Nature Outlook : Autism: Free issue

 "As recently as the mid-1990s, autism was thought to be a rare disorder that led to severe mental disability. But since then its reported incidence has ballooned, and it is thought to encompass conditions that vary widely in character and severity. Still, its causes, treatments and even definition remain to be pieced together."

Mechanism Found For Destruction Of Key Allergy-Inducing Complexes

Researchers have learned how a man-made molecule destroys complexes that induce allergic responses - a discovery that could lead to the development of highly potent, rapidly acting interventions for a host of acute allergic reactions. 

Study finds that just one high-fat meal can affect your heart health

High-fat diets are associated with developing atherosclerosis (narrowing of the arteries) over a lifetime. But how quickly can damage start? Just one day of eating a fat-laden breakfast sandwich – processed cheese and meat on a bun – and "your blood vessels become unhappy," says Heart and Stroke Foundation researcher Dr. Todd Anderson, director of the Libin Cardiovascular Institute of Alberta and head of cardiac science at the University of Calgary.

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New study reveals that every single junk food meal damages your arteries

A single junk food meal – composed mainly of saturated fat – is detrimental to the health of the arteries, while no damage occurs after consuming a Mediterranean meal rich in good fats such as mono-and polyunsaturated fatty acids, according to researchers at the University of Montreal-affiliated ÉPIC Center of the Montreal Heart Institute. The Mediterranean meal may even have a positive effect on the arteries. The findings are being presented at the Canadian Cardiovascular Congress, which runs in Toronto until Wednesday, by the head of the study, Dr. Anil Nigam, Director of Research at the Cardiovascular Prevention and Rehabilitation Centre (ÉPIC) and associate professor at the university's Faculty of Medicine.

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High prevalence of serum antibodies reacting with simian virus 40 capsid protein mimotopes in patients affected by malignant pleural mesothelioma

Human malignant pleural mesothelioma (MPM) is considered a rare tumor, but recent estimations indicate that one-quarter million people will die of this neoplasm in Europe in the next three decades. The mineral asbestos is considered the main causative agent of this neoplasm. MPM is largely unresponsive to conventional chemotherapy/radiotherapy. In addition to asbestos exposure, genetic predisposition to asbestos carcinogenesis and to simian virus (SV)40 infection has also been suggested. SV40 is a DNA tumor virus found in some studies to be associated at high prevalence with MPM. SV40 sequences have also been detected, although at a lower prevalence than in MPM, in blood specimens from healthy donors. However, some studies have failed to reveal SV40 footprints in MPM and its association with this neoplasm. These conflicting results indicate the need for further investigations with new approaches. We report on the presence of antibodies in serum samples from patients affected by MPM that specifically react with two different SV40 mimotopes. The two SV40 peptides used in indirect ELISAs correspond to viral capsid proteins. ELISA with the two SV40 mimotopes gave overlapping results. Our data indicate that in serum samples from MPM-affected patients (n = 97), the prevalence of antibodies against SV40 viral capsid protein antigens is significantly higher (26%, P = 0.043) than in the control group (15%) represented by healthy subjects (n = 168) with the same median age (66 y) and sex. Our results suggest that SV40 is associated with a subset of MPM and circulates in humans.
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Peripheral inflammatory disease associated with centrally activated IL-1 system in humans and mice.

During peripheral immune activation caused by an infection or an inflammatory condition, the innate immune response signals to the brain and causes an up-regulation of central nervous system (CNS) cytokine production. Central actions of proinflammatory cytokines, in particular IL-1β, are pivotal for the induction of fever and fatigue. In the present study, the influence of peripheral chronic joint inflammatory disease in rheumatoid arthritis (RA) on CNS inflammation was investigated. Intrathecal interleukin (IL)-1β concentrations were markedly elevated in RA patients compared with controls or with patients with multiple sclerosis. Conversely, the anti-inflammatory IL-1 receptor antagonist and IL-4 were decreased in RA cerebrospinal fluid (CSF). Tumor necrosis factor and IL-6 levels in the CSF did not differ between patients and controls. Concerning IL-1β, CSF concentrations in RA patients were higher than in serum, indicating local production in the CNS, and there was a positive correlation between CSF IL-1β and fatigue assessments. Next, spinal inflammation in experimental arthritis was investigated. A marked increase of IL-1β, IL-18, and tumor necrosis factor, but not IL-6 mRNA production, in the spinal cord was observed, coinciding with increased arthritis scores in the KBxN serum transfer model. These data provide evidence that peripheral inflammation such as arthritis is associated with an immunological activation in the CNS in both humans and mice, suggesting a possible therapeutic target for centrally affecting conditions as fatigue in chronic inflammatory diseases, for which to date there are no specific treatments.

Toxicology: The learning curve : Nature News & Comment: Toxic effects of low doses

Endocrine disrupters include a large group of synthetic chemicals that interact with cellular hormone receptors. These compounds, which range from the common weed killer atrazine and the plasticizer bisphenol A (BPA) to the antibacterial agent triclosan (used in cleansers) and the vineyard fungicide vinclozolin, don't play by the usual rules of toxicology. On the basis of conventional high-dose testing, regulators have set maximum acceptable levels for each of them that assume all doses below that level are safe. But academic researchers who have studied a wider range of doses, including very low ones found in the everyday environment, say that their experiments usually do not generate the tidy, familiar 'ski-slope' dose-response graphs of classic toxicology. Instead, most endocrine disrupters have 'non-monotonic' dose-response curves, meaning that their slopes change at least once from negative to positive, or vice versa, forming 'U' shapes, inverted 'U's or even stranger shapes that resemble undulating Chinese dragons. 
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Carotid Atherosclerosis and Prospective Risk of Dementia.

