deet has been researched along with Persian Gulf Syndrome in 26 studies
N,N-diethyl-m-toluamide : A monocarboxylic acid amide resulting from the formal condensation of the carboxy group of m-toluic acid with the nitrogen of diethylamine. First developed by the U.S. Army in 1946 for use by military personnel in insect-infested areas, it is the most widely used insect repellent worldwide.
Persian Gulf Syndrome: Unexplained symptoms reported by veterans of the Persian Gulf War with Iraq in 1991. The symptoms reported include fatigue, skin rash, muscle and joint pain, headaches, loss of memory, shortness of breath, gastrointestinal and respiratory symptoms, and extreme sensitivity to commonly occurring chemicals. (Nature 1994 May 5;369(6475):8)
| Excerpt | Relevance | Reference |
|---|---|---|
| "We used a mouse model of GWI by exposing mice repeatedly to a combination of Gulf War chemicals (pyridostigmine bromide, permethrin, DEET, and chlorpyrifos) and mild immobilization stress, followed by investigating their pain susceptibilities and fatigue symptoms." | 4.02 | Exposure to Gulf War Illness-related agents leads to the development of chronic pain and fatigue. ( Clark, JD; Goba, L; Huang, TT; Nguyen, H; Sahbaie, P; Sul, J; Suzaki, A, 2021) |
| " Risk of syndrome 2 ("confusion-ataxia") increased with a scale of advanced adverse effects from pyridostigmine bromide (chi2 for trend, P<." | 3.69 | Self-reported exposure to neurotoxic chemical combinations in the Gulf War. A cross-sectional epidemiologic study. ( Haley, RW; Kurt, TL, 1997) |
| "We investigated whether brain inflammation in GWI is associated with activation of high mobility group box-1 (HMGB1) and complement-related proteins in neurons and astrocytes, and brain inflammation can be tracked through neuron-derived extracellular vesicles (NDEVs) and astrocyte-derived EVs (ADEVs) found in the circulating blood." | 1.51 | Neuroinflammation in Gulf War Illness is linked with HMGB1 and complement activation, which can be discerned from brain-derived extracellular vesicles in the blood. ( Attaluri, S; Gitai, D; Kodali, M; Madhu, LN; Shetty, AK; Shuai, B; Upadhya, R, 2019) |
| " Due to differences in the dermal absorption of DEET between mice and humans, this study eliminated this confounding factor by utilizing sc injection and measured circulating blood levels of DEET to assess bioavailability from sc administration." | 1.35 | N,N,-diethyl-m-toluamide (DEET) suppresses humoral immunological function in B6C3F1 mice. ( Dudley, AC; EuDaly, JG; Gilkeson, GS; Keil, DE; McGuinn, WD; Peden-Adams, MM, 2009) |
| " IPPSFs (n=4/treatment) were topically dosed with mixtures of permethrin, DEET, and permethrin/DEET, in ethanol." | 1.32 | Pyridostigmine bromide modulates topical irritant-induced cytokine release from human epidermal keratinocytes and isolated perfused porcine skin. ( Baynes, RE; Monteiro-Riviere, NA; Riviere, JE, 2003) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 6 (23.08) | 18.2507 |
| 2000's | 7 (26.92) | 29.6817 |
| 2010's | 9 (34.62) | 24.3611 |
| 2020's | 4 (15.38) | 2.80 |
| Authors | Studies |
|---|---|
| Delic, V | 1 |
| Karp, J | 1 |
| Klein, J | 1 |
| Stalnaker, KJ | 1 |
| Murray, KE | 1 |
| Ratliff, WA | 1 |
| Myers, CE | 1 |
| Beck, KD | 1 |
| Citron, BA | 1 |
| Carpenter, JM | 1 |
| Gordon, HE | 1 |
| Ludwig, HD | 1 |
| Wagner, JJ | 1 |
| Harn, DA | 1 |
| Norberg, T | 1 |
| Filipov, NM | 1 |
| Hoffman, JF | 1 |
| Kalinich, JF | 1 |
| Nguyen, H | 1 |
| Sahbaie, P | 1 |
| Goba, L | 1 |
| Sul, J | 1 |
| Suzaki, A | 1 |
| Clark, JD | 1 |
| Huang, TT | 1 |
| Carreras, I | 1 |
| Aytan, N | 1 |
| Mellott, T | 1 |
| Choi, JK | 1 |
| Lehar, M | 1 |
| Crabtree, L | 1 |
| Leite-Morris, K | 1 |
| Jenkins, BG | 1 |
| Blusztajn, JK | 1 |
| Dedeoglu, A | 1 |
| Kodali, M | 2 |
| Hattiangady, B | 2 |
| Shetty, GA | 1 |
| Bates, A | 1 |
