Amare mental wellness business incentive trip to Riviera Maya

Help those with metabolic health issues and build a business on the side in the area of mental health with Amare. Join here

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Call about the trip incentive with Amare , 408-854-1883 , as business owner in this wellness business (in the USA and Mexico, Canada and Europe next, now in its 2nd year).

Mycobacteria,  schizophrenic, epileptic and Osteomyelitis

Immunoelectrophoresis – Semantic Scholar

Cell extracts from four species of mycobacteriaMycobacterium tuberculosis (four strains), M. bovis strain BCG, M. scrofulaceum, and M. phlei, were assayed by 2D-IEPwith four …… alized chronic schizophrenic and epileptic patients. J. Neurol.

Species Identification of Mycobacteria by PCR-Restriction Fragment …


by H Lee – ‎2000 – ‎Cited by 288 – ‎Related articles

Currently, identification of clinical isolates of mycobacteria to the species level …. M. asiaticum; 8, M. chelonae; 9, M. moriokaese; 10, M. phlei; 11, M. pulveris; 12, ….. of microRNA-181b in regulating the schizophrenia susceptibility gene EGR3.

Web results

Osteomyelitis caused by mycobacterium fortuitum – Springer


Zusammenfassung: Osteomyelitis durch Mycobacterium /or- tuitum. Eine Osteomyelitis … A twenty-five year old man with schizophrenia was admit- ted to another …. growth 3–4 weeks. Fast-growing. M. phlei growth within 5 days. M. fortuitum.

Johne’s Disease, Inflammatory Bowel Disease, and Mycobacterium …


Oct 13, 2004 – An extract of Mycobacterium phlei allowed in vitro growth of the microorganisms present in animal tissues by providing mycobactin, …

Periventricular diffuse pinealoma: Report of a case with clinical …


… diffuse pinealoma: Report of a case with clinical features of catatonic schizophrenia. … to Infection by a Crude Cell Wall Preparation from Mycobacterium phlei.

(PDF) Use of DNA probes to identify and classify mycobacteria


Use of DNA probes to identify and classify mycobacteria … 8 (lane 7), 11 (lane 8), 27 (lane 9) M . kansasii (lane lo), M. chelonei (lane 11) and M . phlei (lane 12). … . Two-dimensional PAGE analysis of translation products ,from schizophrenic …

Gut microbes eat our medication for Parkinson

Pills illustration (stock image).
Credit: © georgejmclittle / Adobe Stock
Researchers have discovered one of the first concrete examples of how the microbiome can interfere with a drug’s intended path through the body. Focusing on levodopa (L-dopa), the primary treatment for Parkinson’s disease, they identified which bacteria out of the trillions of species is responsible for degrading the drug and how to stop this microbial interference.

The first time Vayu Maini Rekdal manipulated microbes, he made a decent sourdough bread. At the time, young Maini Rekdal, and most people who head to the kitchen to whip up a salad dressing, pop popcorn, ferment vegetables, or caramelize onions, did not consider the crucial chemical reactions behind these concoctions.

Even more crucial are the reactions that happen after the plates are clean. When a slice of sourdough travels through the digestive system, the trillions of microbes that live in our gut help the body break down that bread to absorb the nutrients. Since the human body cannot digest certain substances — all-important fiber, for example — microbes step up to perform chemistry no human can.

“But this kind of microbial metabolism can also be detrimental,” said Maini Rekdal, a graduate student in the lab of Professor Emily Balskus and first-author on their new study published in Science. According to Maini Rekdal, gut microbes can chew up medications, too, often with hazardous side effects. “Maybe the drug is not going to reach its target in the body, maybe it’s going to be toxic all of a sudden, maybe it’s going to be less helpful,” Maini Rekdal said.

In their study, Balskus, Maini Rekdal, and their collaborators at the University of California San Francisco, describe one of the first concrete examples of how the microbiome can interfere with a drug’s intended path through the body. Focusing on levodopa (L-dopa), the primary treatment for Parkinson’s disease, they identified which bacteria are responsible for degrading the drug and how to stop this microbial interference.