Although vascular risk factors have been implicated in the development of all-cause dementia and Alzheimer disease (AD), few studies have examined the association between subclinical atherosclerosis and prospective risk of dementia.


Participants from the Baltimore Longitudinal Study of Aging (n=364; age, 60-95 years; median age, 73; 60% male; 82% white) underwent initial carotid atherosclerosis assessment and subsequently were assessed for dementia and AD annually for up to 14 years (median, 7.0). Cox proportional hazards models predicting all-cause dementia and AD were adjusted for age, sex, race, education, blood pressure, cholesterol, cardiovascular disease, diabetes mellitus, and smoking.


Sixty participants developed dementia, with 53 diagnosed as AD. Raw rates of future dementia and AD among individuals initially in the upper quintile of carotid intimal medial thickness or with bilateral carotid plaque were generally double the rates of individuals with intimal medial thickness in the lower quintiles or no plaque at baseline. Adjusted proportional hazards models revealed >2.5-fold increased risk of dementia and AD among individuals in the upper quintile of carotid intimal medial thickness, and approximately 2.0-fold increased risk of dementia among individuals with bilateral plaque.


Multiple measures of carotid atherosclerosis are associated with prospective risk of dementia. Individuals in the upper quintile of carotid intimal medial thickness or bilateral carotid plaque were at greatest risk. These findings underscore the possibility that early intervention to reduce atherosclerosis may help delay or prevent onset of dementia and AD.
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Toxoplasma gondii infection induces dendritic retraction in basolateral amygdala accompanied by reduced corticosterone secretion.

Pathological anxiety is thought to reflect a maladaptive state characterized by exaggerated fear. Naturally occurring perturbations that reduce fear can be crucial in the search for new treatments. The protozoan parasite Toxoplasma gondii invades rat brain and removes fear of rats for cat odors, a change believed to be parasitic manipulation of host behavior aimed at increasing parasite transmission. It is likely that mechanisms employed by Toxoplasma gondii can be used as a heuristic tool to understand possible means of fear reduction in clinical settings. Male Long-Evans rats were infected with Toxoplasma gondii and compared with sham-infected animals 8 weeks post-infection. Amount of circulating plasma corticosterone and dendritic arborization of basolateral amygdala principal neurons were quantified. Previous studies have shown that corticosterone, acting within the basolateral amygdala, enhances the fear response to environmental stimuli. Here we show that Toxoplasma gondii infection causes a dendritic retraction in basolateral amygdala neurons. Such dendritic retraction is accompanied by lower amount of circulating corticosterone both at baseline and when induced by an aversive cat odor. The concerted effects of parasitism on two pivotal physiological nodes of fear response provide an animal model relevant to stress hormones interaction with amygdalar plasticity.
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Toxoplasma gondii: A potential role in the genesis of psychiatric disorders

Toxoplasma gondii is the most common protozoan parasite in developed nations. Up to 43% of the French population may be infected, depending on eating habits and exposure to cats, and almost one third of the world human's population may be infected. Two types of infection have been described: a congenital form and an acquired form. Although the medical profession treats these latent cases as asymptomatic and clinically unimportant, results of animal studies and recent studies of personality profiles, behavior, and psychomotor performance have led to reconsider this assumption.


Among rats: parasite cysts are more abundant in amygdalar structures than those found in other regions of the brain. Infection does not influence locomotion, anxiety, hippocampal-dependent learning, fear conditioning (or its extinction) and neophobia in rats. Rats' natural predator is the cat, which is also T. gondii's reservoir. Naturally, rats have an aversion to cat urine, but the parasite suppresses this aversion in rats, thus influencing the infection cycle. Tachyzoites may invade different types of nervous cells, such as neurons, astrocytes and microglial cells in the brain, and Purkinje cells in cerebellum. Intracellular tachyzoites manipulate several signs for transduction mechanisms involved in apoptosis, antimicrobial effectors functions, and immune cell maturation. Dopamine levels are 14% higher in mice with chronic infections. These neurochemical changes may be factors contributing to mental and motor abnormalities that accompany or follow toxoplasmosis in rodents and possibly in humans. Moreover, the antipsychotic haloperidol and the mood stabilizer valproic acid most effectively inhibit Toxoplasma growth in vitro with synergistic activity.


The effects of the parasite are not due to the manipulation in an evolutionary sense but merely due to neuropathological or neuroimmunological effects of the parasite's presence. Toxoplasmosis and schizophrenia: epidemiological studies point to a role for toxoplasmosis in schizophrenia's etiology, probably during pregnancy and early life, this association being congruent with studies in animal models indicating that animal exposures of the developing brain to infectious agents or immune modulating agents can be associated with behavioral changes that do not appear until the animal reaches full maturity. Psychiatric patients have increased rates of toxoplasmic antibodies, the differences between cases and controls being greatest in individuals who are assayed near the time of the onset of their symptoms. The increase of dopamine in the brain of infected subjects can represent the missing link between toxoplasmosis and schizophrenia. Toxoplasmosis and Obsessive Compulsive Disorder (OCD): the seropositivity rate for anti-T. gondii IgG antibodies among OCD patients is found to be significantly higher than the rate in healthy volunteers. Infection of basal ganglia may be implicated in the pathogenesis of OCD among Toxoplasma seropositive subjects. Toxoplasmosis and personality: infected men appear to be more dogmatic, less confident, more jealous, more cautious, less impulsive and more orderly than others. Conversely, infected women seem warmest, more conscientious, more insecure, more sanctimonious and more persistent than others. It is possible that differences in the level of testosterone may be responsible for the observed behavioral differences between Toxoplasma-infected and Toxoplasma-free subjects.


