Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic fatigue syndrome (CFS) is an illness characterized by disabling fatigue associated with complaints of fevers, sore throat, myalgia, lymphadenopathy, sleep disturbances, neurocognitive difficulties, and depression. A striking feature of CFS is its sudden onset following an acute, presumably viral, illness and the subsequent recurrent "flu-like" symptoms. It has been speculated that both CFS and debilitating chronic fatigue (CF) that does not meet strict criteria for CFS may be the direct or indirect result of viral infections. We therefore tested 548 chronically fatigued patients who underwent a comprehensive medical and psychiatric evaluation for antibodies to 13 viruses. Our objectives were to compare the seroprevalence and/or geometric mean titer (GMT) of antibodies to herpes simplex virus 1 and 2, rubella, adenovirus, human herpesvirus 6, Epstein-Barr virus, cytomegalovirus, and Cox-sackie B virus, types 1-6 in patients with CF to healthy control subjects. Other goals were to determine if greater rates of seropositivity or higher GMTs occurred among subsets of patients with CFS, fibromyalgia, psychiatric disorders, a self-reported illness onset with a viral syndrome, and a documented temperature > 37 degrees C on physical examination. Differences in the seroprevalence or GMTs of antibodies to 13 viruses were not consistently found in those with CF compared with control subjects, or in any subsets of patients including those with CFS, an acute onset of illness, or a documented fever. These particular viral serologies were not useful in evaluating patients presenting with CF.
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PMID:Viral serologies in patients with chronic fatigue and chronic fatigue syndrome. 889 37

Various medical conditions that involve activation of the immune system are associated with psychological and neuroendocrine changes that resemble the characteristics of depression. In this review we present our recent studies, designed to investigate the relationship between the behavioral effects of immune activation and depressive symptomatology. In the first set of experiments, we used a double-blind prospective design to investigate the psychological consequences of illness in two models: (1) vaccination of teenage girls with live attenuated rubella virus, and (2) lipopolysaccharide (LPS) administration in healthy male volunteers. In the rubella study, we demonstrated that, compared to control group subjects and to their own baseline, a subgroup of vulnerable individuals (girls from low socioeconomic status) showed a significant virus-induced increase in depressed mood up to 10 weeks after vaccination. In an ongoing study on the effects of LPS, we demonstrated significant LPS-induced elevation in the levels of depression and anxiety as well as memory deficits. These psychological effects were highly correlated with the levels of LPS-induced cytokine secretion. In parallel experiments, we demonstrated in rodents that immune activation with various acute and chronic immune challenges induces a depressive-like syndrome, characterized by anhedonia, anorexia, body weight loss, and reduced locomotor, exploratory, and social behavior. Chronic treatment with antidepressants (imipramine or fluoxetine) attenuated many of the behavioral effects of LPS, as well as LPS-induced changes in body temperature, adrenocortical activation, hypothalamic serotonin release, and the expression of splenic TNF-alpha mRNA. Taken together, these findings suggest that cytokines are involved in the etiology and symptomatology of illness-associated depression.
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PMID:Illness, cytokines, and depression. 1126 75

Appropriate preconception health care improves pregnancy outcomes. When started at least one month before conception, folic acid supplements can prevent neural tube defects. Targeted genetic screening and counseling should be offered on the basis of age, ethnic background, or family history. Before conception, women should be screened for human immunodeficiency virus and syphilis infection and begin treatment to prevent the transmission of disease to the fetus. Immunizations against hepatitis B, rubella, and varicella should be completed, if needed. Women should be counseled on ways to prevent infection with toxoplasmosis, cytomegalovirus, and parvovirus B19. Environmental toxins such as cigarette smoke, alcohol, and street drugs, and chemicals such as solvents and pesticides should be avoided. In women with diabetes, it is important to optimize disease control through intensive management before pregnancy. Medications for hypertension, epilepsy, thromboembolism, depression, and anxiety should be reviewed and changed, if necessary, before the patient becomes pregnant. Counseling about exercise, obesity, nutritional deficiencies, and the overuse of vitamins A and D is beneficial. Physicians may also choose to discuss occupational and financial issues related to pregnancy and to screen patients for domestic violence.
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PMID:Preconception health care. 1261 25

Infections can act as environmental triggers inducing or promoting systemic lupus erythematosus (SLE) in genetically predisposed individuals. The aim of the present study was to compare the titres of antibodies (Abs) to infectious agents with neuropsychiatric (NPSLE) clinical manifestations. The sera of 260 individuals (120 patients with SLE and 140 geographic controls) were evaluated for the titres of Epstein bar virus (EBV), cytomegalovirus (CMV), toxoplasma, rubella and syphilis Abs using the BioPlex 2200 Multiplexed Immunoassay method (BioRad) and by the ELISA method for Helicobacter pylori and Hepatitis B core Ag. All BioPlex 2200 kits used were in developmental stages. Data analysis was performed using SPSS 9.0 statistical analysis software (SPSS Inc., Chicago, IL, USA, 1999). Correlation analysis indicated that rubella IgM Ab titres were marginally, positively associated with psychosis (P = 0.09). No other associations were detected between the 17 infectious Abs and five NP manifestations. When the positivity cut-off for anti-rubella IgM Abs was set at three standard deviations above normal, three positive subjects were identified: one patient with psychosis and one with depression, for a total NPSLE prevalence of 33.3%. On the contrary, the prevalence of NPSLE in the remaining subjects was 6.5%. Marginally significant correlations between elevated titres of rubella IgM Ab with psychosis and depression were found. Although this nearly 5-fold increase is not statistically significant, it appears that in a larger sample size, significance would be reached. This is the first study reported that examined the correlation of NPSLE manifestations with anti-infectious Abs.
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PMID:Neuropsychiatric lupus and infectious triggers. 1849 Apr 12

