Depressive-like behavior likely exacerbated by high-fructose diet in adolescence - Medical News Today

Depressive-like behavior likely exacerbated by high-fructose diet in adolescence - Medical News Today

Prediction and quantification of bioactive microbiota metabolites in the mouse gut :

Metabolites produced by the intestinal microbiota are potentially important physiological modulators. Here we present a metabolomics strategy that models microbiota metabolism as a reaction network and utilizes pathway analysis to facilitate identification and characterization of microbiota metabolites. Of the 2,409 reactions in the model, ~53% do not occur in the host, and thus represent functions dependent on the microbiota. The largest group of such reactions involves amino-acid metabolism. Focusing on aromatic amino acids, we predict metabolic products that can be derived from these sources, while discriminating between microbiota- and host-dependent derivatives. We confirm the presence of 26 out of 49 predicted metabolites, and quantify their levels in the caecum of control and germ-free mice using two independent mass spectrometry methods. We further investigate the bioactivity of the confirmed metabolites, and identify two microbiota-generated metabolites (​5-hydroxy-L-tryptophan and ​salicylate) as activators of the ​aryl hydrocarbon receptor.

Taking antibiotics during pregnancy increases risk for child becoming obese -- ScienceDaily

A study just released by Columbia University's Mailman School of Public
Health found that children who were exposed to antibiotics in the second
or third trimester of pregnancy had a higher risk of childhood obesity
at age 7. The research also showed that for mothers who delivered their
babies by a cesarean section, whether elective or non-elective, there
was a higher risk for obesity in their offspring.

The gut microbiota influences blood-brain barrier permeability in mice

Pivotal to brain development and function is an intact blood-brain barrier (BBB), which acts as a gatekeeper to control the passage and exchange of molecules and nutrients between the circulatory system and the brain parenchyma. The BBB also ensures homeostasis of the central nervous system (CNS). We report that germ-free mice, beginning with intrauterine life, displayed increased BBB permeability compared to pathogen-free mice with a normal gut flora. The increased BBB permeability was maintained in germ-free mice after birth and during adulthood and was associated with reduced expression of the tight junction proteins occludin and claudin-5, which are known to regulate barrier function in endothelial tissues. Exposure of germ-free adult mice to a pathogen-free gut microbiota decreased BBB permeability and up-regulated the expression of tight junction proteins. Our results suggest that gut microbiota–BBB communication is initiated during gestation and propagated throughout life.

Triclosan, a common antimicrobial in personal hygiene products, causes liver fibrosis and cancer in mice

Triclosan is an antimicrobial commonly found in soaps, shampoos,
toothpastes and many other household items. Despite its widespread use,
researchers at University of California, San Diego School of Medicine
report potentially serious consequences of long-term exposure to the
chemical. The study, published Nov. 17 by Proceedings of the National Academy of Sciences,
shows that triclosan causes liver fibrosis and cancer in laboratory
mice through molecular mechanisms that are also relevant in humans.

Reconceptualizing major depressive disorder as an infectious disease

In this article, I argue for a reconceptualization of major depressive disorder (major
depression) as an infectious disease. I suggest that major depression may result from
a parasitic, bacterial, or viral infection and present examples that illustrate possible
pathways by which these microorganisms could contribute to the etiology of major depression.
I also argue that the reconceptualization of the human body as an ecosystem for these
microorganisms and the human genome as a host for non-human exogenous sequences may
greatly amplify the opportunity to discover genetic links to the illness. Deliberately
speculative, this article is intended to stimulate novel research approaches and expand
the circle of researchers taking aim at this vexing illne

Researchers discover type of toxic flame retardant in Americans for first time - Medical News Today


By analyzing phosphate biomarkers in the participants' urine - known as dialkyl or diaryl phosphates (DAPs) - the team was able to identify the presence of phosphates in their body. A previous study showed how these DAPs are present in household dust, leading the researchers to investigate whether they are present in urine.
Results of the analysis revealed that all participants had traces of one or more of the following phosphates in their urine: bis-(1,3-dichloro-2-propyl) phosphate (BDCIPP), tris-(1,3-dichloro-isopropyl) phosphate (TDCIPP) and bis-(2-chloroethyl) phosphate (BCEP). All of these are deemed harmful to human health.
"We found that several toxic flame retardants are in people's bodies. When you sit on your couch, you want to relax, not get exposed to chemicals that may cause cancer," says Dodson.
The researchers say they were surprised to find that almost all participants had traces of TDCIPP in their urine, considering that it had stopped being used in children's pajamas in the 1970s due to the potential harm it may pose to human health.