| Shuai, B | 3 |
| Shetty, AK | 3 |
| Cooper, BY | 2 |
| Flunker, LD | 1 |
| Johnson, RD | 2 |
| Nutter, TJ | 2 |
| Michalovicz, LT | 1 |
| Locker, AR | 2 |
| Kelly, KA | 2 |
| Miller, JV | 1 |
| Barnes, Z | 1 |
| Fletcher, MA | 1 |
| Miller, DB | 2 |
| Klimas, NG | 1 |
| Morris, M | 1 |
| Lasley, SM | 2 |
| O'Callaghan, JP | 2 |
| Madhu, LN | 1 |
| Attaluri, S | 1 |
| Upadhya, R | 1 |
| Gitai, D | 1 |
| Parihar, VK | 1 |
| Flunker, LK | 1 |
| Keil, DE | 2 |
| McGuinn, WD | 1 |
| Dudley, AC | 1 |
| EuDaly, JG | 1 |
| Gilkeson, GS | 1 |
| Peden-Adams, MM | 1 |
| Abdullah, L | 1 |
| Evans, JE | 1 |
| Bishop, A | 1 |
| Reed, JM | 1 |
| Crynen, G | 1 |
| Phillips, J | 1 |
| Pelot, R | 1 |
| Mullan, MA | 1 |
| Ferro, A | 1 |
| Mullan, CM | 1 |
| Mullan, MJ | 1 |
| Ait-Ghezala, G | 1 |
| Crawford, FC | 1 |
| Schoenig, GP | 1 |
| Riviere, JE | 2 |
| Monteiro-Riviere, NA | 2 |
| Baynes, RE | 2 |
| Peden-Adam, MM | 1 |
| Eudaly, J | 1 |
| Eudaly, E | 1 |
| Dudley, A | 1 |
| Zeigler, J | 1 |
| Lee, A | 1 |
| Robbs, J | 1 |
| Gilkeson, G | 1 |
| Abdel-Rahman, A | 1 |
| Abou-Donia, S | 1 |
| El-Masry, E | 1 |
| Shetty, A | 1 |
| Abou-Donia, M | 1 |
| Bischoff, EW | 1 |
| Soetekouw, PM | 1 |
| De Vries, M | 1 |
| Scheepers, PT | 1 |
| Bleijenberg, G | 1 |
| van der Meer, JW | 1 |
| Pennisi, E | 1 |
| Meehan, SK | 1 |
| Wadman, M | 1 |
| Haley, RW | 1 |
| Kurt, TL | 1 |
| Landrigan, PJ | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Randomized, Double-blind, Placebo-controlled Clinical Trial of Oleoylethanolamide (OEA) for Targeting Lipid Metabolism in Gulf War Illness[NCT05252949] | 52 participants (Anticipated) | Interventional | 2021-06-10 | Recruiting | |||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
26 other studies available for deet and Persian Gulf Syndrome
| Article | Year |
|---|---|
Pyridostigmine bromide, chlorpyrifos, and DEET combined Gulf War exposure insult depresses mitochondrial function in neuroblastoma cells.
Topics: Adenosine Triphosphate; Animals; Apoptosis; Cell Line, Tumor; Chlorpyrifos; DEET; Humans; Mice; Mito | 2021 |
Neurochemical and neuroinflammatory perturbations in two Gulf War Illness models: Modulation by the immunotherapeutic LNFPIII.
Topics: Amino Sugars; Animals; Biogenic Monoamines; Brain; Brain Chemistry; DEET; Disease Models, Animal; En | 2020 |
Effects of Incubation of Human Brain Microvascular Endothelial Cells and Astrocytes with Pyridostigmine Bromide, DEET, or Permethrin in the Absence or Presence of Metal Salts.
Topics: Astrocytes; Brain; Cells, Cultured; DEET; Endothelial Cells; Humans; Metals, Heavy; Permethrin; Pers | 2020 |
Exposure to Gulf War Illness-related agents leads to the development of chronic pain and fatigue.
Topics: Animals; Chlorpyrifos; Chronic Pain; DEET; Disease Models, Animal; Fatigue; Humans; Mice; Permethrin | 2021 |
Anxiety, neuroinflammation, cholinergic and GABAergic abnormalities are early markers of Gulf War illness in a mouse model of the disease.
Topics: Acetylcholine; Animals; Anxiety; Astrocytes; Brain; DEET; Disease Models, Animal; Encephalitis; Fema | 2018 |
Curcumin treatment leads to better cognitive and mood function in a model of Gulf War Illness with enhanced neurogenesis, and alleviation of inflammation and mitochondrial dysfunction in the hippocampus.
Topics: Affect; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cognition; Curcumin; DEET; Disease Models, | 2018 |
Behavioral, cellular and molecular maladaptations covary with exposure to pyridostigmine bromide in a rat model of gulf war illness pain.
Topics: Adaptation, Physiological; Animals; Behavior, Animal; Chlorpyrifos; DEET; Disease Models, Animal; Ga | 2018 |
Corticosterone and pyridostigmine/DEET exposure attenuate peripheral cytokine expression: Supporting a dominant role for neuroinflammation in a mouse model of Gulf War Illness.
