DAVID GRANOVSKY

Archive for the ‘DISEASE INFO’ Category

LYME DISEASE UPDATE (good news!)

In DISEASE INFO, HEALTH AND WELLNESS, HOPE AND INSPIRATION, OFF THE BEATEN PATH, VICTORIES & SUCCESS STORIES on June 14, 2017 at 2:23 pm
LYME DISEASE UPDATE:
One of the many problems with the Lyme disease bacteria is that when under attack, they can coat themselves with a biofilm. Think ‘getting slimed from ghostbusters…

bill-murray-ghostbusters-slimed

…in fact:
 
“A biofilm is any group of microorganisms in which cells stick to each other and often these cells adhere to a surface. Biofilm is a polymeric conglomeration generally composed of extracellular DNA, proteins, and polysaccharides. These adherent cells are frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS) which may also be referred to as SLIME (although not everything described as slime is a biofilm).” wiki
 
Is this mucous-y armor-y biofilm strong? Strong enough to withstand the antibiotics used to kill them and tadpole biofilm has even been found intact from the Miocene era so, yeah. Lyme disease bacteria can morph back and forth into this armor-like biofilm when attacked and remove it when it is going about its normal (destructive) life cycle. In fact, antibiotics like doxycycline, the standard treatment for Lyme disease, actually trigger the bacteria into producing this biofilm armor.

“The culprit behind Lyme disease, which is a bacterial infection, is spirochete bacterium Borrelia burgdorferi. The antibiotics proven to kill this form of bacteria are doxycycline and amoxicillin. However, Borrelia burgdorferi can be found in morphological forms, including spirochetes, spheroplast (or L-form), round bodies, and biofilms. When conditions are considered unfavourable for the bacteria, it morphs into the dormant round body, then hides in a biofilm form. When conditions are favourable, however, it can shift back to its spirochete form.”
 
So what’s a Lyme disease sufferer to do when THE TREATMENT essentially STRENGTHENS the antibiotic resistance of the PATHOGEN?
lyme-disease-What-should-I-
THE GOOD NEWS:
A new study shows there is increased hope for Lyme disease sufferers. The use of Stevia, a common sugar, has been fond to destroy the biofilm. Taking STEVIA and ANTIBIOTICS will destroy the biofilm and the bacteria more effectively:

“Subculture experiments with Stevia and antibiotics treated cells were established for 7 and 14 days yielding, no and 10% viable cells, respectively compared to the above-mentioned antibiotics and antibiotic combination. When Stevia and the three antibiotics were tested against attached biofilms, Stevia significantly reduced B. burgdorferi forms. Results from this study suggest that a natural product such as Stevia leaf extract could be considered as an effective agent against B. burgdorferi.”

 
“Stevia Kills Lyme Disease Pathogen Better Than Antibiotics, Study Confirms – http://www.collective-evolution.com/2017/01/25/study-finds-stevia-kills-lyme-disease-pathogen-better-than-antibiotics/
 
 
 

STEM CELLS FOR CYSTIC FIBROSIS

In DISEASE INFO, HEALTH AND WELLNESS, SCIENCE & STEM CELLS on January 31, 2017 at 10:56 am

“[Bob]  received an infusion of cells called allogeneic human mesenchymal stem cells (hMSC), adult stem cells collected from the bone marrow of healthy volunteers”

“CF’s main effect is on the lungs. They fill with a sticky mucus as a reaction – really an over-reaction – by the body’s immune system to bacteria. The lungs are the source for much of the illness and shortened lifespan seen in CF.”

cystic-fibrosis-the_fluorescent_microscopy_image_of_cftr_tagged_with_eyfp

CYSTIC FIBROSIS The_fluorescent_microscopy_image_of_CFTR_tagged_with_EYFP

First stem cell study could lead to development of therapy to reduce inflammation caused by CF

Published on January 31, 2017 at 3:24 AM · 

A 39-year-old man with cystic fibrosis (CF) made history by becoming the first person to receive human adult stem cells in a new research study that researchers hope will someday lead to the development of a therapy to reduce the inflammation and infection caused by CF.

The pioneering subject in the study is Bob Held from Alliance, Ohio, who on Jan. 26 received an infusion of cells called allogeneic human mesenchymal stem cells (hMSC), adult stem cells collected from the bone marrow of healthy volunteers. Mr. Held was diagnosed with CF when he was 16 months old.

Currently, there is no cure for CF, and life expectancy for patients who survive into adulthood is approximately 41 years of age.

“It was a very exciting day for us with the very first participant in the first stem cell trial for cystic fibrosis,” said James Chmiel, MD, the principal investigator of the study at University Hospitals Rainbow Babies & Children’s Hospital.

The Phase 1 trial will assess the safety and tolerability of hMSCs in adult patients with CF.

“This is an early phase trial, and the most important thing is to ensure safety,” said Dr. Chmiel. “This study consists of a single infusion of stem cells. We will follow the study participants for a year to make sure it’s safe. Before applying any therapy on a broad basis, we want to make sure that it’s safe.”

While the goal of the study is safety, Dr. Chmiel hopes this is a first step towards the ultimate goal of developing a therapy to reduce lung inflammation and infection, resulting in longer and healthier lives for people with CF.

“While there’s been a tremendous increase in survival for people with CF from when I entered the field in the 1990s, that’s still not good enough,” said Dr. Chmiel, Director of the Cystic Fibrosis Therapeutics Development Center at UH Rainbow Babies & Children’s Hospital and Professor of Pediatrics at Case Western Reserve University School of Medicine. “While we’ve made great progress, we still have a long way to go.”
The stem cells that Mr. Held received were collected from the bone marrow of a healthy adult volunteer. UH is a national leader in the use of stem cell therapy with hMSCs. Researchers from UH, along with the CWRU School of Medicine, discovered hMSCs. The hMSCs possess many properties that are ideal for the treatment of inflammatory and degenerative diseases, and they possess natural abilities to detect changes in their environment, such as inflammation. The hope is that hMSCs can reduce the inflammation in the lungs caused by CF.