In the future two major avenues for research seem essential. On one hand, prospective studies and research efforts must still be carried out to understand the mechanisms by which the parasite induces these psychiatric disorders. On the other hand, it has not yet been demonstrated that patients with positive toxoplasmic serology may better respond to haloperidol's or valproic acid's antiparasitic activity. These results may appear as a major issue in the drug's prescribing choices and explain variability in response to the treatment of patients with schizophrenia that is not explained by the genetic polymorphism.
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IgGs containing λ- and κ-type light chains and of all subclasses (IgG1-IgG4) from the sera of patients with autoimmune diseases and viral and bacterial infections hydrolyze DNA.

We present the first evidence demonstrating that small fractions of IgGs of all four subclasses (IgG1-IgG4) from patients with viral (tick-borne encephalitis), bacterial infections (streptococcal infection or erysipelas), and suppurative surgical infections caused by epidermal staphylococci as well as from patients with autoimmune diseases (systemic lupus erythematosus and multiple sclerosis) are catalytically active in the hydrolysis of supercoiled DNA. The hydrolysis of DNA was analyzed by agarose gel electrophoresis. The catalytic activities of nonfractionated IgGs increased in the following order: tick-borne encephalitis < suppurative surgical infection < streptococcal infection < multiple sclerosis < systemic lupus erythematosus, whereas IgGs of healthy donors were inactive. However, the pools of antibodies corresponding to any particular disease were characterized by a specific ratio of IgGs of all four subclasses (IgG1-IgG4) and IgGs containing λ- and κ-type light chains, and each of these subfractions of immunoglobulins demonstrated characteristic relative DNase activity. The relative activities of IgGs containing λ-type light chains may on average be higher, lower, or comparable with those for IgGs with κ-type light chains. The relative contributions of IgGs of different subclasses to the total activity of IgGs also varied widely in the case of various diseases: IgG1 (7%-45%), IgG2 (0.4%-73%), IgG3 (0%-12%), and IgG4 (9%-66%). Thus, immune systems of patients with different diseases can generate a variety of anti-DNA abzymes of different types and with different catalytic properties, which can play an important role in the pathogenesis or protection from the development of these diseases.

WHO | Atlasof health and climate

The Atlas of health and climate is a product of this unique collaboration between the meteorological and public health communities. It provides sound scientific information on the connections between weather and climate and major health challenges. These range from diseases of poverty to emergencies arising from extreme weather events and disease outbreaks. They also include environmental degradation, the increasing prevalence of noncommunicable diseases and the universal trend of demographic ageing.
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Risk factors predict childhood obesity, researchers find

ScienceDaily (Oct. 29, 2012) — High birth weight, rapid weight gain and having an overweight mother who smokes can all increase the risk of a baby becoming obese later in childhood, research by experts at The University of Nottingham has found.

Stay-at-home transcription factor prevents neurodegeneration

A study in The Journal of Cell Biology shows how  the STAT3  transcription factor remains in the axon of nerve cells to help prevent neurodegeneration. The findings could pave the way for future drug therapies to slow nerve damage in patients with neurodegenerative diseases.
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Flu Vaccine Could Decrease Risk For Heart Disease And Death: MNT

A flu shot can prevent you from getting sick and also stop heart disease. It can lessen the risk of a major cardiac happening by 50 percent and deaths from a cardiac event by 40 percent, according to new research presented at the 2012 Canadian Cardiovascular Congress.
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Sex-dependent neurotransmitter level changes in brains of Toxoplasma gondii infected mice.

The protozoan parasite Toxoplasma gondii has the ability to alter intermediate host behavior, most impressively the natural aversion to cat scent, to favor the predation by the definitive host. However, the underlying mechanism of the observed phenomenon still remains unknown. Since changes in the neurotransmitter level are postulated as a possible contributing factor, the aim of this work was to assess the monoamine systems activity in specified brain regions involved in the natural defense behaviors, emotion evaluation, and motor and sensory stimuli integration in experimentally T. gondii infected mice compared to uninfected controls. Taking into account the natural differences between genders, the experiments were carried out on both male and female mice. Our results revealed statistically significant changes in all tested monoamine systems with regard to both gender and time after T. gondii invasion. Acute toxoplasmosis was accompanied by a decrease in noradrenergic system activity in females and its slight increase in some brain areas of males. Acute invasion also induced a rise in serotonin system activity, mostly in males. The most striking observation was an increase in the dopamine release noted in acutely infected males. We discuss our results in terms of their possible contribution to T. gondii-induced intermediate host behavior alterations and parasite transmission and with regard to postulated relationship between T. gondii seroprevalence and occurrence of certain disorders such as schizophrenia in humans.
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Cause of high cholesterol discovered

ScienceDaily (Oct. 28, 2012) — Canadian scientists have discovered that a protein called resistin, secreted by fat tissue, causes high levels of "bad" cholesterol (low-density lipoprotein or LDL), increasing the risk of heart disease.
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Scientists step up hunt for bacterial genes tied to Lyme disease

Investigators at The University of Texas Health Science Center at Houston (UTHealth) have accelerated the search for the bacterial genes that make the Lyme disease bacterium so invasive and persistent. The discovery could advance the diagnosis and treatment of this disease, which affects an estimated 30,000 Americans each year.
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Genetic risk for Parkinson's disease correlates with alterations in neuronal manganese sensitivity between two human subjects.