Topics: Animals; Cholinesterase Inhibitors; Corticosterone; Cytokines; DEET; Disease Models, Animal; Gene Ex | 2019 |
Neuroinflammation in Gulf War Illness is linked with HMGB1 and complement activation, which can be discerned from brain-derived extracellular vesicles in the blood.
Topics: Animals; Astrocytes; Brain; Complement Activation; Cytokines; DEET; Disease Models, Animal; Encephal | 2019 |
Mood and memory deficits in a model of Gulf War illness are linked with reduced neurogenesis, partial neuron loss, and mild inflammation in the hippocampus.
Topics: Animals; Anxiety; Cell Death; Cholinesterase Inhibitors; DEET; Depression; Disease Models, Animal; H | 2013 |
Corticosterone primes the neuroinflammatory response to DFP in mice: potential animal model of Gulf War Illness.
Topics: Animals; Anti-Inflammatory Agents; Chemical Warfare Agents; Cholinesterase Inhibitors; Corticosteron | 2015 |
DEET potentiates the development and persistence of anticholinesterase dependent chronic pain signs in a rat model of Gulf War Illness pain.
Topics: Animals; Cholinesterase Inhibitors; Chronic Pain; DEET; Disease Models, Animal; Drug Synergism; Inse | 2017 |
N,N,-diethyl-m-toluamide (DEET) suppresses humoral immunological function in B6C3F1 mice.
Topics: Analysis of Variance; Animals; Antibody Formation; B-Lymphocytes; Biological Availability; CD4-Posit | 2009 |
Lipidomic profiling of phosphocholine-containing brain lipids in mice with sensorimotor deficits and anxiety-like features after exposure to Gulf War agents.
Topics: Animals; Anxiety; Ataxia; Brain Chemistry; Cerebral Cortex; DEET; Dentate Gyrus; Disease Models, Ani | 2012 |
Locomotor and sensorimotor performance deficit in rats following exposure to pyridostigmine bromide, DEET, and permethrin. Alone and in combination.
Topics: Acetylcholinesterase; Animals; Behavior, Animal; Brain; Cholinesterase Inhibitors; DEET; Drug Intera | 2002 |
Gulf War related exposure factors influencing topical absorption of 14C-permethrin.
Topics: Animals; Cholinesterase Inhibitors; DEET; Dermatologic Agents; Environmental Exposure; Humans; Hydro | 2002 |
Pyridostigmine bromide modulates topical irritant-induced cytokine release from human epidermal keratinocytes and isolated perfused porcine skin.
Topics: Administration, Cutaneous; Animals; Cells, Cultured; Cholinesterase Inhibitors; Cytokines; DEET; Din | 2003 |
Evaluation of immunotoxicity induced by single or concurrent exposure to N,N-diethyl-m-toluamide (DEET), pyridostigmine bromide (PYR), and JP-8 jet fuel.
Topics: Animals; Cholinesterase Inhibitors; DEET; Disease Models, Animal; Drug Interactions; Female; Hydroca | 2001 |
Stress and combined exposure to low doses of pyridostigmine bromide, DEET, and permethrin produce neurochemical and neuropathological alterations in cerebral cortex, hippocampus, and cerebellum.
Topics: Animals; Cerebellum; Cerebral Cortex; Cholinesterase Inhibitors; Cognition Disorders; DEET; Disease | 2004 |
Chemical sensitivity in symptomatic Cambodia veterans.
Topics: Adult; Cambodia; Case-Control Studies; DEET; Environmental Exposure; Humans; Incidence; Insect Repel | 2003 |
Menace in the mix.
Topics: DEET; Drug Synergism; Humans; Insect Repellents; Multiple Chemical Sensitivity; Permethrin; Persian | 1995 |
Chemicals behind Gulf War syndrome?
Topics: Animals; Chickens; DEET; Drug Interactions; Humans; Insect Repellents; Insecticides; Military Person | 1996 |
The search for solutions: veterinarians explore causes of Gulf War syndrome.
Topics: Animals; Chickens; Cholinesterase Inhibitors; DEET; Humans; Insect Repellents; Insecticides; Militar | 1996 |
US claims of 'no chemical links' to Gulf War illnesses under fire.
Topics: Chemical Warfare; Chlorpyrifos; DEET; Environmental Exposure; Government; Humans; Persian Gulf Syndr | 1997 |
Self-reported exposure to neurotoxic chemical combinations in the Gulf War. A cross-sectional epidemiologic study.
Topics: Adult; Ataxia; Carboxylic Ester Hydrolases; Chemical Warfare; Cholinesterase Inhibitors; Cognition D | 1997 |
Illness in Gulf War veterans. Causes and consequences.
Topics: Chemical Warfare; Cholinesterase Inhibitors; DEET; Environmental Exposure; Factor Analysis, Statisti | 1997 |