Thursday, May 18, 2017

A New Way to Fight Against Cavities

Most of us brush at least once a day, many do it after each meal, floss daily, but then still end with cavities ! One of the worst thing is to sit on the dental chair, with all the drilling, which gives you not just headache, but jaw pain due to opening your jaws wide for long. Above all the dentist charges are at times equal to a minor surgery ! Quite often dentists makes sure that they take the fees in advance, so you've to keep going to them as and when you're told ! You pay for the transport/ fuel and above waste couple of hours commuting, waiting and the pain to add to your woes. Now when you read about the new possible treatment to overcome all those dreadful days of visiting the dentist, you'll be amazed !

The best defense against cavities might not be your own attentiveness, much less those fillings, sealants, or fluoride treatments. In fact, what could work better is warm, moist, and a bit slimy. That's correct, mucus.

Mucus, along with tears and skin, makes up our first line of defense against disease. They all form a barrier against invading germs. And, as it turns out, according to a study published recently in the "Applied and Environmental Microbiology" journal, the crucial proteins found in mucus known as salivary mucins can protect our teeth from cavity causing bacteria known as Streptococcus mutans. Unlike toothpaste and mouthwash, which destroy bacteria, mucins prevent bacteria from attaching themselves onto your teeth and secreting acid that bores holes through the enamel. Now,the researchers who led the study are trying to engineer synthetic mucus that could be added to toothpaste or bubble gum. Sounds lovely doesn't it?

As disgusting as this sounds, synthetic mucus might go well beyond just preventing cavities. Studies have suggested that mucins might also be able to defend against respiratory infections, stomach ulcers, and even HIV. Since mucins do not actually kill bacteria (they merely prevent bacteria from causing damage), they are seen by some as a much better alternative to antibiotics, which may kill not only harmful bacteria, but helpful bacteria as well, allowing more dangerous strains to take their place. This means that synthetic mucin might offer a less intrusive alternative, used "not necessarily to resolve infections but to stabilize or prevent infections," says Katharina Ribbeck, an assistant professor in the department of biological engineering at MIT, who co-authored this study alongside Erica Shapiro Frenkel, a Ph.D student in her lab. 


We get cavities when bacteria such as S. mutans cling to our teeth, forming an intricate, mesh-like arrangement known as biofilm. The bacteria that make up this biofilm feed on the sugars found in the food we eat to produce acid that can then dissolve the tooth enamel. To investigate how much mucus might be needed to guard against this process, Ribbeck's group got down to the molecular level and homed in on a mucin known as MUC5B. This is the most commonly found mucin in the mouth.


 First, the researchers isolated MUC5B from saliva samples of some volunteers. Then, they grew S. mutans bacteria with sugar and a special broth in plates containing wells that were made from a plastic which imitates a tooth's enamel. Some of the wells also contained MUC5B. At the end of the experiment, Ribbeck and Frenkel counted the number of attached S. mutans bacteria at several points in time and found more of them floating in the growth broth than attached to the plastic in the wells containing MUC5B. This suggests that the mucin somehow prevents S. mutans from sticking to the surface of the tooth.

How, exactly? The researcher aren't sure, but, according to Ribbeck, it's possible that MUC5B encases S. mutans in a "3-D spiderweb" that traps the acid that they secrete. MUC5B might even form a bacteria-repellent coating over the tooth's surface, or even turn off S. mutans genes that are involved in attachment and biofilm formation. Ribbeck and Frenkel are still trying to find the most likely mechanism, though they suspect that mucins might maintain bacterial diversity in the mouth by not only keeping S. mutans alive, but by also neutralizing the toxins that different bacterial strains release to outdo each other.


Of course, scientists still need to confirm the protective role of mucins before investigating the mechanisms involved. William Bowen, a professor at the University of Rochester's School of Medicine and Dentistry, also points out that cavity-causing bacteria embed themselves in plaque - not directly to the surface of the tooth. And many other bacteria in the mouth cause cavities, not just S. mutans, which is not a "major acid producer."


 Still, having said that, Ribbeck and Frenkel have reported similar results with other surfaces, hinting at "a more general mechanism" of MUC5B. Translation? Benefits of synthetic mucus could extend far beyond human health, and could be used to prevent food spoilage, and the accumulation of bacteria on ship hulls and other surfaces, for example. "The applications are enormous," Ribbeck declared.

 this is only for your information, kindly take the advice of your doctor for medicines, exercises and so on.   
https://gscrochetdesigns.blogspot.com. one can see my crochet creations 
https://gseasyrecipes.blogspot.com. feel free to view for easy, simple and healthy recipes    
https://kneereplacement-stickclub.blogspot.com. for info on knee replacement   

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Tuesday, January 31, 2017

Changes in gene contribute independently to breast and ovarian cancer

Defects in a key gene - long thought to drive cancer by turning off the protection afforded by the well-known BRCA genes - spur cancer growth on their own, according to a study led by researchers from NYU Langone Medical Center.