Manganese (Mn) is an environmental risk factor for Parkinson's disease (PD). Recessive inheritance of PARK2 mutations is strongly associated with early onset PD (EOPD). It is widely assumed that the influence of PD environmental risk factors may be enhanced by the presence of PD genetic risk factors in the genetic background of individuals. However, such interactions may be difficult to predict owing to the complexities of genetic and environmental interactions. Here we examine the potential of human induced pluripotent stem cell (iPS)-derived early neural progenitor cells (NPCs) to model differences in Mn neurotoxicity between a control subject (CA) with no known PD genetic risk factors and a subject (SM) with biallelic loss-of-function mutations in PARK2 and family history of PD but no evidence of PD by neurological exam. Human iPS cells were generated from primary dermal fibroblasts of both subjects. We assessed several outcome measures associated with Mn toxicity and PD. No difference in sensitivity to Mn cytotoxicity or mitochondrial fragmentation was observed between SM and CA NPCs. However, we found that Mn exposure was associated with significantly higher reactive oxygen species (ROS) generation in SM compared to CA NPCs despite significantly less intracellular Mn accumulation. Thus, this report offers the first example of human subject-specific differences in PD-relevant environmental health related phenotypes that are consistent with pathogenic interactions between known genetic and environmental risk factors for PD.
Enhanced by Zemanta – To slow Parkinson’s, shut out calcium

The new compounds target and shut a relatively rare membrane protein that allows the destructive calcium to flood into dopamine neurons. Previously published research showed that calcium entry through this protein stresses dopamine neurons, potentially leading to premature aging and death. The earlier research  identified the precise protein involved—the Cav1.3 channel.

Immunoreactivity of Nanoparticles « Pharmaceutical Intelligence

As nanotechnology progresses from research and development to commercialization and use, it is likely that manufactured nanomaterials and nanoproducts will be released into the environment.
Adverse effects of nanoparticles on human health depend on individual factors such as genetics and existing disease, as well as exposure, and nanoparticle chemistry, size, shape, agglomeration state, and electromagnetic properties. Animal and human studies show that inhaled nanoparticles are lessefficiently removed than larger particles by the macrophage clearance mechanisms in the lung,causing lung damage, and that nanoparticles can translocate through the circulatory, lymphatic, and nervous systems to many tissues and organs, including the brain.
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Researchers develop cocktail of bacteria that eradicates Clostridium difficile infection

In a new study out today, researchers used mice to identify a combination six naturally occurring bacteria that eradicate a highly contagious form of Clostridium difficile, an infectious bacterium associated with many hospital deaths. Three of the six bacteria have not been described before. This work may have significant implications for future control and treatment approaches.

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Drug shows promise in animal model of Alzheimer's and Parkinson's with dementia

New research presented in October at the 6th Neurodegenerative Conditions Research and Development Conference in San Francisco demonstrates the role of the investigational compound IRX4204 in alleviating cognitive decline in animal models of Alzheimer's disease (AD). The presentation entitled "Investigation of the RXR-specific agonist IRX4204 as a Disease Modifying Agent of Alzheimer's Disease Neuropathology and Cognitive Impairment" was made by lead researcher Giulio Maria Pasinetti, MD, PhD, of the Mount Sinai School of Medicine in New York City.

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Schizophrenia Research Forum: Live Discussion: Neurotropic Infectious Agents and Cognitive Impairment in Schizophrenia

Join us on Tuesday, 13 November 2012 at 12:00 noon, U.S. Eastern time, for another installment in our Schizophrenia Bulletin theme section Webinar series to learn about and discuss this topic. Registration is required, and don't forget to log in to the Webinar a few minutes early to make certain you have time to familiarize yourself with the Webinar software.
Enhanced by Zemanta – Sea sponge chemical fixes cystic fibrosis defect

A chemical from a marine sponge found in the South Pacific Ocean restores function in a defective protein that causes cystic fibrosis, a fatal genetic disease.
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Neuroprotective Mitochondrial Glutamate Receptors -- Gough 5 (247): ec272 -- Science Signaling

Glutamate receptors of the N-methyl-D-aspartate (NMDA) type participate in both physiological and pathological synaptic events, with excessive activation of these receptors resulting in calcium overload and excitotoxicity. Korde and Maragos prepared isolated mitochondria from rat brains and found that these preparations responded to glutamate or NMDA agonists with increased calcium uptake, compared with the calcium uptake by mitochondria in the absence of these ligands. The NR2a subunit of the NMDA receptor was detected to be associated with mitochondria by electron microscopy of purified mitochondrial preparations or hippocampal slices, and Western blotting of submitochondrial preparations indicated that the NR1 and NR2a subunits were associated with the inner mitochondrial membrane. Mitochondria prepared from GT1-7, a neuronal cell line, in which the NR1 subunit was knocked down exhibited only basal calcium uptake that was not enhanced by the addition of NMDA. In contrast, expression of NR1 and NR2a targeted specifically to the mitochondria resulted in cells that had enhanced ATP production and exhibited less death in response to cytotoxic concentrations of glutamate. Mitochondria from these NMDA receptor–targeted cells had increased calcium uptake, suggesting that increased capacity for calcium buffering may contribute to the protective effects. Although compared with their abundance in the synaptic plasma membrane, the abundance of NMDA receptors in mitochondria is low, these data suggest that mitochondrial NMDA receptors may play a role in the calcium buffering capacity of mitochondria.

Placebo Effect Could Be Genetic

The placebo effect, where treatments with no active ingredients help to alleviate symptoms in some patients and not others, has been a mystery to medical science for the last 70 years. Now for the first time, researchers in the US reporting in PLoS ONE this week, describe how they found clues that might explain why the placebo effect works for some people and not others: it's in their genes, they suggest. An important gene is catechol-O-methyltransferase (COMT).
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Resurrection of endogenous retroviruses in antibody-deficient mice : Nature : Nature Publishing Group

