Children who have had enterovirus infection are around 50 percent more likely to have type 1 diabetes -- ScienceDaily

Children who have been infected with enterovirus are 48 percent more
likely to have developed type 1 diabetes, a study shows. "Type 1
diabetes is considered to be caused by complex interaction between
genetic susceptibility, the immune system, and environmental factors,"
say the authors. "Though the cue for genetic predisposition has been
elucidated, evidence also points to involvement of enterovirus (EV)
infection, including viruses such as poliovirus, Coxsackievirus A,
Coxsackievirus B, and echovirus."

Research reveals likelihood, onset of multiple sclerosis diagnosis among patients with inflammatory eye disease -- ScienceDaily

The results of the largest retrospective study of multiple sclerosis
(MS) in uveitis patients has revealed that nearly 60 percent of patients
with both diseases were diagnosed with each within a five-year span.
While it has long been known that there is an association between the
eye condition and MS, this is the first study to provide a detailed
description of the relative onset of uveitis and MS and to calculate the
likelihood of an MS diagnosis among uveitis patients.
Based on the prevalence of MS in American and European populations, the researchers found that MS is 18 times and 21 times more likely in an American and European population with uveitis, respectively, relative to the general population. The study found that MS was diagnosed before uveitis in 28 (29 percent) of patients, simultaneously in 15 (15 percent) of patients and after uveitis diagnosis in 54 (56 percent) of patients.


Major breakthrough could help detoxify pollutants -- ScienceDaily

Scientists at The University of Manchester hope a major breakthrough could lead to
more effective methods for detoxifying dangerous pollutants like PCBs
and dioxins. The result is a culmination of 15 years of research and has
been published in Nature. It details how certain organisms manage to lower the toxicity of pollutants.
The team at the Manchester Institute of Biotechnology were
investigating how some natural organisms manage to lower the level of
toxicity and shorten the life span of several notorious pollutants.

Professor David Leys explains the research: "We already know that
some of the most toxic pollutants contain halogen atoms and that most
biological systems simply don't know how to deal with these molecules.
However, there are some organisms that can remove these halogen atoms
using vitamin B12. Our research has identified that they use vitamin B12
in a very different way to how we currently understand it."

Oncogenic induction of cellular high CpG methylation by Epstein-Barr virus in malignant epithelial cells.

Epstein-Barr virus (EBV) is a well-known human herpesvirus associated
with virtually all nasopharyngeal carcinoma (NPC) and ~10% of gastric
cancer (GC) worldwide. Increasing evidence shows that acquired genetic
and epigenetic alterations lead to the initiation and progression of NPC
and GC. However, even deep whole exome sequencing studies showed a
relatively low frequency of gene mutations in NPC and EBV-associated GC
(EBVaGC), suggesting a predominant role of epigenetic abnormities,
especially promoter CpG methylation, in the pathogenesis of NPC and
EBVaGC. High frequencies of promoter methylation of tumor suppressor
genes (TSGs) have been frequently reported in NPC and EBVaGC, with
several EBV-induced methylated TSGs identified. Further characterization
of the epigenomes (genome-wide CpG methylation profile -- methylome) of
NPC and EBVaGC shows that these EBV-associated tumors display a unique
high CpG methylation epigenotype with more extensive gene methylation
accumulation, indicating that EBV acts as a direct epigenetic driver for
these cancers. Mechanistically, oncogenic modulation of cellular CpG
methylation machinery, such as DNA methyltransferases (DNMTs), by
EBV-encoded viral proteins accounts for the EBV-induced high CpG
methylation epigenotype in NPC and EBVaGC. Thus, uncovering the
EBV-associated unique epigenotype of NPC and EBVaGC would provide new
insight into the molecular pathogenesis of these unique EBV-associated
tumors and further help to develop pharmacologic strategies targeting
cellular methylation machinery in these malignancies.

How gut bacteria ensures a healthy brain – and could play a role in treating depression

How gut bacteria ensures a healthy brain – and could play a role in treating depression

Scientists prove link between viral infection (cytomegalovirus) and autoimmune disease

Published in the leading journal Immunity, the Australian
research found that chronic cytomegalovirus (CMV) infection could lead
to the development of Sjogren's (SHOW-grins) syndrome.

