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The absence of a one specific species of gut bacteria causes social deficits in mice, researchers at Baylor College of Medicine report June 16, 2016 in Cell. By adding this bacteria species back to…
Source: Gut bacteria can reverse autism-related social behavior in mice
The absence of a one specific species of gut bacteria causes social deficits in mice, researchers at Baylor College of Medicine report June 16, 2016 in Cell. By adding this bacteria species back to the guts of affected mice, the researchers were able to reverse some of their behavioral deficits, which are reminiscent of symptoms of autism spectrum disorders (ASDs) in humans. The investigators are now looking to explore the effects of probiotics on neurodevelopmental disorders in future work.
“Other research groups are trying to use drugs or electrical brain stimulation as a way to reverse some of the behavioral symptoms associated with neurodevelopmental disorders — but here we have, perhaps, a new approach,” says senior author Mauro Costa-Mattioli, a neuroscientist at Baylor College of Medicine. “Whether it would be effective in humans, we don’t know yet, but it is an extremely exciting way of affecting the brain from the gut.”
The inspiration for the paper came from human epidemiological studies that have found that maternal obesity during pregnancy could increase children’s risk of developing neurodevelopmental disorders, including ASDs. In addition, some individuals with ASD also report recurring gastrointestinal problems. With emerging research showing how diet can change the gut microbiome and how gut microbes can influence the brain, Costa-Mattioli and his co-authors suspected there could be a connection.
To begin, the researchers fed approximately 60 female mice a high-fat diet that was the rough equivalent of consistently eating fast food multiple times a day. They bred the mice daily and waited for them to bear young. The offspring stayed with their mother for three weeks and then were weaned onto a normal diet. After a month, these offspring showed behavioral deficits, such as spending less time in contact with their peers and not initiating interactions.
“First we wanted to see if there was a difference in the microbiome between the offspring of mouse mothers fed a normal diet versus those of mothers fed a high-fat diet. So, we used 16S ribosomal RNA gene sequencing to determine the bacterial composition of their gut. We found a clear difference in the microbiota of the two maternal diet groups,” says first author Shelly Buffington, a postdoctoral fellow in Costa-Mattioli’s lab. “The sequencing data was so consistent that by looking at the microbiome of an individual mouse we could predict whether its behavior would be impaired.”
Buffington next tested whether the specific differences in the microbiome were causative factors underlying the social impairments in offspring of mothers fed a high-fat diet. Because mice eat each other’s excrement, the researchers housed the animals together so that they would acquire microbiota from their cagemates. When socially impaired three-week-old mice born to mothers on a high-fat diet were paired with normal mice, a full restoration of the gut microbiome and a concurrent improvement in behavior was observed within four weeks. The investigators concluded that one or more beneficial bacterial species might be important for normal social behavior. Fecal-transplant experiments in mice without microbiota (germ-free mice) provided causal evidence that an imbalanced microbial ecology in the mice born to mothers on a high-fat diet is responsible for their social deficits.
The investigators next wanted to know the specific bacterial species that could be affecting the social behavior of the mice. Whole-genome shotgun sequencing revealed one type of bacteria, Lactobacillus reuteri, which was reduced more than nine-fold in the microbiome of mice born to mothers on the high-fat diet.
“We cultured a strain of Lactobacillus (L.) reuteri originally isolated from human breast milk and introduced it into the water of the high-fat-diet offspring. We found that treatment with this single bacterial strain was able to rescue their social behavior,” Buffington says. Other ASD-related behaviors, such as anxiety, were not restored by the reconstitution of the bacteria. Interestingly, the authors found that L. reuteri also promoted the production of the “bonding hormone” oxytocin, which is known to play a crucial role in social behavior and has been associated with autism in humans.
The authors wondered whether the reward circuitry in the socially impaired mice was dysfunctional. “We found that in response to social interaction there was a lack of synaptic potentiation in a key reward area of the brain that could be seen in the normal control mice,” Costa-Mattiol says. “When we put the bacteria back in the maternal-high-fat-diet offspring, we could also restore the changes in synaptic function in the reward circuitry.”
The researchers believe that their work, which uses a human bacteria species to promote oxytocin levels and improve social behavioral deficits in deficient mice, could be explored as a probiotic intervention for the treatment of neurodevelopmental disorders in humans. “This is where the science is unexpectedly leading us. We could potentially see this type of approach developing quite quickly not only for the treatment of ASD but also for other neurodevelopmental disorders; anyway, this is my gut feeling,” Costa-Mattioli says.
