Sentences with phrase «of plaque forming»

After removing the plaque, we apply a dental polish to smooth any roughened areas and decrease the chances of plaque forming again on the teeth.

There may even be patches of plaque forming that look just like psoriasis.

Not exact matches

Our championship banners — New Jersey accolades including top family business, best small manufacturing firm and fastest growing company — do not hang in the warehouse rafters as they come in the form of fancy plaques, but still they are available for all to admire.

After the night with disrupted sleep, the researchers found people had higher levels of beta - amyloid proteins, the proteins that clump together and form the plaque found in Alzheimer's - afflicted brains, in the volunteers» spinal fluid.

The donation / rewards model, on the other hand, allows people to give money without getting anything in return — other than rewards in the form of whatever the company is selling or providing (e.g., their name on a funders plaque, a free meal at the restaurant, etc.).

A plaque on the wall, commemorating the first pastor, a Bengali missionary whose descendants still form a strong arm of the church, placed the date of its construction at about 80 years ago.

The clock and plaque in remembrance of the Munich Air Disaster of just as poignant and form a special place at The Theatre of Dreams.

The water flosser has a high accessibility to interdental areas, removing plaque that forms between your teeth as well stopping the bleeding of gums.

Have a higher prevalence of stroke, atherosclerosis [a common form of arteriosclerosis in which fatty substances form a deposit of plaque on the inner lining of arterial walls], chronic obstructive pulmonary disease (COPD), Crohn's disease, lymphoma, metabolic syndrome [a collection of heart disease risk factors], cancer, and liver disease.

ORLANDO, Fla. — Adding a pharmaceutical form of the B vitamin niacin — but not the drug ezetimibe — to a cholesterol - lowering statin drug appears to reduce artery plaque buildup in patients with coronary artery disease, according to much - anticipated results announced at a press conference November 15.

Sleep deprivation also caused more plaques to develop, while an insomnia drug reduced the amount of plaque - forming protein (Science, DOI: 10.1126 / science.1180962).

A mouse engineered to have Alzheimer's disease and a gradual reduction in levels of the brain enzyme BACE1 stopped forming plaques (arrows in the first panel) as it aged.

Specifically, rodents genetically modified to express human amyloid precursor protein (hAPP), which can lead to the debilitating plaques that form in the brains of Alzheimer's patients, seem to struggle to find the hidden platform relative to their healthy peers.

Interestingly, they showed that these three organisms worked together to form robust digestive plaque biofilms capable of exacerbating intestinal inflammation.

Nevertheless, the astrocytes must «feel» something when plaques are formed, as when this happens they produce more of their characteristic protein, GFAP.

IRON overload may accelerate Alzheimer's disease, according to research that also reveals the role of beta - amyloid precursor protein (APP), which forms plaques in affected brains.

Dental calculus, also known as tartar, is a calcified form of dental plaque that acquires human DNA and proteins passively, primarily through the saliva and other host secretions.

In rats and tissue cultures of human nerve cells, these «beta sheet breakers» not only prevent amyloid plaques from forming, but also dissolve existing plaques.

Early but not advanced forms of atherosclerotic plaques in the vessel wall disappear when the levels of «bad» cholesterol are lowered, according to a study in mice from Karolinska Institutet, Sweden.

The pathological form is a misfolded version of this molecule and known to initiate the formation of toxic plaques in the brain.

The UCLA researchers, led by David Eisenberg, director of the UCLA - Department of Energy Institute of Genomics and Proteomics and a Howard Hughes Medical Institute investigator, report the first application of this technique in the search for molecular compounds that bind to and inhibit the activity of the amyloid - beta protein responsible for forming dangerous plaques in the brain of patients with Alzheimer's and other degenerative diseases.

Because the protein is normally found outside of blood vessels in the human brain, this suggests that plaques may form in a different way in chimps.

Such fibrils form plaques, or areas of tissue damage, that researchers can observe with microscopes.

The researchers also tracked 592 people who had low levels of A-beta in their cerebral spinal fluid — a clue that plaques have formed in the brain — and who showed symptoms of Alzheimer's.

These plaques, which are believed to cause the dementia associated with the disease, are made up of tangles of amyloid beta (Aβ), a protein that is found in soluble form in healthy individuals.