CMV - a member of the herpes family - is a common viral infection
that causes mild flu-like symptoms in healthy people but can lead to
more serious illness in those with compromised immune systems.

Between 50 and 80 per cent of people in developed countries are
infected with CMV.  Although normally innocuous, given the right genetic
background, chronic viral infection with CMV can trigger autoimmunity.

"Sjogren's syndrome (SS) is the second most common autoimmune disease
in humans, affecting up to three per cent of the population or more
than four million people in the United States alone," Professor
Degli-Esposti said.

Energy drinks may pose danger to public health, researchers warn -- ScienceDaily

Increased consumption of energy drinks may pose danger to public health, especially among young
people, warns a team of researchers. Energy drinks are non-alcoholic
beverages that contain caffeine, vitamins, and sometimes other
ingredients such as taurine, ginseng, and guarana. They are typically
marketed as boosting energy and increasing physical and mental

Researcher adds to evidence linking autism to air pollutants -- ScienceDaily

A researcher at the University of Wisconsin-Milwaukee (UWM) has added to a growing body of evidence that links autism to air pollutants such as those generated by cars and trucks.

Amy Kalkbrenner's study, published this week online at the journal Epidemiology, showed that pollution's impact on autism rates in North Carolina is similar to results of pollution-autism studies in California -- despite weather and climate differences between the two states.

In addition, the work of Kalkbrenner and her colleagues, building on previous studies, showed that women in the third trimester of pregnancy were more susceptible to the damaging effects of air pollution on their unborn child.

Hospital contacts with infection and risk of schizophrenia: a population-based cohort study with linkage of danish national registers.

Infections and immune responses have been suggested to play an important role in the etiology of schizophrenia. Several studies have reported associations between maternal infections during pregnancy and the child's risk of schizophrenia; however, infection during childhood and adolescence unrelated to maternal infection during pregnancy has not been studied to nearly the same extent and the results are far from conclusive. Data were drawn from 2 population-based registers, the Danish Psychiatric Central Register and the Danish National Hospital Register.
We used a historical population-based cohort design and selected all individuals born in Denmark between 1981 and 1996 (n = 843 390). We identified all individuals with a first-time hospital contact with schizophrenia from 1991 through 2010. Out of the 3409 individuals diagnosed with schizophrenia, a total of 1549 individuals had had a hospital contact with infection before their schizophrenia diagnosis (45%). Our results indicate that individuals who have had a hospital contact with infection are more likely to develop schizophrenia (relative risk [RR] = 1.41; 95% CI: 1.32-1.51) than individuals who had not had such a hospital contact. Bacterial infection was the type of infection that was associated with the highest risk of schizophrenia (RR = 1.63; 95% CI: 1.47-1.82). Our study does not exclude that a certain type of infection may have a specific effect; yet, it does suggest that schizophrenia is associated with a wide range of infections. This association may be due to inflammatory responses affecting the brain or genetic and environmental risk factors aggregating in families.

Relationship between arsenic, heart disease and diabetes discovered

Associated with various types of cancer such as
skin and liver, the intake of arsenic it is also linked to
cardiovascular disease and diabetes. According to a long-term study
conducted by experts from the Center for Research and Advanced Studies
(CINVESTAV) it was determined that this metalloid inhibits enzymes
associated with antioxidant protection.

The study focused on analyzing children that had ingested arsenic
through maternal consumption of contaminated water, and it was
determined that oxidizing properties favor generation of fatty plaque in the arteries.

To corroborate the relationship between cardiovascular disease
with arsenic consumption, blood samples were also obtained from the
study group to identify the presence of an amino acid called asymmetric
dimethylarginine (ADMA), which is associated with problems in the

Direct evidence of Parkinson pathology spread from the gastrointestinal tract to the brain in rats -