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The above post is reprinted from materials provided by Cell Press. Note: Materials may be edited for content and length.
Journal Reference:
Cell Press. “A single species of gut bacteria can reverse autism-related social behavior in mice.” ScienceDaily. ScienceDaily, 16 June 2016. <www.sciencedaily.com/releases/2016/06/160616140723.htm>.
Cleveland Clinic researchers have, for the first time, linked trimethylamine N-oxide (TMAO) — a gut metabolite formed during the digestion of egg-, red meat- or dairy-derived nutrients cholin…
Cleveland Clinic researchers have, for the first time, linked trimethylamine N-oxide (TMAO) — a gut metabolite formed during the digestion of egg-, red meat- or dairy-derived nutrients choline and carnitine — to chronic kidney disease.
TMAO has been linked to heart disease already, with blood levels shown to be a powerful tool for predicting future heart attacks, stroke and death. TMAO forms in the gut during digestion of choline and carnitine, nutrients that are abundant in animal products such as red meat and liver. Choline is also abundant in egg yolk and high-fat dairy products.
The research team was led by Stanley Hazen, M.D., Ph.D., Chair of the Department of Cellular & Molecular Medicine for the Lerner Research Institute and section head of Preventive Cardiology & Rehabilitation in the Miller Family Heart and Vascular Institute at Cleveland Clinic, and W.H. Wilson Tang, M.D., Department of Cardiovascular Medicine in the Miller Family Heart and Vascular Institute and Lerner Research Institute. The research will be published online on January 29th and in the January 30th print edition of Circulation Research.
According to the Centers for Disease Control and Prevention, more that 20 million Americans are estimated to have chronic kidney disease, many of whom are undiagnosed. It is caused by a gradual loss of kidney function over time. As the disease worsens, waste products can accumulate in the blood and can be fatal without interventions. It has long been known that patients with chronic kidney disease are at an increased risk for cardiovascular disease, but the exact mechanisms linking the two diseases are not known. This newly discovered TMAO link offers further insight into the relationship between cardiovascular disease and chronic kidney disease.
“It’s a triple whammy” said Dr Hazen. “Elevated plasma TMAO levels in subjects are linked to future cardiac risks, and in subjects with normal renal function, elevated levels predict long-term future risk for development of chronic kidney disease; animal model studies show that long-term exposure to higher levels of TMAO promotes renal functional impairment and atherosclerosis; and as the kidneys lose function, TMAO isn’t eliminated as easily, and levels further rise, increasing cardiovascular and kidney disease risks further.”
Drs. Hazen and Tang measured fasting TMAO levels in 521 patients with chronic kidney disease and in 3,166 subjects without chronic kidney disease, following all subjects over five years. They found that TMAO levels were higher in patients with chronic kidney disease, and elevated TMAO levels were associated with greater mortality risk in both subject groups. In animal models, the researchers also found that chronic dietary exposures to choline and TMAO were associated with development and progression of chronic kidney disease. Further studies are needed to determine if dietary interventions can delay disease progression of both chronic kidney disease and associated cardiovascular disease.
“Our studies raise the exciting prospects of nutritional interventions to help retard development and progression of chronic kidney disease. Regrettably, very little is known about diet and renal disease progression,” said Dr. Tang.
This research strongly implies the need to focus preventive efforts on dietary interventions and therapeutic targeting of gut microbiota-dependent TMAO pathways, potentially to halt development and progression of chronic kidney disease, as well as cardiovascular disease risks
Story Source:
The above post is reprinted from materials provided by Cleveland Clinic.
Trillions of microbes colonize the adult body. Changes in this community have already been tied to the risk and presence of arthritis, multiple sclerosis, irritable bowel syndrome and cancer. With more information on how these microbes are connected with cancer and cancer risk factors, such as genetic predispositions, smoking and other environmental factors, researchers hope to create individualized screening and treatment plans for cancer patients and for those at an increased cancer risk.
For this study, Guerrero-Preston and his colleagues extracted bacterial DNA from the saliva of 42 patients. Seventeen samples were drawn from people with head and neck squamous cell carcinoma, seven of which were positive for HPV and 10 of which were HPV-negative. Twenty-five noncancerous samples were used as a control.
The bacterial DNA found in the saliva was sequenced and sorted into groups of highly related populations. Through further DNA analysis, researchers were then able to determine the category, or genus, of bacteria to which each group belonged.
The researchers found differences in the bacterial populations present in cancerous versus noncancerous samples. Samples from patients with tumors, for example, showed increased populations of Streptococcus, Dialister and Veillonella genera, as well as decreased populations of Neisseria, Aggregatibacter, Haemophilus and Leptotrichia genera with respect to controls. Tumor samples also showed an increased prevalence of the Lactobacillus genus, which was present in 9.1 percent of tumor samples and in only 0.1 percent of the healthy controls. In addition, the researchers found correlations between the types of bacteria present and the patients’ HPV statuses. HPV-positive samples had increased abundances of Gemellaceae, Leuconostoc and Veillonella genera when compared to HPV-negative samples. Veillonella, for example, was present in 15 percent of HPV-positive tumor samples but was only present in 9.4 percent of HPV-negative tumor samples.
Explore further: New colon cancer culprit found in gut microbiome
More information: Rafael Guerrero-Preston et al, 16S rRNA amplicon sequencing identifies microbiota associated with oral cancer, Human Papilloma Virus infection and surgical treatment, Oncotarget (2014). DOI: 10.18632/oncotarget.9710
Jerry Brown on Monday signed into law a bill that limits the state’s seizure of assets from the estates of low-income residents ages 55 to 64. Beginning Jan. 1, 2017, California will join man…
Source: Gov. Brown signs bill that limits seizure of assets of many Medi-Cal recipients
Jerry Brown on Monday signed into law a bill that limits the state’s seizure of assets from the estates of low-income residents ages 55 to 64.
Beginning Jan. 1, 2017, California will join many other states in the country that only recover the costs of enrollees’ long-term care and related costs after they die.
“They can still come after me if I end up in a nursing home or need home care,” said the 64-year-old Richmond resident. “But other than that, the standard stuff I was so up in arms about will no longer exist. My home will go to my kids.”
The new law, signed as part of the 2016-17 state budget, also would prohibit recovery from the estate of a deceased Medi-Cal member who is survived by a spouse or registered domestic partner. And it prohibits estate recovery if a home is of “modest value” — with a fair market value of 50 percent or less of the average price of homes in the county where it’s is located.
Darling once labeled Brown “the Tin Man of California” with “no heart” after the governor vetoed a previous version of the bill in September 2014 over its costs. Yet Brown’s signing message at the time did not completely close the door on an issue that has riled many Medi-Cal recipients between 55 and 64 years.
Since 2014, millions of people joined Medicaid, called Medi-Cal in California, under a special provision in the nation’s new health care law that expanded the program to low-income adults ages 18 to 64 without children if they earn up to 138 percent of the federal poverty level.
In 2016, that amounts to $16,394 a year for an individual or $22,107 for a couple.
Many of the 735,000 California homeowners ages 55 to 64 who have been laid off and are now getting by on dwindling savings said they did not realize that signing up for the expanded health care program for the poor came with a catch: The state could recover a broad array of costs and assets — including homes — from Medi-Cal recipients 55 and older after they die.
The logic behind the rule is simple: It may be fair for low-income Americans to take advantage of the program, now expanded to 32 states under Obamacare, without having to sacrifice their home or other investments. But when they die, so the thinking goes, the government ought to get reimbursed for its contribution to their medical care.
The provision to dock the estates of older recipients didn’t start with Obamacare; it kicked in when Medicaid was signed into law by President Lyndon Johnson in 1965.
Then, the rule was originally optional and applied only to people 65 or older. But in 1993, the law was changed to require all states to recoup the expenses of long-term care for Medicaid recipients 55 or older. States also were given the option to recover all other Medicaid costs, and California jumped in.
Yet the fear of losing their homes to the state led many low-income Americans to shy away from the health plan of last resort.
Legislation introduced in early 2014 by state Sen. Ed Hernandez , D-West Covina, sought to limit Medi-Cal recovery only to what’s required under federal law: the cost of long-term care in nursing homes.
California Gov. Jerry Brown gestures to a chart showing the unpredictable capital gains revenues as he discusses his revised 2016-17 state budget plan
California Gov. Jerry Brown gestures to a chart showing the unpredictable capital gains revenues as he discusses his revised 2016-17 state budget plan released Friday, May 13, 2016, in Sacramento, Calif.(AP Photo/Rich Pedroncelli) (Rich Pedroncelli)
But in 2014, Brown’s budget advisers balked, warning him that California would lose $15 million annually in general fund revenues as a result.
The federal government is paying 100 percent of the cost for these newly eligible Medicaid recipients until 2017, and 90 percent starting in 2020. But Brown’s advisers feared the state couldn’t afford to cover the rest of the bill in 2020 without getting reimbursed by estates.
Brown’s advisers say that today’s $171 billion spending plan can now accommodate both the costs of Medi-Cal expansion to 3.5 million Californians, and the costs associated with the new law on estate recovery, estimated to cost the general fund $5.7 million in 2016-17 fiscal year, and $28.9 million annually thereafter.
“It is a huge victory that this year’s budget limits estate recovery so that people with modest family homes can pass it on to their children,” Hernandez said in a statement.
Still, Department of Finance spokesman H.D. Palmer cautioned that if budget circumstances change going forward the state would have to “revisit a whole host of issues.”
Contact Tracy Seipel at 408-920-5343. Follow her at Twitter.com/taseipel.
WHAT THE NEW LAW WILL DO
Starting Jan. 1, 2017, Medi-Cal will limit estate recovery to only what the federal government requires. It will:
Prohibit estate recovery for costs of Medi-Cal services other than long-term care services
Prohibit estate recovery for a deceased Medi-Cal member who is survived by a spouse or registered domestic partner.
Allow a hardship exemption from estate recovery for a home of modest value (fair market value is 50 percent or less of the average price of homes in the same county).
Source: California Department of Finance
By combining an electronic health record system with genetic testing results, psychiatrists at the Mayo Clinic are able to personalize treatment for patients taking antidepressants. The confluence …
Source: Mayo Clinic uses EHRs, genetics to tailor patients’ antidepressants
By combining an electronic health record system with genetic testing results, psychiatrists at the Mayo Clinic are able to personalize treatment for patients taking antidepressants.
The confluence of EHRs and precision medicine is proving to be a powerful tool for optimizing the prescriptions of antidepressant medication tailored to individual patients.
According to Mark Frye, MD, department chair of psychiatry and psychology at the Mayo Clinic in Rochester, Minn., there are more than 20 treatments approved by the Food and Drug Administration for depression. However, based on a patient’s genetic makeup and the way their body metabolizes medication, he contends that there can be different patient reactions to the drugs—both positive and negative.
In particular, two major genetic tests are used to screen for pharmacokinetic metabolizing genes CYP2D6 and CYP2C19, which are enzymes that metabolize selective serotonin reuptake inhibitors (SSRI) such as Prozac. As Frye points out, there are differences in genetic variations for these two pathways, and knowing how a drug gets metabolized is very valuable information for clinicians. “We’re trying to be better and smarter about the type of antidepressants we use.”
Armed with the results of this genetic testing and an EHR, he believes physicians can now make more precise pharmacotherapy recommendations that are optimized for specific patients.
“The field of medicine is potentially changing quite significantly as it tries to accommodate new genomic research and how to interface that as best we can with electronic health records,” observes Frye. “We’ve been doing testing like this for some time now, and the other thing we’ve struggled with are EHRs, which have millions of data points, and how we can get this sort of information to the clinician where it might really be relevant—as in, they are looking to write a prescription for one of these antidepressants.”
As a physician is about to prescribe such medication, he argues that is the critical moment at which an alert could be issued through the EHR to flag in real time for the doctor the importance of genetic test results for the metabolizing genes. According to Frye, data in the hands of clinicians at the right time is crucial for helping them to make the right drug choice for their patients.
“Generating that information and having it readily available in an electronic health record interface can really facilitate decision support tools,” adds Frye. “It is currently available at Mayo in our Rochester campus. It is our own Mayo-based EHR, but we are going to Epic.”
The Mayo Clinic selected Epic to be its vendor in creating a single, integrated EHR-revenue cycle management system, replacing three EHR systems. “I would hope that this would be viewed as compatible and that we could do something similar with Epic,” he says.
Writing in the current issue of Mayo Clinic Proceeding, Frye and his colleagues discuss pharmacokinetic pharmacogenetic prescribing guidelines for antidepressants primarily metabolized by CYP2D6 and CYP2C19 as a template for psychiatric precision medicine.
“The purpose of the paper was to review the potential merits of such transformative care changes,” he concludes. “This is very early in the field, but there’s no question that genomic medicine has great potential for our practice. At the end of the day, there is not a clear set of antidepressants that have superior effectiveness for all patients, which means we need more tools to get more of a profile of the sort of person that might do well with antidepressant A versus antidepressant B.”
There were indications that c-Abl activity leads to Parkinson’s disease, and our experiments show there is indeed a connection,” says Ted Dawson, M.D., Ph.D., professor of neurology and…
There were indications that c-Abl activity leads to Parkinson’s disease, and our experiments show there is indeed a connection,” says Ted Dawson, M.D., Ph.D., professor of neurology and director of the Institute for Cell Engineering at the Johns Hopkins University School of Medicine. “There is already a Food and Drug Administration-approved c-Abl inhibiting drug in use for leukemia,” he adds, “so we’re interested in whether it could be used safely against Parkinson’s disease or as a starting point to develop other treatments.”
Autopsies have revealed that c-Abl is especially active in the brains of people with Parkinson’s disease, a progressive disorder of the nervous system that affects movement. Additionally, studies in mice bred to be prone to the disease found drugs that block c-Abl may prevent or slow it. But, says Han Seok Ko, Ph.D., assistant professor of neurology at Johns Hopkins, “the drugs used in those studies could also have been blocking similar proteins, so it wasn’t clear that blocking c-Abl was what benefited the animals by either preventing symptoms or influencing disease progression.”
About c-ablNon-receptor tyrosine kinases Arg and c-abl is differently modulated in B lymphoid cells at different stages of differentiation
https://en.wikipedia.org/wiki/ABL2
“Glutathione peroxidase 1 is regulated by the c–Abl and Arg tyrosine kinases”. Glutathione peroxidase 1 is characterized in a polyalanine sequence polymorphism in the N-terminal region, which includes three alleles with five, six or seven alanine (Ala) repeats in this sequence. The allele with five Ala repeats is significantly associated with breast cancer risk
https://en.wikipedia.org/wiki/GPX1
The tyrosine kinase ABL1 (acronym for As elson murine l eukemia viral oncogene homolog 1, also c-Abl, p150) is in various body cells occurring protein from the family of tyrosine kinases .
This protein is available in many cellular processes such as cell migration , cell adhesion , cell differentiation , and apoptosis involved and is an important element for the signal transduction via the T cell receptor . c-Abl is the gene product of the same proto-oncogene c-abl, a precursor of a potentially cancer-causing gene. Through exchange (translocation) of chromosome fragments between the c-abl harboring chromosome 9 and the bcr gene harboring chromosome 22 to the so-called Philadelphia chromosome may result, creates a new bcr-abl gene, which is the by clicking the link found chromosomal abnormalities resulting oncogene was and among others in 95% of chronic myelogenous leukemia (CML) can be detected. Therefore Abl proteins are popular targets for drug development .
c-Abl is a protein with a molecular mass of about 145 kDa, which by a gene on the chromosome 9 locus is encoded q34. It consists of a respective SH2 and SH3 domain that are responsible for the regulation of c-Abl, and the enzyme function bearing kinase domain . The C-terminus carrying a binding domain for interaction with the DNA and actin . Through different splicing two different N-terminal protein sequences can be formed. The N-terminus of c-Abl, the addition in the case of a splice variant 1B myristylation bears, is responsible for the autoinhibition. A binding site for Myristinsäurereste could be identified in the C-lobe of the kinase function. [1]
Comparison of the structural organization of c-Abl (splice variants 1a and 1b) with BCR / Abl. (BD: binding domain, NLS: nuclear localization signal , NES: nuclear export signal )
Activation and regulation
c-Abl is present in a basal inactive state. For the inactivity of the N-terminal part of the protein and myristyl is made responsible, although the splice variant 1A does not have such myristylation. But can to stabilize the inactive state also with fatty acids , modified proteins, such as Fus1 be involved. [2] A complete absence of the term, such as in the case of oncogenic viral offspring v-Abl and the oncogenic mutant BCR-Abl, is associated with the constitutive activity of the kinase function and a cancer-causing potential.
c-Abl, by receptor Tyrosikinasen such as the EGF receptor , and by non-receptor tyrosine kinases such as c-Src are activated. [
https://de.wikipedia.org/wiki/Tyrosinkinase_ABL1
Further reading
Lin J., Arlinghaus R. (2008). . Activated c-Abl tyrosine kinase in malignant solid tumors Oncogene 27: 4385-4391.
References
Dear Readers, My name is Connie Dello Buono, mother of two young adults in college in the bay area and an aunt to 7 nieces/nephews in the Philippines who are in college. As a health blogger, I have…
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