CF’s main effect is on the lungs. They fill with a sticky mucus as a reaction – really an over-reaction – by the body’s immune system to bacteria. The lungs are the source for much of the illness and shortened lifespan seen in CF.

“One of the issues in CF is that people with the disease get bacterial infections in their lungs, and these bacteria incite a vigorous and excessive inflammatory response,” explained Dr. Chmiel. “It’s actually the body’s inflammatory response that damages the lungs. The inflammatory response tries to eliminate the bacteria, but it’s not successful. Instead, the inflammatory system releases molecules that damage the individual’s own airways. The lung disease causes much of the illness and is responsible for the majority of the mortality of the disease.”

The stem cells are donated by healthy adult volunteers who go through a rigorous screening process. The stem cells are cultured in the UH stem cell facility. Volunteers with CF who are in the study receive an infusion through an IV.
“Once in the patient’s body, the stem cell tracks to the area where there’s a significant amount of inflammation, and they take up residence there. The stem cells then respond to the environment, and hopefully reverse some of the abnormalities,” said Dr. Chmiel. “We hope in future studies to demonstrate that the stem cells reduce the infection and inflammation and return the lungs to a more normal state.”

“This therapy aims to turn down the inflammatory response, not eliminate it because we still have to keep the bacteria in check. We want to reduce inflammation and the subsequent lung damage caused by inflammation without allowing the bacteria to proliferate,” said Dr. Chmiel.

A total of 15 clinically stable adults with CF will be enrolled in the study. Support for the study is from the Cystic Fibrosis Foundation.

The patient, Mr. Held, considers himself fortunate to be close to 40 with CF. When he was growing up, he said he’d miss 50 days of school each year because of the disease. Every day, he needs to breathe in aerosols for about two hours in the morning and 1-1/2 hours before bed to keep his lungs functioning. While he hasn’t been sick from the illness since his late teens, he does check himself into the hospital a couple of times a year for precautionary measures and to prevent himself from “getting into a valley” with CF.

His late wife, Michelle, died of CF seven years ago. They had met when they were kids, but didn’t get married until 2012. She died from the disease suddenly 28 days after they married.

“My only regret is that I didn’t ask her out sooner,” said Mr. Held.
He is participating in the study to carry on Michelle’s legacy, and “I am hoping the future generations of CF patients can get better treatments and that eventually a cure will be found for them,” he said.

WHY SMOKING CAUSES CANCER

In DISEASE INFO, HEALTH AND WELLNESS, SCIENCE & STEM CELLS on January 30, 2017 at 7:30 pm
Lung stem cells cultured in the laboratory. The green, blue and purple colors emerging from behind the orbs are a protein expressed by lung basal stem cells. Photo: Clare Weeden, Walter and Eliza Hall Institute of Medical Research

For four years straight medical researcher Clare Weeden would go on alert whenever lung surgery was underway anywhere across Melbourne. No matter the time, she would have to be ready in her lab to receive samples of fresh tissue as part of a project to isolate and research the stem cells that repair our lungs as they constantly breathe in contaminants from air pollution to cigarette smoke.

She didn’t know it at the time, but she was hot on the trail of the lung’s basal stem cells that now appear to be the likely culprits that trigger a major lung cancer closely tied to smoking – squamous cell carcinoma. It is the second most common form of lung cancer.

Basal stems cells are very quick at repairing DNA damage caused by inhaled chemicals such as those from cigarette smoke, but they are prone to making mistakes. It means that the more repair work they have to do, the greater the chance of a cancer-causing mutation.

“What we have found is a genetic fingerprint in squamous cell carcinoma that has been left from basal stem cells in the lung whose repair work has gone awry and led to the cancer,” says Weeden, from the Walter and Eliza Hall Institute of Medical Research and a PhD candidate at the University of Melbourne.

“It isn’t definitive but the evidence is that lung basal stem cells are the likely cells of origin.”

The unmasking of basal stem cells, published in the Public Library of Science: Biology, is the culmination of years of painstaking laboratory work and data-crunching that has now provided a crucial new target for developing drugs that may be able to turn off the progress of the cancer.

Weeden was sometimes up until to 3am at the Institute isolating and processing cells from the freshly operated-on lung tissue, especially when there was a flurry of samples in one day. It is a complex process that took up to six hours for each of the eventual 140 samples.

The Clue

But one day she came across a sample that she could barely get to grow at all.

Intrigued, she contacted the Victorian Cancer Biobank for basic information on the donor. It was likely that the donor was a smoker or ex-smoker since most people having lung surgery have a history of smoking. But this patient had never smoked. Sensing a possible link she went back to the Biobank to get information on all the previous tissue donors, and over that weekend plotted out a chart.

The correlation was stark. Samples from those that had never smoked had low basal cell growth, and the more heavily a patient had smoked, the higher the growth rate.

“It completely grabbed my curiosity,” she says. “I remember on Monday morning going straight into my supervisor’s office (Marie-Liesse Asselin-Labat) and putting the chart down in front of her. We both realized we were onto something significant. The question was what?”

By using the same process that Weeden had developed to accurately isolate lung stem cells, she and Asselin-Libat set to examine how the basal stem cells worked.

They discovered that basal stem cells were very efficient at repairing damaged DNA but that the process the cells use, called non-homologous repair, is prone to making errors that can lead to cancer-causing mutations. In non-homologous repair the break in a damaged DNA chain is simply closed over rather than copied. They also found evidence of the accumulation of mutations in the basal stem cells of the smokers.

“While we need more experimentation, this gave us a model of what may be happening,” says Weeden. “Our lungs are constantly being exposed to what we inhale. When we breathe in something like cigarette smoke that causes lung damage, these basal cells receive a signal to grow and repair the damage.

But they have to first repair their own DNA damage and the process they use is very quick. The advantage is that it helps the cells to survive, but the disadvantage is that they are prone to making errors that can lead to cancer.”