The cellular hallmarks of Parkinson’s disease (PD) are the loss of
nigral dopaminergic neurons and the formation of α-synuclein-enriched
Lewy bodies and Lewy neurites in the remaining neurons. Based on the
topographic distribution of Lewy bodies established after autopsy of
brains from PD patients, Braak and coworkers hypothesized that Lewy
pathology primes in the enteric nervous system and spreads to the brain,
suggesting an active retrograde transport of α-synuclein (the key
protein component in Lewy bodies), via the vagal nerve. This hypothesis,
however, has not been tested experimentally thus far. Here, we use a
human PD brain lysate containing different forms of α-synuclein
(monomeric, oligomeric and fibrillar), and recombinant α-synuclein in an
in vivo animal model to test this hypothesis. We demonstrate that
α-synuclein present in the human PD brain lysate and distinct
recombinant α-synuclein forms are transported via the vagal nerve and
reach the dorsal motor nucleus of the vagus in the brainstem in a
time-dependent manner after injection into the intestinal wall. Using
live cell imaging in a differentiated neuroblastoma cell line, we
determine that both slow and fast components of axonal transport are
involved in the transport of aggregated α-synuclein. In conclusion, we
here provide the first experimental evidence that different α-synuclein
forms can propagate from the gut to the brain, and that
microtubule-associated transport is involved in the translocation of
aggregated α-synuclein in neurons.

Endocrine Disruption in Human Placenta: Expression of the Dioxin-Inducible Enzyme, Cyp1a1, Is Correlated With That of Thyroid Hormone-Regulated Genes: The Journal of Clinical Endocrinology & Metabolism: Vol 0, No 0

Thyroid hormone (TH) is essential for normal development; therefore, disruption
of TH action by a number of industrial chemicals is critical to
identify. Several chemicals including polychlorinated biphenyls are
metabolized by the dioxin-inducible enzyme CYP1A1; some of their
metabolites can interact with the TH receptor. In animals, this
mechanism is reflected by a strong correlation between the expression of
CYP1A1 mRNA and TH-regulated mRNAs. If this mechanism occurs in humans,
we expect that CYP1A1 expression will be positively correlated with the
expression of genes regulated by TH.

The objective of the study was to test the hypothesis that CYP1A1 mRNA
expression is correlated with TH-regulated mRNAs in human placenta.

One hundred sixty-four placental samples from pregnancies with no thyroid
disease were obtained from the GESTE study (Sherbrooke, Qéubec, Canada).
Maternal and cord blood TH levels were measured at birth. The mRNA
levels of CYP1A1 and placental TH receptor targets [placental lactogen
(PL) and GH-V] were quantitated by quantitative PCR.

CYP1A1 mRNA abundance varied 5-fold across 132 placental samples that had
detectable CYP1A1 mRNA. CYP1A1 mRNA was positively correlated with PL (r = 0.64; P < .0001) and GH-V (P < .0001, r = 0.62) mRNA. PL and GH-V mRNA were correlated with each other (r = 0.95; P < .0001), suggesting a common activator. The mRNAs not regulated by TH were not correlated with CYP1A1 expression.

CYP1A1 mRNA expression is strongly associated with the expression of
TH-regulated target gene mRNAs in human placenta, consistent with the
endocrine-disrupting action of metabolites produced by CYP1A1.

Could loss of a hormone drive colon cancer? - Medical News Today

A new study suggests that colon cells may become cancerous when they lose the ability to produce a hormone essential for maintaining their normal biology. If this finding is verified in subsequent studies, then colon cancer will be distinct as the only cancer driven by the lack of a hormone.diagram showing the colon
If the signals that replenish the skin of the gut are unable to maintain cell division, then it becomes more likely that cell division will be irregular and lead to cancer.

The research was conducted by a team at Thomas Jefferson University in Philadelphia, PA, and they publish their findings in the journal Cancer, Epidemiology, Biomarkers & Prevention.

Colon cancer samples were taken from 281 patients and compared with non-cancerous colon tissue from the same patients.

The researchers found that production of the hormone guanylin was decreased by 100-1,000 times in 85% of the colon cancers tested.

Toxicogenetics: in search of host susceptibility to environmental toxicants.

Heavy metals, various pesticide and herbicides are implicated as risk
factors for human health. Paraquat, maneb, and rotenone, carbamate, and
organophosphorous insecticides are examples of toxicants for which acute
and chronic exposure are associated with multiple neurological
disorders including Parkinson's disease. Nevertheless, the role of
pesticide exposure in neurodegenerative diseases is not clear-cut, as
there are inconsistencies in both the epidemiological and preclinical
research. The aim of this short review is to show that at least, some of
the inconsistencies are related to individual differences in
susceptibility to the effects of neurotoxicants, individual differences
that can be traced to the genetic constitution of the individuals and
animals studies, i.e., host-based susceptibility.

Bacterial protein implicated in eating disorders - Medical News Today

Eating disorders (ED) such as anorexia nervosa, bulimia, and binge eating disorder affect approximately 5-10% of the general population, but the biological mechanisms involved are unknown.

Researchers at Inserm Unit 1073, "Nutrition, inflammation and dysfunction of the gut-brain axis" (Inserm/University of Rouen) have demonstrated the involvement of a protein produced by some intestinal bacteria that may be the source of these disorders. Antibodies produced by the body against this protein also react with the main satiety hormone, α-melanocyte-stimulating hormone, which is similar in structure. According to the researchers, it may ultimately be possible to correct this mechanism that causes variations in food intake.

These results are published in the journal Translational Psychiatry, in the online issue of 7 October 2014.
Bacterial ClpB heat-shock protein, an antigen-mimetic of the anorexigenic peptide α-MSH, at the origin of eating disorders

Obesogens: epigenetics and obesity

he debate between nature and nurture has persisted through history. Both
have long been considered for their influence on incidence rates of
diseases like obesity. While technologies have improved our ability to
examine the underlying genetic causes, both have failed to sufficiently
account for the observed incidence of obesity. Such rapid changes in
incidence produces an apparent disparity between genetic and
environmental factors. Although the most widely accepted cause of
obesity is overconsumption of calorically dense food coupled with
diminished physical activity, emerging evidence indicates that
environmental factors can predispose individuals to gain weight,
irrespective of diet and exercise. In line with this, there is a high
rate of obesity in very young children, including infants .
Whereas one can argue that adolescents, and adults may be consuming more
and exercising less than in the past, it is implausible that this would
apply to infants. A more probable explanation is that obesity results
from prolonged disturbances in the homeostatic regulation of energy
metabolism that favors triglyceride storage and adipocyte hypertrophy.
This could occur through the prenatal environment causing these infants
to be born with an increased level of fat and predisposing them to
accumulate fat more readily, or through significant changes in the
postnatal environment. In support of the later, animals living in close
proximity to humans (e.g. dogs, cats, and laboratory animals such as
mice, rats, and primates) have exhibited pronounced increases in obesity
over the past few decades .

Could Multiple Sclerosis Begin in the Gut?

Very low concentrations of heavy metals, antibiotics contribute to resistance -- ScienceDaily

New Swedish research shows that plasmids containing genes that confer resistance to antibiotics can be enriched by very low concentrations of antibiotics and heavy metals. These results strengthen the suspicion that the antibiotic residues and heavy metals (such as arsenic, silver and copper) that are spread in the environment are contributing to the problems of resistance. These findings have now been published in the journal mBio.

mBIO paper Selection of a Multidrug Resistance Plasmid by Sublethal Levels of Antibiotics and Heavy Metals

Viral Infection May Trigger Childhood Diabetes in Utero

The incidence of type 1 childhood diabetes has been increasing rapidly
worldwide. If blood sugar levels aren't well-controlled, juvenile
diabetes can affect nearly every organ of a child's body. And while
long-term complications of the disease develop gradually, they may
become disabling and even life-threatening. The exact cause of juvenile
diabetes has eluded scientists, but a new study from Tel Aviv University suggests a likely trigger before birth.

In a recent paper published in Diabetic Medicine, Prof. Zvi Laron, Professor Emeritus of Pediatric Endocrinology at TAU's Sackler Faculty of Medicine,
Director of the Endocrinology and Diabetes Research Unit at Schneider
Children's Medical Center of Israel, and Head of the WHO Collaborating
Center for the Study of Diabetes in Youth, puts forth evidence that the
autoimmune disease is initiated in utero. According to the
research, conducted in collaboration with an international team of
researchers, women who contract a viral infection during pregnancy
transmit viruses to their genetically susceptible fetuses, sparking the
development of type 1 diabetes.