The mammalian host has developed a long-standing symbiotic relationship with a considerable number of microbial species. These include the microbiota on environmental surfaces, such as the respiratory and gastrointestinal tracts1, and also endogenous retroviruses (ERVs), comprising a substantial fraction of the mammalian genome23. The long-term consequences for the host of interactions with these microbial species can range from mutualism to parasitism and are not always completely understood. The potential effect of one microbial symbiont on another is even less clear. Here we study the control of ERVs in the commonly used C57BL/6 (B6) mouse strain, which lacks endogenous murine leukaemia viruses (MLVs) able to replicate in murine cells. We demonstrate the spontaneous emergence of fully infectious ecotropic4 MLV in B6 mice with a range of distinct immune deficiencies affecting antibody production. These recombinant retroviruses establish infection of immunodeficient mouse colonies, and ultimately result in retrovirus-induced lymphomas. Notably, ERV activation in immunodeficient mice is prevented in husbandry conditions associated with reduced or absent intestinal microbiota. Our results shed light onto a previously unappreciated role for immunity in the control of ERVs and provide a potential mechanistic link between immune activation by microbial triggers and a range of pathologies associated with ERVs, including cancer.
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Moss Harbors Foreign Genes (viral, bacterial and fungal)| The Scientist Magazine®

Land plants emerged around half a billion years ago, having evolved from green aquatic algae. Today, a representative of these early land-dwelling species—a moss—hints that genes from other kingdoms of life may have helped the ancient colonizers flourish on land.

New vitamin-based treatment that could reduce muscle degeneration in muscular dystrophy

Boosting the activity of a vitamin-sensitive cell adhesion pathway has the potential to counteract the muscle degeneration and reduced mobility caused by muscular dystrophies, according to a research team led by scientists at the University of Maine.

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Are schizophrenia and autism close relations?

(Medical Xpress)—Autism Spectrum Disorders (ASD), a category that includes autism, Asperger Syndrome, and Pervasive Developmental Disorder, are characterized by difficulty with social interaction and communication, or repetitive behaviors. The U.S. Centers for Disease Control and Management says that one in 88 children in the US is somewhere on the Autism spectrum—an alarming ten-fold increase in the last four decades.

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Effect of Helicobacter pylori infection on platelet activation and coagulation function in patients with acute cerebral infarction

To investigate the effect of Helicobacter pylori (Hp) on platelet activation and coagulation function in patients with acute cerebral infarction. Methods: Sixty-six patients with acute cerebral infarction and 50 health individuals were enrolled in the study. Hp antibody,expression of CD62p on platelets and clotting indexes were measured and compared between two groups. Results: The positive rate of Hp-IgG and Hp-CagA in cerebral infarction patients were higher than that in controls (P<0.05). The positive rate of CD62p in patients with positive Hp-IgG and Hp-CagA was significantly higher than that in negative patients and also controls (P<0.05). The APTT and TT were lower and FIB was higher in patients with positive Hp antibody than those in patients with negative Hp antibody (P<0.05),but there was no difference in PT,PTR and INR (P>0.05). Conclusion: Hp infection can activate platelets and affect coagulation function,which may be involved in the development of cerebral infarction.

Link found between Alzheimer's disease and protein regulation in the brain -- hope for new treatments

A link has been discovered between Alzheimer's disease and the activity level of a protein called eIF2alpha. This has been reported in a new study conducted at the University of Haifa's Sagol Department of Neurobiology, recently published in the journalNeurobiology of Aging. According to Prof. Kobi Rosenblum, head of the Department, altering the performance of this protein via drug therapy could constitute a treatment for Alzheimer's, which is incurable.

Clue to cause of Alzheimer's dementia found in brain samples

Researchers at Washington University School of Medicine in St. Louis have found a key difference in the brains of people with Alzheimer's disease and those who are cognitively normal but still have brain plaques that characterize this type of dementia.

Specific bacterial species may initiate, maintain Crohn’s

ScienceDaily (Oct. 22, 2012) — Patients newly diagnosed with pediatric Crohn's disease had significantly different levels of certain types of bacteria in their intestinal tracts than age-matched controls, according to a paper in the OctoberJournal of Clinical Microbiology. The work may ultimately lead to treatment involving manipulation of the intestinal bacteria.
Enhanced by Zemanta – ‘Tube’ view of nerve fibers may monitor Multiple sclerosis

A new discovery could be a powerful tool for the diagnosis and monitoring of brain diseases like multiple sclerosis that have links to myelin loss.

Paradoxical downregulation of HLA-A expression by IFNγ associated with schizophrenia and noncoding genes.

Neuronal MHC/HLA regulates the synapses of the central nervous system (CNS). The expression of MHC/HLA is, in turn, regulated by immune cytokines. We were therefore interested in the regulation of schizophrenia-associated HLA antigens, specifically their regulation of expression by interferons. We had previously observed a moderately increased frequency of HLA-A10 expression in schizophrenic patients. While searching for the "true" disease gene near the HLA-A gene, we discovered that homozygosity of the HLA-J M80469 pseudogene allele, in combination with HLA-A10 or HLA-A9, was associated with a high risk of schizophrenia (HLA-A10 relative risk=29.33, p=0.00019, patients N=77, controls N=214). The allele HLA-J M80468, which codes for interferon-inducible mRNA, conferred protection on carriers of HLA-A9 and HLA-A10 (HLA-A10 relative risk=0.022, p=0.00017). Functional analysis revealed that interferon γ (IFNγ) downregulated the expression of HLA-A9 and HLA-A10 in monocytes from HLA-J M80469 homozygous patients but not from carriers of the HLA-J M80468 allele. This is the first demonstration of an inverse effect of IFNγ on HLA expression that is associated with non-coding gene variants and schizophrenia. Our findings suggest that the interferons secreted during acute and chronic infections may interfere in synaptic regulation via neuronal HLA and that this disturbance in synaptic regulation may induce the symptoms of mental illness.
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Natural process activating brain's immune cells could point way to repairing damaged brain tissue

The brain's key "breeder" cells, it turns out, do more than that. They secrete substances that boost the numbers and strength of critical brain-based immune cells believed to play a vital role in brain health. This finding adds a new dimension to our understanding of how resident stem cells and stem cell transplants may improve brain function.
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Increase in dopaminergic, but not serotoninergic, receptors in T-cells as a marker for schizophrenia severity.