To test that model they turned to Institute bioinfomaticians Professor Gordon Smyth and Yunshun (Andy) Chen who used statistics and computer science to extract a genetic “signature” for lung basal stem cells. They then compared that signature with the genetics of various lung cancers.

clear evidence

They discovered that this same signature was highly correlated with lung squamous cell carcinoma, the second most common form of lung cancer and the most closely linked to smoking – some 96 per cent of people with lung squamous cell carcinoma are either smokers or ex-smokers. It was clear evidence that basal stem cells are the likely culprits in how the cancer is triggered.

By identifying a cell of origin Weeden says we now have a drug target to aim at that has the potential to stop the progress of the cancer. Previous Institute research in 2009 lead by Professor Jane Visvader and Professor Geoff Lindeman had similarly identified a likely cell of origin for inherited breast cancer, and last year that same team identified an existing drug, denosumab, that in laboratory models could switch off the problematic cell growth and curtail the cancer. Clinical trials are now underway.

“In the breast cancer research they similarly used correlations to identify a cell of origin like we have and now further work has solidified that,” says Weeden.

Does this mean that at some point in the future smokers could breathe easier by taking a drug that could stop the cancer being triggered? No. Weeden points out that if someone took such a drug and continued to smoke the damage could be even worse than the cancer.

“Basal stem cells have a job to do in the lung, they repair any damage. If a person was treated with a drug that turned off basal cells and continued to smoke, I would imagine that other lung problems may develop due to the inability of the stem cell to repair the lung airways from cigarette smoke-induced damage,” says Weeden. She points out that smoking also causes other lung cancers that don’t arise from basal stem cells.

She says the biggest beneficiaries of any such drug could be ex-smokers. “This is particularly relevant as lung squamous cell carcinoma can occur in ex-smokers who have quit perhaps 20 or 30 years ago.

“But the best way to reduce the risk of lung cancer is to simply quit smoking because no matter how long you’ve smoked for, the risk of lung cancer is reduced when you quit.”

(NOT) FIRST PARALYZED HUMAN TREATED WITH STEM CELLS FOR SCI

In ALL ARTICLES, DISEASE INFO, SCIENCE & STEM CELLS, STEM CELLS IN THE NEWS, THIS IS SPINAL... on January 27, 2017 at 12:05 pm

First paralyzed human treated with stem cells has now regained his upper body movement http://theheartysoul.com/stem-cells-cure-paralysis/

stem-cell-patient

CONGRATS! But…
NOT the FIRST!

This is the sort of article which makes me crazy because on the one hand, it is a triumph!  A mainstream coverage of a stem cell success, increasing awareness and helping to erode our entrenched concepts of what can be done with medicine and what is and isn’t really “incurable.”

On the other….it grossly misrepresents the long history of stem cell successes versus spinal cord injury. It devalues the patients who have recovered, the loved ones who supported them during their treatments and the doctors who worked their butts off developing the protocols and pushing the envelops, often in the face of massive popular skepticism.

 
These people, these patients and loved ones and doctors who risked everything; life, limb, money, time and more…they are the mavericks, the trail blazers, the ones who sacrificed everything for the one pure goal of advancing medicine, of advancing healing. They deserve to be honored and credited with their barrier breaking work, not dismissed in some ill conceived misinformation campaign, weakly relying upon the un-sturdy columns of anti-Piaget-ian Object Permanence.

hear_speak_see_no_evil_toshogu_cropped_enhanced

And no mention of Spinal Cord Injury and Stem Cell Treatment should be made without a HUGE nod to the God-Fathers, Prof Mackay-Sim and Dr Carlos Lima.

Dr Mackay-Sim was researching olfactoric mucosal stem cell applications for spinal cord injury in murine models as far back as 2001:

  1. Lu, J.; Feron, F.; Ho, S. H.; Mackay-Sim, A.; Waite, P. M. E. Transplantation of nasal olfactory tissue promotes partial recovery in paraplegic adult rats. Brain Research 2001, 889, 344-357.
  2. Lu, J.; Feron, F.; Mackay-Sim, A.; Waite, P. M. E. Olfactory ensheathing cells promote locomotor recovery after delayed transplantation into transected spinal cord. Brain 2002, 125, 14-21.

Dr Lima was “improving” and “recovering” Spinal Cord Injury patients with stem cells derived from their own noses as far back as…wait for it…2003.

“Olfactory stem cells have been shown to be most versatile. Indeed, Adult stem cells from the nose have now helped paraplegic patients walk. From the primary source, Carlos Lima et al., Olfactory mucosal autografts and rehabilitation for chronic traumatic spinal cord injury, Neurorehabil Neural Repair 24(1):10–22 | doi: 10.1177/1545968309347685.”

“Of the 13 patients assessed by functional studies, 1 paraplegic patient (patient 9) can ambulate with 2 crutches and knee braces with no physical assistance and 10 other patients can ambulate with walkers with or without braces with physical assistance.

One tetraplegic [paralyzed in both arms and legs] patient (patient 13) ambulates with a walker, without knee braces or physical assistance.”

Why haven’t you heard of this?  I don’t know.  Perhaps you missed the “Testimony of Ms. Laura Dominguez, delivered at a hearing held by the United States Senate Subcommittee on Science, Technology, and Space on July 14, 2004. Accessed at: http://commerce.senate.gov/hearings/testimony.cfm?id=1268andwit_id=3673

If that doesn’t work, go here and skip ahead to 1 hour, 16 minutes to 2hrs 21min: https://www.c-span.org/video/?182693-1/stem-cell-research-treatment

Laura Dominguez, also featured in the article  here, was treated in 2004.  By then,

Dr “Lima’s procedure had proven successful in 26 patients, states Dr. Jean D. Peduzzi-Nelson, a co-researcher at the University of Alabama in Birmingham. [9] Dominguez was the tenth person in the world and the second American to undergo the surgery.