Parkinson’s disease attacks nerve cells in the brain that produce dopamine, without which the body can suffer tremors, muscle rigidity, and problems with balance and coordination. L-dopa delivers dopamine to the brain to relieve symptoms. But only about 1 to 5% of the drug actually reaches the brain.

This number — and the drug’s efficacy — varies widely from patient to patient. Since the introduction of L-dopa in the late 1960s, researchers have known that the body’s enzymes (tools that perform necessary chemistry) can break down L-dopa in the gut, preventing the drug from reaching the brain. So, the pharmaceutical industry introduced a new drug, carbidopa, to block unwanted L-dopa metabolism. Taken together, the treatment seemed to work.

“Even so,” Maini Rekdal said, “there’s a lot of metabolism that’s unexplained, and it’s very variable between people.” That variance is a problem: Not only is the drug less effective for some patients, but when L-dopa is transformed into dopamine outside the brain, the compound can cause side effects, including severe gastrointestinal distress and cardiac arrhythmias. If less of the drug reaches the brain, patients are often given more to manage their symptoms, potentially exacerbating these side effects.

Maini Rekdal suspected microbes might be behind the L-dopa disappearance. Since previous research showed that antibiotics improve a patient’s response to L-dopa, scientists speculated that bacteria might be to blame. Still, no one identified which bacterial species might be culpable or how and why they eat the drug.

So, the Balskus team launched an investigation. The unusual chemistry — L-dopa to dopamine — was their first clue.

Few bacterial enzymes can perform this conversion. But, a good number bind to tyrosine — an amino acid similar to L-dopa. And one, from a food microbe often found in milk and pickles (Lactobacillus brevis), can accept both tyrosine and L-dopa.

Using the Human Microbiome Project as a reference, Maini Rekdal and his team hunted through bacterial DNA to identify which gut microbes had genes to encode a similar enzyme. Several fit their criteria; but only one strain, Enterococcus faecalis (E. faecalis), ate all the L-dopa, every time.

With this discovery, the team provided the first strong evidence connecting E. faecalis and the bacteria’s enzyme (PLP-dependent tyrosine decarboxylase or TyrDC) to L-dopa metabolism.

And yet, a human enzyme can and does convert L-dopa to dopamine in the gut, the same reaction carbidopa is designed to stop. Then why, the team wondered, does the E. faecalis enzyme escape carbidopa’s reach?

Even though the human and bacterial enzymes perform the exact same chemical reaction, the bacterial one looks just a little different. Maini Rekdal speculated that carbidopa may not be able to penetrate the microbial cells or the slight structural variance could prevent the drug from interacting with the bacterial enzyme. If true, other host-targeted treatments may be just as ineffective as carbidopa against similar microbial machinations.

But the cause may not matter. Balskus and her team already discovered a molecule capable of inhibiting the bacterial enzyme.

“The molecule turns off this unwanted bacterial metabolism without killing the bacteria; it’s just targeting a non-essential enzyme,” Maini Rekdal said. This and similar compounds could provide a starting place for the development of new drugs to improve L-dopa therapy for Parkinson’s patients.

The team might have stopped there. But instead, they pushed further to unravel a second step in the microbial metabolism of L-dopa. After E. faecalis converts the drug into dopamine, a second organism converts dopamine into another compound, meta-tyramine.

To find this second organism, Maini Rekdal left behind his mother dough’s microbial masses to experiment with a fecal sample. He subjected its diverse microbial community to a Darwinian game, feeding dopamine to hordes of microbes to see which prospered.

Eggerthella lenta won. These bacteria consume dopamine, producing meta-tyramine as a by-product. This kind of reaction is challenging, even for chemists. “There’s no way to do it on the bench top,” Maini Rekdal said, “and previously no enzymes were known that did this exact reaction.”

The meta-tyramine by-product may contribute to some of the noxious L-dopa side effects; more research needs to be done. But, apart from the implications for Parkinson’s patients, E. lenta’s novel chemistry raises more questions: Why would bacteria adapt to use dopamine, which is typically associated with the brain? What else can gut microbes do? And does this chemistry impact our health?

“All of this suggests that gut microbes may contribute to the dramatic variability that is observed in side effects and efficacy between different patients taking L-dopa,” Balskus said.