Cysts that resulted from loss of contact inhibition proliferated like plaques along the walls of the nephron, then buckled to form «disorganized» cysts.

As we age, fat and blood cells form hard plaques on the walls of our arteries.

Taken together, the animal data suggest that a range of different microbes can induce amyloid plaques to form, Tanzi says.

Candida can't effectively form plaque biofilms on teeth on its own nor can it bind S. mutans, unless in the presence of sugar.

While previous investigations into the protein's effects have used either mice in which gene expression was knocked out or transgenic animals that expressed human gene variants throughout their lifetimes, the MGH - MIND - led study used a different approach to investigate the effects of introducing the variant forms of the protein into brains in which plaque formation had already begun.

More than 40 illnesses known as amyloid diseases — Alzheimer's, Parkinson's and rheumatoid arthritis are a few — are linked to the buildup of proteins after they have transformed from their normally folded, biologically active forms to abnormally folded, grouped deposits called fibrils or plaques.

Secreted by certain brain cells, APOE is known to regulate cholesterol metabolism within the brain and can bind to A-beta peptides, suggesting that the different forms of the protein may affect whether and how toxic A-beta plaques form.

We don't fully understand what it means, but it may combine with other forms of amyloid - beta to stimulate plaque formation.»

In several diseases of the brain, long fibres of protein form, and eventually become tangled to form dense bodies known as «plaque» or «aggregates.»

They may pave the way for better diagnosis of neurodegenerative diseases, such as Alzheimer's disease, in which plaque forms from the amyloid beta or tau proteins.

They also gained fame as the first carriers of messages designed for other civilizations, in the form of etched plaques about humans and Earth.

A definitive diagnosis of Alzheimer's includes dementia and two distortions in the brain: amyloid plaques, sticky accumulations of misfolded pieces of protein known as amyloid beta peptides; and neurofibrillary tangles, formed when proteins called tau clump into long filaments that twist around each other like ribbons.

Researchers at Rice's Center for Theoretical Biological Physics used computer models to analyze proteins suspected of misfolding and forming plaques in the brains of patients with neurological diseases.

Previously, researchers have shown that treating cells with neuregulin - 1, for example, dampens levels of amyloid precursor protein, a molecule that generates amyloid beta, which aggregate and form plaques in the brains of Alzheimer's patients.

Neurons responsible for producing key neurotransmitters — among them acetylcholine, noradrenaline and 5 - hydroxytryptophan — begin to fail, traces of the plaques and tangles that infest the brains of Alzheimer's patients begin to form, and the organ as a whole shrinks.

In the brains of patients with Alzheimer's, amyloid peptides aggregate to form oligomers and plaques that are thought to be responsible for the disease symptoms.

Together, these plaques and neurofibrillary tangles form the pathological hallmarks of the disease.

Particulate matter in the body, such as the cholesterol crystals associated with vascular disease and the amyloid plaques that form in the brain in Alzheimer's disease, can also cause inflammation but the exact mechanism of action remains unclear.

In the brains of patients with Alzheimer's disease (AD), amyloid precursor protein is broken apart, and the resulting fragments — β - amyloid peptides, or Aβ peptides — aggregate to form plaques.

The disease is largely attributed to an abnormal buildup of proteins, which can form amyloid beta plaques and tangles in the brain that trigger inflammation and result in the loss of brain connections called synapses, the effect most strongly associated with cognitive decline.

The drug also appeared to reduce the amount of the protein amyloid beta (which forms toxic plaques in the brains of Alzheimer's patients) by decreasing the levels of metals such as zinc and copper.

A study of temperature sensitive clear - plaque - forming mutants of bacteriophage P22 demonstrates that the c1 and c2 loci must function in a temporal sequence in the establishment of lysogeny in Salmonella typhimurium.

Rather than being a secondary effect of these protein pathologies, as experts had previously thought, this process may begin well before plaques form.

A 67 - year - old woman had sky - high levels of the form of cholesterol long seen as protective against heart disease, and yet her arteries were lined with plaque.

But recent research indicates that smaller, soluble forms of amyloid - beta — rather than the solid plaques — are responsible for the death of nerve cells that leads to cognitive decline.