Completion of the surgery permitted a return to the United States, which ushered in the continuation of the therapeutic process and the resumption of home life in San Antonio. After an MRI was conducted, physicians informed her that her spinal cord had begun healing and that 70 percent of the lesion had recovered into normal spinal tissue. Within six months she had acquired sensation down to the abdominal region. By 2004, she had gained upper body agility and the ability to stand for extended periods of time with the aid of a walker. In addition, she reported improved motor skills, including the ability to stand on her toes and contract her quadriceps and hamstring muscles. She also announced that she had walked more than 1400 feet with the use of braces and outside help. Laura is inspired by the results and hopes to walk unassisted by the time she turns 21. [10]

Not first.  Missed it by just a baker’s dozen of years.

Here are just a small selection of more stem cell heroes from the past:

SPINAL CORD SUCCESSES

 https://repairstemcell.wordpress.com/2009/03/25/spinal-cord-injury-success/

 

MORE SPINAL CORD SUCCESSES

https://repairstemcell.wordpress.com/2009/03/25/more-spinal-cord-injury-success-from-adult-stem-cells/

 

STEM CELLS FOR SPINAL CORD

https://repairstemcell.wordpress.com/2009/03/20/stem-cell-surgery-spinal-cord-injury/

 

16 YEAR OLD PARALYZED KARTING CHAMP

https://repairstemcell.wordpress.com/2009/09/07/16-year-old-paralyzed-karting-champ-undergoing-stem-cell-treatment/

 

PARALYZED WOMAN WALKS ON 21ST BIRTHDAY
https://repairstemcell.wordpress.com/2009/04/23/strength-and-determination-help-paralyzed-woman-walk-on-21st-birthday/

 

QUEST TO CURE HIS DAUGHTER

https://repairstemcell.wordpress.com/2009/04/14/a-father%e2%80%99s-quest-to-cure-his-daughter-well-blog-nytimescom/

 

PARALYSIS IN RATS REVERSED

https://repairstemcell.wordpress.com/2009/04/02/adult-spinal-stem-cells-reverse-paralysis-in-rats/

 

ADULT STEM CELL PROGRAMS

https://repairstemcell.wordpress.com/2009/03/30/il-sussidiarionet-raisman-the-best-results-are-coming-from-the-adult-stem-cell-research-programmes/

 

IMPROVED QUALITY OF LIFE FOR THE PARALYZED

https://repairstemcell.wordpress.com/2009/03/26/adult-stem-cell-study-demonstrates-improved-quality-of-life-for-patients-suffering-from-spinal-cord-injury/

 

A PERSONAL NOTE

http://reflectionsofaparalytic.com/?p=2052

 

FUNDRAISING FOR SPINAL CORD/STEM CELL THERAPY

https://repairstemcell.wordpress.com/2009/03/20/fundraiser-for-spinal-cord-injury-patient-for-stem-cell-treatment/

 

STEM CELLS HELP 52 SPINAL CORD INJURY PATIENTS

https://repairstemcell.wordpress.com/2009/03/19/stem-cell-research-helps-52-spinal-cord-injury-patients-stem-cell-research-adult-stem-cell-research-spinal-cord-injury/

 

PARALYZED LAWMAKER MAKES STEM CELL DECISION

https://repairstemcell.wordpress.com/2009/03/11/paralyzed-ri-lawmaker-hails-stem-cell-decision-international-herald-tribune/

 

JAPAN AHEAD OF USA IN STEM CELLS FOR SCI

https://repairstemcell.wordpress.com/2009/02/10/spinal-cord-injury-sci-stem-cell-trials-japan-plays-catch-up/

 

CHINA AHEAD OF USA FOR STEM CELL TREATMENTS/SCI

https://repairstemcell.wordpress.com/2009/02/27/stem-cell-research-yields-benefits-for-american-man-traveling-to-china/

 

WHY DO WE PRETEND STEM CELLS DON’T WORK?

https://repairstemcell.wordpress.com/2009/02/18/adult-stem-cells-get-the-shaft-none-are-so-blind-as-those-who-will-not-see/

 

IRAN AHEAD OF USA IN STEM CELLS

https://repairstemcell.wordpress.com/2009/02/12/stem-cells-in-iran-catch-up/

 

 

TODDLER, CANCER, STEM CELLS, SPINAL CORD INJURY

https://repairstemcell.wordpress.com/2009/02/08/toddler-helps-bring-about-a-medical-miracle-cancer-spimal-cord-injury/

 

REGENERATING THE CENTRAL NERVOUS SYSTEM https://repairstemcell.wordpress.com/2011/10/17/regenerating-the-central-nervous-system/

 

Stepping Towards A Paralysis Cure, A Tale Of Two Supermen Stem Cells Cure 23 Year Old Male of Paralysis – C6…-C7 injury

https://repairstemcell.wordpress.com/2009/03/28/stepping-towards-a-paralysis-cure-a-tale-of-two-supermen-stem-cells-cure-23-year-old-male-of-paralysis-c6-c7-injury/

 

Paraplegic – Adult Stem Cell Success Stories – Laura Dominguez

https://repairstemcell.wordpress.com/2010/05/05/paraplegic-adult-stem-cell-success-stories-laura-dominguez/

 

PARALYZED COUSINS PLEASED WITH STEM CELL TREATMENT

https://repairstemcell.wordpress.com/2010/02/15/paralyzed-cousins-pleased-with-stem-cell-treatment/

 

Successful Stem Cell Treatment of Spinal Cord Injury in Dogs

https://repairstemcell.wordpress.com/2010/02/08/successful-stem-cell-treatment-of-spinal-cord-injury-in-dogs/

 

Spinal Cord Injury Patient Wins…and Loses

https://repairstemcell.wordpress.com/2010/02/08/spinal-cord-injury-patient-wins-and-loses/

 

STEM CELLS FOR SPINAL CORD INJURY

https://repairstemcell.wordpress.com/2009/12/31/stem-cells-for-spinal-cord-injury/

 

Adult Stem Cell Grafts Help Paralyzed Heal

https://repairstemcell.wordpress.com/2009/10/21/adult-stem-cell-grafts-help-paralyzed-heal/

 

Medical hope as paralysed dog cured by stem cell therapy

https://repairstemcell.wordpress.com/2009/10/08/medical-hope-as-paralysed-dog-cured-by-stem-cell-therapy-mirror-co-uk/

 

and even, Major the Roseville police dog gets stem cell treatment

http://blogs.citypages.com/blotter/2011/01/major_police_dog_stem_cell.php

 

Time to set the record straight.  Too many have waited too long to get news which blacks out a dozen years of research and progress.

