RNAs in the Sera of Persian Gulf War Veterans Have Segments Homologous to Chromosome 22q11.2

Urnovitz, Howard B.; Tuite, James J.; Higashida, Jean; Murphy, William H.

doi:10.1128/cdli.6.3.330-335.1999

Cited by 27 publications

(3 citation statements)

References 48 publications

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“…When only a single military unit is studied, the results cannot be generalized [18,23]. Controls were regularly not included or were inadequate [18,31,32,37,68,77]. Healthy warrior bias can be present if only military personnel on active duty are examined and if veterans rejected as medically un®t are omitted.…”

Section: Discussionmentioning

confidence: 99%

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Somatic hypotheses of war syndromes

Soetekouw

Vries

Bergen

et al. 2000

Eur J Clin Investigation

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Since the end of the American Civil War, unexplained symptoms in military personnel arising after a war or peace mission have frequently been described. The pattern of symptoms is highly similar for all of the various war syndromes although the conditions of each war or peace mission are widely different. Many somatic hypotheses have been formulated to explain these syndromes; a considerable proportion of them are already outdated. In the last few years much attention has been given to Gulf War Syndrome and to unexplained symptoms of military personnel who were sent to Cambodia, Rwanda, Burundi, Zaire, or the former Yugoslavia. In this review the symptoms of war syndromes will be considered in more detail and the suggested somatic explanations will be discussed. During the last decade the following somatic causes have been suggested as possible explanations for these symptoms: (persistent) infection, abnormal immune response, administration of multiple vaccinations within a short period of time, use of malaria chemoprophylaxis, neurological abnormalities, exposure to toxicological substances and environmental factors. The various investigations performed to study these hypotheses are discussed. The fact that bias regularly occurs in the course of these investigations is pointed out. For the future, a reliable investigation of a war syndrome should be a prospective multidisciplinary study and should distinguish between causative and sustaining factors.

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Section: Discussionmentioning

confidence: 99%

“…Recently, speci®c polyribonucleotides were detected in sera from veterans with Gulf War Syndrome and not in those of nonmilitary controls [77]. It is suggested that exposure to environmental genotoxins during the Gulf War could have led to genetic alterations in a region on chromosome 22q11.2.…”

Section: Exposure To Toxic Agentsmentioning

confidence: 99%

Somatic hypotheses of war syndromes

Soetekouw

Vries

Bergen

et al. 2000

Eur J Clin Investigation

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“…More specifically, sequences within short interspersed element DNA, or Alu sequences, are activated by human immunodeficiency virus type 1 (HIV-1) infection (16). Moreover, activation and Alumediated recombination are recognized as contributing factors in the progression of some chronic disorders (27). In addition, with the development of xenogenic therapies for human diseases, there is the potential for nonhuman retroelements to be unintentionally incorporated into the human genome.…”

mentioning

confidence: 99%

Antibody to Human Endogenous Retrovirus Peptide in Urine of Human Immunodeficiency Virus Type 1-Positive Patients

Stevens¹,

Baltch

Smith

et al. 1999

Clin Diagn Lab Immunol

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Human endogenous retrovirus (HERV)-like sequences are normal inherited elements that constitute several hundredths of the human genome. The expression of genes located within these elements can occur as a consequence of several different events, including persistent inflammation or genotoxic events. Antibodies to endogenous retroviral gene products have been found in a number of infectious, chronic, and malignant diseases, suggesting a role in disease initiation and progression. We studied human immunodeficiency virus type 1 (HIV-1)-infected patients for evidence of urine antibody to a HERV peptide and investigated correlates with clinical and laboratory parameters. Forty-three HIV-1-infected patients in documented asymptomatic, symptomatic, or AIDS stages of disease and 21 age- and gender-matched, uninfected controls were tested for antibody to HERV-related peptide 4.1. Urine specimens were examined in a blinded fashion with the Calypte Biomedical Corp. experimental enzyme immunoassay for antibody to peptide 4.1. Results were compared with demographic data, medical history, clinical state of disease, and results of other laboratory tests. Thirty-six percent of the asymptomatic (Centers for Disease Control and Prevention [CDC] category A) and 81.3% of both the symptomatic (CDC category B) and AIDS (CDC category C) patients were positive for antibody to HERV-related peptide 4.1. None of the controls were positive. In this study, antibodies to HERV-related peptide 4.1 were found more frequently in patients with advanced stages (categories B and C) of HIV-1 disease than in those patients with an earlier stage (category A) of HIV disease. In HIV patients, severe immunosuppression, defined as having had at least one opportunistic infection, correlated with the expression of antibody to a HERV-related peptide.

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Differential mRNA expression of acetylcholinesterase in the central nervous system of rats with acute and chronic exposure of sarin & physostigmine

Bansal

Waghmare

Anand

et al. 2009

J of Applied Toxicology

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A time-course study was carried out to measure the acetylcholinesterase (AChE) gene expression in the brain of female rats exposed to different doses of sarin and physostigmine. Short-term effects were studied with an acute single subcutaneous dose (s.c.) of 80 microg kg(-1) (0.5 x LD(50)) sarin. Cortex and cerebellum showed a significant decline in AChE mRNA expression at 2.5, 24 and 72 h. Biochemical studies showed that plasma butrylcholinesterase (BChE) and brain AChE activities were significantly decreased at 2.5 h, which came back to near control values by 24 h in both cases. For long-term chronic studies, three groups of female rats received daily doses of physostigmine (0.1 mg kg(-1) day(-1)) intramuscularly (i.m.), sarin (15 microg kg(-1) day(-1)) s.c. independently and a combined dose of physostigmine (i.m.) (0.1 mg kg(-1) day(-1)) followed by sarin (s.c.) (15 microg kg(-1) day(-1)) continuously for 30 days. Differential AChE mRNA levels in cortex and cerebellum of rat brain were observed after 30 days and after a lag period of another 30 days with no further administration. Plasma (BChE) and brain (AChE) showed irregular inhibition profile in biochemical studies at 30 days and returned to control levels after 60 days. The acute single subcutaneous administration of sarin for short-term as well as chronic long-term studies showed that AChE inhibition alone does not lead to observed changes in mRNA expression of AChE gene. These observations further suggest that route of administration as well as dose exposure regimen also contributes to the regulation of AChE mRNA expression.

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RNAs in the Sera of Persian Gulf War Veterans Have Segments Homologous to Chromosome 22q11.2

Cited by 27 publications

References 48 publications

Somatic hypotheses of war syndromes

Somatic hypotheses of war syndromes

Antibody to Human Endogenous Retrovirus Peptide in Urine of Human Immunodeficiency Virus Type 1-Positive Patients

Differential mRNA expression of acetylcholinesterase in the central nervous system of rats with acute and chronic exposure of sarin & physostigmine

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