The Human Protein Atlas

The Human Protein Atlas portal is a publicly available database with
millions of high-resolution images showing the spatial distribution of
proteins in 44 different normal human tissues and 20 different cancer
types, as well as 46 different human cell lines. The data is released
together with application-specific validation performed for each
antibody, including immunohistochemisty, Western blot analysis and, for a
large fraction, a protein array assay and immunofluorescent based
confocal microscopy. The database has been developed in a gene-centric
manner with the inclusion of all human genes predicted from genome
efforts. Search functionalities allow for complex queries regarding protein expression profiles, protein classes and chromosome location.

Premature infants are exposed to unsafe levels of phthalates in medical products used to save their lives -- ScienceDaily

The chemical, di(2-ethylhexyl)phthalate (DEHP), is used to increase
flexibility of many plastic devices. These products, made from polyvinyl
chloride (PVC), include most intravenous tubing, catheters,
endotracheal tubes, and fluid and blood product bags. DEHP doesn't bind
chemically to PVC, and is able to leach into fluids and body tissues in
contact with it. New Johns Hopkins Bloomberg School of Public Health
research suggests that critically ill preterm infants may be exposed to
DEHP at levels approximately 4,000 to 160,000 times higher than those
believed to be safe. Infants can receive high exposures to DEHP during
weeks to months of treatment in a hospital's neonatal intensive care
unit (NICU).


The results are reported online Nov. 13 date by the Journal of Perinatology.

Research links tobacco smoke and roadway air pollution with childhood obesity

The source of virtually all roadway air pollut...
The source of virtually all roadway air pollution emissions is the exhaust (Photo credit: Wikipedia)
The study, to be posted online Wednesday, Nov. 12, 2014 in Environmental Health Perspectives, shows increased weight gain during adolescence in children exposed to secondhand tobacco smoke or near-roadway air pollution, compared to children with no exposure to either of these air
pollutants. The study is one of the first to look at the combined
effects on body mass index of exposure to both near-roadway air pollution and tobacco smoke. The
effects were substantially greater in children exposed to both air
pollutant mixtures than to either alone.

Is the number of fast-food outlets in the neighbourhood related to screen-detected type 2 diabetes mellitus and associated risk factors?

Objective We investigated whether a higher number of fast-food outlets in an individual’s home neighbourhood is associated with increased prevalence of type 2 diabetes mellitus and
related risk factors, including obesity.

Design Cross-sectional study.

Three UK-based diabetes screening studies (one general population, two
high-risk populations) conducted between 2004 and 2011. The primary
outcome was screen-detected type 2 diabetes. Secondary outcomes were
risk factors for type 2 diabetes.

Subjects In total 10 461 participants (mean age 59 years; 53 % male; 21 % non-White ethnicity).

Results There was a higher number of neighbourhood (500 m radius from home postcode) fast-food outlets among non-White ethnic groups (P<0·001) and in socially deprived areas (P<0·001).
After adjustment (social deprivation, urban/rural, ethnicity, age,
sex), more fast-food outlets was associated with significantly increased
odds for diabetes (OR=1·02; 95 % CI 1·00, 1·04) and obesity (OR=1·02;
95 % CI 1·00, 1·03). This suggests that for every additional two outlets
per neighbourhood, we would expect one additional diabetes case,
assuming a causal relationship between the fast-food outlets and
diabetes.

Conclusions
These results suggest that increased exposure to fast-food outlets is
associated with increased risk of type 2 diabetes and obesity, which has
implications for diabetes prevention at a public health level and for
those granting planning permission to new fast-food outlets.

Deletion of Virus-specific T-cells Enhances Remyelination in a Model of Multiple Sclerosis.

We used transgenic expression of capsid antigens to Theiler's murine
encephalomyelitis virus (TMEV) to study how the immune response to VP1
and VP2 influences spinal cord demyelination, remyelination and axonal
loss during the acute and chronic phases of infection. Expression from
birth of capsid antigen under the ubiquitin promoter resulted in
tolerance to the antigen and absence of an immune response to the
respective capsid antigen following virus infection. The transgenic mice
were crossed to B10.Q mice normally susceptible to demyelination but
which, when compared to FVB mice of the same H2 q
haplotype, show poor remyelination. The major finding in this study was
that VP1+ and VP2+ animals featured more remyelination at all three
chronic time points (90, 180 and 270 dpi) than transgene-negative
controls. Interestingly, at 270 dpi, remyelination in VP1+ mice tended
to be higher and more complete than that in VP2+ mice. Compared with
transgene- negative controls, VP1+ and VP2+ animals showed similar
demyelination in but less only late in the disease (270 dpi). The number
of mid-thoracic axons at the last time point correlated with the levels
of remyelination. The increase in number of axons in VP1+ mice with
remyelination was driven by counts in medium- and large-caliber axons.
This study supports the hypothesis that expression of viral capsid
proteins as self and subsequent genetic deletion of capsid-specific T
cells influences the extent of spinal cord remyelination following
Theiler's virus-induced demyelination. We propose that VP1- and, to a
lesser extent, VP2-specific CD8+ T cells limit and/or prevent
the naturally occurring process of remyelination. This finding may have
relevance to human multiple sclerosis, as targeted removal of CD8+ T cells specific for a yet-to-be-discovered causative peptide may enhance remyelination and prevent axonal loss in patients.

β-Amyloid peptides display protective activity against the human Alzheimer’s disease-associated herpes simplex virus-1 - Online First - Springer

Amyloid plaques, the hallmark of Alzheimer’s disease (AD), contain
fibrillar β-amyloid (Aβ) 1-40 and 1-42 peptides. Herpes simplex virus 1 (HSV-1)
has been implicated as a risk factor for AD and found to co-localize
within amyloid plaques. Aβ 1-40 and Aβ 1-42 display anti-bacterial,
anti-yeast and anti-viral activities. Here, fibroblast, epithelial and
neuronal cell lines were exposed to Aβ 1-40 or Aβ 1-42 and challenged
with HSV-1. Quantitative analysis revealed that Aβ 1-40 and Aβ 1-42 inhibited HSV-1
replication when added 2 h prior to or concomitantly with virus
challenge, but not when added 2 or 6 h after virus addition. In
contrast, Aβ 1-40 and Aβ 1-42 did not prevent replication of the
non-enveloped human adenovirus. In comparison, antimicrobial peptide
LL-37 prevented HSV-1 infection independently of its sequence of addition. Our findings showed also that Aβ 1-40 and Aβ 1-42 acted directly on HSV-1
in a cell-free system and prevented viral entry into cells. The
sequence homology between Aβ and a proximal transmembrane region of HSV-1 glycoprotein B suggested that Aβ interference with HSV-1 replication could involve its insertion into the HSV-1
envelope. Our data suggest that Aβ peptides represent a novel class of
antimicrobial peptides that protect against neurotropic enveloped virus
infections such as HSV-1.
Overproduction of Aβ peptide to protect against latent herpes viruses
and eventually against other infections, may contribute to amyloid
plaque formation, and partially explain why brain infections play a
pathogenic role in the progression of the sporadic form of AD.

Gut Microbiome Heritability | The Scientist Magazine®

Previous
research suggested host genetic variation can influence microbial
phenotype, but an analysis of data from a large twin study published in Cell today
(November 6) solidifies the connection between human genotype and the
composition of the gut microbiome. Studying more than 1,000 fecal
samples from 416 monozygotic and dizygotic twin pairs, Cornell
University’s Ruth Ley and her colleagues have homed in on one bacterial taxon, the family Christensenellaceae, as the most highly heritable group of microbes in the human gut. The researchers also found that Christensenellaceae—which was first described
just two years ago—is central to a network of co-occurring heritable
microbes that is associated with lean body mass index (BMI). They
determined that introducing at least one member this bacterial family
was associated with reduced weight gain in mice.

New study shows strong link between selenium levels and depression

The results of this research, a collaboration between the University's
Psychology and Human Nutrition departments, and published in the
prestigious Journal of Nutrition today, suggests that there is a
relationship between selenium concentration and depressive symptoms and
negative mood among young adults. Young adults with either too low, or
too high, levels of selenium showed the highest risk of depressive
symptoms and poorer mood. However, lower concentrations of selenium were
found to be even more detrimental to these outcomes.

Breathing dirty air during pregnancy raises odds of childhood ADHD-related behavior problems

Prenatal exposure to polycyclic aromatic hydrocarbons, or PAH, a
component of air pollution, raises the odds of behavior problems
associated with attention deficit hyperactivity disorder, or ADHD, at
age 9, according to researchers at the Columbia Center for Children's
Environmental Health at the Mailman School of Public Health. Results are
published online in the journal PLOS ONE.

Antibodies to Toxoplasma gondii in individuals with mania.

Increased rates of infection with Toxoplasma gondii have been found in individuals with schizophrenia as compared to control groups but this issue has not been studied in mania.

METHODS:

We measured immunoglobulin G (IgG) and IgM class antibodies to T. gondii in 57 individuals with mania who were assessed at up to three time-points. We also measured these antibodies in 743 individuals in other psychiatric groups and in 314 non-psychiatric controls. T. gondii antibody levels were compared among groups by multivariate analyses. IgG class and IgM class antibodies to cytomegalovirus were also measured in the same samples. T. gondii antibody levels were also compared over time in the mania group.

RESULTS:

The mania group had a significantly elevated level of IgM antibodies to T. gondii as compared to the control individuals without a psychiatric diagnosis [odds ratio (OR) = 2.33, p < 0.04 at hospital admission  and OR = 2.32, p < 0.02 at study entry during the hospital stay]. Elevated IgM class antibodies to T. gondii were not found in individuals with the other psychiatric diagnoses. We also did not find an increased level of IgG class antibodies to T. gondii or IgG or IgM class antibodies to CMV in the individuals with mania. Within the mania group, there was a significant difference between the prevalences of increased levels of T. gondii IgM at the baseline and the follow-up time-point (t = 2.97, p < 0.003).

CONCLUSIONS:

Infection with T. gondii may confer risk for mania.

Amyloid beta reduces cytopathic effects of Herpes Simplex virus type I

Alzheimer’s disease (AD) is a neurodegenerative disorder that is
characterized by memory loss and other types of dementia. Amyloid β (Aβ)
is a main cause of senile plaques detected in the brains of patients
with AD and other forms of dementia. Recent evidence suggests that the
buildup of Aβ is may be in response to microbial infections in the
central nervous system. Aβ has been shown to inhibit the growth of
bacteria and yeast; however, little work has tested its role in reducing
viral activity. The present work tests the hypothesis that Aβ
suppresses the cytopathic effects induced by the neurotropic Herpes
Simplex Virus Type I (HSV-1). To test this hypothesis, we treated
SH-SY5Y neuroblastoma cells with varying concentrations of Aβ one hour
before HSV-1 infection (1716 strain). Forty-eight hours after infection,
cell viability and morphology was assayed. First we determined cell
viability by utilizing the
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)
assay. The MTT assay indicated that pretreatment of Aβ (100nM, 1μM,
10μM) reduced HSV-1 induced cell death by 40% (p<0.01).
Photomicrographs of neuroblastoma cells infected with HSV-1
(multiplicity of infection; MOI=1) also demonstrated that Aβ
pretreatment reduced cytopathic effects of HSV-1. To more directly test
HSV-1 activity, plaque formation assays are ongoing. These data indicate
that the antimicrobial activities of Aβ are not limited to bacteria.
Overall, the results provide another link connecting HSV-1 infection and
the progression of AD.

A fifth of schizophrenia cases 'may be attributable to T. gondii infection' - Medical News Today

Smith wanted to determine the proportion of schizophrenia cases that could be attributable to T.gondii
infection. He did this by calculating the population attributable
fraction (PAF) - a measure used by epidemiologists to understand the
importance of a risk factor.
"In other words," explains Smith, "we ask, if you could stop infections
with this parasite, how many [schizophrenia] cases could you prevent?"
Smith calculated the PAF fraction throughout an average lifetime
to be 21.4%, meaning that a fifth of all schizophrenia cases over a
lifetime could be prevented by stopping T. gondii infections from occurring. "That, to me, is significant," says Smith.

He notes that many countries have a much higher prevalence of T. gondii infections than the US, and such countries also have a higher prevalence of schizophrenia.
Schizophrenia is one of the leading causes of disability in the US, affecting more than 3.5 million people.
Smith believes that his findings indicate the importance of gaining a better understanding of the link between T. gondii infection and schizophrenia. He adds:

Relationship between herpes simplex virus-1-specific antibody titers and cortical brain damage in Alzheimer’s disease and amnestic mild cognitive impairment

Alzheimer’s disease (AD) is a multifactorial disease with a still barely
understood etiology. Herpes simplex virus 1 (HSV-1) has long been
suspected to play a role in the pathogenesis of AD because of its
neurotropism, high rate of infection in the general population, and
life-long persistence in neuronal cells, particularly in the same brain
regions that are usually altered in AD. The goal of this study was to
evaluate HSV-1-specific humoral immune responses in patients with a
diagnosis of either AD or amnestic mild cognitive impairment (aMCI), and
to verify the possible relation between HSV-1-specific antibody (Ab)
titers and cortical damage; results were compared to those obtained in a
group of healthy controls (HC). HSV-1 serum IgG titers were measured in
225 subjects (83 AD, 68 aMCI, and 74 HC). HSV-specific Ab avidity and
cortical gray matter volumes analyzed by magnetic resonance imaging
(MRI) were evaluated as well in a subgroup of these individuals (44 AD,
23 aMCI, and 26 HC). Results showed that, whereas HSV-1 seroprevalence
and IgG avidity were comparable in the three groups, increased Ab titers
(p < 0.001) were detected in AD and aMCI compared to HC.
Positive significant correlations were detected in AD patients alone
between HSV-1 IgG titers and cortical volumes in orbitofrontal (region
of interest, ROI1 RSp0.56; p = 0.0001) and bilateral temporal cortices (ROI2 RSp0.57; p < 0.0001; ROI3 RSp0.48; p
= 0.001); no correlations could be detected between IgG avidity and MRI
parameters. Results herein suggest that a strong HSV-1-specific humoral
response could be protective toward AD-associated cortical damage.