But this microbial interference may not be limited to L-dopa and Parkinson’s disease. Their study could shepherd additional work to discover exactly who is in our gut, what they can do, and how they can impact our health, for better or worse.

Story Source:

Materials provided by Harvard University. Original written by Caitlin McDermott-Murphy. Note: Content may be edited for style and length.

My scientist friend asked how to detox or clean his body from toxins

Over the years, I have experienced family and friends dying of cancer. I observed their lifestyle and toxins they are exposed to. So to answer my friend’s question on how to detox and the mechanism of cleaning our body or getting rid of toxins, I listed some items for Dos and Donts.

Our lymphatic system which travels opposite our blood is responsible for cleaning our blood.  Search for lymphatic, massage and detox in this site http://www.clubalthea.com

When we clean the many bad foods or toxins that entered our body, we must clean our liver first, our laboratory.  It is closely linked to our heart that during our last breath, our liver is the first and last signal that our heart gets to shut down.

Detox or cleaning our cells from toxins is the key to living longer, the anti-aging process we all are seeking for. In my 50s, I could have died long time ago if I was born centuries ago with no clean water, fresh produce and raising a dozen children. Each child is minus 5 years of a woman’s age.

Detox is like cleaning the toilet. The following are detox tips and anti-aging tips to clean your cells:

Dos in cleansing your body from toxin, also detoxes your liver

  • Massage
  • Adequate sleep
  • Filtered water
  • Lemon
  • Baking soda (pinch in your drinking water)
  • Activated charcoal
  • Digestive enzymes from pineapple and papaya
  • Apple cider vinegar
  • Wash produce with salt or diluted vinegar
  • No over ripe fruits and left over foods or 3-day old rice ( aflatoxin , mycotoxin )
  • No charred BBQ
  • Whole foods ; sulfur rich as they are anti-inflammatory (ginger, garlic, turmeric, coconut, walnuts)
  • Deep breathing thru nose and blow out thru mouth
  • Prayer: May God’s light energy be with you and say Amen to accept it.
  • Resveratrol from Berries, kiwi, citrus fruit
  • Fasting
  • Activated charcoal
  • Clean air

Donts are ways that when practiced or consumed can kills our nerve cells and produce toxins in our cells.

  • Avoidance of too much caffeine, iron and sugar, these are food for cancer
  • Other metal toxins
  • TRANS fat
  • Processed
  • Plastics in food
  • Stress
  • Shift work: not sleeping from 10pm to 4 am
  • Radiation
  • Over medications, chemo, other carcinogens
  • Avoid exposure to fumes, chemicals (formaldehydes,carcinogens,toxins)

 

——-

Hi Connnie,

And what is your recipe for liver detox and the mechanism by which it works to accomplish that?

From: Male friend in his late 50s whose brother died of pancreatic cancer

Researchers connect brain blood vessel lesions to intestinal bacteria

bac 111.JPGNIH-funded pre-clinical study links gut microbes and the immune system to a genetic disorder that can cause stroke and seizures.

 A study in mice and humans suggests that bacteria in the gut can influence the structure of the brain’s blood vessels, and may be responsible for producing malformations that can lead to stroke or epilepsy.

The research, published in Nature, adds to an emerging picture that connects intestinal microbes and disorders of the nervous system. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health.

Cerebral cavernous malformations (CCMs) are clusters of dilated, thin-walled blood vessels that can lead to seizures or stroke when blood leaks into the surrounding brain tissue. A team of scientists at the University of Pennsylvania investigated the mechanisms that cause CCM lesions to form in genetically engineered mice and discovered an unexpected link to bacteria in the gut. When bacteria were eliminated the number of lesions was greatly diminished.

“This study is exciting because it shows that changes within the body can affect the progression of a disorder caused by a genetic mutation,” said Jim I. Koenig, Ph.D., program director at NINDS.

The researchers were studying a well-established mouse model that forms a significant number of CCMs following the injection of a drug to induce gene deletion. However, when the animals were relocated to a new facility, the frequency of lesion formation decreased to almost zero.