The study gene, known as EMSY, has some of the same functions as BRCA1 and BRCA2, which are known to protect against breast and ovarian cancer when normal. When defective, BRCA genes block the body's self-defense against cancer-causing genetic mistakes.

The new study, published online Jan. 13 in Oncotarget, helps to explain why some women with healthy BRCA1 and BRCA2 genes develop cancer. The findings may also expand treatment options for the roughly 11 percent of women with breast and ovarian cancer and normal BRCA genes, say the study authors.

"Now that we know exactly how changes in EMSY spur cancer cell growth, we can start to design therapies to specifically target that activity and hopefully stop it," says senior author Douglas Levine, MD, director of the Division of Gynecologic Oncology at NYU Langone and its Perlmutter Cancer Center.

"This work also suggests that treatments that work for patients with BRCA1 or BRCA2 mutations might also be effective against EMSY-driven cancers because the disease mechanism is similar," says first study author Petar Jelinic, PhD, a research assistant professor at NYU Langone. "The best way to go rapidly from bench to bedside is to find new ways to use existing treatments."

When normal, EMSY, BRCA1 and BRCA2 give the body's cells instructions to create proteins that help to repair DNA damage that can cause cancer. When those genes are altered, the repair process fails and cancer grows. Overly active EMSY, like mutated BRCA1 or BRCA2, changes those instructions, so that the DNA damage repair process is blocked.

This new study dispels prior theories that EMSY's activation merely turned off the cancer suppression function of BRCA2, says Jelinic.

Earlier work by Levine and others pointed toward EMSY activation as a culprit in breast and ovarian cancer, but had only examined certain parts of the EMSY protein. The new study was the first to evaluate the full-length EMSY protein and to show that it acts independently of BRCA1 or BRCA2.

Furthermore, the research revealed the part of the EMSY protein is changed by an enzyme called protein kinase A. When there is more active EMSY than normal, this enzyme reacts with the EMSY protein to more thoroughly suppress the DNA repair process.

Breast cancer is the second most common cancer among women in the United States, after skin cancer. Ovarian cancer is the fifth leading cause of cancer death among women, according to the National Cancer Institute.





this is only for your information, kindly take the advice of your doctor for medicines, exercises and so on.
https://gscrochetdesigns.blogspot.com. one can see my crochet creations
https://gseasyrecipes.blogspot.com. feel free to view for easy, simple and healthy recipes 
https://kneereplacement-stickclub.blogspot.com. for info on knee replacement

Defects in a key gene - long thought to drive cancer by turning off the protection afforded by the well-known BRCA genes - spur cancer growth on their own, according to a study led by researchers from NYU Langone Medical Center.
The study gene, known as EMSY, has some of the same functions as BRCA1 and BRCA2, which are known to protect against breast and when normal. When defective, BRCA genes block the body's self-defense against cancer-causing genetic mistakes.
The new study, published online Jan. 13 in Oncotarget, helps to explain why some women with healthy BRCA1 and BRCA2 genes develop cancer. The findings may also expand treatment options for the roughly 11 percent of women with breast and ovarian cancer and normal BRCA genes, say the study authors.
"Now that we know exactly how changes in EMSY spur , we can start to design therapies to specifically target that activity and hopefully stop it," says senior author Douglas Levine, MD, director of the Division of Gynecologic Oncology at NYU Langone and its Perlmutter Cancer Center.
"This work also suggests that treatments that work for patients with BRCA1 or BRCA2 mutations might also be effective against EMSY-driven cancers because the disease mechanism is similar," says first study author Petar Jelinic, PhD, a research assistant professor at NYU Langone. "The best way to go rapidly from bench to bedside is to find new ways to use existing treatments."
When normal, EMSY, BRCA1 and BRCA2 give the body's cells instructions to create proteins that help to repair DNA damage that can cause cancer. When those genes are altered, the repair process fails and cancer grows. Overly active EMSY, like mutated BRCA1 or BRCA2, changes those instructions, so that the DNA damage repair process is blocked.
This new study dispels prior theories that EMSY's activation merely turned off the cancer suppression function of BRCA2, says Jelinic.
Earlier work by Levine and others pointed toward EMSY activation as a culprit in breast and ovarian cancer, but had only examined certain parts of the EMSY protein. The new study was the first to evaluate the full-length EMSY protein and to show that it acts independently of BRCA1 or BRCA2.
Furthermore, the research revealed the part of the EMSY protein is changed by an enzyme called protein kinase A. When there is more active EMSY than normal, this enzyme reacts with the EMSY protein to more thoroughly suppress the DNA .
Breast cancer is the second most common cancer among women in the United States, after skin cancer. Ovarian cancer is the fifth leading cause of death among women, according to the National Cancer Institute.


Read more at: https://medicalxpress.com/news/2017-01-gene-contribute-independently-breast-ovarian.html#jCp

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