Europe with Italian ophthalmologist Dr Giancarlo Falcinelli, who developed the MOOKP procedure from the original OOKP technique developed in the 1960s by another Italian eye specialist, Professor Benedetto Strampelli.

However, not all surgeons feel positive about MOOKP.

A member of the American Academy of Ophthalmology, Dr Ivan Schwab, told CNN that they've known about MOOKP since the 1980s and view it with skepticism. It needs a large team and several operations, and although it seems to be reasonably successful on the small numbers of patients that have received it, it results in disfigurement.

Schwab said the procedure was just an "extreme variation on techniques we're already doing" and that the alternatives were nearly as good. But in defense of Perez and his team he said "they are working on the worst of the worst, people with no other alternatives".

Another doctor who brought MOOKP to England from Italy, Dr Christopher Liu from the Sussex Eye Hospital in Brighton, told CNN that he didn't think the procedure would take off in the US because it was too lengthy.

"Each stage takes hours to perform," said Liu , adding that although the person can see again, the eye does not look natural.

However, one patient at least is very happy that US surgeons made the effort. Thornton told the press:

"I'm so thankful that the doctors at Bascom Palmer never gave up on me -- they kept searching."

Thornton said she was excited about seeing her three grown children and nine grandchildren, and rediscovering simple joys like playing cards and watching clouds go by.

"Without sight, life is really hard. I'm hoping this surgery will help countless people," she said.

Heart pumps, hooked with wires to power themselves, end up seriously infecting nearly 40 percent of patients.

Scientists have now developed the technology to power heart pump wirelessly thus saving thousands of lives, and eventually offering an alternative to heart transplants.

The wireless pump uses magnetic fields to transfer power through skin rather than using wire cables and can be powered this way 24 hours a day for a lifetime.

The new technology came out of collaboration among scientists from University of Auckland's Bio-engineering Institute, departments of electrical and computer engineering and physiology.

A new company, TETCor, was created to market the technology for powering a wide range of such implanted devices.

TETCor CEO Simon Malpas says heart pumps need a huge amount of power. The only way to power current artificial heart pumps is through a wire cable that goes through a patient's stomach and chest, according to an Auckland University release.

These wires cause serious infections, sometimes leading to death, in about forty percent of patients. The wires are also prone to breaking and restrict a patient's activities, said Malpas.

"This new wireless heart pump weights only 92 grams and measures just seven cm by three cm. It uses a coil outside a person's body to generate a magnetic field. A second coil placed inside a person's body, near the collar bone, picks up the signal from this field and creates power for the pump."

Malpas says previous attempts at making wireless heart pumps produced too much heat. These earlier pumps would have ended up "cooking a person from the inside".

A network of proteins underlying the plasma membrane keeps epithelial cells in shape and maintains their orderly hexagonal packing in the mouse lens, say Nowak et al. The study will appear in the September 21, 2009 issue of the Journal of Cell Biology (online September 14).

Spectrin, F-actin, and associated proteins form a meshwork that supports and shapes the plasma membrane of red blood cells. A similar network underlies the membranes of other cell types, including lens fiber cells: elongated epithelial cells that encircle vertebrate lenses in concentric layers, appearing in cross section as tightly packed hexagons. Actin filaments within this membrane skeleton are stabilized by their association with members of the tropomyosin and tropomodulin families of actin-binding proteins.

In mice lacking tropomodulin1, gamma-tropomyosin was also lost from the membrane skeleton of lens fiber cells. F-actin and spectrin remained associated with the cell membrane, but gaps appeared in the usually continuous protein network, suggesting that the two actin-binding proteins stabilize a subset of actin filaments required to link the network together. Scanning electron microscopy revealed that fiber cell membrane protrusions, which interlock with neighboring cells, were distorted and irregularly arranged in the absence of tropomodulin1. And although the fiber cells appeared hexagonal when first forming at the lens' equator, they often became misshapen and disorganized as they matured and moved toward the lens' center.

Senior author Velia Fowler thinks that disruption of the spectrin-actin network alters the adhesive interactions between neighboring cells, causing their shapes and packing to become disordered in response to the mechanical stresses associated with lens growth and eye movements.

A team of scientists at the University of California, Riverside has found that even second-hand tobacco smoke exposure can result in nonalcoholic fatty liver disease (NAFLD), a common disease and rising cause of chronic liver injury in which fat accumulates in the liver of people who drink little or no alcohol.

The researchers found fat accumulated in liver cells of mice exposed to second-hand cigarette smoke for a year in the lab. Such fat buildup is a sign of NAFLD, leading eventually to liver dysfunction.

In their study, the researchers focused on two key regulators of lipid (fat) metabolism that are found in many human cells as well: SREBP (sterol regulatory element-binding protein) that stimulates synthesis of fatty acids in the liver, and AMPK (adenosine monophosphate kinase) that turns SREBP on and off.

They found that second-hand smoke exposure inhibits AMPK activity, which, in turn, causes an increase in activity of SREBP. When SREBP is more active, more fatty acids get synthesized. The result is NAFLD induced by second-hand smoke.

"Our study provides compelling experimental evidence in support of tobacco smoke exposure playing a major role in NAFLD development," said Manuela Martins-Green, a professor of cell biology, who led the study. "Our work points to SREBP and AMPK as new molecular targets for drug therapy that can reverse NAFLD development resulting from second-hand smoke. Drugs could now be developed that stimulate AMPK activity, and thereby inhibit SREBP, leading to reduced fatty acid production in the liver."

Results of the study appear in the September issue of the Journal of Hepatology.

The study emphasizes that discouraging cigarette smoking helps prevent not only cardiovascular disease, pulmonary disease and cancer, but now also liver disease.

Second-hand smoke is the combination of smoke exhaled by a smoker and smoke given off by the burning end of a tobacco product. Lingering in the air long after tobacco products have been extinguished, it is involuntarily inhaled by nonsmokers in the vicinity.

Second-hand smoke is a major toxicant that affects children, the elderly and nonsmokers living in the household of adults who smoke. Many state and local governments have passed laws prohibiting smoking in public facilities. Diseases associated with second-hand smoking include cancer, heart disease, atherosclerosis, pneumonia, bronchitis and severe asthma.

Despite the large body of scientific evidence documenting the effects of passive or active smoking on the heart and lungs, reports investigating how smoking causes liver injury are scant.

"Until our study, second-hand smoking had not been linked to NAFLD development," Martins-Green said.