NON SMOKERS GET LUNG CANCER

In DISEASE INFO, HEALTH AND WELLNESS, SCIENCE & STEM CELLS on January 26, 2017 at 2:00 pm

‘Lung cancer is almost always fatal because it is asymptomatic. “Symptoms of lung cancer (chronic cough, shortness of breath, phlegm in lungs) are very similar to common respiratory illnesses”’

Can people get lung cancer if they don’t smoke?

smoke-industrial-sky

Lung cancer is responsible for almost one-quarter of all cancer deaths in the nation.

Although this type is especially common in people who smoke cigarettes, it is possible for the disease to occur in non-smokers and yes, sometimes even in those who aren’t often breathing secondhand smoke.

A Texas A&M College of Medicine Radiation Oncologist breaks down the science behind lung cancer and the environmental hazards that could result in a diagnosis.

The American Cancer Society (ACS) estimates 224,000 new cases of lung cancer will be diagnosed in 2016.

“This means up to 13 percent of all projected cancers this year could be lung cancer,” said Niloy J. Deb, MD, Assistant Professor of radiology with the Texas A&M College of Medicine and Chairman.

“The leading cause of diagnosis is due to smoking cigarettes, but there are other instances where the cancer can occur.”

Secondhand smoke—like breathing car exhaust into your lungs

Do you live with friends or family who smoke cigarettes? If so, you’re at a much higher risk for developing lung cancer.

“Exposure to secondhand smoke is the number one cause of lung cancer in non-smokers,” Deb said. “Non-smokers who are constantly exposed to secondhand smoke increase their likelihood of getting lung cancer by 20 percent.”

buttout

So, how exactly does secondhand smoke up your chances for lung cancer? Deb said even smoke indirectly inhaled from a cigarette is damaging to the lungs.

“Chronic smoking impairs the tiny alveoli (small sacs that move oxygen and carbon dioxide between the lungs and bloodstream) in our lungs, and these alveoli start ‘trapping’ air,” he said.

“Cigarette smoke, with all the dissolved carcinogens, will then ‘sit’ in the alveoli, which causes the genetic mutations (changes) that cause cancerous transformation.”

Important to know: The most harmful part of cigarette smoke comes from the burning paper. This is because compounds are added to the wrapping to allow the tobacco and paper to burn at the same rate.

“To do this, companies add tar and other petroleum derivatives to the paper around cigarettes,” Deb said. “So, when you inhale smoke from a cigarette, it’s essentially like breathing car exhaust directly into your lungs.”

butt-car-exhaust-fumes-325x294

Carcinogens activate the ‘switch’ for cancer cell mutation

Cancer happens when a cell’s DNA is changed, and there are certain known substances and exposures that can lead to cancer; these are called carcinogens.

According to the ACS, carcinogens don’t always cause cancer in every case, but they may predispose to cancer in other ways.

“Some environmental carcinogens like asbestos, silica, benzene, ethylene oxide, and exposure to nickel compounds and by-products of petroleum distillation from vehicle exhaust and fossil fuels, can lead to lung cancer,” Deb said.

“These substances flip the genetic switches in our body by turning on a cancer activator or turning off a cancer suppressor.”

For example: For a cancer cell to form in our lungs, there must be an on/off switch flipped in the genetic code of the lung cells. “When a carcinogen flicks the ‘on’ switch, it turns on a gene that converts a normal cell into a cancer cell,” Deb said.

“When a carcinogen hits the ‘off’ switch, it’s turning off a gene that has been preventing a cancerous process or cancer cell formation. These switches can be flipped because of exposure to environmental carcinogens.”

Why lung cancer is a killer

Lung cancer is almost always fatal because it is asymptomatic. “Symptoms of lung cancer (chronic cough, shortness of breath, phlegm in lungs) are very similar to common respiratory illnesses,” Deb said.

“Most patients (both smokers and non-smokers) do not know their symptoms may be caused by cancer instead of a relatively benign illness.”

Most people who are diagnosed with lung cancer live with symptoms for years before seeking any medical opinion, and by then, it’s too late.

“This is why most lung cancers are diagnosed at Stage 3 or Stage 4 and the reason approximately 158,000 people die from lung cancer each year,” Deb said.

“The death rate increases when you can’t catch the cancer at an earlier stage, when there are more treatment options available.”

LEAKY GUT + BLOOD BRAIN BARRIER =AUTISM?

In DISEASE INFO, HEALTH AND WELLNESS, SCIENCE & STEM CELLS on January 24, 2017 at 10:55 am

leaking

Does leaking cause autism and schizophrenia?

Remember those hysterical soccer Moms who said Autism has to do with the gut, the immune system and the brain.  Guess what, they were pretty spot on…it looks like in ASD and schizophrenia patients, there is a significant incidence of leaking in both the intestines and the blood-brain barrier

  1. “Blood-brain-barrier integrity and function and with inflammation was detected in ASD tissue samples, supporting the hypothesis that an impaired blood-brain barrier associated with neuroinflammation contributes to ASD”
  2. Gut: “75 percent of the individuals affected by ASD had reduced expression of barrier-forming cellular components, compared with controls, and 66 percent showed a higher expression of molecules that increase intestinal permeability”

autism-awareness

Wednesday, January 18, 2017

Study finds alterations in both blood-brain barrier and intestinal permeability in individuals with autism

Autism spectrum disorder (ASD) has the dubious distinction of being the fastest-growing developmental disability in the U.S., according to the Centers for Disease Control and Prevention. With 1 in every 68 children born in this country diagnosed with ASD, parents are looking everywhere for answers about best treatments. Along with selective medication to treat certain symptoms, traditional treatments include intensive behavioral approaches. But with no “one-size-fits-all” treatment approach, parents often turn to diverse complementary and alternative therapies.