Human alpha-fetoprotein is a pregnancy-associated protein with an undetermined physiological role. As human alpha-fetoprotein binds retinoids and inhibits estrogen-dependent cancer cell proliferation, and because retinoic acid (a retinol metabolite) and estradiol (an estrogen) can both initiate cellular gene transcription, it is hypothesized here that alpha-fetoprotein functions during critical gestational periods to prevent retinoic acid and maternal estradiol from inappropriately stimulating gene expression in developing brain regions which are sensitive to these chemicals. Prenatal/maternal factors linked to increased autism risk include valproic acid, thalidomide, alcohol, rubella, cytomegalovirus, depression, schizophrenia, obsessive-compulsive disorder, autoimmune disease, stress, allergic reaction, and hypothyroidism. It will be shown how each of these risk factors may initiate expression of genes which are sensitive to retinoic acid and/or estradiol - whether by direct promotion or by reducing production of alpha-fetoprotein. It is thus hypothesized here that autism is not a genetic disorder, but is rather an epigenetic disruption in brain development caused by gestational exposure to chemicals and/or conditions which either inhibit alpha-fetoprotein production or directly promote retinoic acid-sensitive or estradiol-sensitive gene expression. This causation model leads to potential chemical explanations for autistic brain morphology, the distinct symptomatology of Asperger's syndrome, and the differences between high-functioning and low-functioning autism with regard to mental retardation, physical malformation, and sex ratio. It will be discussed how folic acid may cause autism under the retinoic acid/estradiol model, and the history of prenatal folic acid supplementation will be shown to coincide with the history of what is popularly known as the autism epidemic. It is thus hypothesized here that prenatal folic acid supplementation has contributed to the post-1980 increase in US autism diagnoses. In addition to explaining the epidemic within the wider retinoic acid/estradiol model of causation, this theory leads to potential explanations for certain genetic findings in autism, autistic regression, and changing trends in autism symptomatology with regard to mental retardation, wheat allergy, and gastrointestinal problems.
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PMID:A novel embryological theory of autism causation involving endogenous biochemicals capable of initiating cellular gene transcription: a possible link between twelve autism risk factors and the autism 'epidemic'. 2138 46

Patterns of serum and C.S.F. IgG, IgA and IgM, and haemagglutination inhibiting (HI) antibodies and complement fixing (CF) antibodies against rubella and cytomegaloviruses respectively and total CSF protein were investigated in 30 depressives, 20 each in neurological and surgical patients. Significant changes in total CSF protein and immunoglobulins in depressives and neurological patients in comparison to surgical subjects indicate an etiological similarity between the two groups. Failure to detect antibodies in C.S.F. of these subjects and statistically insignificant seropositivity refute the claim of viral hypothesis for depression but similar alterations in these body proteins in depressives and neurological patients raise other aetiological possibilities.
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PMID:Immunoglobulins and viral antibodies in depressive patients. 2192 84

Congenital rubella syndrome (CRS) is caused by rubella virus infection of the pregnant mother leading to teratogenic effects on the fetus. Although rare in the developed world, manifestations reach far into adulthood and underscore the importance of careful evaluation before surgery. We present a case of an adult with CRS in whom unexpected prolonged postoperative respiratory depression occurred. Perioperative workup of CRS and investigations pertaining to the patient's respiratory insufficiency are discussed.
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PMID:Prolonged respiratory depression after general anesthesia in an adult with congenital rubella syndrome. 2561 47

The impact of infections and inflammation during pregnancy on the developing fetal brain remains incompletely defined, with important clinical and research gaps. Although the classic infectious TORCH pathogens (ie, Toxoplasma gondii, rubella virus, cytomegalovirus [CMV], herpes simplex virus) are known to be directly teratogenic, emerging evidence suggests that these infections represent the most extreme end of a much larger spectrum of injury. We present the accumulating evidence that prenatal exposure to a wide variety of viral and bacterial infections-or simply inflammation-may subtly alter fetal brain development, leading to neuropsychiatric consequences for the child later in life. The link between influenza infections in pregnant women and an increased risk for development of schizophrenia in their children was first described more than 30 years ago. Since then, evidence suggests that a range of infections during pregnancy may also increase risk for autism spectrum disorder and depression in the child. Subsequent studies in animal models demonstrated that both pregnancy infections and inflammation can result in direct injury to neurons and neural progenitor cells or indirect injury through activation of microglia and astrocytes, which can trigger cytokine production and oxidative stress. Infectious exposures can also alter placental serotonin production, which can perturb neurotransmitter signaling in the developing brain. Clinically, detection of these subtle injuries to the fetal brain is difficult. As the neuropsychiatric impact of perinatal infections or inflammation may not be known for decades after birth, our construct for defining teratogenic infections in pregnancy (eg, TORCH) based on congenital anomalies is insufficient to capture the full adverse impact on the child. We discuss the clinical implications of this body of evidence and how we might place greater emphasis on prevention of prenatal infections. For example, increasing uptake of the seasonal influenza vaccine is a key strategy to reduce perinatal infections and the risk for fetal brain injury. An important research gap exists in understanding how antibiotic therapy during pregnancy affects the fetal inflammatory load and how to avoid inflammation-mediated injury to the fetal brain. In summary, we discuss the current evidence and mechanisms linking infections and inflammation with the increased lifelong risk of neuropsychiatric disorders in the child, and how we might improve prenatal care to protect the fetal brain.
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PMID:The fetal origins of mental illness. 3218 52


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