Schizophrenia is characterized by a slow deteriorating mental illness. Although the pathophysiology mechanisms are not fully understood, different studies have suggested a role for the immune system in the pathogenesis of schizophrenia. To date, an altered expression or signaling of neurotransmitters receptors is observed in immune cells during psychiatric disorders. In the present study, we investigated the expression of different serotonin and dopamine receptors in T-cells of schizophrenic and control patients. We used flow cytometry to determine the pattern of expression of dopamine (D2 and D4) and serotonine receptors (SR1A, SR1C, SR2A, SR2B), as well as serotonin transporter (ST), in T-cell subsets (CD4 and CD8). Expression of serotonin receptors and ST in T-cells of schizophrenic patients were not different from controls. However, the percentages of CD4+D4+ and CD8+D4+ were increased in schizophrenic patients as compared to controls. In addition, increased percentages of CD8+D2+ cells were also observed in schizophrenic patients, albeit this population revealed lower CD4+D2+ cells in comparison to controls. Interestingly, a relationship between clinical symptoms and immunological parameters was also observed. We showed that the Brief Psychiatric Rating Scale (BPRS), the Positive and Negative Syndrome Scale (PANSS) and the Abnormal Involuntary Movement Scale (AIMS) were positively related to CD8+D2+ cells, though AIMS was inversely related to CD4+D4+ cells. In conclusion, the alteration in the pattern of cell population and molecules expressed by them might serve as a promising biomarker for diagnosis of schizophrenia.

Helicobacter pylori serology in autoimmune diseases - fact or fiction?

The pathogenesis of autoimmunity is presumed to be a complex process including genetic predisposition, hormonal balance and environmental factors such as infectious agents. Helicobacter pylori, a common bacterial infectious agent has been associated with a variety of autoimmune disorders. However, this bacteria is also thought to play a protective role in the development of multiple sclerosis (MS), systemic lupus erythematosus (SLE) and inflammatory bowel disease (IBD). We tested various links between anti-H. pylori (anti-HP) antibodies and a wide profile of autoimmune diseases and autoantibodies. Methods: A total of 1290 patients diagnosed with 14 different autoimmune diseases from two geographical areas (Europe and Latin America) and two groups of healthy matching controls (n=385) were screened for the presence of H. pylori IgG antibodies by "pylori detect" kit. In parallel, a large profile belonging to three groups of autoantibodies was tested in all sera (anti-nuclear antibodies, autoantibodies associated with thrombophilia and gastrointestinal diseases). Results: Our data demonstrate associations between anti-HP antibodies and anti-phospholipid syndrome, giant cell arteritis, systemic sclerosis and primary biliary cirrhosis. Our data also support a previously known negative association between the prevalence of anti-HP antibodies and IBD. Additionally, links were made between seropositivity to H. pylori and the presence of anti-nuclear antibodies, dsDNA, anti-Ro and some thrombophilia-associated antibodies, as well as negative associations with gastrointestinal-associated antibodies. Conclusions: Whether these links are epiphenomenal or H. pylori does play a causative role in the autoimmune diseases remains uncertain. The negative associations could possibly support the notion that in susceptible individuals infections may protect from the development of autoimmune diseases.
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Response to valganciclovir in chronic fatigue syndrome patients with human herpesvirus 6 and Epstein-Barr virus IgG antibody titers.

Valganciclovir has been reported to improve physical and cognitive symptoms in patients with chronic fatigue syndrome (CFS) with elevated human herpesvirus 6 (HHV-6) and Epstein-Barr virus (EBV) IgG antibody titers. This study investigated whether antibody titers against HHV-6 and EBV were associated with clinical response to valganciclovir in a subset of CFS patients. An uncontrolled, unblinded retrospective chart review was performed on 61 CFS patients treated with 900 mg valganciclovir daily (55 of whom took an induction dose of 1,800 mg daily for the first 3 weeks). Antibody titers were considered high if HHV-6 IgG ≥1:320, EBV viral capsid antigen (VCA) IgG ≥1:640, and EBV early antigen (EA) IgG ≥1:160. Patients self-rated physical and cognitive functioning as a percentage of their functioning prior to illness. Patients were categorized as responders if they experienced at least 30% improvement in physical and/or cognitive functioning. Thirty-two patients (52%) were categorized as responders. Among these, 19 patients (59%) responded physically and 26 patients (81%) responded cognitively. Baseline antibody titers showed no significant association with response. After treatment, the average change in physical and cognitive functioning levels for all patients was +19% and +23%, respectively (P < 0.0001). Longer treatment was associated with improved response (P = 0.0002). No significant difference was found between responders and non-responders among other variables analyzed. Valganciclovir treatment, independent of the baseline antibody titers, was associated with self-rated improvement in physical and cognitive functioning for CFS patients who had positive HHV-6 and/or EBV serologies. Longer valganciclovir treatment correlated with an improved response.
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Human Stool Transplant Effective Treatment For C-diff

An unconventional therapy that uses donated human stool to treat the highly contagious and potentially fatal C.diff is safe and beneficial, according to a new study being presented at the annual Infectious Disease Society of America Meeting in San Diego.
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After PhIII flops, Alzheimer's R&D turns to prevention instead of cure - FierceBiotech

Now that three of the world's biggest drug developers--J&J ($JNJ), Pfizer ($PFE) and Eli Lilly ($LLY)--have failed to demonstrate the efficacy of their leading Alzheimer's drugs among afflicted patients in Phase III, investigators have started off on a lengthy journey to see if one of the therapies in the pipeline can save people before they succumb to this memory-wasting ailment.