Just as parents are looking for answers, scientists are trying to tease out the causes of this multifactorial and complex condition. “Although we are fairly certain that there is a genetic component, there are many pathways for an individual to arrive at autism’s final destination,” says Alessio Fasano, MD, director of the Center for Celiac Research and Treatment at Massachusetts General Hospital (MGH) and co-senior author of a study published in the journal Molecular Autism. “What might dispose one person to develop ASD – either pre- or post-natally – might have no such effect on another person,” he adds.

Looking at the interconnectivity of the gut-brain axis – the biochemical signaling between the gastrointestinal and central nervous systems – researchers led by Maria Rosaria Fiorentino, PhD, of the Mucosal Immunology and Biology Research Center at MassGeneral Hospital for Children (MGHfC), have opened up a new avenue of research into the pathophysiology of ASD and other neurodevelopmental disorders. “As far as we know, this is the first study to look at the molecular signature of blood-brain barrier dysfunction in ASD and schizophrenia in samples from human patients,” says Fiorentino. In collaboration with researchers from the University of Maryland School of Medicine and others, Fiorentino’s group found an altered blood-brain barrier in tissue samples from people with ASD when compared with healthy controls.

The group analyzed postmortem cerebral cortex and cerebellum tissues from 33 individuals – 8 with ASD, 10 with schizophrenia and 15 healthy controls. Altered expression of genes associated with blood-brain-barrier integrity and function and with inflammation was detected in ASD tissue samples, supporting the hypothesis that an impaired blood-brain barrier associated with neuroinflammation contributes to ASD.

In keeping with the hypothesis that the interplay within the gut-brain axis is a crucial component in the development of neurodevelopmental disorders, the group also analyzed intestinal epithelial tissue from 12 individuals with ASD and 9 without such disorders. That analysis revealed that 75 percent of the individuals affected by ASD had reduced expression of barrier-forming cellular components, compared with controls, and 66 percent showed a higher expression of molecules that increase intestinal permeability.

The study was driven in part by the high number of gastrointestinal problems that occur in people with ASD. Although considered controversial by some health care practitioners, a gluten- and casein-free diet has been shown to produce some improvement in behavioral and gastrointestinal symptoms in a subgroup of children with ASD. “This is the first time anyone has shown that an altered blood-brain barrier and impaired intestinal barrier might both play a role in neuroinflammation in people with ASD,” says Fiorentino.

Fasano adds, “As well as information on the blood-brain barrier, we were looking for more information on how increased intestinal permeability, otherwise known as a ‘leaky gut,’ might affect the development of ASD in the context of a dysfunctional gut-brain axis.”

Fiorentino’s next project involves looking more mechanistically at how microbiota – the collection of microorganisms in the gut – are linked with intestinal permeability and behavior. “There is definitely something going on between the gut and the brain with ASD and other neurodevelopmental disorders, and of course the microbiome has a big role to play,” she says. “It has already been shown that ASD kids have an altered composition of gut microbial communities. If we can figure out what is required or missing, then maybe we can come up with a treatment that might be able to improve some of the behavioral issues and/or the gastrointestinal symptoms.”

Fasano is a professor of Pediatrics, and Fiorentino is an assistant professor of Pediatrics at Harvard Medical School. Additional co-authors of the Molecular Autism paper are Anna Sapone, PhD, Stefania Senger, PhD, and Stephanie Camhi, MGHfC Mucosal Immunology and Biology Research Center; Sarah Kadzielski, MD, and Timothy Buie, MGHfC Gastoenterology and Lurie Center for Autism; Deanna L. Kelly, PharmD, BCPP, University of Maryland School of Medicine, and Nicola Cascella, MD, Sheppard Pratt Health System, Baltimore.

Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH Research Institute conducts the largest hospital-based research program in the nation, with an annual research budget of more than $800 million and major research centers in HIV/AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, photomedicine and transplantation biology. The MGH topped the 2015 Nature Index list of health care organizations publishing in leading scientific journals and earned the prestigious 2015 Foster G. McGaw Prize for Excellence in Community Service. In August 2016 the MGH was once again named to the Honor Roll in the U.S. News & World Report list of “America’s Best Hospitals.”

20 MINUTES EXERCISE = INFLAMMATION REDUX

In DISEASE INFO, HEALTH AND WELLNESS on January 23, 2017 at 11:17 am

Does exercise increase or reduce inflammation?  One look at Arnold Schwarzenegger’s  incredibly pumped physique and you might think exercise increases inflammation…but this is a different KIND of inflammation.
Scientists have found that just
one session of moderate exercise can stimulate the immune system, producing an anti-inflammatory cellular response.  “The findings have encouraging implications for chronic diseases like arthritis, fibromyalgia and for more pervasive conditions, such as obesity.”
schwarzenegger

Exercise … It does a body good: 20 minutes can act as anti-inflammatory

One moderate exercise session has a cellular response that may help suppress inflammation in the body

Date:January 12, 2017 – Source: University of California – San Diego
Summary:
It’s well known that regular physical activity has health benefits, including weight control, strengthening the heart, bones and muscles and reducing the risk of certain diseases. Recently, researchers have found how just one session of moderate exercise can also act as an anti-inflammatory. The findings have encouraging implications for chronic diseases like arthritis, fibromyalgia and for more pervasive conditions, such as obesity.

It’s well known that regular physical activity has health benefits, including weight control, strengthening the heart, bones and muscles and reducing the risk of certain diseases. Recently, researchers at University of California San Diego School of Medicine found how just one session of moderate exercise can also act as an anti-inflammatory. The findings have encouraging implications for chronic diseases like arthritis, fibromyalgia and for more pervasive conditions, such as obesity.

The study, recently published online in Brain, Behavior and Immunity, found one 20-minute session of moderate exercise can stimulate the immune system, producing an anti-inflammatory cellular response.

