Paints, pesticides, and other consumer products now add as much to air pollution as cars | Science | AAAS

Cars are no longer the top contributor to urban air pollution. That’s
the conclusion of a new study presented here at the annual meeting of
AAAS, which publishes Science, that finds pesticides,
paints, adhesives, and other consumer and industrial products add about
as much to air pollution as transportation does. For the new work,
researchers examined volatile organic compounds (VOCs). VOCs react with
air to create ozone and, separately, produce fine particulate matter,
which contributes to haze. Both of these air pollutants are health
hazards and contribute to respiratory diseases, particularly in urban
areas where emissions tend to be highest. Emissions from cars and other
automobiles have long been considered the major contributor to these
kinds of air pollutants. But the new work, which examined the chemical
productions statistics from industrial and government agencies, found
pesticides, coatings, inks, adhesives, and personal care products such
as perfumes produce more than double the emissions of cars.
That means U.S. inventories underestimate VOC emissions from these
products by as much as a factor of three while overestimating car VOC
emissions by 40%, researchers also report today in Science.
Because most people use the products that make VOCs indoors, the
researchers also compared emissions from residential and commercial
buildings to outdoor measurements in Los Angeles, California. They found
the concentration of emission compounds indoors was seven times higher
than in ambient air. That means air pollution is increasingly from
consumer and industrial products rather than from the transportation
sector. These products are used indoors where people spend most of their
time, which means their use poses a health risk that requires updated
regulations, the researchers say.

Half of all dementias start with damaged 'gatekeeper cells': Once the cells are compromised, the brain's protective fort becomes leaky and allows blood toxins to trespass into the brain, damaging critical connections between brain areas, esearchers say. -- ScienceDaily

Half of all dementias start with damaged 'gatekeeper cells', or Pericytes: Once the cells are compromised, the brain's protective fort becomes leaky and allows blood toxins to trespass into the brain, damaging critical connections between brain areas, researchers say. -- ScienceDaily

Dye kills malaria parasites at speed not seen before -- ScienceDaily

Research shows that the dye methylene blue is a safe antimalarial that
kills malaria parasites at an unprecedented rate. Within two days,
patients are cured of the disease and no longer transmit the parasite if
they are bitten again by a mosquito. This discovery was made by Radboud
university medical center scientists and international colleagues
during a research project conducted in Mali. The results are
published in The Lancet Infectious Diseases .

Epstein-Barr virus is present in the brain of most cases of multiple sclerosis and may engage more than just B cells. - PubMed - NCBI

 Multiple sclerosis (MS) is a chronic neuroinflammatory condition of the
central nervous system (CNS). It is a major cause of neurological
disability in young adults, particularly women. What triggers the
destruction of myelin sheaths covering nerve fibres is unknown. Both
genetic and infectious agents have been implicated. Of the infectious
agents, Epstein-Barr virus (EBV), a common herpesvirus, has the
strongest epidemiological and serological evidence. However, the
presence of EBV in the CNS and demonstration of the underlying
mechanism(s) linking EBV to the pathogenesis of MS remain to be
elucidated. We aimed at understanding the contribution of EBV infection
in the pathology of MS. We examined 1055 specimens (440 DNA samples and
615 brain tissues) from 101 MS and 21 non-MS cases for the presence of
EBV using PCR and EBER-in situ hybridization (EBER-ISH). EBV was
detected by PCR and/or EBER-ISH in 91/101 (90%) of MS cases compared to
only 5/21 (24%) of non-MS cases with other neuropathologies. None of the
samples were PCR positive for other common herpesviruses (HSV-1, CMV,
HHV-6). By quantitative PCR, EBV viral load in MS brain was mainly low
to moderate in most cases. However, in 18/101 (18%) of MS cases,
widespread but scattered presence of EBV infected cells was noted in the
affected tissues by EBER-ISH. Immunohistochemical analysis of EBV gene
expression in the 18 heavily infected cases, revealed that the EBV
latent protein EBNA1, and to a lesser extent the early lytic protein
BZLF1 were expressed. Furthermore, using double-staining we show for the
first time that astrocytes and microglia, in addition to B-cells can
also be infected. To the best of our knowledge, this is the most
comprehensive study demonstrating that EBV is present and
transcriptionally active in the brain of most cases of MS and supports a
role for the virus in MS pathogenesis. Further studies are required to
address the mechanism of EBV involvement in MS pathology.

Study finds bacteria in milk linked to rheumatoid arthritis

A team of UCF College of Medicine researchers has discovered a link between rheumatoid arthritis and Mycobacterium avium subspecies paratuberculosis,
known as MAP, a bacteria found in about half the cows in the United
States. The bacteria can be spread to humans through the consumption of
infected milk, beef and produce fertilized by cow manure.

$1 Million Prize for Alzheimer’s Disease Germ Announced by Dr. Leslie Norins on

Leslie Norins, MD, PhD, CEO of Alzheimer’s Germ Quest, Inc., announces a
$1 million challenge award for the scientist who provides persuasive
evidence that an infectious agent is the root cause of Alzheimer’s
disease. The three-year contest begins January 16, 2018. Details are
provided at

Benefits of a healthy diet greater in people at high genetic risk for obesity: Genetic predisposition to obesity is no barrier to successful weight management -- ScienceDaily

The benefits of sticking to a healthy diet to prevent long term weight gain are greater in people at high genetic risk for obesity than in those with low genetic risk, finds a study in The BMJ today.
The researchers say their findings indicate that improving dietquality over time might lead to greater weight loss for people who are genetically susceptible to obesity. The study also indicates that the
genetic risk of weight gain is attenuated by improving diet quality.

Comment: In other words, certain susceptibility genes are no longer susceptibility genes when unhealthy eating is replaced by healthy eating.  

The paper is published in The British Medical Journal

Improving adherence to healthy dietary patterns, genetic risk, and long term weight gain: gene-diet interaction analysis in two prospective cohort studies

Monocyte activation detected prior to a diagnosis of schizophrenia in the US Military New Onset Psychosis Project (MNOPP)

 : Low-grade inflammation is present in some cases of schizophrenia, particularly in
the early stages of this disorder. The inflammation source is not known but may be
the result of dysbiotic processes occurring in the gut. We examined peripheral biomarkers
of bacterial translocation, soluble CD14 (sCD14) and lipopolysaccharide binding protein
(LBP), and of general inflammation, C-reactive protein (CRP), in a unique, pre-onset
study of schizophrenia. This sample was composed of 80 case-control matched pairs
of US military service members from whom blood samples were obtained at time of entry
to service, before a psychiatric diagnosis was made.

Defective cholesterol clearance limits remyelination in the aged central nervous system | Science

Age-associated decline in regeneration capacity limits the restoration of nervous system functionality after injury. In a model for demyelination, we found that old mice fail to resolve the inflammatory response initiated after myelin damage. Aged phagocytes accumulated excessive amounts of myelin debris, which triggered cholesterol crystal formation, phagolysosomal membrane rupture, and stimulated inflammasomes. Myelin debris clearance required cholesterol transporters including apolipoprotein E. Remarkably, stimulation of reverse cholesterol transport was sufficient to restore the capacity of old mice to remyelinate lesioned tissue. Thus, cholesterol-rich myelin debris can overwhelm the efflux capacity of phagocytes, resulting in a phase transition of cholesterol into crystals thereby inducing a maladaptive immune response that impedes tissue regeneration.

Artificial Sugar Trehalose Linked to Clostridium difficile Epidemics | Medicine |

An artificial sugar called trehalose enhances the virulence of epidemic lineages of Clostridium difficile, a Gram-positive spore forming bacterium that causes life-threatening inflammation of the colon, according to a new study published in the journal Nature.

Hydraulic fracturing negatively impacts infant health -- ScienceDaily

Health risks increase for infants born to mothers living within 2 miles
of a hydraulic fracturing site, according to a study published Dec. 13
in Science Advances. The research team found that infants born
within a half a mile from a fracking site were 25 percent more likely to
be born at low birth weights, leaving them at greater risk of infant
mortality, ADHD, asthma, lower test scores, lower schooling attainment
and lower lifetime earnings.

Hydraulic fracturing and infant health: New evidence from Pennsylvania
Science Advances  13 Dec 2017:
Vol. 3, no. 12, e1603021

Frontiers | The Porphyromonas gingivalis/host interactome shows enrichment in GWASdb genes related to Alzheimer’s disease, diabetes and cardiovascular diseases | Frontiers in Aging Neuroscience

Periodontal disease is of established aetiology in which polymicrobial
synergistic ecology has become dysbiotic under the influence of
Porphyromonas gingivalis. Following breakdown of the host’s protective
oral tissue barriers, P. gingivalis migrates to developing inflammatory
pathologies that associate with Alzheimer’s disease (AD). Periodontal
disease is a risk factor for cardiovascular disorders (CVD), type II
diabetes mellitus (T2DM), AD and other chronic diseases, whilst T2DM
exacerbates periodontitis. This study analysed the relationship between
the P. gingivalis/host interactome and the genes identified in
genome-wide association studies (GWAS) for the aforementioned conditions
using data from GWASdb (P<1E-03) and, in some cases, from the
NCBI/EBI GWAS database (P< 1E-05). Gene expression data from
periodontitis or P. gingivalis microarray was compared to microarray
datasets from the AD hippocampus and/or from carotid artery plaques. The
results demonstrated that the host genes of the P. gingivalis
interactome were significantly enriched in genes deposited in GWASdb
genes related to cognitive disorders, AD and dementia, and its co-morbid
conditions T2DM, obesity, and CVD. The P. gingivalis/host interactome
was also enriched in GWAS genes from the more stringent NCBI-EBI
database for AD, atherosclerosis and T2DM. The misregulated genes in
periodontitis tissue or P. gingivalis infected macrophages also matched
those in the AD hippocampus or atherosclerotic plaques. Together, these
data suggest important gene/environment interactions between P.
gingivalis and susceptibility genes or gene expression changes in
conditions where periodontal disease is a contributory factor.

Building Bridges Between Infectious Disease Physicians and Psychiatrists

Complex problems require complex solutions with interdisciplinary cooperation.
When state mental hospitals were filled with mentally ill patients who
had syphilis, everyone recognized the close association between
infectious disease and psychiatric illness. In fact, in 1927, the first
Nobel prize in Psychiatry was awarded to Dr. Julius Wagner-Jauregg who
recognized the association between infections and mental illness and
introduced malaria inoculation, which proved to be very successful in
treating dementia paralytica. After the introduction of penicillin, the
gap between these two specialties widened with specialization and
fragmentation in medicine resulting in few physicians maintaining
updated capability in both infectious disease and psychiatry. Most
infectious disease physicians have very little current training in
neurochemistry, psychoimmunology, or the pathophysiology of mental
illness. Likewise, many psychiatrists have little current training in
infectious diseases and psychoimmunology.

More recently, this gap has been bridged by advances in evolutionary
medicine, a growing recognition of the significance of the microbiome,
improved brain imaging and testing capabilities and discoveries in
psychoimmunology which have greatly expanded our knowledge of the
pathophysiology of mental illness. Now, many, including the Center for
Disease and Prevention recognize chronic diseases and the mental
illnesses can stem from infectious agents.

Evidence of increased exposure to Toxoplasma gondii in individuals with recent onset psychosis but not with established schizophrenia. - PubMed - NCBI

A possible role for Toxoplasma gondii in the etiopathogenesis of
schizophrenia is supported by epidemiological studies and animal models
of infection. However, recent studies attempting to link Toxoplasma to
schizophrenia have yielded mixed results. We performed a nested
case-control study measured serological evidence of exposure to
Toxoplasma gondii in a cohort of 2052 individuals. Within this cohort, a
total of 1481 individuals had a psychiatric disorder and 571 of were
controls without a psychiatric disorder. We found an increased odds of
Toxoplasma exposure in individuals with a recent onset of psychosis (OR
2.44, 95% Confidence Interval 1.4-4.4, p < .003). On the other hand,
an increased odds of Toxoplasma exposure was not found in individuals
with schizophrenia or other psychiatric disorder who did not have a
recent onset of psychosis. By identifying the timing of evaluation as a
variable, these findings resolve discrepancies in previous studies and
suggest a temporal relationship between Toxoplasma exposure and disease

Exposure to BPA during pregnancy may cause health problems for offspring

Bisphenol A -- BPA -- used in plastic packaging and in the linings of food and beverage cans, may be passed from a mother to her offspring during pregnancy and cause changes in the gut bacteria of the offspring, according to an international team of researchers.
In a study on rabbits, the researchers observed that exposure to BPA during pregnancy caused chronic inflammation in the offspring's intestines and liver. The researchers also noted signs of increased gut permeability -- or leaky gut -- and a decrease in the diversity of gut bacteria and anti-inflammatory bacterial metabolites, such as short-chain fatty acids, said Jairam K.P. Vanamala, associate professor of food sciences, Penn State.
Leaky gut and decreased gut-bacteria diversity and metabolites are considered biomarkers -- or indicators -- of inflammation-related chronic diseases, he added.
"Obesity and inflammation-promoted chronic diseases like colon cancer and type 2 diabetes are increasing not just in America, but worldwide," said Vanamala. "We know that many types of cancers are inflammation-promoted, like colon cancer. But, we have not understood what causes inflammation in the intestine and liver. We have previously shown that food is a double-edge sword. Some foods can promote inflammation in the intestine, whereas bright-colored fruits and vegetables, like purple potatoes, can suppress intestinal inflammation. This study shows that we also need to think about the toxins in the environment."

Sulfites inhibit the growth of four species of beneficial gut bacteria at concentrations regarded as safe for food

Sulfites and other preservatives are considered food additives to limit
bacterial contamination, and are generally regarded as safe for
consumption by governmental regulatory agencies at concentrations up to
5000 parts per million (ppm). Consumption of bactericidal and
bacteriostatic drugs have been shown to damage beneficial bacteria in
the human gut and this damage has been associated with several diseases.
In the present study, bactericidal and bacteriostatic effects of two
common food preservatives, sodium bisulfite and sodium sulfite, were
tested on four known beneficial bacterial species common as probiotics
and members of the human gut microbiota. Lactobacillus species casei, plantarum and rhamnosus, and Streptococcus thermophilus
were grown under optimal environmental conditions to achieve early log
phase at start of experiments. Bacterial cultures were challenged with
sulfite concentrations ranging between 10 and 3780 ppm for six hours. To
establish a control, a culture of each species was inoculated into
media containing no sulfite preservative. By two hours of exposure, a
substantial decrease (or no increase) of cell numbers (based on OD600
readings) were observed for all bacteria types, in concentrations of
sulfites between 250–500 ppm, compared to cells in sulfite free media.
Further testing using serial dilution and drop plates identified
bactericidal effects in concentrations ranging between 1000–3780 ppm on
all the Lactobacillus species by 4 hours of exposure and bactericidal effects on S. thermophilus in 2000ppm NaHSO3 after 6 hours of exposure.

Could lupus raise dementia risk?

 The researchers identified 4,886 individuals who had received a
diagnosis of systemic lupus erythematosus , and these were matched by age and sex in a 1:5 ratio
to 24,430 people without the condition (the controls). The incidence of
dementia was assessed for each group.
The study revealed that people with SLE were 51 percent more
likely to develop dementia than people without SLE, and this association
persisted across all age groups.
Based on their results, the researchers conclude that "systemic lupus erythematosus is significantly associated with dementia."

Two new studies support the link between the gut microbiome and multiple sclerosis

Previous research has found that multiple sclerosis (MS) patients may
have a specific microbial signature in their gut microbiota that could
impact disease pathogenesis. However, it is
not known to what extent structural and functional changes in the gut
microbiota are primary contributors to MS pathogenesis and which
underlying mechanisms are involved.

A new study, led by Dr. Sergio Baranzini from the Department of
Neurology at the University of California San Francisco (USA), has found
that specific gut bacteria from multiple sclerosis patients regulate
immune responses and exacerbate MS-like symptoms in mice.

The researchers used 16S ribosomal ribonucleic acid (rRNA) gene
sequencing of stool samples from 71 untreated relapsing-remitting MS
patients and 71 healthy controls.

Although they did not find shifts in the gut microbiota structure,
specific bacterial taxa were significantly associated with MS. Both
Akkermansia muciniphila and Acinetobacter calcoaceticus were increased
in MS patients. Although the role of A. muciniphila has been extensively
studied in the context of metabolism, little is known about its role in
regulating immune responses and these results are in agreement with
previous research supporting A. muciniphila as a bacterial species that
exacerbates inflammation during infection. In contrast, MS patients
exhibited decreased levels of Parabacteroides distasonis.

Immune Cells Mistake Heart Attacks for Viral Infections

 What is it about dying cells in the heart that stimulates the immune
system? To answer this, researchers looked deep inside thousands of
individual cardiac immune cells and mapped their individual
transcriptomes using a method called single cell RNA-Seq. This led to
the discovery that after a heart attack, DNA from dying cells
masquerades as a virus and activates an ancient antiviral program called
the type I interferon response in specialized immune cells. ¬¬ The
researchers named these "interferon inducible cells (IFNICs)."

When investigators blocked the interferon response, either
genetically or with a neutralizing antibody given after the heart
attack, there was less inflammation, less heart dysfunction, and
improved survival. Specifically, blocking antiviral responses in mice
improved survival from 60 percent to over 95 percent. These findings
reveal a new potential therapeutic opportunity to prevent heart attacks
from progressing to heart failure in patients.

Here's the paper:-

IRF3 and type I interferons fuel a fatal response to myocardial infarction

Clemastine fumarate as a remyelinating therapy for multiple sclerosis (ReBUILD): a randomised, controlled, double-blind, crossover trial - The Lancet

Multiple sclerosis is a degenerative inflammatory disease of the CNS characterised by immune-mediated destruction of myelin and progressive neuroaxonal loss. Myelin in the CNS is a specialised extension of the oligodendrocyte plasma membrane and clemastine fumarate can stimulate differentiation of oligodendrocyte precursor cells in vitro, in animal models, and in human cells. We aimed to analyse the efficacy and safety of clemastine fumarate as a treatment for patients with multiple sclerosis.

We did this single-centre, 150-day, double-blind, randomised, placebo-controlled, crossover trial (ReBUILD) in patients with relapsing multiple sclerosis with chronic demyelinating optic neuropathy on stable immunomodulatory therapy. Patients who fulfilled international panel criteria for diagnosis with disease duration of less than 15 years were eligible. Patients were randomly assigned (1:1) via block randomisation using a random number generator to receive either clemastine fumarate (5·36 mg orally twice daily) for 90 days followed by placebo for 60 days (group 1), or placebo for 90 days followed by clemastine fumarate (5·36 mg orally twice daily) for 60 days (group 2). The primary outcome was shortening of P100 latency delay on full-field, pattern-reversal, visual-evoked potentials. We analysed by intention to treat. The trial is registered with, number NCT02040298.

Between Jan 1, 2014, and April 11, 2015, we randomly assigned 50 patients to group 1 (n=25) or group 2 (n=25). All patients completed the study. The primary efficacy endpoint was met with clemastine fumarate treatment, which reduced the latency delay by 1·7 ms/eye (95% CI 0·5–2·9; p=0·0048) when analysing the trial as a crossover. Clemastine fumarate treatment was associated with fatigue, but no serious adverse events were reported.

To our knowledge, this is the first randomised controlled trial to document efficacy of a remyelinating drug for the treatment of chronic demyelinating injury in multiple sclerosis. Our findings suggest that myelin repair can be achieved even following prolonged damage."

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