Neurotensin Level Linked To Various Diseases | Medical News and Health Information

What do diabetes, cardiovascular disease, breast cancer, and death all have in common? Researchers say it’s plasma levels of proneutrotensin, a precursor of the hormone neurotensin.
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Imbalanced Oxidative Stress Causes Chlamydial Persistence during Non-Productive Human Herpes Virus Co-Infection.

Both human herpes viruses and Chlamydia are highly prevalent in the human population and are detected together in different human disorders. Here, we demonstrate that co-infection with human herpes virus 6 (HHV6) interferes with the developmental cycle of C. trachomatis and induces persistence. Induction of chlamydial persistence by HHV6 is independent of productive virus infection, but requires the interaction and uptake of the virus by the host cell. On the other hand, viral uptake is strongly promoted under co-infection conditions. Host cell glutathione reductase activity was suppressed by HHV6 causing NADPH accumulation, decreased formation of reduced glutathione and increased oxidative stress. Prevention of oxidative stress restored infectivity of Chlamydia after HHV6-induced persistence. We show that co-infection with Herpes simplex virus 1 or human Cytomegalovirus also induces chlamydial persistence by a similar mechanism suggesting that Chlamydia -human herpes virus co-infections are evolutionary shaped interactions with a thus far unrecognized broad significance.

No antibodies, no problem: Researchers identify how mosquito immune system attacks specific infections

Researchers at the Johns Hopkins Bloomberg School of Public Health have determined a new mechanism by which the mosquitoes' immune system can respond with specificity to infections with various pathogens, including the parasite that causes malaria in humans, using one single gene. Unlike humans and other animals, insects do not make antibodies to target specific infections. According to the Johns Hopkins researchers, mosquitoes use a mechanism known as alternative splicing to arrange different combinations of binding domains, encoded by the same AgDscam gene, into protein repertoires that are specific for different invading pathogens.

Predicting the Outcome of Infectious Diseases: How one infection (influenza) influences another (H.Pylori)

"when we infected mice first with Hpylori and then 2 months later with influenza A virus, Hpylori colonization densities in the stomachs of individual mice showed a strong positive correlation with the influenza viral loads in their lungs. In other words, knowledge of the Hpylori bacterial load in the stomach could have predicted the influenza viral load in the lung. Weight loss is an indication of influenza severity in mice and is correlated with viral titers ). Interestingly, the Hpylori burden was also highly correlated with weight change after influenza virus infection and, in fact, was a better predictor than the influenza virus titer . Thus, the bacterial load ofHpylori in the stomach predicts both virologic and clinical outcomes of influenza virus infection among inbred mice. Together, these data suggest that individual inbred mice differ in the capacity to control disparate infections in two distinct tissue compartments".
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Global pattern of experienced and anticipated discrimination reported by people with major depressive disorder: a cross-sectional survey : The Lancet

Depression is the third leading contributor to the worldwide burden of disease. We assessed the nature and severity of experienced and anticipated discrimination reported by adults with major depressive disorder worldwide. Moreover, we investigated whether experienced discrimination is related to clinical history, provision of health care, and disclosure of diagnosis and whether anticipated discrimination is associated with disclosure and previous experiences of discrimination.
In a cross-sectional survey, people with a diagnosis of major depressive disorder were interviewed in 39 sites (35 countries) worldwide with the discrimination and stigma scale (version 12; DISC-12). Other inclusion criteria were ability to understand and speak the main local language and age 18 years or older. The DISC-12 subscores assessed were reported discrimination and anticipated discrimination. Multivariable regression was used to analyse the data.


1082 people with depression completed the DISC-12. Of these, 855 (79%) reported experiencing discrimination in at least one life domain. 405 (37%) participants had stopped themselves from initiating a close personal relationship, 271 (25%) from applying for work, and 218 (20%) from applying for education or training. We noted that higher levels of experienced discrimination were associated with several lifetime depressive episodes (negative binomial regression coefficient 0·20 [95% CI 0·09—0·32], p=0·001); at least one lifetime psychiatric hospital admission (0·29 [0·15—0·42], p=0·001); poorer levels of social functioning (widowed, separated, or divorced 0·10 [0·01—0·19], p=0·032; unpaid employed 0·34 [0·09—0·60], p=0·007; looking for a job 0·26 [0·09—0·43], p=0·002; and unemployed 0·22 [0·03—0·41], p=0·022). Experienced discrimination was also associated with lower willingness to disclose a diagnosis of depression (mean discrimination score 4·18 [SD 3·68] for concealing depression vs 2·25 [2·65] for disclosing depression; p<0·0001). Anticipated discrimination is not necessarily associated with experienced discrimination because 147 (47%) of 316 participants who anticipated discrimination in finding or keeping a job and 160 (45%) of 353 in their intimate relationships had not experienced discrimination.


Discrimination related to depression acts as a barrier to social participation and successful vocational integration. Non-disclosure of depression is itself a further barrier to seeking help and to receiving effective treatment. This finding suggests that new and sustained approaches are needed to prevent stigmatisation of people with depression and reduce the effects of stigma when it is already established.
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Researchers elucidate transport pathway of immune system substances

To transport substances from the site of their production to their destination, the body needs a sophisticated transport and sorting system. Various receptors in and on the cells recognize certain molecules, pack them and ensure that they are transported to the right place. One of these receptors is Sortilin. It is present in the cells of the nervous system, the liver, and the immune system. Studies by Stefanie Herda and Dr. Armin Rehm (Max Delbrück Center for Molecular Medicine, MDC, Berlin-Buch and Charité–Universitätsmedizin Berlin) and the immunologist Dr. Uta Höpken (MDC) have now shown that the receptor Sortilin plays an important role in the function of the immune system.