“Each time we exercise, we are truly doing something good for our body on many levels, including at the immune cell level,” said senior author Suzi Hong, PhD, in the Department of Psychiatry and the Department of Family Medicine and Public Health at UC San Diego School of Medicine. “The anti-inflammatory benefits of exercise have been known to researchers, but finding out how that process happens is the key to safely maximizing those benefits.”

The brain and sympathetic nervous system — a pathway that serves to accelerate heart rate and raise blood pressure, among other things — are activated during exercise to enable the body to carry out work. Hormones, such as epinephrine and norepinephrine, are released into the blood stream and trigger adrenergic receptors, which immune cells possess.

This activation process during exercise produces immunological responses, which include the production of many cytokines, or proteins, one of which is TNF — a key regulator of local and systemic inflammation that also helps boost immune responses.

exercise

“Our study found one session of about 20 minutes of moderate treadmill exercise resulted in a five percent decrease in the number of stimulated immune cells producing TNF,” said Hong. “Knowing what sets regulatory mechanisms of inflammatory proteins in motion may contribute to developing new therapies for the overwhelming number of individuals with chronic inflammatory conditions, including nearly 25 million Americans who suffer from autoimmune diseases.”

The 47 study participants walked on a treadmill at an intensity level that was adjusted based on their fitness level. Blood was collected before and immediately after the 20 minute exercise challenge.

“Our study shows a workout session doesn’t actually have to be intense to have anti-inflammatory effects. Twenty minutes to half-an-hour of moderate exercise, including fast walking, appears to be sufficient,” said Hong. “Feeling like a workout needs to be at a peak exertion level for a long duration can intimidate those who suffer from chronic inflammatory diseases and could greatly benefit from physical activity.”

Inflammation is a vital part of the body’s immune response. It is the body’s attempt to heal itself after an injury; defend itself against foreign invaders, such as viruses and bacteria; and repair damaged tissue. However, chronic inflammation can lead to serious health issues associated with diabetes, celiac disease, obesity and other conditions.

“Patients with chronic inflammatory diseases should always consult with their physician regarding the appropriate treatment plan, but knowing that exercise can act as an anti-inflammatory is an exciting step forward in possibilities,” said Hong.


Story Source:

Materials provided by University of California – San Diego. Original written by MIchelle Brubaker. Note: Content may be edited for style and length.


Journal Reference:

  1. Stoyan Dimitrov, Elaine Hulteng, Suzi Hong. Inflammation and exercise: Inhibition of monocytic intracellular TNF production by acute exercise via β2-adrenergic activation. Brain, Behavior, and Immunity, 2016; DOI: 10.1016/j.bbi.2016.12.017

TZAP! GOES THE TELOMERE FUSE

In DISEASE INFO, HEALTH AND WELLNESS, OFF THE BEATEN PATH, PHARMA AND DRUGS, SCIENCE & STEM CELLS on January 21, 2017 at 9:44 am

burning-cancle-both-emds

EVERY TIME A CELL DIVIDES, A TELOMERE LOSES IT’S WINGS

  • The length of a telomere controls cell age.
  • Each time a cell splits, the telomere gets smaller.
  • Too long and cancer risk increases.
  • Too short and no more cell division.

Scripps Research Institute discovered the TZAP that controls telomere length.  “TZAP: a Telomere-Associated Protein involved in telomere length control”

Master regulator of cellular aging discovered

Date: January 12, 2017 – Source: Scripps Research Institute – Summary: Scientists have discovered a protein that fine-tunes the cellular clock involved in aging.
Cell culture under microscope (stock image).
Credit: © sinitar / Fotolia
 Scientists at The Scripps Research Institute (TSRI) have discovered a protein that fine-tunes the cellular clock involved in aging.

This novel protein, named TZAP, binds the ends of chromosomes and determines how long telomeres, the segments of DNA that protect chromosome ends, can be. Understanding telomere length is crucial because telomeres set the lifespan of cells in the body, dictating critical processes such as aging and the incidence of cancer.

“Telomeres represent the clock of a cell,” said TSRI Associate Professor Eros Lazzerini Denchi, corresponding author of the new study, published online today in the journal Science. “You are born with telomeres of a certain length, and every time a cell divides, it loses a little bit of the telomere. Once the telomere is too short, the cell cannot divide anymore.”

Naturally, researchers are curious whether lengthening telomeres could slow aging, and many scientists have looked into using a specialized enzyme called telomerase to “fine-tune” the biological clock. One drawback they’ve discovered is that unnaturally long telomeres are a risk factor in developing cancer.

“This cellular clock needs to be finely tuned to allow sufficient cell divisions to develop differentiated tissues and maintain renewable tissues in our body and, at the same time, to limit the proliferation of cancerous cells,” said Lazzerini Denchi.

In this new study, the researcher found that TZAP controls a process called telomere trimming, ensuring that telomeres do not become too long.

“This protein sets the upper limit of telomere length,” explained Lazzerini Denchi. “This allows cells to proliferate — but not too much.”

For the last few decades, the only proteins known to specifically bind telomeres is the telomerase enzyme and a protein complex known as the Shelterin complex. The discovery TZAP, which binds specifically to telomeres, was a surprise since many scientists in the field believed there were no additional proteins binding to telomeres.

“There is a protein complex that was found to localize specifically at chromosome ends, but since its discovery, no protein has been shown to specifically localize to telomeres,” said study first author Julia Su Zhou Li, a graduate student in the Lazzerini Denchi lab.

“This study opens up a lot of new and exciting questions,” said Lazzerini Denchi.

In addition to Lazzerini Denchi and Li, authors of the study, “TZAP: a telomere-associated protein involved in telomere length control,” were Tatevik Simavorian, Cristina Bartocci and Jill Tsai of TSRI; Javier Miralles Fuste of the Salk Institute for Biological Studies and the University of Gothenburg; and Jan Karlseder of the Salk Institute for Biological Studies.

The study was supported by the American Cancer Society (grant RSG-14-186-01), the Swedish Research Council International (grant D0730801) and the National Institutes of Health (grant R01GM087476 and R01CA174942).


Story Source:

Materials provided by Scripps Research Institute. Note: Content may be edited for style and length.