“It was a complete mystery. Suddenly, our normally reliable mouse model was no longer forming the lesions that we expected,” said Mark L. Kahn, M.D., professor of medicine at the University of Pennsylvania, and senior author of the study. “What’s interesting is that this variability in lesion formation is also seen in humans, where patients with the same genetic mutation often have dramatically different disease courses.”

While investigating the cause of this sudden variability, Alan Tang, a graduate student in Dr. Kahn’s lab, noticed that the few mice that continued to form lesions had developed bacterial abscesses in their abdomens — infections that most likely arose due to the abdominal drug injections.

The abscesses contained Gram-negative bacteria, and when similar bacterial infections were deliberately induced in the CCM model animals, about half of them developed significant CCMs.

“The mice that formed CCMs also had abscesses in their spleens, which meant that the bacteria had entered the bloodstream from the initial abscess site,” said Tang. “This suggested a connection between the spread of a specific type of bacteria through the bloodstream and the formation of these blood vascular lesions in the brain.”

The question remained as to how bacteria in the blood could influence blood vessel behavior in the brain. Gram-negative bacteria produce molecules called lipopolysaccharides (LPS) that are potent activators of innate immune signaling. When the mice received injections of LPS alone, they formed numerous large CCMs, similar to those produced by bacterial infection. Conversely, when the LPS receptor, TLR4, was genetically removed from these mice they no longer formed CCM lesions.  The researchers also found that, in humans, genetic mutations causing an increase in TLR4 expression were associated with a greater risk of forming CCMs.

“We knew that lesion formation could be driven by Gram-negative bacteria in the body through LPS signaling,” said Kahn.

“Our next question was whether we could prevent lesions by changing the bacteria in the body.”

The researchers explored changes to the body’s bacteria (microbiome) in two ways. First, newborn CCM mice were raised in either normal housing or under germ-free conditions. Second, these mice were given a course of antibiotics to “reset” their microbiome. In both the germ-free conditions and following the course of antibiotics, the number of lesions was significantly reduced, indicating that both the quantity and quality of the gut microbiome could affect CCM formation. Finally, a drug that specifically blocks TLR4 also produced a significant decrease in lesion formation. This drug has been tested in clinical trials for the treatment of sepsis, and these findings suggest a therapeutic potential for the drug in the treatment of CCMs, although considerable research remains to be done.

“These results are especially exciting because they show that we can take findings in the mouse and possibly apply them at the human patient population,” said Koenig. “The drug used to block TLR4 has already been tested in patients for other conditions, and it may show therapeutic potential in the treatment of CCMs, although considerable research still remains to be done.”

Kahn and his colleagues plan to continue to study the relationship between the microbiome and CCM formation, particularly as it relates to human disease. Although specific gene mutations have been identified in humans that can cause CCMs to form, the size and number varies widely among patients with the same mutations. The group next aims to test the hypothesis that differences in the patients’ microbiomes could explain this variability in lesion number.

This work was supported by the NINDS (NS092521, NS075168, NS100252, NS065705), the National Heart, Lung, and Blood Institute (HL094326, HL07439), NIDDK (DK007780), the DFG (German Research Foundation), Penn-CHOP, and the National Health and Medical Research Council, Australia.

The NINDS is the nation’s leading funder of research on the brain and nervous system. The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.

Part of the National Institutes of Health, the National Heart, Lung, and Blood Institute (NHLBI) plans, conducts, and supports research related to the causes, prevention, diagnosis, and treatment of heart, blood vessel, lung, and blood diseases; and sleep disorders. The Institute also administers national health education campaigns on women and heart disease, healthy weight for children, and other topics. NHLBI press releases and other materials are available online at https://www.nhlbi.nih.gov.

The NIDDK conducts and supports research on diabetes and other endocrine and metabolic diseases; digestive diseases, nutrition, and obesity; and kidney, urologic, and hematologic diseases. Spanning the full spectrum of medicine and afflicting people of all ages and ethnic groups, these diseases encompass some of the most common, severe, and disabling conditions affecting Americans. For more information about the NIDDK and its programs, visit www.niddk.nih.gov.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

NIH…Turning Discovery Into Health®

Article

Tang et al. Endothelial TLR4 and the microbiome drive cerebral cavernous malformations. Nature. May 10, 2017.