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Mutations in BCKD-kinase Lead to a Potentially Treatable Form of Autism with Epilepsy

Autism spectrum disorders are a genetically heterogeneous constellation of syndromes characterized by impairments in reciprocal social interaction. Available somatic treatments have limited efficacy. We have identified inactivating mutations in the gene BCKDK (Branched Chain Ketoacid Dehydrogenase Kinase) in consanguineous families with autism, epilepsy, and intellectual disability. The encoded protein is responsible for phosphorylation-mediated inactivation of the E1α subunit of branched-chain ketoacid dehydrogenase (BCKDH). Patients with homozygous BCKDK mutations display reductions in BCKDK messenger RNA and protein, E1α phosphorylation, and plasma branched-chain amino acids. Bckdk knockout mice show abnormal brain amino acid profiles and neurobehavioral deficits that respond to dietary supplementation. Thus, autism presenting with intellectual disability and epilepsy caused by BCKDK mutations represents a potentially treatable syndrome.

Influenza infection induces neuroinflammation, alters hippocampal neuron morphology, and impairs cognition in adult mice.

Influenza is a common and highly contagious viral pathogen, yet its effects on the structure and function of the CNS remain largely unknown. Although there is evidence that influenza strains that infect the brain can lead to altered cognitive and emotional behaviors, it is unknown whether a viral strain that is not neurotropic (A/PR/8/34) can result in a central inflammatory response, neuronal damage, and neurobehavioral effects. We hypothesized that neuroinflammation and alterations in hippocampal neuron morphology may parallel cognitive dysfunction following peripheral infection with live influenza virus. Here, we show that influenza-infected mice exhibited cognitive deficits in a reversal learning version of the Morris water maze. At the same time point in which cognitive impairment was evident, proinflammatory cytokines (IL-1β, IL-6, TNF-α, IFN-α) and microglial reactivity were increased, while neurotrophic (BDNF, NGF) and immunomodulatory (CD200, CX3CL1) factors were decreased in the hippocampus of infected mice. In addition, influenza induced architectural changes to hippocampal neurons in the CA1 and dentate gyrus, with the most profound effects on dentate granule cells in the innermost portion of the granule cell layer. Overall, these data provide the first evidence that neuroinflammation and changes in hippocampal structural plasticity may underlie cognitive dysfunction associated with influenza infection. In addition, the heightened inflammatory state concurrent with reduced neurotrophic support could leave the brain vulnerable to subsequent insult following influenza infection. A better understanding of how influenza impacts the brain and behavior may provide insight for preventing inflammation and neuronal damage during peripheral viral infection.

Vitamin D supplements may benefit lupus patients

A new clinical study published in BioMedCentral's open access journal Arthritis Research and Therapy provides preliminary evidence that vitamin D supplementation could be considered an immunomodulatory agent for systemic lupus erythematosus (SLE), a debilitating autoimmune disease characterized not only by skin, joint, neurological and renal symptoms, but also by inflammation of tissue linings in the body.
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Nurture trumps nature in a longitudinal survey of salivary bacterial communities in twins from early adolescence to early adulthood.

Variation in the composition of the human oral microbiome in health and disease has been observed. We have characterized inter- and intra-individual variation of microbial communities of 107 individuals in one of the largest cohorts to date (264 saliva samples), using culture-independent 16S rRNA pyrosequencing. We examined the salivary microbiome in up to three time-points during 10 yr spanning adolescence, and determined the influence of human genotype, gender, age, and weight class. Participants, including 27 monozygotic and 18 dizygotic twin pairs, were sampled mainly at ages 12-13, 17-18, and 22-24, with a few sampled as early as 8 yr of age. In contrast to gut or skin microbiomes, there is a core genus-level salivary microbiome. Individuals are more similar to themselves and their co-twins in the 12-17 and in the 17-22 cohorts than to the whole sample population, but not over the 10 yr from 12 to 22; and monozygotic twin pairs are statistically not more similar than dizygotic twin pairs. The data are most consistent with shared environment serving as the main determinant of microbial populations. Twins resemble each other more closely than the whole population at all time-points, but become less similar to each other when they age and no longer cohabit. Several organisms have age-specific abundance profiles, including members of the genera Veillonella, Actinomyces, and Streptococcus. There is no clear effect of weight class and gender. The results of this work will provide a basis to further study oral microbes and human health.

Mitochondrial dysfunction and immune activation are detectable in early Alzheimer's disease blood.

Alzheimer's disease (AD), like other dementias, is characterized by progressive neuronal loss and neuroinflammation in the brain. The peripheral leukocyte response occurring alongside these brain changes has not been extensively studied, but might inform therapeutic approaches and provide relevant disease biomarkers. Using microarrays, we assessed blood gene expression alterations occurring in people with AD and those with mild cognitive changes at increased risk of developing AD. Of the 2,908 differentially expressed probes identified between the three groups (p < 0.01), a quarter were altered in blood from mild cognitive impairment (MCI) and AD subjects, relative to controls, suggesting a peripheral response to pathology may occur very early. There was strong evidence for mitochondrial dysfunction with decreased expression of many of the respiratory complex I-V genes and subunits of the core mitochondrial ribosome complex. This mirrors changes previously observed in AD brain. A number of genes encoding cell adhesion molecules were increased, along with other immune-related genes. These changes are consistent with leukocyte activation and their increased transition from circulation into the brain. In addition to expression changes, we also found increased numbers of basophils in people with MCI and AD, and increased monocytes in people with an AD diagnosis. Taken together this study provides both an insight into the functional response of circulating leukocytes during neurodegeneration and also identifies potential targets such as the respiratory chain for designing and monitoring future therapeutic interventions using blood.
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Study examines how Alzheimer's kills brain cells

(Medical Xpress)—Exactly how Alzheimer's disease kills brain cells is still somewhat of a mystery, but University of Michigan researchers have uncovered a clue that supports the idea that small proteins prick holes into neurons.

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