Journal Reference:

  1. Julia Su Zhou Li, Javier Miralles Fuste, Tatevik Simavorian, Cristina Bartocci, Jill Tsai, Jan Karlseder, Eros Lazzerini Denchi. TZAP: A telomere-associated protein involved in telomere length control. Science, 2017; DOI: 10.1126/science.aah6752

MOSES, STEM CELL PATHWAYS AND MAYBE METASTATIC CANCERS

In ALL ARTICLES, DISEASE INFO, SCIENCE & STEM CELLS, STEM CELLS IN THE NEWS on January 20, 2017 at 9:32 am

When white blood cells leave a vessel through the vessel wall, they contort their shape to pass through.  But when stem cells exit a blood vessel, they don’t change their shape.  They just pass on through the wall and the endothelial cells lining the vessel do the work by stretching around them and then actively expelling them.   In other words, the stem cells are the Moses to the parting of the cells of the blood vessels:
“…when we looked at therapeutic stem cells… the endothelial cells not only changed their shape in order to surround the stem cell, they actually pushed the stem cells out of the blood vessel. We’ve named this process angiopellosis, and it represents an alternative way for cells to leave blood vessels.”  Which begs the question…is this how cancer cells move around too?

Stem Cell Finding May Improve Understanding of Metastatic Cancers

  • A stem cell exits the bloodstream through angiopellosis. [Alice MacGregor Harvey, North Carolina State University]

  • Researchers at North Carolina State University have discovered that therapeutic stem cells exit the bloodstream in a different manner than was previously thought. This process, called angiopellosis by the researchers, has implications for improving our understanding of not only intravenous stem cell therapies, but also metastatic cancers.

    When white blood cells need to get to the site of an infection, they can exit the bloodstream via a process known as diapedesis. In diapedesis, the white blood cell changes its shape to squeeze between or through the epithelial cells that form the walls of the blood vessel. Diapedesis is a well-understood process, and researchers believed that other types of cells, like therapeutic stem cells or even metastatic cancer cells, exited blood vessels in a similar way, with the cells pushing or squeezing themselves out.

    But a group of researchers led by Ke Cheng, Ph.D., associate professor of molecular biomedical sciences at NC State with a joint appointment in the NC State/University of North Carolina (UNC)-Chapel Hill Department of Biomedical Engineering, found that these stem cells behaved differently. Their study (“Angiopellosis as an Alternative Mechanism of Cell Extravasation”) appears online in Stem Cells.

    Therapeutic stem cells share the same ability to exit the bloodstream and target particular tissues that white blood cells do. But the precise way that they did so was not well understood, so Dr. Cheng and his team used a zebrafish model to study the process. The genetically modified zebrafish embryos were transparent and had fluorescently marked green blood vessels. Researchers injected the embryos with white blood cells and cardiac stem cells from humans, rats, and dogs. These cells had all been marked with a red fluorescent protein.

    Through time-lapse, three-dimensional, light sheet microscopic imaging, Dr. Cheng and his team could trace the progress of these cells as they left the blood vessel. The white blood cells exited via diapedesis, as expected. When stem cells exited the blood vessel, however, the endothelial cells lining the vessel actively expelled them. Membranes surrounding the endothelial cells on either side of the stem cell stretched themselves around the stem cell, then met in the middle to push the stem cell out of the vessel.

    “When you’re talking about diapedesis, the white blood cell is active because it changes its shape in order to exit. The endothelial cells in the blood vessel are passive,” Dr. Cheng says. “But when we looked at therapeutic stem cells, we found the opposite was true—the stem cells were passive—and the endothelial cells not only changed their shape in order to surround the stem cell, they actually pushed the stem cells out of the blood vessel. We’ve named this process angiopellosis, and it represents an alternative way for cells to leave blood vessels.”

    The researchers found two other key differences between angiopellosis and diapedesis: one, that angiopellosis takes hours, rather than minutes, to occur and two, that angiopellosis allows more than one cell to exit at a time.

    “Angiopellosis is really a group ticket for cells to get out of blood vessels,” notes Dr. Cheng. “We observed clusters of cells passing through in this way. Obviously, this leads us to questions about whether other types of cells, like metastatic cancer cells, may be using this more effective way to exit the bloodstream, and what we may need to do to stop them.”

 

via

PROOF THE ENVIRONMENT CONTRIBUTES TO DISEASE

In ALL ARTICLES, DISEASE INFO, HEALTH AND WELLNESS on November 26, 2014 at 4:33 pm

Science has poo-pooed the effect of environmental toxins for years citing that the miniscule concentrations of toxins couldn’t possibly cause harm to the human body. Everything from GMOs to toxins in vaccines were ignored based on this premise. New science reveals though that the environment can not only effect the human body but it can change DNA and contribute to diseases. Now that there’s proof, it’s time to get the crap out of our lives. -David Granovsky toxin-problem HOW ENVIRONMENT CONTRIBUTES TO SEVERAL HUMAN DISEASES National Institute of Environmental Health Sciences (NIEHS) Using a new imaging technique, researchers have found that the biological machinery that builds DNA can insert molecules into the DNA strand that are damaged as a result of environmental exposures. These damaged molecules trigger cell death that produces some human diseases, according to the researchers. The work provides a possible explanation for how one type of DNA damage may lead to cancer, diabetes, hypertension, cardiovascular and lung disease, and Alzheimer’s disease… Samuel Wilson, M.D., senior NIEHS researcher on the team, explained that the damage is caused by oxidative stress, or the generation of free oxygen molecules, in response to environmental factors, such as ultraviolet exposure, diet, and chemical compounds in paints, plastics, and other consumer products… “When one of these oxidized nucleotides is placed into the DNA strand, it can’t pair with the opposing nucleotide as usual, which leaves a gap in the DNA,” Wilson said. “Until this paper, no one had actually seen how the polymerase did it or understood the downstream implications.” http://www.niehs.nih.gov/news/newsroom/releases/2014/november25/index.cfm http://www.sciencedaily.com/releases/2014/11/141125101703.htm

%d bloggers like this: