all Clifford Woolf stories

Simple bedside test improves diagnosis of chronic back pain

50443248 — Mon, 06 Apr 2009 15:07:59 -0400

A simple and inexpensive method of assessing pain, developed by Harvard researchers at Massachusetts General Hospital (MGH), is better than currently used techniques for distinguishing neuropathic pain – pain caused by damage to the nervous system — from other types of chronic back pain. Being able to more precisely determine the underlying nature of the pain is essential to choosing the best treatment. The report appears in tomorrow's edition of the open-access journal PLoS Medicine.

GlaxoSmithKline and Harvard Stem Cell Institute announce major collaboration agreement

404132862 — Mon, 21 Jul 2008 15:00:05 -0400

GlaxoSmithKline (GSK) and the Harvard Stem Cell Institute (HSCI) today announced that they have entered into a five-year, $25 million-plus collaborative agreement to build a unique alliance in stem cell science to hasten the development of treatments and cures for a range of diseases.

Chili pepper cocktail points to wide-awake surgery

Mon, 22 Oct 2007 11:56:32 -0400

Imagine an epidural or a shot of Novocain that doesn’t paralyze your legs or make you numb yet totally blocks your pain. This type of pain management is now within reach. As a result, childbirth, surgery, and trips to the dentist might be less traumatic in the future, thanks to researchers at Massachusetts General Hospital (MGH) and Harvard Medical School (HMS) who have succeeded in selectively blocking pain-sensing neurons in rats without interfering with other types of neurons.

The pint-sized subjects received injections near their sciatic nerves, which run down their hind limbs, and subsequently lost the ability to feel pain in their paws. But they continued to move normally and react to touch.

Sensitivity to pain explained

Thu, 12 Jul 2007 09:25:40 -0400

Stabbing back pain or the aches of arthritis send some people to bed in misery while the same distress seems easily tolerated by others. Why does pain hurt some people more than others? Scientists finally have an answer.

It involves a single molecule under control of a gene that acts like a dimmer switch. A "bright" or high setting excites sensory nerves to produce more of a chemical called BH4. For scientists, BH4 has one meaning, but for sufferers, it might as well mean "Big Hurt." Lower settings block BH4, protecting people from the wrench and bite of chronic pain.

Barrier found to nerve regeneration

70652986 — Mon, 26 Mar 2007 05:41:31 -0400

Scientists have long dreamed of prompting adult neurons of the central nervous system to regenerate. But these cells have the deck stacked against them in several ways. Molecules from the myelin sheath surrounding their axons actively discourage growth. After injury, nearby astrocytes form a dense scar to block them. Even the signals that once guided axons as they formed during development now seem to prevent regeneration. And most neurons also have lost the internal factors that enabled them to stretch their axons out in the first place - even if allowed to, they wouldn't grow.

Regeneration seems like a daunting task with all of these circumstances conspiring against it. Still, most researchers in the field believe it will be possible to remove the brakes on growth in the centrall nervous system if they can identify the restraints. An encouraging study in the Oct. 7, 2005 Science from the lab of Zhigang He, Harvard Medical School assistant professor of neurology at Children's Hospital Boston, uncovers a surprising new player on the side of inhibition - the well-known epidermal growth factor (EGF) receptor. The molecule appears to mediate the inhibitory signals of both myelin and proteoglycans from the glial scar - a convergence of pathways in a field that has become increasingly complex.

Research in brief

50443248 — Wed, 25 Jul 2007 16:23:17 -0400

Dramatic gains for American Indians

Identified for decades as the poorest group in the United States, American Indians living on reservations made substantial gains, both economically and socially, during the final decade of the 20th century. A new report released by the Harvard Project on American Indian Economic Development at the Kennedy School of Government compiles the data from the 1990 and 2000 U.S. Censuses for 15 key socioeconomic indicators. The data on measures ranging from income and poverty to unemployment, education, and housing conditions indicate that although substantial gaps remain between America's Native population and the rest of U.S. society, rapid economic and social development is taking place among gaming and non-gaming tribes alike.

Protector protein part of nerve cell defense

70652986 — Mon, 26 Mar 2007 05:24:32 -0400

Heat shock proteins are known to protect all cell types from various general assaults. They were originally discovered when cultured cells that were heated expressed the proteins at high levels and proved more resistant to other injuries and toxins. They help fold proteins that are misfolded in times of crisis, help maintain structural integrity of the cell, and serve as a counterbalance to apoptosis. But their specific role in the nervous system is not well known. Now a new study led by Clifford Woolf, the Richard J. Kitz professor of anesthesia research at Massachusetts General Hospital, suggests that a small heat shock protein, Hsp27, helps determine whether injured sensory and motor neurons live or die. The study, published in the Sept.

Chili peppers and inflammation

70652986 — Mon, 26 Mar 2007 05:25:03 -0400

Researchers have discovered that the burinng pain of arthritis is similar to the pain associated with eating chili peppers. "The receptor activated by chili peppers in the mouth and other tissues also increases in the terminals of sensory neurons in the skin after inflammation, and this contributes to pain hypersensitivity," says Clifford Woolf, director of the Neural Plasticity Research Group in the Department of Anesthesia and Critical Care at Massachusetts General Hospital (MGH). A receptor is a protein that transports a chemical signal into a cell. Woolf and study lead author Ru-Rong Ji, also of the MGH Neural Plasticity Research Group, found that the increased production of the receptor following inflammation is mediated by a signal molecule called p38, located within sensory neurons. The chili pepper receptor responds to capsaicin, the chemical that is responsible for the "hot" in peppers. It also responds to actual heat and to low pH, a condition that occurs with inflammation. "With these findings, we're starting to understand why patients with arthritis or other inflammatory conditions are likely to have increased pain and sensitivity to heat," says Woolf, who also is Richard J. Kitz Professor of Anaesthesia Research at Harvard Medical School.

First domino falls in research on sense of touch

70652986 — Mon, 26 Mar 2007 05:10:35 -0400

Unlike the other four senses, touch is ubiquitous, involving sensory terminals dispersed over the outside and on the inside of the body. This system encodes a variety of sensations in addition to touch, such as pain, vibration, pressure, stretch, itch, texture, and temperature. The system is sensitive to certain chemical states like painful tissue acidity, the result of inflammation or infection. Touch also underlies the brain's sense of where parts of the body are positioned at any given moment, crucial to motor control. Research reported in April 2001 focuses on an ion channel in mammals that appears to mediate the sense of touch. It is the first molecule identified in the macromolecular complex that converts touch stimuli to a neural signal.

Pain promoter plays unexpected role in central nervous system

70652986 — Mon, 26 Mar 2007 05:06:58 -0400

Despite all the attention it draws in patients, pain has only in recent years been deemed a subject worthy of scientific scrutiny. "It really was the Cinderella of medicine," said researcher Clifford Woolf. "Pain was always seen as part of some other problem, whether it's orthopedic or gastrointestinal or whatever." Woolf's own efforts for the past 20 years have been directed toward understanding how pain signals at the site of a wound or infection are received and interpreted by neurons in the spinal cord. For years researchers believed that longer-lasting pain was due to changes near the site of injury or infection.

Memories of pain can come back to hurt

70652986 — Mon, 26 Mar 2007 05:08:59 -0400

"As we search for the molecular basis of pain, we keep uncovering associations between pain and memory," says researcher Clifford Woolf. "Blocking such associations can provide a new basis for treating pain." The key is controlling the excitation of cells that register memories of pain. In one example, to decrease excitability, patients were given spinal injections of painkillers before prostate surgery. Compared with those not so treated, they experienced less pain while hospitalized and were more active after surgery. The pain reduction lasted as long as nine-and-a-half weeks. "When you think about it, the link makes sense," Woolf points out. "During evolution, animals had to learn to recognize what causes pain and to remember to avoid such things.